Screening Guidelines For Primary Care

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This material may be freely reproduced for educational and not for profit
purposes. No reproduction by or for commercial organizations is permitted without the
express written permission from the Family Medicine Specialists Association of Malaysia.
First Edition 2015
Published by:
Family Medicine Specialists Association of Malaysia
Room14, Level 5,
Malaysian Medical Association Building
124, Jalan Pahang, 53000 Kuala Lumpur
Fms.association@yahoo.com.my
http://fms-malaysia.org
ISBN 978-967-11389-2-2
FOREWORD
Congratulations to the Family Medicine Specialists Association
(FMSA) of Malaysia on publishing this Consensus Guide on Adult
Health Screening in Primary Care. In particular, the chairperson,
committee members, authors, reviewers and editors deserve
mention for their enormous efforts in providing guidance to
practitioners on appropriate, beneficial and cost-effective tools in
primary care.
The decision to screen for diseases must be made on a sound

basis and take into consideration elements of treatability and
progression. As the pillar of health services in a country, primary care plays a very important
role in identifying diseases early. Focussing on screening and early intervention for selected
medical conditions has much lower costs than treating after late detection. The saying
‘prevention is better than cure’ is very true. Therefore, a good screening tool based on sound
evidence is very essential.
The review on screening for each disease condition in this Consensus Guide was done quite
extensively. I am proud that this is the first evidence-based guide in Malaysia. It is my hope
that these screening guidelines will be used by all primary care providers in both government
and private sectors and become a useful tool at point of first contact with healthcare services
in this country.
DATUK DR NOOR HISHAM BIN ABDULLAH

Director General of Health
Ministry of Health Malaysia
Foreword iii
FOREWORD
Screening is a process of identifying apparently healthy people
who may be at increased risk of a disease or condition. They can
be offered information, further tests and appropriate treatment
to reduce their risk and/or any complications arising from the
disease or condition. Screening for diseases, and their risk factors,
has been implemented in many countries. Via screening, early
intervention can be done. Moreover, the treatment outcome may
differ compared to late detection. Screening is generally done,
and is worth doing, if early intervention proves to be beneficial in
terms of outcome and cost-effectiveness.
Primary care is a suitable place to conduct medical screening due its role as the point of first
contact to health services in a country, and the point to incorporate the wellness element in
patient care apart from the disease-oriented approach. Primary care providers also manage
patients with various risk factors and medical conditions. There is a need, therefore, to guide
primary care providers on medical screening.
To meet this need, the Family Medicine Specialists Association (FMSA) of Malaysia took
the initiative to produce evidence-based guidelines on screening at primary care level to
facilitate primary care providers in their day-to-day practice. The screening guidelines herein
provides information on the epidemiology and magnitude of each medical problem, the
benefits of screening and treatment, specific recommended screening tests as well as any
harm from screening. Due to the challenge of having a wide variety of medical conditions
seen at primary care level, the committee decided to prioritize certain conditions that can be
intervened early in this country.
FMSA hopes that this Guide will assist primary care providers to optimize their roles and
functions based on evidence, locally available resources and cost effectiveness.
DR NORSIAH ALI
President
Family Medicine Specialists Association
iv Foreword
PREFACE
This is a consensus guide on recommendations for health
screening in primary care clinic settings. The recommendations
are based on the best available evidence tailored to local context.
In a broader sense, health screening is one of the components

of preventive health care. Other components of preventive
health care include promoting a healthy life-style, immunisation
and chemoprevention. Although health screening is relevant
to all stakeholders in the health sector, primary care is directly
responsible for it because it is the first point of contact for people
seeking healthcare and, thereafter, provides continued care to individual patients.
There are credible screening guidelines, such as, the Canadian Taskforce for Preventive
Services, the United States Preventive Service Task Force and the Royal Australian College
of General Practice. However, the local context has to be considered when recommending
screening due to differences in morbidity and mortality patterns which affects the predictive
ability and, thus, cost-effectiveness of screening tests. At face value, health screening
appears compelling as it may be seen as a one-stop health assessment to ensure one is
free of specific diseases. However, there are shortcomings in some health screening tests.
The benefits of health screening can also be misunderstood by health care providers and
the public. Although many screening tests are beneficial, there are also tests that may cause
more harm than good. These recommendations aim to provide a summary of evidence for
or against screening in order to guide decisions when offering health screening to patients
at primary care settings.
PROFESSOR DR TONG SENG FAH

Chair
Consensus working group
Screening Guidelines 2015

Preface v
CONSENSUS WORKING GROUP
Chair
Dr Tong Seng Fah
Professor, Department of Family Medicine
Faculty of Medicine, Universiti Kebangsaan Malaysia
Contributors
(in alphabetical order)
Cardiovascular Dr Ambigga Devi A/P S. Krishnapillai

risk assessment Associate Professor, Discipline of Primary Care Medicine
Faculty of Medicine and Defence Health, National Defence University of
Malaysia
Dr Maizatullifah Miskan
Senior Lecturer, Discipline of Primary Care Medicine
Malaysia
Dr Mazapuspavina Md. Yasin

Senior Lecturer, Discipline of Primary Care Medicine,
Faculty of Medicine, Universiti Teknologi MARA
Dr Ng Kien Keat
Senior Lecturer, Discipline of Primary Care Medicine
Malaysia
Osteoporosis Dr Adibah Hanim Ismail

and Thyroid Associate Professor, Department of Family Medicine,
dysfunction Faculty of Medicine and Health Sciences, Universiti Putra Malaysia
Dr Cheong Ai Theng
Associate Professor, Department of Family Medicine,
Faculty of Medicine and Health Sciences, Universiti Putra Malaysia
Dr Tong Seng Fah

Professor, Department of Family Medicine,
Dr Zuhra Hamzah
Senior Lecturer, Department of Family Medicine,
Chronic obstructive Dr Ching Siew Mooi

pulmonary disease Senior Lecturer, Department of Family Medicine,
vi Consensus Working Group

Chronic obstructive Dr Verna Lee Kar Mun
pulmonary disease Associate Professor, Department of Family Medicine,
International Medical University
Cervical cancer Dr Fuziah Paimin

Breast cancer Consultant Family Medicine Specialist
Colorectal cancer Klinik Kesihatan Kajang
Prostate cancer
Dr Hasliza Hassan
Family Medicine Specialist
Klinik Kesihatan Sungai Pelek
Dr Harmy bin Mohamed Yusoff

Faculty of Medicine, Universiti Sultan Zainal Abidin
Dr Irmi Zarina Ismail

Dr Norhayati Mohd Noor

Associate Professor, Department of Family Medicine
School of Health Science, Universiti Sains Malaysia
Depression Dr Baizury Bashah

Nicotine addiction Consultant Family Medicine Specialist
Alcohol addiction Klinik Kesihatan Putrajaya Precint 18
Illicit substance
addiction Dr Faezah Hassan
Dr Norizzati Bukhari
Klinik Kesihatan Bangi
Dr Norsiah Ali
Consultant Family Medicine Specialist
Klinik Kesihatan Masjid Tanah
Dr Sherina Mohd Sidik

Professor, Department of Psychiatry
Human immuno Dr Vickneswari A/P Ayadurai

deficiency virus Consultant Family Medicine Specialist
Infection Klinik Kesihatan Taman Medan
Consensus Working Group vii

CONSENSUS WORKING GROUP
Domestic violence Dr Inderjit Singh Ludher

Family Physician
Academy of Family Physicians of Malaysia
Dr Sajaratulnisah Binti Othman,

Associate Professor, Department of Primary Care Medicine
Faculty of Medicine, University of Malaya
Scoliosis in Dr Sri Wahyu Taher

adolescent Consultant Family Medicine Specialist
Klinik Kesihatan Simpang Kuala
Older age group: Dr Ambigga Devi A/P S. Krishnapillai

Hearing loss Associate Professor, Discipline of Primary Care Medicine
Visual impairment Faculty of Medicine and Defence Health,
Fall risk National Defence University of Malaysia
Dementia
Urinary incontinence Dr Ho Bee Kiau
Klinik KesihatanBotanik
Dr Lee Ping Yein

Dr Noorlaili Mohd Tohit @ Mohd Tauhid

Dr Ruziaton Hasim
Klinik Kesihatan Pandamaran
Dr Sazlina Shariff Ghazali

Dr Zaiton Ahmad (Late)

viii Consensus Working Group

REVIEWERS
(in alphabetical order)
Internal reviewers Dr Harmy bin Mohamed Yusoff

Faculty of Medicine, Universiti Sultan Zainal Abidin
Dr Khoo Ee Ming
Professor, Department of Primary Care Medicine
Dr Mastura Ismail
Klinik Kesihatan Seremban 2
Dr Norsiah Ali
Klinik Kesihatan Tampin
Dr Teng Cheong Lieng

International Medical University
Dr Tong Seng Fah

External Reviewers Professor James Dickinson

(international) Family Medicine and Community Health Science
University of Calgary
Professor Mark Harris,

Centre for Primary Health Care and Equity,
University of New South Wales
External Reviewers Dr Asma Abdullah

(national) Professor, Department of Otorhinolaryngology
Dr Feisul Idzwan Mustapha

Public Health Physician, Non-Communicable Disease Section
Disease Control Division, Ministry of Health
Dr Lee Fatt Soon

Geriatrician, Department of Medicine
Hospital Kuala Lumpur
Dr Lee Tong Weng

Family Physician
Klinik T W Lee Sdn Bhd
Reviewers ix
REVIEWERS
External Reviewers Dr Lee Wai Khew

(national) Family Medicine Specialist
Klinik Kesihatan Luyang
Dr. Marhani Midin

Professor, Department of Psychiatry
Dr. Mohamad Aziz Salowi

Public Health Ophthalmologist, Department of Ophthalmology
Hospital Selayang
Dr Nor Azmi Kamarudin

Professor, Department of Medicine
Dr Ong Teng Aik

Associate Professor, Department of Surgery
Dr Pang Yong Kek

Professor, Department of Medicine
Dr Sabarul Afian Mokhtar

Professor, Department of Orthopaedic
Dr Salmiah Sharif
Family Medicine Specialist,
Klinik Kesihatan Batu 9 Cheras
Dr Shaiful Bahari Ismail

Professor, Department of Family Medicine
School of Health Science, Universiti Sains Malaysia
Dr Sheila A/P Marimuthu

Paediatrician, Department of Paediatric
Hospital Kuala Lumpur
Dr Suresh Kumar A/L Chidambaram

Infectious Disease Physician, Department of Medicine
Hospital Sungai Buluh
Dr Tan Chow Wei

Family Physicians
The People’s Dispensary
x Reviewers
ACKNOWLEDGMENTS
Since health screening covers a wide range of illnesses across various systems, age groups
and gender, a large team of experts was involved in drawing up these guidelines. I wish
to thank all the editors, contributors and reviewers for contributing to the content of this
guide. On behalf of the guideline development team, we wish to acknowledge the support
of the Division of Family Health Development of the Ministry of Health, Family Medicine
Specialists Association, the Department of Family Medicine of Universiti Putra Malaysia and
other contributors for either funding or providing the infrastructural support for the group.
We would like to also thank the following colleagues who provided input during the
development of the guides:
Dr. Feisul Idzwan Mustapha

Public Health Physician, Non-Communicable Disease Section
Disease Control Division, Ministry of Health
Dr Mohd Aminuddin Mohd Yusof

Public Health Physician, Health Technology Assessment
Ministry of Health
Dr. Noridah bt. Mohd Saleh

Public Health Physician, Primary Health Division,
Acknowledgments xi
Defining Health Screening
Conventional health screening and health checks are different although they have
similar underlying concepts. Health screening aims to identify asymptomatic
populations who are at higher risk of a disease. At primary care settings, however,
health screening should go beyond identifying the at-risk asymptomatic population
for a particular disease – as in the definition of screening. It should also identify
risk behaviours, such as smoking, and unreported symptomatic illnesses, such as
domestic violence and depression. These are not necessarily asymptomatic. Thus,
for these guidelines, it is more appropriate to expand the above definition of health
screening, which is essentially the same concept as health checks, to include the
following:
1. Screening for asymptomatic conditions such as hypertension, diabetes,

hypercholesterolaemia and colon cancer.
2. Screening for symptomatic conditions that are under-reported by patients

such as depression.
3. Assessing health risk behaviours such as smoking and nutritional status.
Determining the evidence for health screening
By evidence-based practice, health screening should only be recommended if

its benefit is proven to outweigh harm. However, proving that health screening
is beneficial can be challenging. Most people presenting or being offered health
screening are in good health to begin with. Therefore, subjecting them to any harm
arising from health screening is unjustified. Furthermore, evidence of any benefit from
health screening is difficult to establish. Proving that an illness is prevented - the
main benefit resulting from health screening – is more difficult than proving that its
symptoms have improved and the illness has been cured. In addition, the benefit
is often delayed. Although randomized controlled trials (RCTs) are the highest level
of evidence to inform practice, RCTs evaluating the benefit of health screening take
years to complete. In contrast, the harmful effects of screening often emerge earlier.
Hence, many recommendations put forward for health screening may not be
supported by robust evidence. Instead, many inferences are made to justify the
recommendations. These may have contributed to the inconsistencies in screening
guidelines over the years and from different expert committees.
xii Define Health Screening

Given the limited resources, we proposed our recommendations based on evidence
from the following:
1. Review of primary literature from MEDLINE and Cochrane database
2. Review of screening guidelines from the United States Preventive Service

Task Force (USPSTF), Canadian Task Force for Preventive Care (CTFPC)
and Guidelines for preventive activities in general practice 8th edition
For each condition, the evidence was appraised by the authors before making their
recommendation on screening. The reviews and recommendations were subjected to
internal and external reviewers.
Determining the benefits of health screening
The final aim of health screening is to reduce morbidity and mortality associated
with the disease screened. Achieving the final benefits requires a series of actions
from initiating screening to management of the disease detected. Potential harms
associated with the series of actions and factors diluting the benefits of screening have
to be considered before the final benefits are ascertained. (Figure 1)
Fig 1: Process of screening and factors diluting the benefit of screening
Referral for Referral for Morbidity and

Patients Screening diagnosis treatment Mortality benefits
Risk of False
disease negative 1. Non adherence to
test follow up tests
2. Psychosocial Non adherence
impact of false to treatment
Adverse
positive test
effect of
3. Adverse effects of
procedure
False sense procedure Adverse effect
of security of treatment on
patient’s quality
of life (patient
Long term impact of
started off as
missed diagnosis
healthy
Many factors can dilute the net benefits of screening. A lower risk of disease will result
in a higher chance of obtaining a false positive results, and adverse effects associated
with it. False positive results may lead to an adverse impact on the psychological and
Determining the benefits of health screening xiii

social wellbeing of patients. On the other hand, a false negative result due to poor
test sensitivity is a concern as well because disease diagnosis will be missed, and a
false sense of security will be created. Adverse effects can occur from the screening
test, diagnostic test and treatment. Documenting and quantifying some of these
factors, such as a false sense of security, can be challenging. Since many studies do
not formally assess these factors, many recommendations are based on consensus
expert opinion.
Objectives and scope of the recommendations
Objectives
The aim of these recommendations is to assist clinicians in making evidence-based
decisions on health screening. There are many possible areas for screening ranging
from cardiovascular risk factors to cancers and mental health. In each of these areas,
we asked the following questions to justify our recommendations:
a. How common is the condition?

b. What is the disease burden?
c. What are the benefits of screening and treating the condition?
d. What are the optimal screening tools available?
e. What are the harm of screening?
Target user
The recommendations are intended for use by doctors and allied health care workers
who offer health screening to their patients. They would include:
a. Primary care physicians (at various levels: medical officers running primary
care clinics, general practitioners, family physicians or family medicine
specialists)
b. Allied health professionals who are given the responsibility to provide health
screening
Scope and limitations of the recommendations

The recommendations do not include all preventive activities and are limited to only
health screening in primary care settings. Hence, counselling, health promotion, health
education, immunisation, life-style advice and management of health risk factors are
not included in these recommendations. For patients attending outpatient clinics, the
recommendations include the assessment of risk factors and screening tests, which
may consist of questionnaires, laboratory or radiological tests. The recommendations
are not applicable to pre-employment health checks which serve different objectives.
These recommendations also do not cover management strategies for detected
xiv Objectives and scope of the recommendations

diseases (e.g., treatment for diabetes or cervical cancer). Screening for disease
complications is not considered as health screening because patients diagnosed with
a medical condition represent different risks and should be considered under disease
surveillance (e.g., screening for diabetic retinopathy).
These recommendations are based on evidence up to the date of publishing. They are
generally valid for up to three years unless new evidence becomes available.
Statement of Intent
These recommendations are meant to guide clinical practice. Adherence to these
recommendations should take into consideration the strength of the recommendations,
individual patient’s risk profile, patient’s values and the setting of the health services.
Every healthcare provider is responsible for the management of his or her unique
patient population. These recommendations also consider local data and options of
tests available, or potentially available, locally.
Consensus Development Methods
The development of consensus involved a central committee and the contributors

of specific chapters. The central committee members are appointed by the Family
Medicine Specialists Association, whereas the contributors of specific chapters
are primary care providers with special interest in the respective chapter topic. The
central committee was responsible for deciding on the topics/chapters to be included,
reviewing the content of each chapter and making suggestions to improve the drafts
submitted. The committee also standardized the approach to writing each chapter.
Guide for contributors

1. Perform a literature review using primary literature and reviewing established
screening guidelines on the following key clinical questions:
a. What is the magnitude of the problem (e.g., the prevalence and

burden of breast cancer, and its mortality and morbidity)?
b. What are the benefits of treatment if disease or risk factors are
detected early?
c. Does screening improve disease mortality and morbidity?
d. What is the validity of screening tools or tests?
e. What are the harms associated with screening?
2. Search the literature to include major electronic data of PubMed, and Cochrane
Systematic Reviews.
Consensus Development Methods xv

3. Use major preventive guidelines as reference points as these guidelines have
undergone rigorous development protocols.
4. Appraise, summarise and synthesise information adopting the classification of

strength of evidence developed by the United States Preventive Service Task
Force.
5. Summarise the evidence and make recommendations based on the following

criteria:
• The condition has significant disease burden, i.e., the condition is prevalent
and associated with high mortality and morbidity
• Effective management of the condition or risk factors is available, which
leads to significant morbidity and mortality benefit
• Screening of the condition leads to improvement in disease mortality and
morbidity
• Valid and acceptable screening tests are available for early detection of the
condition
• Harm from screening is justifiable
Grading of evidence
Level
I Evidence obtained from at least one properly randomized controlled trial
II - 1 Evidence obtained from well-designed controlled trials without randomisation
II - 2 Evidence obtained from well-design cohort or case-control analytic studies,

preferably from more than one centre or research group
II - 3 Evidence obtained from multiple time series with or without the intervention.
Dramatic results in uncontrolled experiments (such as the results of the
introduction of penicillin treatment in the 1940s) could also be regarded as this
type of evidence
III Opinions of respected authorities based on clinical experience; descriptive

studies and case reports; or reports of expert committees
Source: U.S. / Canadian preventive services task force (adopted by Health Technology Assessment of Malaysia)
Grading of recommendation
The grades range from A, B, C, D and I (see the table below). Grade D is unique
grade of recommendation. It denotes good certainty that the test has no benefit.
xvi Grading
Hence, we recommend against offering such tests. The grading of recommendations
is not necessarily consistent with the level of evidence, however. Some recommended
screening, such as asking about smoking, may not have direct level I evidence of benefit
i.e., that asking about smoking results in reduced risk of mortality or morbidity. However,
supporting evidence is sufficiently strong to warrant a grade A recommendation.
Key to Grade of recommendation (adopted from the USPSTF 2012)
Grade Definition Suggestions for Practice
The USPSTF recommends the service. Offer or provide this service.

A There is high certainty that the net
benefit is substantial.
The USPSTF recommends the service. Offer or provide this service.

There is high certainty that the
B net benefit is moderate or there is
moderate certainty that the net benefit
is moderate to substantial.
The USPSTF recommends Only offer or provide this service

selectively offering or providing this for selected patients depending on
C service to individual patients based individual circumstances.
on professional judgment and patient
preferences. There is at least moderate
certainty that the net benefit is small.
The USPSTF recommends against the Discourage the use of this service.
service. There is moderate or high
D certainty that the service has no net
benefit or that the harms outweigh the
benefits.
The USPSTF concludes that the current If the service is offered, patients
evidence is insufficient to assess the should understand the uncertainty
I balance of benefits and harms of the about the balance of benefits and
Statement service. Evidence is lacking, of poor harms.
quality, or conflicting, and the balance
of benefits and harms cannot be
determined.
Source: U.S. preventive services task force
Process of reviewing
The draft of the guidelines was sent to reviewers for appraisal. Feedback from the
reviewers was discussed in the group meeting before finalizing the guidelines.
Grading xvii
Implementing health screening
Proactive and Opportunistic health screening

In order to be effective, discussions about health screening tests that have proven to
be beneficial should be initiated proactively or opportunistically. The public may not be
aware of the recommended health screening or have inaccurate or false beliefs about
health screening. Primary care settings offer great opportunities for personal contact
between the community and health care. These contacts are potential encounters
where such discussions can be initiated.
Universal health screening

Screening with level A or B recommendations has clear benefits outweighing harm.
Universal health screening is recommended where patients are routinely screened
according to the criteria stated. However, the benefits of screening should be
discussed. A system needs to be created to record the screening test, follow through
with the results, remind patients for screening or repeat screening, manage patients
with positive results and counsel patients with negative results at appropriate screening
intervals.
Shared decision approach in selecting tests for health screening

Screening with level C or I recommendation requires careful discussion with patients.
This should involve informing on direct medical benefit, harms of screening, cost
incurred, and patients’ values and beliefs.
In most instances, because of the difficulty in getting good evidence to support the
recommendations, a discussion is needed to avoid undue anxiety and unnecessary
tests. Health care providers need to inform patients on:
1. The test procedures

2. The aim of the test, i.e., benefit of screening and treatment following
screening
3. The screening process including the steps after the test results
4. Harms from the screening and diagnostic procedures, and from treatment
resulting from positive diagnosis upon confirmation of screening tests.
5. Patient’s personal goals for undertaking the screening
Patients should then participate in the decision-making of undertaking the tests.

This shared decision approach aims to provide sufficient information to patients, and
allows them to examine their own values and perspective in undertaking such tests.
This may be done with decision aids (if available), printed information or counselling
by allied health care workers or doctors. Patients should be aware of the conditions
they are being assessed or tested on, the implications of a positive or negative test,
the need fora confirmatory test, and the harm and benefit of the diagnostic test
xviii Implementing health screening

and the treatment resulting from a positive diagnosis. Doctors also need to actively
participate in recommending tests after a thorough assessment of the patients’ risks.
This balanced approach will minimise negative experiences and regret over an initial
health screening decision.
Using this consensus recommendations
These recommendations were drafted with the intention of ease of use at the point
of care during clinic consultation. This booklet is also meant to provide a summary
of information concerning screening to help counsel patients while discussing health
screening. We aimed to include sufficient details to justify the recommendations made.
This booklet is presented in two sections:
1. Summary of recommendations of health screening according to gender and

age
2. Description of each condition to (or not to) justify screening
The summary charts, 1, 2 and 3, provide a list of recommendations according to

grade level for screening for different age groups. The charts should provide a
quick reference at the point of care, and practitioners can use the chart to track the
recommended screening as patients are being followed up. Some tests, requiring
initial risk assessment, should only be offered to specific risk groups while other tests
can be offered routinely. The tests that are offered to specific risk groups are shaded
yellow while the checks offered routinely are shaded red. The alphabets within the box
represent the grade of the recommendation. The grade of recommendations are A, B
or C (see previous section for their definitions). Chart 1 is for male patients and chart 2
for female. Grades D and I are not included in charts 1 and 2 because those tests are
not recommended or there is insufficient evidence to support undertaking the tests.
These are summarized in Chart 3.
Practitioners may want to read further on the justification for the screening in Section 2.
In this section, the description of screening for each condition starts with a summary
Box in yellow with the recommendation for it in blue. This is followed by narrative
reviews of the information and evidence for the screening. Where appropriate, the
steps needed before offering the test are provided.
Where appropriate, assessment of risk factors should be undertaken and

patients assigned to different risk categories (e.g., high risk for colon cancer). The
recommendations should then be provided accordingly.
An Appendix at the end of each chapter in Section 2 provides a description of relevant

screening tools (e.g., for cardiovascular risk calculator and for illicit drug use).
Using this consensus recommendations xix

TABLE OF CONTENTS
Foreword iii
Foreword iv
Preface v
Consensus Working Group vi
Reviewers ix
Acknowledgments xi
Defining Health Screening xii
Determining the Evidence for Health Screening xii
Determining the Benefits of Health Screening xiii
Objectives and Scope of the Recommendations xiv
Consensus Development Methods xv
Implementing Health Screening xviii
Using this Consensus Recommendations xix
Table of Contents xx
Health Screening Schedule for Adult Male xxv
Health Screening Schedule for Adult Female xxvi
Conditions Not Recommended for Health Screening xxvii

1. Cardiovascular Disease (CVD) Risk Factors: Screening for Adults 1
1.1 Introduction 2
1.2 Benefits of screening and treating CVD risk factors 3
1.3 Screening Tools & Tests 4
1.4 Harm of CVRFs assessment 10

2. Thyroid Dysfunction 21
2.1 Introduction 22
2.2 Benefit of screening and treating subclinical thyroid dysfunction 23
2.3 Screening test 23
2.4 Harm of screening 23

3. Osteoporosis 26
3.1 Introduction 26
3.2 Benefit of screening and treating osteoporosis 27
3.3 Screening tests 28

4. Chronic Obstructive Pulmonary Disease (COPD) 32
4.1 Introduction 32
4.2 Benefit of treatment or early intervention 33

xx Contents
5. Cervical Cancer 35
5.1 Introduction 35
5.2 Benefit of screening and treating cervical abnormalities 36
6. Breast Cancer 42
6.1 Introduction 42
6.2 Benefit of screening and treating breast cancer 43
7. Colorectal Cancer 49
7.1 Introduction 49
7.2 Benefit of screening and treating colorectal cancer 51
7.3 Screening Tests 52
7.4 Harm of Screening 53
8. Prostate Cancer 58
8.1 Introduction 58
8.2 The benefit of screening and treating prostate cancer 59
9. Tobacco 63
9.1 Introduction 63
9.2 Benefit of screening and treating tobacco addiction 63
10. Alcohol 66
10.1 Introduction 66
10.2 Benefit of screening and treating alcohol use 67

11. Illicit Drugs 70
11.2 Benefit of screening and treating illicit drug use 70
Contents xxi
TABLE OF CONTENTS
12. Human Immunodeficiency Virus Infection 72
12.2 Benefit of screening and treating HIV infection 73
13. Domestic Violence 78

13.2 Benefit of screening and managing domestic violence 79
14. Depression 83
1.1 Introduction 83
14.1 Benefit of screening and treating depression 84
15. Scoliosis in Adolescents 91

15.2 Benefit of screening and treating adolescent idiopathic scoliosis 92
16. Hearing Loss in Older People 95

16.2 Benefit of screening and treating hearing impairment 96
17. Visual Impairment in Older Persons 99

17.2 Benefit of screening visual impairment and treating common
causes of visual impairment 100
18. Risk of Fall in Older People 103

18.2 Benefit of screening and intervention for fall prevention 104
xxii Contents
19. Dementia in Older People 107
19.2 Benefit of screening and treating dementia 108
20. Urinary Incontinence in Older People 111

20.2 Benefit of screening urinary incontinence and treating
urinary incontinence 112
Contents xxiii
SECTION 1
Health Screening Schedule for Adult Male
Tests recommended for male Reference Age

Frequency Notes
page 18 20 25 30 40 50 60 65 70 75 80
low risk 2 -5 years

Global CV
risk intermediate 6/12 -1year B B B B B B B
assessment
high Individualised
Smoking or
Should be done as part of
nicotine Opportunistic A A A A A A A A A A A
clinic vital sign recording
addiction
More frequent for
Hypertension Yearly individual with higher CV A A A A A A A A A A A
risk
Diabetes Earlier for individual with 2
Yearly A A A A A A A A A A A
Mellitus DM risk
Cardiovascular
(CV) risk
At any age for individual
Dyslipidaemia Yearly A A A A A A A A A A A
with CV risk
Family history
Once at first
of premature B
presentation
CVD
More frequent for
Obesity 2-yearly individual with higher CV B B B B B B B B B B B
risk
More frequent for
Unhealthy
2-yearly individual with higher CV B B B B B B B B B B B
diet
risk
More frequent for
Physical
2-yearly individual with higher CV B B B B B B B B B B B
inactivity
risk
average Yearly (FOBT) A A A A A A

Colon cancer
10 years earlier than the 47
5-yearly
high age of first diagnosis of A A A A A A A
(colonoscopy)
CRC in the family
HIV infection At any age for high risk
Opportunistic 70 A A A A A A A A A A A
individuals
Alcohol misuse Opportunistic Among at risk individual 65 B B B B B B B B B B B
Screening is appropriate
Depression
Opportunistic in setting with support for 83 C C C C C C C C C C C
treatment
Fall risk assessment Yearly Among at risk individual 104 C C C C C
The alphabet in each cell denotes the grade of recommendation.
Colour coding: Offer to all patients

Offer to patients with risk factors
Health screening schedule for adult female xxv

Health Screening Schedule for Adult Female
Tests recommended for female Reference Age

Frequency Notes
page 12 18 20 25 30 40 50 60 65 70 75 80
Screening is through
Scoliosis
Once school based 88 B
programme
low risk 2-5 years
Global CV
risk intermediate 6/12 -1year B B B B B B B
assessment
high Individualised
Smoking or Should be done as part
nicotine Opportunistic of clinic vital signs A A A A A A A A A A A
addiction recording
More frequent for
Hypertension Yearly individual with higher A A A A A A A A A A A
CV risk
Diabetes Earlier for individual
Yearly A A A A A A A A A A A
Mellitus with DM risk
Cardiovascular
2
(CV) risk
At any age for individual
Dyslipidaemia Yearly A A A A A A A A A A A
with CV risk
Family history
Once at first
of premature B
presentation
CVD
More frequent for
Obesity 2-yearly individual with higher B B B B B B B B B B B
CV risk
More frequent for
Unhealthy
2-yearly individual with higher B B B B B B B B B B B
diet
CV risk
More frequent for
Physical
2-yearly individual with higher B B B B B B B B B B B
inactivity
CV risk
Every 3 years Start screening 3 years
(5 -yearly after sexually active. A A A A A C
Cervical Cancer interval for Screening can be done 32
co-testing of up to 70 years old if no
cytology) prior pap-smear
Discuss earlier
Breast cancer
2-yearly screening for high-risk 39 B B B B
group.
Yearly
average A A A A A A
(FOBT)
Colon cancer 10 years earlier than 47
5-yearly the age of first
high A A A A A A A
(colonoscopy) diagnosis of CRC in the
family
Start screening for
2-yearly
Osteoporosis (BMD) individual with higher of 21 C C C C C C
fragility fracture
HIV infection At any age for high risk
Opportunistic 70 A A A A A A A A A A A
individuals
Domestic Violence For pregnant women 77 B B B B B B B B B B B
Alcohol misuse Opportunistic For at risk individuals 65 B B B B B B B B B B B

Screening is
Depression appropriate in setting
Opportunistic 83 C C C C C C C C C C C
with support for
treatment
Among at risk
Fall risk assessment Yearly 104 C C C C C
individuals
Colour coding: Offer to all patients

Offer to patients with risk factors
xxvi Health screening schedule for adult female

Conditions Not Recommended for Health Screening
Universal health screening is not recommended for the following conditions – the conditions
that do not have sufficient evidence to support screening (Grade I recommendation) or have
evidence of harm from screening (Grade D recommendation):
Conditions Reference Grade of

page recommendation
Thyroid dysfunction 16 I
Osteoporosis in male 21 I
Chronic obstructive pulmonary disease 28 D
Prostate cancer 55 D
Illicit substances 67 I
Hearing loss in older age group 92 I
Visual impairment in older age group 96 I
Dementia in older age group 104 I
Urinary incontinence in older age group 108 I
Note: Older age group is individual ≥ 65 years old

Conditions Not Recommended for Health Screening xxvii

SECTION 2
xxviii
01 Cardiovascular Disease (CVD) Risk
Factors: Screening for Adults
SUMMARY
CVD is a leading cause of morbidity and mortality in Malaysia and globally.

Major modifiable risk factors for CVD include smoking, hypertension,
dyslipidaemia, diabetes, obesity and physical inactivity.
Treatment of major cardiovascular risk factors reduces CVD mortality.
Given the high prevalence of various CVD risk factors in Malaysia, a targeted-
individual risk factor screening approach is likely justifiable for adults above 18
years of age.
Global CVD risk scoring may be beneficial for individuals aged 40 years and
above without prior known CVD risk factors.
For individuals aged above 30 years with identified CVD risk factors, a global
CVD risk estimation may be helpful in deciding on management strategies and
treatment target.
RECOMMENDATIONS
Screening for hypertension, smoking, is indicated for all adults (18 Grade A
years and above) at all appropriate primary care visits.
Screening for overweight and obesity, unhealthy diet and physical Grade B
inactivity and family history of premature CVD is indicated for all
adults (18 years and above) at all appropriate primary care visits.
Early screening (18 years and above) for diabetes mellitus and Grade A
dyslipidaemia is indicated for high risk individuals.
Framingham Risk Score (10-Year General Cardiovascular Risk Grade B
Model) is indicated for all adults above 40 years old or with prior
known CVD risk as a guide to identify high-risk individuals for more
comprehensive measures.
Regular assessment of cardiovascular risk factors is required for Grade C
asymptomatic adults based on their initial risk classification.
Generally, cardiovascular risk screening using new biomarkers is Grade D
not indicated.
CVD risk factors: Screening for adults 1

1.1 Introduction
Cardiovascular disease (CVD) is a group of disorders of the heart and blood vessels (1). In
the context of this consensus guide, CVD refers to coronary heart disease, cerebrovascular
disease and peripheral artery disease where atherosclerosis is the main underlying
pathological process (2).
CVD is a leading cause of morbidity and mortality worldwide (2-4). In Malaysia, 24.4% of
deaths in government hospitals were attributed to CVD (5). In terms of the number of years
of life lost due to premature death in Malaysia, coronary heart disease and cerebrovascular
disease were the highest in the ranking of causes in 2010. Moreover, both disease burdens,
as measured by disability-adjusted life years (DALYs), have increased by 85% and 39%,
respectively, compared to 1990 statistics (6).
Cardiovascular risk factors (CVRFs) are biomedical, behavioural and genetic conditions that
promote the process of atherosclerosis and lead to a greater risk of CVD. The likelihood
of CVD developing and manifesting over a certain period will be based on the presence,
intensity and interplay among the multiple risk factors (7, 8).
The recognized CVD risk factors are listed in Table 1 (2, 9-13) Level II-2, III:
Table 1: Recognized CVD Risk Factors
Modifiable risk factors Non-modifiable risk factors
• Smoking (tobacco use) a • Advancing age a,b

• Physical inactivity a • Male gender
• Raised blood pressure (hypertension) a • Inherited (genetic) predisposition
• Raised blood glucose (diabetes) a (ethnicity, family history of premature
• Raised blood lipids (dyslipidaemia) a CVD c and familial hypercholesterolaemia) a
• Overweight and obesity (central obesity and
high body mass index) a
• Unhealthy diet (high salt, fat and calorie
intake; low fibre intake)
• Harmful use of alcohol
• Psychosocial factors (stress, depression,
poverty and low educational status)
a Considered as major CVD risk factors; play a key role in the aetiology of atherosclerosis
b >55 years for men, >65 years for women
c < 55 years for men, <65 years for women
According to the annual report of the Acute Coronary Syndrome (ACS) Registry 2010, a five-
year national cardiovascular database (2006-2010), 90% of patients with ACS had at least
2 Introduction
one established CVRF. BMI > 23 kg/m2 (overweight and obesity) was the most prevalent
modifiable CVRF (75%), followed by hypertension (61%), diabetes (43%), smoking (33%)
and hypercholesterolaemia (33%) (14).
In the National Health and Morbidity Survey 2011 report, the most prevalent modifiable
CVRF among adults of 18 years and above in Malaysia is unhealthy diet (inadequate fibre
intake, 92.5%), followed by overweight and obesity (60.5%), physical inactivity (35.7%),
hypercholesterolaemia (35.1%), hypertension (32.7%), smoking (25%) and diabetes (15.2%).
The survey also highlighted the high proportion of adults with undiagnosed CVRFs, namely,
hypercholesterolaemia (26.6%), hypertension (19.8%) and diabetes (8%) (15).
Given the high proportion of undiagnosed CVRFs, screening and management of these risk
factors potentially can reduce cardiovascular morbidity and mortality in Malaysia.
1.2 Benefits of screening and treating cvd risk factors
Treating major CVD risk factors has been proven to reduce cardiovascular mortality (16-
18). Interventions, such as blood pressure lowering, glucose lowering, lipid lowering, weight
reduction, smoking cessation, dietary modification, and increasing physical activities, are
effective measures to treat individuals diagnosed with known CVRFs (9-11, 19-29).
On the other hand, evidence showing the benefits of screening is less established. A
Cochrane Review by Krogsbøll LT et al. (2012) did not find a beneficial effect of CVD risk
factor screening on CVD mortality (RR 1.03, 95% CI 0.91-1.17)(30) level I. However, the trials
included in the review were old with different treatment strategies recommended compared
to the present. A large good quality retrospective cohort study from Korea using national
representative samples demonstrated the benefit of cardiovascular screening in reducing
cardiovascular mortality and overall mortality (RR 0.58, 95% CI 0.53-0.63, RR 0.63, 95%
CI 0.60-0.64 respectively) (31) Level II. In a local study modelling Malaysian NHMS 2006 data,
which used the Framingham Risk Score (FRS) in its analysis, targeted screening at older
ages was shown to be more cost effective than universal screening. Coverage for the high-
risk population was estimated to be higher than 99%, even if screening started at 40 years
of age compared to universal screening of all age groups (32) Level III.
Since there is a multiplicative effect of CVD risk when clustering various CVRFs on CVD
mortality and morbidity, a standardized tool to assess global CVD risk is advocated to help
clinicians to individualise CVRF management (33-35). However, evidence of its benefit in
screening is weak because the advantage of this total CVD risk approach compared to an
ad hoc single risk factor approach has not been assessed by a randomized controlled trial
(36).
Benefits of screening and treating CVD risk factors 3

Although several risk prediction algorithms have been developed and validated for clinical
use, FRS is the most widely used assessment tool for the purpose of total CVD risk estimation
(37) Level II-2. In fact, it has been incorporated into local clinical practice guidelines to manage
hypertension and hypercholesterolaemia (9, 10). However, the FRS-prediction model was not
validated nor recalibrated for the local population prior to its adoption into clinical practice (38,
39). In individuals with certain clustering of CVRFs (e.g., age, ethnicity, gender, family history
of premature CVD, familial hypercholesterolemia, etc.), FRS often over- or underestimates
the global cardiovascular risk of different risk groups from various origins and regions (40-44)
Level II-2
. For this reason, FRS should be applied as a guide tool to identify those adults who
are asymptomatic but at high risk for CVD and require a more comprehensive intervention
(45). Global risk scoring per se does not translate to better clinical outcomes unless it is used
appropriately by health care providers with effective communication so that individuals fully
understand the global CVD risks and are able to make sustainable lifestyle changes (46, 47).
Given the high prevalence of various CVRFs in Malaysia, a targeted-individual based screening
approach is likely justifiable. Global CVD risk scoring may be beneficial for individuals 40
years old and above without prior known CVRFs. However, individual CVRF screening is
recommended as the benefits of identifying risk factors at a younger age have been shown in
many major reviews. Once a CVRF is detected in the individual, a global CVD risk estimation
may be helpful for adults over 30 years old* for decisions on management strategies and
treatment target.
* In the Framingham Heart Study, the studied population of interest was adults aged 30 -74
years old without CVD at baseline enrolment (48-50). Therefore, FRS is not applicable for
those under 30 years old in terms of global CVD risk assessment.
1.3 Screening Tools & Tests
According to the Framingham Study Group, the FRS has been recalibrated and validated
for use as a general CVD risk assessment tool (37) rather than coronary heart disease (CHD)
risk. This FRS risk prediction function is recommended as the basis for FRS because it
performed better than the previously used Framingham CHD risk prediction in predicting
CVD risk. Based on the FRS assessment, each individual’s total CVD risk is stratified as
low (< 10%), intermediate (10 - 20%), or high (> 20%) for a CVD event over a 10-year
period. To encourage the use of FRS in primary care practice, the main prediction model
has been simplified by using only clinic-based predictors that do not require laboratory
testing. These variables include age, gender, body mass index (replacing lipids), systolic
blood pressure, anti-hypertensive medication use, current smoking and diabetes status (50).
The recommendations for global CVD risk assessment and individual CVRF screening are
summarized in Table 2 and Table 3.
4 Screening Tools & Tests

In addition to conventional risk factors, the use of newer blood and urine biomarkers
(high-sensitivity C-reactive protein, apolipoprotein B, fibrinogen, homocysteine, estimated
glomerular filtration rate, uric acid, microalbuminuria, and genetic biomarkers) has shown
only marginal benefit in predicting cardiovascular outcomes. None of these markers has
been evaluated as a screening test in randomized controlled trials with clinical events as
outcomes (51-55). Thus, the following screening assessments are not recommended for
re-stratification of general CVD risk:
i. Uric acid (56) Level III, Grade D

ii. Genomic Testing (35, 53) Level III, Grade D
iii. Lipoprotein Apo B (35, 54) Level III, Grade D
Whereas, the following screening assessments are not recommended for re-stratification
of general CVD risk for low or high-risk sub-groups. But, there is insufficient evidence for or
against the use of these screening tests for the intermediate risk sub-group. They might be
useful for revision or re-classification of CVD risk for therapeutic intervention:
i. HS-C-Reactive Protein (35, 51, 54) Level II-2, Grade I

ii. Homocysteine (54) Level II-2, Grade I
iii. Haemoglobin A1C (35) Level II-2, Grade I
Microalbuminuria (urine albumin excretion of 30 - 300 mg/24 hour or urine protein:

creatinine ratio of 15-44 mg/mmol/L) might be useful in further risk-stratifying individuals
with intermediate risk or there is a coexistence of CVRFs of hypertension, diabetes mellitus
or hypercholesterolaemia (35, 54) Level II-2.
Generally, these new biomarkers are not necessary in the initial assessment of CVD risk.
Screening Tools & Tests 5

6 6
Table 2
Recommendation for CVRFs Assessment of Asymptomatic Adults (Aged ≥ 18 years old):
Table 2: Global CVD risk assessment with risk prediction function
Level of
Level of Evidence
Recommended Screening Age Evidence
No Tools Reference Interval Grade of Reference
Prediction Model (Years) Grade of
recommendation
recommendation
1.
Framingham Risk Scoring ≥ 30, with prior known FRS using lipid or Level II-2 (37,38) Low CVD risk: 2 - 5 Level III (12, 29, 57)
(FRS) for 10 - Year General CVRFs FRS using BMI years
CVD risk: Grade B Grade C
i. Age (Refer to Appendix CV1) Intermediate CVD
ii. Gender ≥ 40, without prior risk: 6 months to 1
iii. Smoking known CVRFs year
iv. Diabetes
v. Treated and untreated
Systolic Blood High CVD risk:
Pressure Individualized
vi. Total cholesterol according to clinical
vii. HDL cholesterol context
viii. BMI (replacing lipids
in a simplified model)
Table 3: Individual CVRF screening
Level of
Level of Evidence
Cardiovascular risk Evidence Reference Interval
No Screening Age (Year) Tools/ methods Grade of Reference
factors Grade of
recommendation
recommendation
1.
Obesity: All adults ≥ 18 Waist circumference (WC) Level II-2 (34, 57-59) For normal WC & Level III (34, 57)
2 and BMI should be assessed
• BMI ≥ 27.5 kg/m BMI:
• WC ≥ 90 cm in males (at all appropriate Grade B • Every 2 years if Grade C
& 80 cm in females primary care visits) without any CVD
risk factor
Overweight:
2 • Annually if
• BMI 23 to < 27.5 kg/m increased CVD
risk
6 monthly if there is
overweight or obesity
Check more
frequently if high CVD
risk
2.
Hypertension All adults ≥ 18 Any of the following devices Level III (9, 57,60) Annually if systolic BP Level III (9, 57,60)
can be used: < 130 and diastolic BP
BP ≥ 140/90 mmHg (at all appropriate • mercury column Grade A < 85 mmHg Grade B
primary care visits) sphygmomanometer
(Gold standard) Within 3 - 6 months if
• aneroid systolic BP 130 -139
sphygmomanometer
and diastolic BP 85 -
• certified electronic devices
89 mmHg
• automated ambulatory BP
devices
Check more
frequently if high CVD
risk
Table 3
7 7
8 8
Table 3
Level of
Level of Evidence
factors Grade of
recommendation
recommendation
7.
Dyslipidaemia ≥ 18, with prior known Complete fasting lipid profile Level III (10, 34) Annually if the lipid Level III (10)
CVRFs (e.g., HPT, (TC, LDL-C, HDL-C and TG) profile is normal
Diabetes, obesity) Grade A Grade B
(Refer to Appendix CV3)
≥ 40, without prior
known CVRFs
8.
Diabetes Mellitus ≥ 18, with known Random blood glucose, fasting Level III (11, 22) 1 - 3 years if no Level III (11, 22, 34,
diabetes risk factor blood glucose, oral glucose diabetes risk factors 57)
FBG ≥ 7.0 mmol/L tolerance test or HbA1C Grade A Grade B
RBG ≥ 11.1 mmol/L (Refer to appendix More frequent with
2-Hour OGTT ≥ 11.1 CV4) (Refer to Appendix CV5) diabetes risk factors
mmol/L
≥ 30, without known
diabetes risk factors
9.
Familial ≥ 18, with known risk Assess the probability of Level III (57, 61-63) At first presentation Level III (57, 61, 62)
Hypercholesterolemia (FH) factors having FH using Modified UK
Simon Broome criteria Grade B Grade B
(Refer to Appendix
CV6) (Refer to Appendix CV7)
Genetic testing is generally not

needed for screening
Level of
Level of Evidence
factors Grade of
recommendation
recommendation
7.
Dyslipidaemia ≥ 18, with prior known Complete fasting lipid profile Level III (10, 34) Annually if the lipid Level III (10)
CVRFs (e.g., HPT, (TC, LDL-C, HDL-C and TG) profile is normal
Diabetes, obesity) Grade A Grade B
(Refer to Appendix CV3)
≥ 40, without prior
known CVRFs
8.
Diabetes Mellitus ≥ 18, with known Random blood glucose, fasting Level III (11, 22) 1 - 3 years if no Level III (11, 22, 34,
diabetes risk factor blood glucose, oral glucose diabetes risk factors 57)
FBG ≥ 7.0 mmol/L tolerance test or HbA1C Grade A Grade B
RBG ≥ 11.1 mmol/L (Refer to appendix More frequent with
2-Hour OGTT ≥ 11.1 CV4) (Refer to Appendix CV5) diabetes risk factors
mmol/L
≥ 30, without known
diabetes risk factors
9.
Familial ≥ 18, with known risk Assess the probability of Level III (57, 61-63) At first presentation Level III (57, 61, 62)
Hypercholesterolemia (FH) factors having FH using Modified UK
Simon Broome criteria Grade B Grade B
(Refer to Appendix
CV6) (Refer to Appendix CV7)
Genetic testing is generally not

needed for screening
Table 3
9 9
1.4 Harm of CVRFs assessment
No systematic review or meta-analysis has been done to evaluate the evidence on clinically
important harms associated directly with the screening of CVFRs: false positives, false
negatives, psychological effects and socioeconomic impact. An examination of potential harms
resulting from pharmacotherapy for hypertension, diabetes mellitus, hypercholesterolaemia,
smoking cessation and obesity was outside the scope of this screening guideline review.
Although there are no local studies of asymptomatic adults’ values and preferences regarding
CVRFs screening, it can be inferred from undertaking the population-based National Health
and Morbidity Survey every 10 years, which used similar CVR assessment tools, that the
recommended screening tools for common CVRFs are acceptable to the general public.
REFERENCES
1. World Health Organisation. Cardiovascular diseases of Hypertension. 4th ed. Putrajaya: Ministry of Health
(CVDs). [updated January 2015; assessed 10th April Malaysia; 2013.
2015]. Available from: http://www.who.int/mediacentre/ 10. National Heart Association of Malaysia, Academy
factsheets/fs317/en/#. of Medicine Malaysia. Clinical Practice Guidelines:
2. Mendis S, Puska P, Norrving B. Global Atlas on Management of Dyslipidaemia. 4th ed. Putrajaya:
Cardiovascular Disease Prevention and Control. Geneva: Ministry of Health Malaysia; 2011.
WHO, 2011. 11. Malaysian Endocrine & Metabolic Society, Malaysian
3. World Health Organisation. Global status report on non- Association of Diabetes, Academy of Medicine Malaysia.
communicable diseases 2014. Geneva: WHO; 2014. Clinical Practice Guidelines: Management of Type 2
4. Roth GA, Forouzanfar MH, Moran AE, Barber R, Nguyen Diabetes Mellitus. 4th ed. Putrajaya: Ministry of Health
G, Feigin VL, et al. Demographic and epidemiologic Malaysia; 2009.
drivers of global cardiovascular mortality. N Engl J Med 12. National Vascular Disease Prevention Alliance. Guidelines
2015;372(14):1333-41. for the assessment of absolute cardiovascular disease
5. Health Informatics Centre, Ministry of Health (MOH). risk. Melbourne: National Heart Foundation of Australia;
Health Facts 2014. Putrajaya, Malaysia; 2014. 2009.
6. Institute for Health Metrics and Evaluation. Country 13. Scottish Intercollegiate Guidelines Network. Risk
Profile: Malaysia (Global Burden of Disease Study 2010). estimation and the prevention of cardiovascular disease:
[updated 5th March 2013; assessed 16th April 2015]. A national clinical guideline. Edinburgh: SIGN; 2007.
Available from: http://www.healthdata.org/sites/default/ 14. Wan Ahmad WA, Sim KH. Annual report of the Acute
files/files/country_profiles/GBD/ihme_gbd_country_ Coronary Syndrome (ACS) Registry 2009 and 2010
report_malaysia.pdf. (Malaysia: National Cardiovascular Disease Database).
7. Raitakari OT, Juonala M, Ronnemaa T, Keltikangas- Kuala Lumpur: National Heart Association of Malaysia
Jarvinen L, Rasanen L, Pietikainen M, et al. Cohort and Ministry of Health Malaysia; 2013.
profile: the cardiovascular risk in Young Finns Study. Int 15. Institute for Public Health. National Health and Morbidity
J Epidemiol 2008;37(6):1220-6. Survey (Interim) 2011 (NHMS 2011). Vol. II: Non-
8. World Health Organisation. Global health risks: Mortality Communicable Diseases. Kuala Lumpur: Ministry of
and burden of disease attributable to selected major Health Malaysia; 2011.
risks. Geneva: WHO; 2009. 16. Non-communicable Diseases and Mental Health.
9. Malaysian Society of Hypertension, Academy of Medicine Integrated management of cardiovascular risk: Report
Malaysia. Clinical Practice Guidelines: Management of a WHO Meeting, Geneva, 9-12 July 2002. Geneva:
10 Harm of CVRFs assessment

World Health Organisation; 2002. 28. Tamakoshi A, Tamakoshi K, Lin Y, Yagyu K, Kikuchi S,
17. Erhardt L, Moller R, Puig JG. Comprehensive Group JS. Healthy lifestyle and preventable death:
cardiovascular risk management--what does it mean in findings from the Japan Collaborative Cohort (JACC)
practice? Vasc Health Risk Manag 2007;3(5):587-603. Study. Prev Med 2009;48(5):486-92.
18. Law MR, Morris JK, Wald NJ. Use of blood pressure 29. National Vascular Disease Prevention Alliance
lowering drugs in the prevention of cardiovascular (NVDPA). Guidelines for the management of absolute
disease: meta-analysis of 147 randomised trials in the cardiovascular disease risk [Internet]. 1st ed. Australia;
context of expectations from prospective epidemiological 2012 [cited 5 May 2015]. Available from: http://
studies. BMJ 2009;338:1665. strokefoundation.com.au/site/media/AbsoluteCVD_GL_
19. World Health Organisation. Prevention of cardiovascular webready.pdf
disease: Guidelines for assessment and management of 30. Krogsbøll LT, Jørgensen KJ, Grønhøj Larsen C, Gøtzsche
cardiovascular risk. Geneva: WHO; 2007. PC. General health checks in adults for reducing
20. National Coordinating Committee on Food and Nutrition, morbidity and mortality from disease. Cochrane
Ministry of Health. Malaysian Dietary Guidelines Database Syst Rev 2012:Issue 10.
[Internet]. 1st ed. Malaysia;2010 [cited 5 May 31. Lee H, Cho J, Shin D, Lee S, Hwang S, Oh J et al.
2015]. Available from: http://dg.cnsoc.org/upload/ Association of cardiovascular health screening with
affix/20140818104029708.pdf mortality, clinical outcomes, and health care cost: A
21. International Diabetes Federation. Clinical Guidelines nationwide cohort study. Prev Med 2015;70:19-25.
Task Force Global Guideline for Type 2 Diabetes 32. Sharmini S, Jamaiyah H, Gurpreet K, Gurpreet K, Tee
[Internet]. 1st ed. Belgium;2012 [cited 5 May 2015]. GH, Mohd Adam B, Kee CC, Bots ML. Identification
Available from: http://www.idf.org/sites/default/files/ of effective screening strategies for cardiovascular
IDF%20T2DM%20Guideline.pdf disease prevention in a developing country: using
22. American Diabetes Association. Standards of medical cardiovascular risk-estimation and risk-reduction tools
care in diabetes-2015 abridged for primary care for policy recommendations. BMC Cardiovasc Disord
providers. Clin Diabetes 2015;33(2):97-111. 2013;13:10,2261-13-10Assmann G, Cullen P, Schulte
23. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti H. Simple scoring scheme for calculating the risk of
A, Bohm M, et al. 2013 ESH/ESC guidelines for the acute coronary events based on the 10-year follow-up
management of arterial hypertension: the Task Force of the prospective cardiovascular Munster (PROCAM)
for the Management of Arterial Hypertension of the study. Circulation 2002;105(3):310-5.
European Society of Hypertension (ESH) and of the 33. Goh LG, Chua T, Kang V, Kwong KH, Lim WY, Low LP,
European Society of Cardiology (ESC). Eur Heart J et al. Ministry of health clinical practice guidelines:
2013;34(28):2159-219. screening of cardiovascular disease and risk factors.
24. James PA, Oparil S, Carter BL, Cushman WC, Dennison- Singapore Med J 2011;52(3):220-7.
Himmelfarb C, Handler J, et al. 2014 evidence-based 34. Greenland P, Alpert JS, Beller GA, Benjamin EJ, Budoff
guideline for the management of high blood pressure MJ, Fayad ZA, et al. 2010 ACCF/AHA guideline for
in adults: report from the panel members appointed assessment of cardiovascular risk in asymptomatic
to the Eighth Joint National Committee (JNC 8). JAMA adults: executive summary: a report of the American
2014;311(5):507-20. College of Cardiology Foundation/American Heart
25. Cleeman JI. Executive summary of the third report of the Association Task Force on Practice Guidelines.
National Cholesterol Education Program (NCEP) expert Circulation 2010;122(25):2748-64.
panel on detection, evaluation, and treatment of high 35. Cooney MT, Dudina A, D’Agostino R, Graham IM.
blood cholesterol in adults (adult treatment panel III). Cardiovascular risk-estimation systems in primary
JAMA 2001;285(19):2486-97. prevention: do they differ? Do they make a difference?
26. Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Can we see the future? Circulation 2010;122(3):300-
Blum CB, Eckel RH, et al. 2013 ACC/AHA guideline on the 10.
treatment of blood cholesterol to reduce atherosclerotic 36. D’Agostino RB, Sr., Vasan RS, Pencina MJ, Wolf PA,
cardiovascular risk in adults: a report of the American Cobain M, Massaro JM, et al. General cardiovascular
College of Cardiology/American Heart Association Task risk profile for use in primary care: the Framingham
Force on Practice Guidelines. Circulation 2014;129(25 Heart Study. Circulation 2008;117(6):743-53.
Suppl 2):S1-45. 37. D’Agostino RB, Sr., Grundy S, Sullivan LM, Wilson P,
27. Ammerman AS, Lindquist CH, Lohr KN, Hersey J. The Group CHDRP. Validation of the Framingham coronary
efficacy of behavioral interventions to modify dietary fat heart disease prediction scores: results of a multiple
and fruit and vegetable intake: a review of the evidence. ethnic groups’ investigation. JAMA 2001;286(2):180-7.
Prev Med 2002;35(1):25-41. 38. Selvarajah S, Kaur G, Haniff J, Cheong KC, Hiong TG,
References 11
REFERENCES
van der Graaf Y, et al. Comparison of the Framingham 51. De Backer G, Graham I, Cooney MT. Do novel biomarkers
Risk Score, SCORE and WHO/ISH cardiovascular risk add to existing scores of total cardiovascular risk? Eur J
prediction models in an Asian population. Int J Cardiol Prev Cardiol 2012;19(2 Suppl):14-7.
2014;176(1):211-8. 52. Palomaki GE, Melillo S, Neveux L, Douglas MP, Dotson
39. Bastuji-Garin S, Deverly A, Moyse D, Castaigne A, Mancia WD, Janssens AC, et al. Use of genomic profiling to
G, de Leeuw PW, et al. The Framingham prediction assess risk for cardiovascular disease and identify
rule is not valid in a European population of treated individualized prevention strategies--a targeted
hypertensive patients. J Hypertens 2002;20(10):1973- evidence-based review. Genet Med 2010;12(12):772-
80. 84.
40. Pyörälä K. Cardiovascular risk prediction systems have to 53. Perk J, De Backer G, Gohlke H, Graham I, Reiner
be adapted and updated to current national conditions. Z, Verschuren WM, et al. European Guidelines on
Eur J Cardiovasc Prev Rehabil 2006;13(5):674-5. cardiovascular disease prevention in clinical practice
41. Liu J, Hong Y, D’Agostino RB, Sr., Wu Z, Wang W, Sun (version 2012): the Fifth Joint Task Force of the
J, et al. Predictive value for the Chinese population of European Society of Cardiology and other societies on
the Framingham CHD risk assessment tool compared cardiovascular disease prevention in clinical practice
with the Chinese Multi-Provincial Cohort Study. JAMA (constituted by representatives of nine societies and
2004;291(21):2591-9. by invited experts). Eur J Prev Cardiol 2012;19(4):585-
42. Koller MT, Steyerberg EW, Wolbers M, Stijnen T, Bucher 667.
HC, Hunink MG, et al. Validity of the Framingham point 54. Hlatky MA, Greenland P, Arnett DK, Ballantyne CM, Criqui
scores in the elderly: results from the Rotterdam study. MH, Elkind MS, et al. Criteria for evaluation of novel
Am Heart J 2007;154(1):87-93. markers of cardiovascular risk: a scientific statement
43. Rodondi N, Locatelli I, Aujesky D, Butler J, Vittinghoff from the American Heart Association. Circulation
E, Simonsick E, et al. Framingham risk score and 2009;119(17):2408-16.
alternatives for prediction of coronary heart disease in 55. Genest J, McPherson R, Frohlich J, Anderson T, Campbell
older adults. PloS one 2012;7(3):e34287. N, Carpentier A, et al. Canadian Cardiovascular Society/
44. Chia YC. Review of tools of cardiovascular disease Canadian guidelines for the diagnosis and treatment of
risk stratification: interpretation, customisation and dyslipidemia and prevention of cardiovascular disease
application in clinical practice. Singapore Med J 2011; in the adult - 2009 recommendations. Can J Cardiol
52(2):116-23. 2009;25(10):567-79.
45. Beswick A, Brindle P. Risk scoring in the assessment of 56. Red Book Taskforce. Guidelines for preventive activities
cardiovascular risk. Curr Opin Lipidol 2006;17(4):375- in general practice. 8th ed. East Melbourne: Royal
86. Australian College of General Practitioners; 2012.
46. Brindle P, Beswick A, Fahey T, Ebrahim S. Accuracy and 57. Malaysian Endocrine & Metabolic Society, Malaysian
impact of risk assessment in the primary prevention Association for the Study of Obesity, Academy of
of cardiovascular disease: a systematic review. Heart Medicine Malaysia. Clinical Practice Guidelines:
2006;92(12):1752-9. Management of Obesity. Putrajaya: Ministry of Health
47. Dawber TR, Meadors GF, Moore FE, Jr. Epidemiological Malaysia; 2004.
approaches to heart disease: the Framingham Study. 58. Brauer P, Connor Gorber S, Shaw E, Singh H, Bell N,
Am J Public Health Nations Health 1951;41(3):279-81. Shane AR, et al. Recommendations for prevention of
48. Kannel WB, Feinleib M, McNamara PM, Garrison RJ, weight gain and use of behavioural and pharmacologic
Castelli WP. An investigation of coronary heart disease interventions to manage overweight and obesity in
in families. The Framingham offspring study. Am J adults in primary care. CMAJ 2015;187(3):184-95.
Epidemiol 1979;110(3):281-90. 59. Yusuf S, Islam S, Chow CK, Rangarajan S, Dagenais
49. Framingham Heart Study Group. Cardiovascular Disease G, Diaz R, et al. Use of secondary prevention drugs
Risk Function (10-Year Risk): Risk Score Calculators. for cardiovascular disease in the community in high-
2008 [assessed 16th April 2015]. Available from: income, middle-income, and low-income countries
https://www.framinghamheartstudy.org/risk-functions/ (the PURE Study): a prospective epidemiological survey.
cardiovascular-disease/10-year-risk.php. Lancet 2011;378(9798):1231-43.
50. Goff DC, Jr., Lloyd-Jones DM, Bennett G, Coady S, 60. Goldberg AC, Hopkins PN, Toth PP, Ballantyne CM, Rader
D’Agostino RB, Gibbons R, et al. 2013 ACC/AHA DJ, Robinson JG, et al. Familial hypercholesterolemia:
guideline on the assessment of cardiovascular risk: a screening, diagnosis and management of pediatric
report of the American College of Cardiology/American and adult patients: clinical guidance from the
Heart Association Task Force on Practice Guidelines. National Lipid Association Expert Panel on Familial
Circulation 2014;129(25 Suppl 2):S49-73. Hypercholesterolemia. J Clin Lipidol 2011;5(3):133-40.
12 References
61. National Clinical Guidelines Centre for Acute and
Chronic Conditions. Identification and management of
familial hypercholesterolaemia 2008 (Revised 2014).
National Institute for Health and Care Excellence; 2014.
62. Watts GF, Sullivan DR, Poplawski N, van Bockxmeer
F, Hamilton-Craig I, Clifton PM, et al. Familial
hypercholesterolaemia: a model of care for Australasia.
Atheroscler Suppl 2011;12(2):221-63.
References 13
Appendix CV1
Examples of FRS calculator for general CVD risk prediction:
A) Web-based FRS Calculators:
14 Appendix CV1
B) Paper-based FRS Calculators:
Simple Model with Office-based non-laboratory Predictors

CVD Points for Women
SBP Not SBP
POINTS Age BMI Treated Treated Smoker Diabetic
-3 <120
-2
-1 <120
0 30-34 <25 120-129 NO NO
1 25-<30 130-139
2 35-39 ≥30 120-129
3 140-149 130-139
4 150-159 YES
5 40-44 160+ 140-149 YES
6 45-49 150-159
7
8 50-54 160+
9
10 55-59
11 60-64
12 65-69
13
14 70-74
TOTAL
15 75+ POINTS
Points
Allotted

CVD Risk for Women
POINTS RISK POINTS RISK POINTS RISK
-2 or
less Below 1% 6 3.4% 14 11.6%
-1 1.0% 7 3.9% 15 13.5%
0 1.1% 8 4.6% 16 15.6%
1 1.5% 9 5.4% 17 18.1%
2 1.8% 10 6.3% 18 20.9%
3 2.1% 11 7.4% 19 24.0%
4 2.5% 12 8.6% 20 27.5%
5 2.9% 13 10.0% 21+ Above 30%
Appendix CV1 15
CVD Points for Men
SBP Not SBP
POINTS Age BMI Treated Treated Smoker Diabetic
-2 <120
-1
0 30-34 <25 120-129 <120
1 25-<30 130-139 NO NO
2 35-39 ≥30 140-159 120-129
3 160+ 130-139 YES
4 140-159 YES
5 40-44 160+
6
7 45-49
8 50-54
9
10 55-59
11 60-64
12
13 65-69
14 70-74
TOTAL
15 75+ POINTS
Points
Allotted

CVD Risk for Men
POINTS RISK POINTS RISK POINTS RISK
-5 or
less Below 1% 3 4.0% 11 15.7%
-4 1.1% 4 4.7% 12 18.5%
-3 1.4% 5 5.6% 13 21.7%
-2 1.6% 6 6.7% 14 25.4%
-1 1.9% 7 8.0% 15 29.6%
0 2.3% 8 9.5% 16+ Above 30%
1 2.8% 9 11.2%
2 3.3% 10 13.3%
16 Appendix CV1
Appendix CV2
The following is the listing of key messages proposed in the Malaysian Dietary Guidelines, 2010
Key Message 1 Eat a variety of foods within your recommneded intake
Key Message 2 Maintain body weight in a healthy range
Key Message 3 Be physically active everyday
Key Message 4 Eat adequate amount of rice, other cereal products (preferably whole grain) and tubers
Key Message 5 Eat plenty of fruits and vegetables every day
Key Message 6 Consume moderate amounts of fish, meat, poutry, egg, legumes and nuts
Key Message 7 Consume adequate amounts of milk and milk products
Key Message 8 Limit intake of foods high in fats and minimise fats and oils in food preparation
Key Message 9 Choose and prepare foods with less salt and sauces
Key Message 10 Consume foods and beverages low in sugar
Key Message 11 Drink plenty of water daily
Key Message 12 Practise exclusive breastfeeding
Key Message 13 Consume safe and clean foods
Key Message 14 Make effective use of nutrition information on food labels
(Please refer to the guidelines for details of the recommendations)
Appendix CV3
Screening & evaluation of dyslipidaemia (adopted from the Malaysian Clinical Practice Guidelines
in Management of Dyslipidemia, 4th Edition)
• TC and HDL-C can be measured in fasting and non fasting states.

• TG is best measured in a fasting sample. LDL-C should be the primary target of
1 therapy, LDL-C is calculated using the Friedwald’s equation (LDL-C (mmol/l) = TC
1 -HDL-C - TG / 2.2 ).
• When TG > 2.3mmol/L, non HDL-C is a better indicator of total atherogenic burden.
1 When TG > 4.5 mmol/L, the equation is no longer valid for LDL-C calculation.
• HDL-C < 1.0 mmol/L & TG > 1.7 mmol/L are considered as major CVD risk factors.
Appendix CV3 17
Appendix CV4
Risk factors for type 2 Diabetes Mellitus (T2DM) screening:
• Symptoms suggestive of DM (tiredness, lethargy, polyuria, polydipsia, polyphagia,

weight loss, pruritus vulvae, balanitis)
• Asymptomatic adults who are overweight or obese (BMI >23 kg/m2 or WC ≥80 cm
for women & ≥90 cm for men) with additional risk factors:
o Physical inactivity
o First-degree relative with diabetes
o Hypertension ( ≥ 140/90 mmHg or on therapy for hypertension)
o Dyslipidaemia
n high density lipoprotein (HDL) cholesterol <0.9mmol/L or
n triglycerides (TG) >1.7 mmol/L
o HbA1C ≥ 5.7%, impaired glucose tolerance or impaired fasting glucose on
previous testing
o History of CVD
o Other clinical conditions associated with insulin resistance (e.g., severe
obesity and acanthosis nigricans)
o Women with polycystic ovarian syndrome
o Women who delivered a baby weighing >4 kg or were diagnosed with gestational
diabetes mellitus
(Adapted from the American Diabetes Association: Position Statement on Standards of

Medical Care in Diabetes 2015)

18 Appendix CV4
Appendix CV5
Screening for T2DM at primary care level - without symptoms

(Adopted from the Clinical Practice Guidelines of Management of Type 2 Diabetes Mellitus,
4th Edition)
ASYMPTOMATIC WITH RISK
Capillary Plasma Glucose
<5.6 ≥5.6 Random Venous Plasma

Glucose (RPG)
Fasting Venous Plasma Glucose (FPG)
NORMAL <7.8 7.8 to 11.0

NORMAL OGTT
<6.1 6.1 to 6.9 ≥7.0 ≥11.1
Second FPG Second
RPG
NORMAL
<7.0 ≥7.0
≥11.1
NORMAL DM
DM
FPG 2 hour PPG
<6.1 6.1 to 6.9 ≥7.0 <7.8 7.8 to 11.0 ≥11.1
NORMAL IFG DM NORMAL IGT DM
• For screening of T2DM, measuring either venous or capillary blood using glucometer
is acceptable
• For diagnosis of T2DM, venous plasma glucose value is required
• If FPG ≥ 7.0 mmol/L or 2 hour PPG ≥ 11.1 mmol/L, repeat OGTT is required to make
the diagnosis of diabetes
• All values in mmol/L. Capillary whole blood reading is 12% lower than venous plasma
glucose

Appendix CV5 19
Appendix CV6
Individuals with increased risk of Familial Hypercholesterolaemia (FH):
• History of premature CVD (men aged < 55 years, women aged < 60 years)
• Family history of first-degree relative with premature CVD (men aged < 55 years,
women aged < 60 years)
• Total cholesterol > 7.5 or LDL-cholesterol > 4.9 mmol/L (untreated)
• First-degree relative with a total cholesterol > 7.5 or LDL-C > 4.9 mmol/L (untreated)
• Presence of physical signs of FH: tendon xanthomata or arcus cornealis at age < 45
years; xanthelasma at age < 25 years
Appendix CV7
Modified UK Simon Broome Criteria for FH:
1. DNA mutation
2. Tendon xanthomas in patient or first/second-degree relative
3. Family history MI <50 in second-degree or <60 in first-degree relative
4. Family history of cholesterol >7.5 in first- or second-degree relative
5. Cholesterol >7.5 (adult) or >6.7 (age <16 years)
6. LDL-C >4.9 (adult) or >4.0 (age <16 years)
Definite FH: (5 or 6) + 1
Probable FH: (5 or 6) + 2
Possible FH: (5 or 6) + (3 or 4)

20 Appendix CV7
02 Thyroid Dysfunction
SUMMARY
There is insufficient evidence to recommend universal screening for subclinical

thyroid disorder.
The risk of progression from subclinical thyroid dysfunction to overt thyroid
disorder is relatively low.
Measuring serum TSH and free T4 level should be based on individual merits,
i.e., high risk of overt clinical disease.
RECOMMENDATIONS
Routine screening for thyroid dysfunction should not be offered. Grade I
2.1 Introduction
Thyroid dysfunction ranges from subclinical to overt thyroid disease. Screening

can detect patients with subclinical disease or undiagnosed overt thyroid
disease. Patients with overt disease have derangement in both thyroid stimulating
hormone and free thyroxine level. Overt thyroid disease is noted to be associated
with multiple co-morbidities including adverse cardiovascular, musculo–skeletal,
neuropsychiatric, dermatologic and gastrointestinal effects (1). Although the
prevalence of overt undiagnosed thyroid dysfunction was reported to vary
between countries, it was consistently noted to be less common than subclinical
dysfunction (2-4).
Subclinical hypothyroidism is defined as an elevated serum thyroid stimulating

hormone level (TSH: reference range of 0.45-4.5 mIU/L) with a normal serum
free thyroxine (T4) and triiodothyroxine levels (T3) (5). In the United States, the
prevalence of subclinical hypothyroidism in adults is noted to range from 4 to
10% (5, 6) Level II. No local data is available at present. Untreated subclinical
hypothyroidism progresses to overt hypothyroidism at the rate of 2–5% per
year. The rate of progression is faster in patients with higher levels of TSH, older
patients, female gender and positive thyroid antibody status (7 -9) Level II-2. The
risks of cardiovascular disease and cardiovascular mortality are increased with
increasing level of TSH in patients with subclinical hypothyroidism (10) Level II.
Thyroid Dysfunction 21
Participants with TSH ≥ 10 mIU/L have a significantly increased risk of CHD events (HR, 1.89
[95% CI, 1.28–2.80]) and CHD mortality (HR, 1.58 [95% CI, 1.10–2.27]) but not all-cause
mortality (10, 11) Level II. All-cause mortality is increased only among those with cardiovascular
risks (RR 1.76, [95% CI 1.36-2.30]) (12, 13) (14) Level II. However, the associations between
subclinical hypothyroidism and other clinical conditions, e.g., neuropsychiatric syndromes
and systemic hypothyroid symptoms, are not clear, except dyslipidemia which is increased
in patients with a TSH >10 mU/L” (15-18) Level II.
Subclinical hyperthyroidism is defined as condition characterized by low serum TSH levels

with a normal serum T4 and T3 (13, 19). The prevalence of subclinical hyperthyroidism
ranges from 0.6-12.4% (13) Level II. In untreated subclinical hyperthyroidism, a great majority
of patients remain subclinically hyperthyroid or revert to euthyroid status (20) Level II-2. It may
develop into overt disease at a rate of 1–5% per year especially in elderly patients with
multinodular goitre or those with total suppression of TSH level (TSH < 0.1) (11, 21) Level
I (22) Level II-2. Furthermore, there is an increased relative risk of atrial fibrillation (RR 2.2, CI
1.4-3.3) in those aged 65 years and above with TSH < 0.1 mU/L (19) Level II-1 (23, 24) Level II-2.
However, the evidence for increased cardiovascular disease risk is conflicting (19) Level I (25) Level
II-2
(13) Level I (26) Level I. Cardiovascular mortality may be increased only among undetectable
TSH (<0.1 mU/L) (27). It is also associated with reduced BMD in post-menopausal women
(13) Level I, but there is no clear evidence to support its association with osteoporotic fracture
(13, 19) Level I. In addition, there is no clear evidence linking subclinical hyperthyroidism with
mental health (13, 18) Level I or overall mortality risk (25, 28 -32) Level II (14, 26) Level I.
2.2 Benefit of screening and treating subclinical thyroid

dysfunction
Significant morbidities associated with subclinical thyroid dysfunction are uncommon. No
study has looked at the benefit of screening for subclinical thyroid dysfunction (1). There
is no clear clinical benefit of treating subclinical hypothyroidism (1, 33 -37) and subclinical
hyperthyroidism (38 -43); moreover, the evidence is of poor quality. There could be positive
effects on lipid profile (reduced total and LDL cholesterol) with thyroxine treatment but
its clinical benefit is uncertain (1, 44). Treating subclinical hyperthyroidism is noted to be
associated with a positive benefit of improving daytime blood systolic blood pressure, but a
small increase in BMI. Again, however, the quality of evidence is poor (44). There could be
benefit in treating patients with TSH > 10mIU/L or those with increased cardiovascular risk,
i.e., patients with documented diastolic dysfunction, diastolic hypertension, atherosclerosis,
dyslipidemia or diabetes mellitus, and smokers (13) Level III. However, screening of patients
with CVD risk factors for thyroid disorders yield low prevalence thus it is not justified.
22 Benefit of screening and treating subclinical thyroid dysfunction

2.3 Screening test
TSH test is the initial evaluation because of its ability to detect abnormalities prior to
abnormal serum free T4 and T3 levels(13). The TSH test has sensitivity above 98% and
specificity above 92% in detecting thyroid dysfunction among patients suspected to have
thyroid disorder (45). Among healthy people, normal TSH concentration has a high negative
predictive value in ruling out thyroid disease (45). Nevertheless, thyroid function results in the
elderly (>70 years) should be interpreted with caution as the normal range may be different
from that in younger population. (46)
2.4 Harm of screening
A review by USPFTF finds scarce evidence documenting harm of screening (1). Harm
generally associated with screening, such as overtreatment and anxiety resulting from
overdiagnosis, is a potential problem.
REFERENCES
1. Rugge J, Bougatsos C, Chou R. Screening and treatment 7. Vanderpump M, Tunbrldge W, French J, Appleton D,
of thyroid dysfunction: an evidence review for the Bates D, Clark F et al. The incidence of thyroid disorders
U.S. Preventive Services Task Force. Ann Intern Med in the community: a twenty-year follow-up of the
2015;162(1):35. Whickham Survey. Clin Endocrinol 1995;43(1):55-68.
2. Delitala A, Pilia M, Ferreli L, Loi F, Curreli N, Balaci L 8. Diez JJ, Iglesias P. Spontaneous subclinical
et al. Prevalence of unknown thyroid disorders in a hypothyroidism in patients older than 55 years: an
Sardinian cohort. Eur J Endocrinol 2014;171(1):143-9. analysis of natural course and risk factors for the
3. Unnikrishnan A, Bantwal G, John M, Kalra S, Sahay R, development of overt thyroid failure. J Clin Endocrinol
Tewari N. Prevalence of hypothyroidism in adults: An Metab 2004;89(10):4890-7
epidemiological study in eight cities of India. Indian J 9. Huber G, Staub JJ, Meier C, Mitrache C, Guglielmetti
Endocrinol Metab 2013;17(4):647. M, Huber P, Braverman LE. Prospective study of the
4. Benseñor I, Goulart A, Lotufo P, Menezes P, Scazufca spontaneous course of subclinical hypothyroidism:
M. Prevalence of thyroid disorders among older people: prognostic value of thyrotropin, thyroid reserve,
results from the São Paulo Ageing and Health Study. Cad and thyroid antibodies. J Clin Endocrinol Metab
Saude Publica 2011; 27(1):155-61. 2002;87(7):3221-6.
5. Hollowell JG, Staehling NW, Flanders WD, et al. Serum 10. Rodondi N, den Elzen W, Bauer D, Cappola A, Razvi
TSH, T4 and thyroid autoantibodies in the United States S, Walsh J et al. Subclinical hypothyroidism and the
population (1988–1994): National Health and Nutrition risk of coronary heart disease and mortality. JAMA
Examination Survey (NHANES III). J Clin Endocrinol 2010;304(12):1365.
Metab 2002;87:489–99. 11. Gencer B, Collet T, Virgini V, Auer R, Rodondi N.
6. Canaris G J, Manowitz NR, Mayor G, Ridgway EC. The Subclinical thyroid dysfunction and cardiovascular
Colorado thyroid disease prevalence study. Arch Intern outcomes among prospective cohort studies. Endocr
Med 2000;160:526-34. Metab Immune Disord Drug Targets 2013;13(1):4-12.
References 23
REFERENCES
12. Singh S, Duggal J, Molnar J, Maldonado F, Barsano Subclinical thyroid dysfunction and the risk for
C, Arora R. Impact of subclinical thyroid disorders on coronary heart disease and mortality. Ann Intern Med
coronary heart disease, cardiovascular and all-cause 2008;148(11):832-45.
mortality: A meta-analysis. Int J Cardiol 2008;125(1):41- 27. Biondi B. How could we improve the increased
8. cardiovascular mortality in patients with overt
13. Biondi B, Cooper D. The clinical significance of subclinical and subclinical hyperthyroidism? Eur J Endocrinol
thyroid dysfunction. Endocr Rev. 2008;29(1):76-131. 2012;167(3):295-9.
14. Haentjens P, Van Meerhaeghe A, Poppe K, Velkeniers 28. Singh S, Duggal J, Molnar J, Maldonado F, Barsano
B. Subclinical thyroid dysfunction and mortality: an C, Arora R. Impact of subclinical thyroid disorders on
estimate of relative and absolute excess all-cause coronary heart disease, cardiovascular and all-cause
mortality based on time-to-event data from cohort mortality: A meta-analysis. Int J Cardiol 2008;125(1):41-
studies. Eur J Endocrinol 2008;159(3):329-41. 8.
15. Kanaya Am, Harris F, Volpato S et al. Association between 29. Boekholdt S, Titan S, Wiersinga W, Chatterjee K, Basart
thyroid dysfunction and total cholesterol level in an D, Luben R et al. Initial thyroid status and cardiovascular
older biracial population: the health, aging and body risk factors: The EPIC-Norfolk prospective population
composition study. Arch Intern Med 2002;162:773-9. study. Clin Endocrinol 2010;72(3):404-10.
16. Bauer Dc, Ettinger B, Browner WS. Thyroid function and 30. Flynn R, Bonellie S, Jung R, MacDonald T, Morris
serum lipids in older women: A population-based study. A, Leese G. Serum thyroid-stimulating hormone
Am J Med 1998;6:546-51. concentration and morbidity from cardiovascular
17. Kung AW, Pang RW, Janus ED. Elevated serum disease and fractures in patients on long-term thyroxine
lipoprotein (a) in subclinical hypothyroidism. Clin therapy. J Clin Endocrinol Metab 2010;95(1):186-93.
Endocrinol 1995;4:445-9 31. Ittermann T, Haring R, Sauer S, Wallaschofski H, Dorr
18. Chaker L, Baumgartner C, Ikram MA, Dehghan A, Medici M, Nauck M et al. Decreased serum TSH levels are not
M, Visser WE, et al. Subclinical thyroid dysfunction associated with mortality in the adult northeast German
and the risk of stroke: a systematic review and meta- population. Eur J Endocrinol 2009;162(3):579-85.
analysis. Eur J Epidemiol 2014;29(11):791-800. 32. Sgarbi J, Matsumura L, Kasamatsu T, Ferreira S, Maciel
19. Helfand M. Screening for subclinical thyroid dysfunction R. Subclinical thyroid dysfunctions are independent
in non-pregnant adults: a summary of the evidence for risk factors for mortality in a 7.5-year follow-up: the
the U.S. Preventive Services Task Force. Ann Intern Med Japanese-Brazilian thyroid study. Eur J Endocrinol
2004;140(2):128. 2009;162(3):569-77.
20. Vadiveloo T, Donnan P, Cochrane L, Leese G. 33. Villar HCCE, Saconato H, Valente O, Atallah ÁN. Thyroid
The thyroid epidemiology, audit, and research hormone replacement for subclinical hypothyroidism.
study (TEARS): the natural history of endogenous Cochrane Libr 2007.
subclinical hyperthyroidism. J Clin Endocrinol Metab 34. Razvi S, Shakoor A, Vanderpump M, Weaver J, Pearce
2011;96(1):E1-E8. S. The influence of age on the relationship between
21. Collet TH, Gussekloo J, Bauer DC, den Elzen WP, Cappola subclinical hypothyroidism and ischemic heart
AR, Balmer P, et al. Subclinical hyperthyroidism and the disease: a meta-analysis. J Clin Endocrinol Metab
risk of coronary heart disease and mortality. Arch Intern 2008;93(8):2998-3007.
Med 2012;172(10):799-809. 35. Razvi S, Ingoe L, Keeka G, Oates C, McMillan C, Weaver
22. Díez J, Iglesias P. An analysis of the natural course J. The beneficial effect of l-thyroxine on cardiovascular
of subclinical hyperthyroidism. Am J Med Sci risk factors, endothelial function, and quality of life in
2009;337(4):225-32. subclinical hypothyroidism: randomized, crossover trial.
23. Cappola A, Fried L, Arnold A, Danese M, Kuller L, Burke J Clin Endocrinol Metab 2007;92(5):1715-23.
G et al. Thyroid status, cardiovascular risk, and mortality 36. Iqbal A, Jorde R, Figenschau Y. Serum lipid levels in
in older adults. JAMA 2006;295(9):1033. relation to serum thyroid-stimulating hormone and the
24. Palmeiro C, Davila MI, Bhat M, Frishman WH, Weiss effect of thyroxine treatment on serum lipid levels in
IA. Subclinical hyperthyroidism and cardiovascular subjects with subclinical hypothyroidism: the Tromso
risk: recommendations for treatment. Cardiol Rev study. J Intern Med 2006;260(1):53-61.
2013;21(6):300-8. 37. Völzke H, Schwahn C, Wallaschofski H, Dörr M. The
25. Vo¨lzke H, Schwahn C, Wallaschofski H, Do¨rr M. Review: association of thyroid dysfunction with all-cause and
the association of thyroid dysfunction with all-cause and circulatory mortality: is there a causal relationship? J
circulatory mortality: is there a causal relationship? J Clin Endocrinol Metab 2007;92(7):2421-9.
Clin Endocrinol Metab 2007;92:2421–9. 38. Forfar J, Feek C, Miller H, Toft A. Atrial fibrillation and
26. Ochs N, Auer R, Bauer DC, et al. Meta-analysis: isolated suppression of the pituitary-thyroid axis:
24 References
response to specific antithyroid therapy. Int J Cardiol
1981;1(1):43-8.
39. Kaminski G, Michalkiewicz D, Makowski K, Podgajny Z,
Szalus N, Ruchala M et al. Prospective echocardiographic
evaluation of patients with endogenous subclinical
hyperthyroidism and after restoring euthyroidism. Clin
Endocrinol (Oxf) 2011;74(4):501-7.
40. Sgarbi J, Villaça F, Garbeline B, Villar H, Romaldini
J. The effects of early antithyroid therapy for
endogenous subclinical hyperthyroidism in clinical
and heart abnormalities. J Clin Endocrinol Metab
2003;88(4):1672-7.
41. Faber, Jensen, Petersen, Nygaard, Hegedus, Siersbaek-
Nielsen. Normalization of serum thyrotrophin by means
of radioiodine treatment in subclinical hyperthyroidism:
effect on bone loss in postmenopausal women. Clin
Endocrinol (Oxf) 1998;48(3):285-90.
42. Yönem Ö, Dökmetas H, Aslan S, Erselcan T. Is antithyroid
treatment really relevant for young patients with
subclinical hyperthyroidism? Endocr J 2002;49(3):307-
14.
43. Mudde A, Houben A, Kruseman A. Bone metabolism
during anti-thyroid drug treatment of endogenous
subclinical hyperthyroidism. Clin Endocrinol (Oxf)
1994;41(4):421-4.
44. Rugge B, Balshem H, Sehgal R. Screening and subclinical
screening and treatment of subclinical hypothyroidism
or hyperthyroidism. Agency Healthc Res Qual US Dep
Heal Hum Serv 2007;24.
45. British Thyroid Association. UK guidelines for the use of
thyroid function tests. Consultant 2006.
46. Brenner AP, Feddema P, Leedman PJ, et al. J Clin
Endocrinol Metab 2012; 97(5): 1554-62.
References 25
03 Osteoporosis
SUMMARY
Osteoporotic fracture is associated with high morbidity and mortality.

Treatment for osteoporosis reduces the incidence of osteoporotic fracture for
women but evidence for the benefit of screening is yet to be established.
Evidence for any benefit in treating and screening men for osteoporosis is
insufficient.
High risks of future osteoporotic fractures include age >50 with previous fragility
fracture or loss of height.
DEXA scan is the recommended screening tool.
RECOMMENDATIONS
Screening for osteoporosis using DEXA scan should only be Grade C

indicated for women at high risk of osteoporotic fracture.
Routine screening for osteoporosis should not be offered to men. Grade I
3.1 Introduction
Osteoporosis is defined as a systemic skeletal disease characterized by low bone

mass and micro-architectural deterioration of bone tissue, with a consequence
of increased bone fragility and susceptibility to fracture (1). Clinically, WHO
working groups defines osteoporosis in women based on the following criteria:
Table 1: The World Health Organisation (WHO) Working Group classification of

osteoporosis (2)
Normal Bone mineral density (BMD) within 1 SD of young adult reference range (T score
> –1)
Osteopenia BMD more than 1 SD but less than 2.5 SD below the young adult mean (T score
between –1 and –2.5)
Osteoporosis BMD value of 2.5 SD or more below the young adult mean (T score < –2.5)
Severe/ BMD value of 2.5 SD or more below the young adult mean
Established Osteoporosis with the presence of 1 or more fragility fractures
• T score is the standard deviation (SD) in comparison with young adult BMD
26 Introduction
The aim of managing osteoporosis is to reduce the risk of future osteoporotic fracture. Hip
fracture is associated with a higher mortality rate in women aged 50 years compared to
those without. It is also associated with a mortality rate of up to 20% in the first year. The
majority of those who survive are disabled and only 25% will resume normal activities (3)
Level II-3
. Osteoporosis-related fractures are estimated to cause 6.7% of women to become
dependent in basic activities of daily living and 7.8% requiring nursing home care for an
average of 7.6 years (4).
In Malaysia, the incidence of hip fracture for individuals over 50 years old have increased
over the years from 70 per 100,000 population in 1989 to 90 per 100,000 in 1996 and
1997 (5, 6). In 1997, the age-adjusted rates of osteoporotic fracture for men and women in
Malaysia were 88 and 218 per 100,000, which were lower than the rates for US Whites (7
-9). Race-specific incidence data have shown that fracture rates are highest among Chinese
Malaysians (160/100 000) followed by ethnic Indians (150/100 000) and Malays (30/100
000) (6). Females are twice as commonly affected compared to males. Countries with a high
incidence of osteoporotic hip fracture have rates over 250/100 000 (9).
The important factors associated with an increased risk of osteoporotic fracture are (10 -17):
• age
• prior fragility fracture
• low body mass index
• low BMD
• parental history of hip fracture
• smoking
• use of systemic corticosteroids
• excess alcohol intake
• low calcium and vitamin D intake
• sedentary life-style
Age is the single most important risk factor. Prior fragility fracture, including a vertebral
fracture, and documented reduced height poses a high risk for another osteoporotic fracture.
Increased risk of a fall is also associated with osteoporotic fracture.
3.2 Benefit of screening and treating osteoporosis
Meta-analyses and reviews have shown that treating post-menopausal women with
established osteoporosis using various agents reduces the rates of osteoporotic fracture
(18 -22) Level I. Effective treatments include calcium and vitamin D (23), bisphophanates (22),
SERMs, teriparatide (24) and denosumab (25). Treating old and frail women with osteoporotic
fracture also reduces their mortality rate (26). Most meta-analyses have included secondary
Benefit of screening and treating osteoporosis 27

prevention studies on patients who have had a prior fragility fracture. The benefit of reducing
fracture risk in primary prevention, i.e., without prior fracture, is smaller or not significant
compared with secondary prevention (27 -30). In men with osteoporosis, meta-analyses
have shown a reduction of vertebral and non-vertebral fractures with alendronate and
risedronate treatments (31, 32) Level I.
On the other hand, the benefit of screening is less uncertain. RCTs on screening programmes
to reduce fracture rates in the community show conflicting results. One RCT on osteoporosis
screening in women aged 45-54 followed by treatment showed reduced osteoporosis
fracture (HR = 0.741, 95% CI = 0.551-0.998) (33) but the absolute benefit was small.
Another screening programme using risk score and spinal radiograph for those at risk did
not show any significant short-term (12 months) benefit in reducing osteoporotic vertebral
fracture (34).
Data on the cost-effectiveness of any particular strategy is lacking. Cost-effectiveness

assessment on osteoporosis screening followed by treatment in a cohort study indicated
that non-adherence with osteoporosis medications substantially increases the incremental
cost-effectiveness ratio of osteoporosis screening (35) Level II-2. A RCT on the benefit of
osteoporosis screening using fracture risk scoring is still ongoing (36).
3.3 Screening tests
Annual measurements of height to detect possible risk vertebral fracture is simple and can
be used to identify patients for lateral spinal radiograph and BMD assessment (37). Those
with high risk of osteoporosis, such as age > 50 with previous fragility fracture and high risk
of fall, should be offered BMD assessment (37).
Dual energy X-ray absorptiometry (DEXA) is the gold standard for diagnosing osteoporosis
and is the recommended screening test, if indicated (38, 39).
Quantitative Ultrasound (QUS) for diagnosing and monitoring treatment is not recommended
because there is a diversity of techniques and a lack of standardised reference range.
The criteria for diagnosis and recommending treatment based on ultrasound are not well
established (40) Level II-2.
There are many risk scoring systems to predict the risk of osteoporosis. However, no tool
is good enough and validated yet for selecting patients for therapy and improving fracture
outcome. Most tools are reported to have sensitivity of 80-90% and specificity of 50%
in detecting osteoporosis (41). Simple tools, such as the Osteoporosis Self-assessment
Tool (OST), Osteoporosis Risk Assessment Instrument (ORAI), and Garvan Fracture Risk
Calculator (Garvan), fare as well or better than more complex tools, such as the Simple
28 Screening tests
Calculated Risk Estimation Score [SCORE], WHO Fracture Risk Assessment Tool [FRAX]
(http://www.shef.ac.uk/FRAX/index.jsp), and Qfracture, in predicting osteoporosis (42), or
osteoporotic fracture (41). RCTs evaluating the use of FRAX tool in prevention of osteoporotic
fracture are still ongoing (36).
Screening programmes have been shown to consistently increase the chance of treatment
but with uncertain fracture risk reduction (33, 34, 43). Meta-analyses on osteoporotic
treatment found harms of increased risk of serious infection with denosumab [OR (95% CI)
4.45 (1.15 to 17.14), p=0.03] (44), and a possible association with adverse cardiovascular
outcomes (45) with calcium intake. However, the risk of harm is small (46).
REFERENCES
1. Consensus Development Conference. Diagnosis, 8. Cummings S, Melton L. Epidemiology and

prophylaxis and treatment of osteoporosis. Am J Med outcomes of osteoporotic fractures. The Lancet
1993;94:646-50. 2002;359(9319):1761-7.
2. WHO technical Report Series 843. Assessment 9. Kanis J, Odén A, McCloskey E, Johansson H, Wahl D,
of fracture risk and its application to screening for Cooper C. A systematic review of hip fracture incidence
postmenopausal osteoporosis. Geneva, World Health and probability of fracture worldwide. Osteoporos Int
Organisation 1994. 2012;23(9):2239-2256.
3. Clayer MT, Bauze RJ. Morbidity and mortality following 10. Lau EM, Suriwongpaisal P, Lee JK, et al. Risk factors
fractures of femoral neck and trochanteric region: for hip fracture in Asian men and women: the Asian
analysis of risk factors journal of trauma-injury infection Osteoporosis Study. J Bone Miner Res 2001;16(3):572-
& critical care. J Trauma 1989;29(12):1673-8. 80.
4. Chrischilles EA, Butler CD, Davis CS, Wallace RB. A 11. Kanis JA, Borgstrom F, De Laet C, et al. Assessment of
model of lifetime osteoporosis impact. Arch Intern Med fracture risk. Osteoporos Int 2005;16(6):581-9.
1991;151(10):2026-32. 12. Kanis JA, Johansson H, Johnell O, et al. Alcohol
5. Lee CM, Sidhu JS, Pan KL. Hip fracture incidence intake as a risk factor for fracture. Osteoporos Int
in Malaysia 1981-1989. Acta Orthop Scand 2005;16(7):737-42.
1993;64(2):178-80. 13. Kanis JA, Johnell O, Oden A, et al. Smoking and fracture
6. Lee JK, Khir ASM. The incidence of hip fracture in risk: a meta-analysis. Osteoporos Int 2005;16(2):155-
Malaysians above 50 years of age: variation in different 62.
ethnic groups. J Rheumatol 2007;10(4):300-5. 14. Kanis JA, Johnell O, Oden A, et al. A family history
7. Lau EM, Lee JK, Suriwongpaisal P, et al. The of fracture and fracture risk: a meta-analysis. Bone
incidence of hip fracture in Four Asian countries: 2004;35(5):1029-37.
the Asian Osteoporosis Study (AOS). Osteoporos Int 15. De Laet C, Kanis JA, Odén A, et al. Body mass index as
2001;12(3):239-43. a predictor of fracture risk: a meta-analysis. Osteoporos
References 29
REFERENCES
Int 2005;16(11):1330-8. 2008(1):Cd004523.

16. Lim PS, Ong FB, Adeeb N, et al. Bone health in urban 29. Wells GA, Cranney A, Peterson J, Boucher M, Shea
midlife Malaysian women: risk factors and prevention. B, Robinson V, et al. Etidronate for the primary and
Osteoporos Int 2005;16(12):2069-79. secondary prevention of osteoporotic fractures in
17. Loh KY, Shong KH, Soo NL, et al. Risk factors for fragility postmenopausal women. Cochrane Database Syst Rev
fracture in Seremban district, Malaysia: a comparison 2008(1):Cd003376.
of patients with fragility fracture in the orthopedic ward 30. Wells GA, Cranney A, Peterson J, Boucher M, Shea
versus those in the outpatient department. Asia Pac J B, Robinson V, et al. Alendronate for the primary and
Public Health 2008;20(3):251-7. secondary prevention of osteoporotic fractures in
18. Adachi JD, Rizzoli R, Boonen S, et al. Vertebral fracture postmenopausal women. Cochrane Database Syst Rev
risk reduction with risedronate in post-menopausal 2008(1):Cd001155.
women with osteoporosis: a meta-analysis of individual 31. Sawka AM, Papaioannou A, Adachi JD, et al. Does
patient data. Aging Clin Exp Res 2005;17(2):150-6. alendronate reduce the risk of fracture in men? A
19. Fraser LA, Vogt KN, Adachi JD, Thabane L. Fracture risk meta-analysis incorporating prior knowledge of anti-
associated with continuation versus discontinuation of fracture efficacy in women. BMC Musculoskelet Disord
bisphosphonates after 5 years of therapy in patients 2005;6:39.
with primary osteoporosis: a systematic review and 32. Zhong ZM, Chen JT. Anti-fracture efficacy of risedronic
meta-analysis. Ther Clin Risk Manag 2011;7:157-66. acid in men: A meta-analysis of randomized controlled
20. Kanis JA, Johansson H, Oden A, McCloskey EV. A meta- trials. Clin Drug Investig 2009;29(5):349-57.
analysis of the effect of strontium ranelate on the risk of 33. Barr RJ, Stewart A, Torgerson DJ, Reid DM. Population
vertebral and non-vertebral fracture in postmenopausal screening for osteoporosis risk: a randomised control
osteoporosis and the interaction with FRAX. Osteoporos trial of medication use and fracture risk. Osteoporos Int
Int 2011;22(8):2347-55. 2010;21(4):561-8.
21. Boonen S, Laan RF, Barton IP, Watts NB. Effect of 34. Clark EM, Gould V, Morrison L, Ades AE, Dieppe P, Tobias
osteoporosis treatments on risk of non-vertebral JH. Randomized controlled trial of a primary care-
fractures: review and meta-analysis of intention-to-treat based screening program to identify older women with
studies. Osteoporos Int 2005;16(10):1291-8. prevalent osteoporotic vertebral fractures: Cohort for
22. Murad M, Drake M, Mullan R, Mauck K, Stuart L, Lane Skeletal Health in Bristol and Avon (COSHIBA). J Bone
M et al. Comparative effectiveness of drug treatments Miner Res 2012;27(3):664-71.
to prevent fragility fractures: a systematic review 35. Hiligsmann M, Gathon HJ, Bruyere O, et al. Cost
and network meta-analysis. J Clin Endocrinol Metab effectiveness of osteoporosis screening followed by
2012;97(6):1871-80. treatment; the impact of medication adherence. Value
23. Avenell A, Mak JC, O’Connell D. Vitamin D and vitamin D in Health 2010;13(4):394-401.
analogues for preventing fractures in post-menopausal 36. Shepstone L, Fordham R, Lenaghan E, Harvey I, Cooper
women and older men. Cochrane Database Syst Rev C, Gittoes N, et al. A pragmatic randomised controlled
2014;4:Cd000227. trial of the effectiveness and cost-effectiveness of
24. Han S, Wan S. Effect of teriparatide on bone mineral screening older women for the prevention of fractures:
density and fracture in postmenopausal osteoporosis: rationale, design and methods for the SCOOP study.
meta-analysis of randomised controlled trials. Int J Clin Osteoporos Int 2012;23(10):2507-15.
Pract 2012;66(2):199-209. 37. Care C. Overview—Appraisal Process [Internet].
25. Silva-Fernández L, Rosario M, Martínez-López J, Canadian Task Force on Preventive Health Care.
Carmona L, Loza E. Denosumab for the treatment 2015 [cited 2 March 2015]. Available from: http://
of osteoporosis: A systematic literature review. canadiantaskforce.ca/appraised-guidelines/overview/
Reumatología Clínica 2013;9(1):42-52. 38. Uspreventiveservicestaskforce.org. Home - US
26. Bolland MJ, Grey AB, Gamble GD, Reid IR. Effect of Preventive Services Task Force [Internet]. 2015
osteoporosis treatment on mortality: a meta-analysis. J [cited 2 March 2015]. Available from: http://www.
Clin Endocrinol Metab 2010;95(3):1174-81. uspreventiveservicestaskforce.org/
27. Holder KK, Kerley SS. Alendronate for fracture prevention 39. Acadmed.org.my. Academy of Medicine of Malaysia
in postmenopause. Am Fam Physician 2008;78(5):579- - Clinical Practice Guidelines (CPGs) [Internet]. 2015
81. [cited 2 March 2015]. Available from: http://www.
28. Wells G, Cranney A, Peterson J, Boucher M, Shea B, acadmed.org.my/index.cfm?&menuid=67
Robinson V, et al. Risedronate for the primary and 40. Flöter M, Bittar CK, Zabeu JL, et al. Review of
secondary prevention of osteoporotic fractures in comparative studies between bone densitometry and
postmenopausal women. Cochrane Database Syst Rev quantitative ultrasound of the calcaneus in osteoporosis.
30 References
Acta Reumatol Port 2011;36(4):327-35.
41. Rubin KH, Friis-Holmberg T, Hermann AP, Abrahamsen
B, Brixen K. Risk assessment tools to identify women
with increased risk of osteoporotic fracture: complexity
or simplicity? A systematic review. J Bone Miner Res
2013;28(8):1701-17.
42. Nayak S, Edwards DL, Saleh AA, Greenspan SL.
Systematic review and meta-analysis of the performance
of clinical risk assessment instruments for screening for
osteoporosis or low bone density. Osteoporos Int 2015.
43. McConaha JL, Berdine HJ, Skomo ML, Laux RV,
Higginbotham SK, O’Neil CK. Impact of the fracture
risk assessment on patient and physician behavior in
osteoporosis prevention. J Pharm Pract 2014;27(1):25-
30.
44. Anastasilakis AD, Toulis KA, Goulis DG, Polyzos SA,
Delaroudis S, Giomisi A, et al. Efficacy and safety of
denosumab in postmenopausal women with osteopenia
or osteoporosis: a systematic review and a meta-
analysis. Horm Metab Res 2009;41(10):721-9.
45. Rojas-Fernandez CH, Maclaughlin EJ, Dore NL, Ebsary
S. Assessing the potential adverse consequences of
supplemental calcium on cardiovascular outcomes:
should we change our approach to bone health? Ann
Pharmacother 2012;46(5):696-702.
46. Varenna M, Bertoldo F, Di Monaco M, Giusti A, Martini G,
Rossini M. Safety profile of drugs used in the treatment
of osteoporosis: a systematical review of the literature.
Reumatismo 2013;65(4):143-66.
References 31
04 Chronic Obstructive Pulmonary
Disease (COPD)
SUMMARY
Chronic obstructive pulmonary disease (COPD) is characterised by progressive,

partially reversible airflow obstruction and lung hyperinflation.
The main factor associated with COPD is cigarette smoking.
An established screening tool is not available.
Early diagnosis management with pharmacological agents does not improve
mortality and morbidity.
Smoking cessation remains the most effective strategy in reducing mortality and
morbidity associated with COPD.
RECOMMENDATIONS
Routine screening of adults for COPD is not indicated. Grade D
4.1 Introduction
Chronic obstructive pulmonary disease (COPD) is characterised by progressive,

partially reversible airflow obstruction and lung hyperinflation (1). It is mainly
caused by cigarette smoking. COPD may initiate or worsen many co-morbid
diseases, such as ischemic heart disease, congestive heart failure, osteoporosis,
anaemia, lung cancer, depression and diabetes. In turn, these diseases may
worsen COPD, which leads to increased hospitalizations, mortality and
healthcare costs (2, 3) Level II-3.
Population-based surveys from seven countries reported overall prevalence of

COPD ranging from 4.5% to 21.1% (4). The estimated prevalence rates of COPD
in Asia Pacific and Malaysian adults were 6.3% and 4.6%, respectively (5) Level
III. The estimation was based on a model calculation of patients with at least
moderately severe COPD. COPD is currently the fifth leading cause of death
worldwide (6). In a cross sectional study at primary care settings in Malaysia,
airflow limitation (defined as FEV1/FVC of < 0.7) was noted in 10.6% of adults
over than 40 years with ≥ 10 pack-years of smoking history. (7)
32 Introduction
4.2 Benefit of treatment or early intervention
The mainstay of COPD management is smoking cessation, which has been shown to
reduce mortality and morbidity at any stage of disease severity (8) Level I. Other management
strategies, such as inhaled bronchodilators, corticosteroids and vaccinations, have been
shown to reduce exacerbations in patients with severe COPD and have a small effect on
all–cause mortality (9 -17) Level I.
4.3 Screening tests
The diagnosis of COPD should be based on careful history-taking on the presence of

symptoms and assessment of airway obstruction (or airflow limitation) (18). The available
screening tools include spirometry and questionnaires. Spirometer is the validated tool
for measuring lung function. Case Finding Questionnaire (CFQ) and COPD Diagnostic
Questionnaire (CDQ) have been developed and studied to identify high-risk chronic smokers
(19). CDQ consists of five questions on symptoms of COPD, with each question carrying
one point. With a score of three and above as the cut-off for COPD, CFQ has a wide range
of sensitivity and specificity of 59%-80% and 58%-77%, respectively, in predicting COPD
(19) Level III. CDQ, which was assessed in various countries in Europe and the UK, as well as
in Australia recently, has shown poor validity (19 -22). None of these tools has been formally
tested in Malaysia.

There is no evidence to conclude potential benefits of early diagnosis and management of
asymptomatic patients through screening (19). Screening may also result in potential harms,
such as false-positive results, leading to subsequent unnecessary therapy with adverse
effects (19, 24, 25) Level II-B. Since, smoking cessation is the only effective intervention to
improve morbidity and mortality among COPD patients, it is arguably more useful to screen
patients for smoking and advise on smoking cessation.
Harm of screening 33
REFERENCES
1. Agusti A. systemic effects of chronic obstructive effects of beta-agonists in patients with asthma and
pulmonary disease: What we know and what we don’t COPD. Chest 2004;125(6):2309-21.
know (but should). Proc Am Thorac Soc 2007;4(7):522- 15. Salpeter SR, Buckley NS, Salpeter EE. Metaanalysis:
5. Anticholinergics, but not beta agonists, reduce severe
2. Barnes PJ, Celli BR. Systemic manifestations and exacerbations and respiratory mortality in COPD. J Gen
comorbidities of COPD. Eur Respir J 2009;33(5):1165- Intern Med 2006;21 (10):1011-9.
85. 16. Barr RG, Bourbeau J, Camargo Jr CA. Inhaled tiotropium
3. Soriano JB, Visick GT, Muellerova H, Payvandi N, Hansell for stable chronic obstructive pulmonary disease.
AL. patterns of comorbidities in newly diagnosed COPD Cochrane Libr 2005.
and asthma in primary care. Chest 2005;128(4):2099- 17. Ferguson GT, Funck-Brentano C, Fischer T, Darken P,
107. Reisner C. Cardiovascular safety of salmeterol in COPD.
4. Wilt TJ, Niewoehner D, Kim C, et al. Use of spirometry Chest 2003;123(6):1817-24.
for case finding, diagnosis, and management of chronic 18. Global Initiative for Chronic Obstructive Lung Disease
obstructive pulmonary disease (COPD). Summary, (GOLD), Spirometry for health care providers [Internet].
Evidence Report/Technology Assessment:121. 2005. 2010 (cited 2012 May 12). Available from: http://
Agency for Healthcare Research and Quality, Rockville, www.goldcopd.org/uploads/users/files/GOLD_
MD. Spirometry_2010.pdf
5. Regional COPD working group. COPD prevalence in 12 19. Hill K, Hodder R, Blouin M, Heels-Ansdell D, Guyatt G,
Asia-pacific countries and regions: Projections based Goldstein R. Identifying adults at risk of COPD who need
on the COPD prevalence estimation model. Respirology confirmatory spirometry in primary care. Do symptom-
2003;8:192-8. based questions help? Can. Fam. Physician 2011; 57:
6. Mannino DM, Buist AS. Global burden of COPD: risk e51–7.
factors, prevalence, and future trends. The Lancet 20. Price DB, Tinkelman DG, Nordyke RJ. Scoring system and
2007;370(9589):765-73. clinical application of COPD diagnostic questionnaires.
7. Ching SM, Pang YK, Price D, et al. Detection of airflow Chest 2006;129(6):1531.
limitation using a handheld spirometer in a primary care 21. Kotz D, Nelemans P, van Schayck CP, Wesseling GJ.
setting. Respirology 2014;19(5):689-93 External validation of a COPD diagnostic questionnaire.
8. Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Eur Respir J 2008;31(2):298-303.
Kanner RE, Connett JE. The effects of a smoking 22. Stanley AJ, Hasan I, Crockett AJ, van Schayck OCP, Zwar
cessation intervention on 14.5-year mortality. Ann Int NA. Validation of the COPD diagnostic questionnaire in
Med 2005;142(4):233. an Australian general practice cohort: a cross-sectional
9. Wongsurakiat P, Maranetra KN, Wasi C, Kositanont U, study. Prim Care Respir J 2014;23(1):92-7.
Dejsomritrutai W, Charoenratanakul S. Acute respiratory 23. Lin K, Watkins B, Johnson T, Rodriguez JA, Barton
illness in patients with copd and the effectiveness of MB. Screening for chronic obstructive pulmonary
influenza vaccination. Chest 2004;125(6):2011-20. disease using spirometry: summary of the evidence
10. Burge PS, Calverley PMA, Jones PW, Spencer S, Anderson for the US Preventive Services Task Force. Ann Int Med
JA, Maslen TK. Randomised, double blind, placebo 2008;148(7):535-43.
controlled study of fluticasone propionate in patients 24. Vedal S, Crapo RO. False positive rates of multiple
with moderate to severe chronic obstructive pulmonary pulmonary function tests in healthy subjects. Bull Eur
disease: the ISOLDE trial. BMJ 2000;320(7245):1297- Physiopathol Respir 1983;19(3):263-6.
303. 25. Hardie JA, Buist AS, Vollmer WM, Ellingsen I, Bakke
11. Calverley PMA, Anderson JA, Celli B, Ferguson GT, PS, MÃ¸rkve O. Risk of over-diagnosis of COPD in
Jenkins C, Jones PW, et al. Salmeterol and fluticasone asymptomatic elderly never-smokers. Eur Respir J
propionate and survival in chronic obstructive pulmonary 2002;20(5):1117-22.
disease. N Engl J Med 2007;356(8):775-89.
12. Sin DD, Wu L, Anderson JA, Anthonisen NR, Buist AS,
Burge PS, et al. Inhaled corticosteroids and mortality
in chronic obstructive pulmonary disease. Thorax
2005;60(12):992-7.
13. Sestini P, Renzoni E, Robinson S, Poole P, Ram FS. Short-
acting beta 2 agonists for stable chronic obstructive
pulmonary disease. Cochrane Database Syst Rev
2002;4.
14. Salpeter SR, Ormiston TM, Salpeter EE. Cardiovascular
34 References
05 Cervical Cancer
SUMMARY
Cervical cancer is the second most common cancer among women in Malaysia.
The incidence rate increases with age after 25 years and peaks at 60-69 years old.
Treating precancerous cervical lesions costs much less than treating the cancer
itself.
Screening with cytology has been proven to reduce cervical cancer mortality and
morbidity.
Co-testing of cytology with HPV DNA every five years confers the benefit of lower
incidence of cervical cancer.
RECOMMENDATIONS
Screening should start at 25 years old for women who have ever Grade A
had sexual activity or 3 years after the initiation of sex
Screening can be done using either conventional cytology testing Grade A
in Pap test or liquid based cytology every 3 years, or co-testing
cytology with HPV DNA every 5 years
Screening can be discontinued in women at age 65 after 3 negative Grade C
consecutive tests.
Screening should still be offered to women aged 65 and above who Grade C
have not had any cervical cancer screening
5.1 Introduction
Cervical cancer is a health concern worldwide. The incidence rate among

Hispanics and African Americans in the USA was reported at 9.0 to 9.8 per
100,000 women in 2011 (1). However, the incidence among Caucasians in
the USA is very low (1). In Malaysia, it is the second most common cancer
among women age 15-44 years old. The incidence has increased from an age-
standardised ratio (ASR) of 12.2 in 2006 to 15.6 per 100,000 in 2012 (2, 3). The
incidence rate starts to increase at the age of 25-29 years old years and peaks
at 60-69 years old (3). By ethnicity, Chinese Malaysian women have the highest
incidence of cervical cancer followed by Indians and Malays (2). Even though it
Introduction 35
is not listed in the top ten of hospitalized cases in Malaysia, neoplasm contribute the fourth
highest cause of death in Ministry of Health hospitals (4).
The risk factors for cervical cancer include:
• Early age of sexual debut (5) Level II-2, (6) Level I, (7) Level I.
• More than 2 sexual partners (5) Level II-2, (7) Level I, (8) Level II-2
• Multi-parity (8) Level II-2
• Persistent and high risk type of HPV infection (9) Level I, (10) Level I, (11) Level II,
(12) Level II-2, (13) Level II-2
• Smoking factor (14), (15) Level I
• HIV infection (16) Level II-2
• In-utero exposure to diethylstilbestrol (17) Level III
Almost all cases of cervical cancer are caused by high-risk human papilloma virus (HPV)
(3), (18) Level III. Chronic and persistent exposure to high-grade type of HPV precedes cervical
metaplasia and dysplasia, and the long duration of its pathology makes screening for
cervical cancer feasible. Although HPV vaccination may prevent cervical cancer, there is still
no strong evidence that it offers total protection. The vaccination does not cover all types of
high-risk HPV. While HPV 16 and 18 are responsible for 70% of cervical cancer cases, there
are at least 13 other types of HPV that are linked to the development of cervical cancer (9)
Level I
. Even though current HPV vaccination has an efficacy of 98% - 100% in preventing HPV
16 and 18 infections, the duration of protection is unclear making the cost-effectiveness of
this program as cancer prevention still under investigation (19) Level I. Thus, cervical cancer
screening is relevant.
5.2 Benefit of screening and treating cervical

abnormalities
The treatment of cervical cancer at an early stage is associated with excellent survival (20).
Therefore, it is imperative to diagnose cervical cancer early as screening for cervical cancer
provides great benefits to women (21) Level I. Screening compared to no screening significantly
reduced the risk of invasive cancer (RR: 0.38, 95%CI: 0.23, 0.63) and reduced the mortality
from advanced cancer (RR: 0.56, 95%CI: 0.42, 0.75) (22) Level I. In Malaysia, even though the
ASR of cervical cancer has declined, the percentage of cervical cancer patients who had
been screened three years before diagnosis was found to be very low (0-12%) (23).
Managing precancerous cervical lesions costs much less than cancer treatment (24). The
average cost of managing atypical squamous cell of undetermined significance (ASCUS) in
Malaysia is estimated to cost RM898 to RM1948 for CIN2/3. This is comparatively much
cheaper than the average cost of managing cervical cancer which is estimated at RM10,
36 Benefit of screening and treating cervical abnormalities

540.24. In addition to the cost-effectiveness, the success rate of ablation and excision
therapy of the pre-cancerous lesion ranges from 90% to 95% (25).
5.3 Screening tests
Screening tests used for cervical cancer include conventional Pap smear, liquid-based
cervical cytology, HPV-DNA test and visual inspection with acetic acid.
Conventional Pap smear test is a well-established screening test for cervical cancer (26).
The liquid-based cervical cytology is neither more sensitive nor more specific for detecting
high-grade cervical abnormality compared with the conventional Pap test (27) Level I, (28) Level I.
The HPV-DNA test for cervical smear is not useful for younger aged women because of the
high rate of clearance observed in infected cases. The infection is shown to decrease after age
29 years and has a clearance rate of 92% within five years (29) Level II-3, (30) Level II-2. However, for
women aged 30 years and above, co-testing of Pap smear and HPV DNA is an alternative.
This combination is more useful as it results in a higher detection of positive screening cases
(31) Level III. Co-testing for three years increases the detection of CIN3 or cancer compared
to Pap smear alone (10% vs 3.1%, p<0.0001) and the increased detection continues to be
seen at year 5 (12.15 vs 5.95, p<0.0001) (32) Level II-2, (33) Level III. In India, a single round of
HPV DNA testing followed by management of positive cases compared to cervical cytology
with no invitation for screening was associated with a significant reduction in the numbers
of CIN2 or advanced cervical cancers and deaths from cervical cancer (22) Level I. In another
study in the Netherlands, however, the added benefit of HPV DNA compared to cytology in
the incidence of cervical cancer after five years was marginal (4 of 19,579 in the intervention
group vs 14 of 19,731; OR: 0.29, 95% CI: 0.10-0.87; p=0·031) (34) Level I. Nonetheless, HPV
DNA as a single primary screening test or co-test every three to five years is an alternative
for women above 30 years old. However, in view of its high cost, it is not offered regularly.
Visual inspection with acetic acid is also an alternative method of screening. It has high
sensitivity and specificity but poor positive predictive value. Furthermore, colposcopy training
and other resources are needed before recommending this for routine use (35) Level I, (36) Level
II-2
.
Age of initiation
A cohort study in Manchester showed that the cumulative risk of developing CIN3/cervical
cancer begins at age 20 years, after which the incidence increases (37) Level II-2. In a 2005-
2009 cohort analysis in US, the incidence rate of cervical cancer among women younger
than 20 years was 0.2%, increasing up to 14% from age 20 years onwards till age 44 after
Screening tests 37
which it decreases (38) Level II-2. Despite a high prevalence of HPV infection among younger
age groups following sexual debut, very few infections persist beyond two and a half years.
Those with persistent infection have an increased risk of cervical abnormalities (39) Level II-3.
Furthermore, the prevalence rates of biopsy-proven dysplasia of any grade and cervical
cancer were highest among women younger than 30 years of age. Screening women aged
20–24 years old had no detectable impact on reducing cervical cancer rates in women
under 30 years. The risk of mortality from screening women age 22-24 years old was not
significant either (OR: 1.1, 95% CI: 0.8-1.5) (40). In addition, CIN2 and CIN3 cases peak at
25-29 years old with an incidence rate of 3.8 and 4.1 /1000 smears, respectively. Screening
women starting at the age of 25 confers benefit in reducing cervical cancer mortality and
morbidity (40).
Interval of screening
In a cohort of women followed up every year for three years in a Pap smear programme, the
prevalence of CIN2 and 3 decreased after two consecutive screenings (41) Level II-2. Among
younger age groups, there was little difference in the prevalence of dysplasia between
women who had one negative test compared to two negative tests but screening once every
three years after the last negative test was anticipated to result in an average of five extra
cases of cancer per 100,000 women (41) Level II-2. For women aged 25 and above, screening
with cytology every three years is adequate. A shorter interval of screening is associated with
increased unnecessary colposcopy (42).
Among women aged 30 to 64 years who have had three or more negative cervical cancer
results from prior screening done once in three years have an excess cancer risk of no
more than 3 in 100,000 compared to annual screening (41) Level II-2. A vast majority of cervical
cancers in older women occurred in those who were not previously screened or who did
not have three consecutive normal cytology results (17) Level III. Screening women above 65
years old who have had two previous normal smears confers minimum benefit (42). Women
aged above 65 who have not had regular cytology screening benefit from three consecutive
screens.
Harm from screening for cervical cancer may occur when cervical abnormalities are over-
interpreted, especially in women with low risk of developing invasive cancer. CIN1 has to
be managed as CIN1 and not looked at as a positive endo–cervical curettage because
most episodes of CIN1 are transient and do not usually progress to CIN3. Similarly, with the
high prevalence of HPV and cervical abnormalities among younger women, the American
Society for Colposcopy and Cervical Pathology in 2011 has made some changes to be
38 Harm of screening
more conservative with younger women with CIN (25). Approximately 55,000 cytologies are
required to detect one case of cervical cancer in women aged less than 24 years old which
does not justify close follow-up for minor cervical abnormalities.
When a young woman knows that she carries a high-risk type HPV, the effect on her
emotional health can be detrimental. The distress that comes from receiving the news may
be accompanied by feelings of shame and also impose a stigma even though subsequent
follow up is reassuring (41, 43).
Some studies have indicated a negative effect on pregnancy when treating a pre-cancerous
lesion. A meta-analysis has shown some evidence of increase in preterm delivery, perinatal
mortality and low birth weight with ablation therapy for pre-cancerous lesion. Loop excision
also carries a small risk (44).
REFERENCES
1. Watson M, Saraiya M, Benard V, et al.Burden of cervical of Cervical Cancer. Cervical Carcinoma and Sexual
cancer in the United States from 1998 -2003. Cancer Behavior: collaborative re-analysis of individual data
2008;113(10 Suppl):2855-64. on 15,461 women with cervical carcinoma and
2. Zainal Ariffin O, Zainudin MA, Nor Saleha IT. Malaysia 29,164 women without cervical carcinoma from 21
cancer statistics-data and figure Peninsular Malaysia epidemiological studies. Cancer Epidemiol Biomarkers
2006.National Cancer Registry 2006, Ministry Of Health Prev 2009;18:1060-9.
Malaysia. 8. Parazzini F, Chatenoud L, La Vecchia C, et al.Determinants
3. Bruni L, Barrioneuvo-Rosas L, Albero G, and et al. ICO of risk of invasive cervical cancer in young women. Br J
information centre on HPV and Cancer (HPV infornation Cancer 1998;77(5):838-41.
centre). Human Papillomavirus and related diseases in 9. Muñoz N, Bosch FX, de Sanjosé S, et al.Epidemiologic
Malaysia. Summary report 2015-03-02. Data accessed classification of Human Papillomavirus types associated
on 10th April 2015. with cervical cancer. N Engl J Med 2003;348:518-27.
4. Ministry of Health Malaysia. Annual Health Report 10. Smith JS, Lindsay L, Hoots B, et al.Human Papillomavirus
2011 [Internet]. Putrajaya; 2011. (cited 29 April type distribution in invasive cervical cancer and high-
2015). Available from: http://vlib.moh.gov.my/ grade cervical lesions: a meta-analysis update. Int J
cms/documentstorage/com.tms.cms.document. Cancer 2007;121:621-32.
Document_433472a1-a02c4149-1b47cc20- 11. Lacey JV Jr, Swanson CA, Brinton LA, et al. Obesity
e49f321e/2012%20(English).pdf as a potential risk factor for adenocarcinomas and
5. Cooper D, Hoffman M, Carrara H, et al. Determinants squamous cell carcinomas of the uterine cervix. Cancer
of sexual activity and its relation to cervical cancer 2003;98:814-21.
risk among South African women. BMC Public Health 12. Kjaer SK, van den Brule AJ, Paull G, et al. Type specific
2007;7:341. persistence of high risk Human Papillomavirus (HPV) as
6. Louie KS, de Sanjose S, Diaz M, et al. Early age at first indicator of high grade cervical squamous intraepithelial
sexual intercourse and early pregnancy are risk factors lesions in young women: population based prospective
for cervical cancer in developing countries .Br J Cancer follow up study. BMJ 2002;325:1-7.
2009;100(7):1191-7. 13. Brown DR, Shew ML, Qadadri B, et al. A longitudinal
7. International Collaboration of Epidemiological Studies study of genital Human Papillomavirus infection in a
References 39
REFERENCES
cohort of closely followed adolescent women. J Infect 27. Arbyn M, Bergeron C, Klinkhamer P, et al. Liquid
Dis 2005;191(2):182-92. compared with conventional cervical cytology: a
14. McIntyre-Seltman K, Castle PE, Guido R, et al. Smoking systematic review and meta-analysis. Obstet & Gynecol
is a risk factor for cervical intraepithelial neoplasia grade 2008 ;111(1):167-77.
3 among oncogenic Human Papillomavirus DNA-positive 28. Evelyn P. Whitlock, MPH; Kimberly K. Vesco, MD, MPH;
women with equivocal or mildly abnormal cytology. Michelle Eder, PhD; Jennifer S. Lin, MD, MCR; Caitlyn
Cancer Epidemiol Biomarkers Prev 2005;14(5):1165- A. Senger, MPH; and Brittany U. Burda, MPH Liquid-
70. Based Cytology and Human Papillomavirus Testing to
15. International Collaboration of Epidemiological Studies of Screen for Cervical Cancer: A Systematic Review for the
Cervical Cancer. Comparison of risk factors for invasive U.S. Preventive Services Task Force. Ann Intern Med.
squamous cell carcinoma and adenocarcinoma of 2011;155:687-97.
the cervix: collaborative reanalysis of individual data 29. Elfgren K, Kalantari M, Moberger B, et al. A population-
on 8,097 women with squamous cell carcinoma based five-year follow-up study of cervical human
and 1,374 women with adenocarcinoma from 12 papillomavirus infection. Am J Obstet Gynecol
epidemiological studies. Int J Cancer 2006;120:885- 2000;188(3):561-7.
91. 30. Datta SD, Koutsky LA, Ratelle S, et al. Human
16. Adjorlolo-Johnson G, Unger ER, Boni-Ouattara E, et al. Papillomavirus infection and cervical cytology in women
Assessing the relationship between HIV infection and screened for cervical cancer in the United States, 2003-
cervical cancer in Côte d’Ivoire: A case-control study. 2005. Ann Intern Med 2008;148:493-500.
BMC Infect Dis 2010;10:242. 31. Moyer VA, U.S. Preventive Services Task Force.
17. American College of Obstetricians and Gynecologists. Screening for cervical cancer: U.S. preventive Services
ACOG Practice Bulletin number 109, December 2009: Task Force Recommendation Statement. Ann Intern Med
Cervical cytology screening. Obstet Gynecol 2009;114: 2012;156;880-91.
1409-20. 32. Katki HA, Kinney WK, Fetterman B, et al. Cervical
18. Du J, Näsman A, Carlson JW, et al. Prevalence of cancer risk for women undergoing concurrent testing
Human Papillomavirus (HPV) types in cervical cancer for Human Papillomavirus and cervical cytology: a
2003 - 2008 in Stockholm, Sweden, before public HPV population-based study in routine clinical practice.The
vaccination. Acta Oncol 2011;50(8):1215-9. Lancet Oncology 2011;12(7):663-72.
19. Damm O, Nocon M, Roll S, et al. Human Papillomavirus 33. Noormah MD, Chandriah H, Rosliza L. HPV DNA based
(HPV) vaccination for the prevention of HPV 16/18 screening test for cervical cancer. Health Technology
induced cervical cancer and its precursors. GMS Health Assessment Report 2010. Ministry of Health Malaysia.
Technol Assess 2009; 5:4. 34. Rijkaart DC, Berkhof J, Rozendaal L, et al. Human
20. Steven E Waggoner. Cervical cancer. Lancet 2003; 361: papillomavirus testing for the detection of high-grade
2217–25 cervical intra-epithelial neoplasia and cancer: final
21. Peirson L, Fitzpatrick-Lewis D, Cliliska D, Warren R. results of the POBASCAM randomised controlled trial.
Screening for cervical cancer: A systematic review and Lancet Oncol 2012;13:78–88
meta-analysis. Systematic Reviews 2013;2:35. 35. Sauvaget C, Favette JM, Muwone R, et al. Accuracy of
22. Sankaranarayanan R, Nene BM, Shastri SS, et al. HPV visual inspection with acetic acid for cervical cancer
screening for cervical cancer in rural india. N Engl J Med screening. Intl J Gynecol & Obstet 2011;113(1):14-24.
2009;360(14):1385-93. 36. Arbyn M, Sankaranarayanan R, Muwonge R, et al.
23. Othman N, Beena CRV, Halimah Y. Cervical Cancer Pooled analysis of the accuracy of five cervical cancer
Screening; patient’s understanding in major hospitals in screening tests assessed in eleven studies in Africa and
Malaysia. Asian Pac J Cancer Prev 2009;10:569-74. India. Inlt J Cancer 2008;123(1):153-60.
24. Aljunid S, Zafar A, Saperi S, Amrizal M. Burden of 37. Peto J, Gilham C, Deacon J, et al. Cervical HPV
disease associated with cervical cancer in Malaysia and infection and neoplasia in a large population-based
potential costs and consequences of HPV vaccination. prospective study: the Manchester cohort. Br J Cancer
Asian Pac J Cancer Prev 2010;11(6):1551-9. 2004;91:942-53.
25. Massad LS, Einstein AH, Huh WK and et al. 2012 38. U.S. Department of Health and Human Services -
Updated consensus guidelines for the management of National Cancer Institute, (NCI) cancer incidence -
abnormal cervical cancer screening tests and cancer surveillance, epidemiology, and end results (SEER 18)
precursors. J Low Genit Tract Dis 2013; 17:S1-27. registries research data (adjustments for areas impacted
26. Waxman AG. Guidelines for cervical cancer screening: by Hurricanes Katrina and Rita, 2005). National Cancer
history and scientific rationale. Clin Obstet Gynecol Institute, Surveillance Systems Branch, Bethesda, USA.
2005;48(1):77–97 39. Rodriguez AC, Burk R, Herrero R, et al. The natural
40 References
history of Human Papillomavirus infection and cervical
intraepithelial neoplasia among young women in the
guanacaste cohort shortly after initiation of sexual life.
Sexually Transmitted Diseases 2007;34(7):494-502.
40. Care Canada. Screening for Cervical Cancer (2013)
[Internet]. Canadian Task Force on Preventive Health
Care. 2013 [cited 28 April 2015]. Available from: http://
canadiantaskforce.ca/ctfphc-guidelines/2013-cervical-
cancer/
41. Sawaya GF, McConnell KJ, Kulasingam SL, et al. Risk of
cervical cancer associated with extending the interval
between cervical-cancer screenings. N Engl J Med
2003;349(16):1501-9.
42. Saslow D, Solomon D, Lawson HW, et al. American
Cancer Society, American Society for Colposcopy and
Cervical Pathology, And American Society for Clinical
Pathology screening guidelines for the prevention and
early detection of cervical cancer. Ca Cancer J Clin
2012;62:147-72.
43. Rogstad KE. The psychological impact of abnormal
cytology and colposcopy. BJOG 2002;109:364–8
44. Arbyn M, Kyrigiou M, Simoens S et al. Perinatal
mortality and other severe adverse pregnancy outcomes
associated with treatment of cervical intraepithelial
neoplasia: meta-analysis. BMJ 2008;337:a1284.
References 41
06 Breast Cancer
SUMMARY
Breast cancer is the most common cancer among women in Malaysia.

Breast cancer in Malaysia starts at a relatively early age from 30-39 years old and
presents at an advanced stage.
Compared to women 50 years and above, screening women aged 40-49 years
leads to a relative reduction in mortality but requires a higher number of women to
be screened to prevent one death.
RECOMMENDATIONS
For women below 50 years of age, the decision to offer screening

depends upon the discussion on harm, benefit, risk and patient’s
preference.
For women aged 50 -74 years, screening with mammogram is Grade B
indicated every two years.
For women aged above 75 years, routine screening is not indicated.
Instructing women on self-breast examination should only be
incorporated as breast health awareness.
6.1 Introduction
Breast cancer is still the most common cancer among women even though
the rate has reduced from an age standardized ratio (ASR) of 47.4 per 100,000
population in 2003 to an ASR of 39.3 per 100,000 population in Malaysia in2005
(1, 2). Although the incidence rate in Malaysia is comparable to some of the
ASEAN countries, it has one of the highest annual mortality rates at 6% per year
over the period 1997-2008 (3). While it peaks at 50-59 years, the incidence in
Malaysia starts to rise at a lower age from 30-39 years compared to the United
States where the risk increases from 40 years onwards (2, 4).
In Malaysia, women with breast cancer tend to present late. Specifically, a

substantial number (up to 40%) of women with breast cancer in this country
present at an advanced stage, with only 14% presenting at stage 1 (3, 5). On
42 Introduction
average, women present with a 4cm lump, mostly at stage 2 of the disease (1, 5, 6,). A larger
tumour is associated with a higher staging of tumour. It was thought that the breast lumps of
women with breast cancer would be smaller if screening modalities were strengthened (7).
However, the recommendations for breast cancer screening remain controversial.
The risk of breast cancer can be stratified according to the table shown below:
Low Risk Moderate Risk High Risk

(RR 1.0 - 1.4) (RR 1.5 - 2.0) (RR > 2.0)
o Alcohol consumption o Increasing age from 40 o Personal history of invasive
o Reproductive factors: years old breast cancer
• Increasing age at first o Reproductive factors: o Lobular Carcinoma In Situ
full term pregnancy • Early menarche (< 12 (LCIS) and Ductal Carcinoma
> 30 years years old) (RR 1.02) In Situ (DCIS)
• Hormone replacement • Late menopause (> 55 o Benign breast disease with
therapy years old) (OR 2.4) atypical hyperplasia
• Oral contraceptive pills • Nulliparity o Ionising radiation from
o Obesity o Benign breast disease with treatment of breast cancer,
proliferation without atypia Hodgkin’s disease, etc
o Dense breast o Carrier of BRCA1 and 2
genetic mutation
o Significant family history, i.e.,
first degree family with
breast cancer
*RR-relative risk compared to the normal population without risk
Adapted from Clinical Practice Guideline 2010, Malaysia (8) with permission from Health Technology Assessment, Ministry of Health Malaysia.
6.2 Benefit of screening and treating breast cancer

A systematic review of trials have identified up to eight randomised controlled trials (RCT)
assessing cancer mortality with screening. In general, a 20% decrease in the relative risk
of breast cancer mortality is expected from systematic cancer screening (9). A Canadian
Task force found a reduction in breast cancer mortality with screening at a median of 11.4
years of follow-up (RR:0.81, 95%CI:0.74-0.88) (10). Another meta-analysis has also shown
a reduction in breast cancer mortality across all ages (RR:0.81, 95%CI:0.74-0.87). However,
due to variations in the quality of randomisation, a sub-analysis of the trials with high qualities
did not reveal a similar significant reduction (RR:0.90, 95%CI:0.79-1.02) (11). Similarly, a
recent RCT in Canada did not demonstrate a reduction in breast cancer mortality with
mammography screening for women aged 40-59 even after25 years of follow-up (RR: 1.05
(95% CI:0.85 to 1.30) (12).
In countries with high breast cancer awareness, it has been argued that screening adds
little benefit to cancer mortality. Women with tumours detected through mammogram have
a better survival rate compared to those detected through routine clinic care (70.6% of
Benefit of screening and treating breast cancer 43

25-year survival compared to 62.8%). This is because a mammogram can detect smaller
tumour sizes, and not because of the screening programme per se. The Canadian breast
screening study shows that the mean size of tumour found during screening was significantly
smaller (19mm) compared to the size from routine clinical care (21mm). Also, women with
tumours less than 20mm have a 25-year survival of 77% compared to 54% among those
with tumours greater than 20mm (HR:0.46, 95% CI:0.37-0.58). However, once palpable, the
25-year survival for women who have had mammography was similar to the control group
(66.3% versus 62.8%) (12). It was concluded that the benefit seen in screening was due to
a higher number of elderly women being diagnosed with tumours which were non-palpable
in the intervention group (12). In the USA, there has been a very small decrease in advanced
cancer mortality attributable to screening (13). Despite the incidence of early-stage breast
cancer in USA increasing from 112 cases in 1976 to 234 cases per 100,000 women in
2008 (a 109% increase), the incidence of late-stage cancer has decreased only by 8%,
from 102 to 94 cases per 100,000 women, while the incidence of distant metastases has
remained similar (11). The declining trend in breast cancer mortality is thought to be due
to advancements in the treatment regime, which is seen to affect all stages of the disease,
and is independent of tumour characteristics (11). There have been considerable recent
advancements in treatment. Treatments using anti-hormones and new poly chemotherapy
are noted to be effective even when the cancer has metastasized (14). Hence, for tumours
beyond 20mm, screening does not confer any benefit in terms of its detection rate (15). It
should be noted that this trend is seen among countries with a high awareness of breast
cancer.
In view of the many controversies with regards to the absolute benefit of screening, especially
with mammography, the decision for or against mammography should be individualized.
It should involve an exchange of information on risks, benefits and alternatives, and
consideration of patients’ preference, values and reservations (9). Support for the decision-
making process has been reported to increase women’s knowledge in screening risks and
benefits. Individuals with better knowledge seem to be less likely to go for unnecessary
screening (9). In a country with a high rate of late presentation and large tumour size at
diagnosis, screening may be beneficial because many would not seek treatment early
despite having clinically palpable tumours (8).
6.3 Screening tests
Over the past many years, a few modalities have been used to screen for breast cancer.
In the general population, there is no evidence to show that clinical breast examination or
breast self-examination reduces mortality from breast cancer or from any other cause (16).
Breast self-examination (BSE) appears to be ineffective in reducing breast cancer mortality
(17). A systematic review did not show any reduction in breast cancer mortality associated
with teaching regular breast self-examination to women aged 31–64 years. Instead,
44 Benefit of screening and treating breast cancer

increased harm was seen from detecting benign biopsies (RR 1.5, 95% CI 1.1–1.9) (16, 17).
BSE is recommended for raising awareness among women at risk rather than as a screening
method. In fact, increasing breast cancer awareness seems to have been an important
motivation for women. In Denmark, before the era of screening, the average tumour size
at diagnosis in 1978-79 was larger at 33 mm compared to 24 mm average at diagnosis in
1988-89. This difference is greater than the size difference found with screening which was
only 5 mm (11, 14).
Current evidence is insufficient to assess the additional benefits and harms of clinical
breast examination (CBE) (18). Studies involving CBE have shown promising outcomes to
downstage the cancer upon diagnosis but the studies have not taken into consideration the
effect of over-diagnosis from other concomitant screening tests nor the quality of the process
done (19). A review on CBE showed many poorly executed CBE performance (19). A recent
RCT has suggested that screening using mammography may have a higher detection rate
if a thorough physical breast examination is done (12). Therefore, CBE can still be used as
part of a screening method as per normal practice especially for women from countries who
present with advanced stage cancer.
Screening using MRI scans for women with average breast cancer risk has not been
evaluated compared with mammography, CBE or SBE. Thus, screening women at average
risk using MRI scans is not recommended (16, 18).
Mammography for women aged 40-49 years
The net benefit of screening this group with mammography is small compared to screening
higher risk groups. In addition to queries on the quality of the supporting evidence, a higher
risk of false-positive results has been noted. (11). The USPSTF has stated that screening with
mammography results in a 15% reduction in breast cancer mortality among women aged
39-49 years old (18). In one systematic review that excluded trials with suspected flawed
randomization, the risk of dying from breast cancer was lower with screening (RR: 0.84,
95%CI: 0.75-0.96)(9). As estimated, if 10,000 of these women had an annual screening
done for 10 years, about 190 would be diagnosed with invasive cancer and up to 16 deaths
could be prevented. At the same time, however, an estimated 6,130 women would have
more than one false positive result over 10 years of screening (9). Meta-analysis also showed
that to prevent one death from breast cancer among women in this age group, 1,904 women
would have to be screened (9).
The Canadian Task Force also agreed that mammography is associated with a reduction in
breast cancer mortality but in view of the lower risk of developing cancer in this age group,
the absolute risk benefit is much lower than for older age groups. The Task Force estimated
that 2,108 women needed to be screened with mammography every two years for a median
of 11 years to prevent one cancer death. In the same analysis, 690 women would have a
Screening tests 45
false-positive result from a mammogram, leading to 75 women having a potentially avoidable
biopsy of their breasts (16).
Thus, the net benefit of screening young women is small and the harm is high with a high
number needed to screen to prevent death. It should be noted, however, that the evidence
described is mostly derived from developed countries. The recommendation on screening
women aged less than 50 in Malaysia needs to consider the tendency for breast cancer to be
diagnosed at younger ages, the high mortality rate and the advanced stage of presentation
seen in this country compared to developed countries. At present, the Malaysian clinical
guideline does not recommend routinely screening women aged 40-49 years old with
average risk but these women should not be denied this procedure if they prefer to have it
done (8). The decision to execute screening has to consider the risks, benefit and harm from
mammography in this age group.
Mammography for women aged 50-69 years
The risk reduction for women aged 50-59 is reported to be similar to younger women (RR:
0.86, 95%CI: 0.75-0.99) but the benefit of screening is estimated to be higher (9). To prevent
one death from breast cancer, 1,339 women need to be screened (9, 18). Similarly, if 10,000
of these women underwent a screening every year for 10 years, a higher number of invasive
cancers would be detected and deaths prevented compared to screening younger women;
an estimated 302 cases and up to 32 deaths. The estimated number of false positive results
would be similar to the one estimated for younger women (6,130) (9).
A review of seven studies by the Canadian Task Force demonstrated that, screening leads
to a reduction in breast cancer mortality (RR 0.79, 95% CI 0.68-0.90) among women aged
50 to 69 years. However, the decrease in risk becomes non-significant when the meta-
analysis was restricted to properly randomized studies (RR 0.91, 95% CI 0.74–1.11) (10).
The Canadian Task Force also stated that in order to prevent one death among women 50-
69 years old, 720 women would have to be screened, 204 of which would produce false
positive results resulting in 26 unnecessary biopsies (16). Regardless, this is more efficient
than screening the younger age group.
In Denmark, after over 17 years of observations, screening for breast cancer is offered only
to 20% of women. A 10-year follow-up cohort study of screened women aged 55 to 74
years showed no reduction in mortality. In fact, a significant reduction was seen among
women who came from non-screened areas (RR: 0.98, 95%CI: 0.97-0.99). In its conclusion,
this reduction was attributed to the use of Tamoxifen as a treatment since changes were
already seen at a premature stage of the screening programme (13). Screening at more
than 24-month intervals resulted in more mortality reduction than the ones at less than 24
months intervals (RR: 0.86; 95%CI 0.75–0.98 vs RR: 0.67; 95%CI: 0.51–0.88). Furthermore,
screening every 33 months portrayed a similar trend in benefit even though the finding was
not statistically significant (RR: 0.70; 95%CI: 0.45-1.09) (16).
46 Screening tests
Mammography for women aged over 74 years
Routine screening for breast cancer is not recommended for women this age group. A
systematic review revealed that a meta-analysis of two studies on mammography screening
for women aged ≥70 years found a non-significant reduction in breast cancer mortality
(RR 0.68, 95% CI 0.45–1.01) (10). Similarly, a comparative study in Denmark showed no
significant changes between the screened and non-screened group of women age 75 to 84
years (13). These women are more likely to die due to other conditions then breast cancer
(18).
Across all ages, the cumulative risk of a false-positive result for women after 10 mammograms
ranges from about 21% to 49%. This rate is most commonly seen among younger women;
97.8 per 1,000 women aged 40-49 years, when their risk for invasive cancer is the lowest
(1.8 per screening round). In Japan, even though the rate is reported to be lower than in
Europe, younger women still have the highest rate of false positive results (20).
Over-diagnosis occurs when tumours with limited malignant potential are diagnosed and
treated, such as cancer in situ, or tumours are diagnosed in women who are at higher
risk of dying from other causes such, as old age (9, 18). A meta-analysis of studies from
six European countries revealed an over-diagnosis of 52% from mammography screening
programmes (21).
Over-diagnosis and overtreatment expose women diagnosed with breast cancer to

unnecessary psychological distress. Women with false positive biopsy results also suffer
unnecessary psychological distress and the effect is prolonged. The severity of the
psychological distress in women with a false positive biopsy result was noted to be between
that for healthy women and those with breast cancer even three years after they have been
declared free from cancer (22).
Many women (26%-77%) reported experiencing varying degrees of pain during a mammogram
and some women decline from going to the second round of screening primarily due to the
pain from a previous mammography (23).
Even though there has been no study evaluating the effect of mammography in inducing
cancer, radiotherapy from the treatment of breast cancer among women aged 70 has been
noted to increase relative mortality due to heart failure and lung cancer by 27% and 78%,
respectively (24). This is particularly important for women with cancer detected through by
screening because the cancer may be over diagnosed and over treated in almost a third of
women (11, 21, 25).
REFERENCES
1. Maznah D, Sofea R, Awang MB. Breast cancer prevention cancer in average-risk women aged 40–74 years.
and control programs in Malaysia. Asian Pacific Journal CMAJ 2011;183(17):1991-2001.
of Cancer Prevention 2011;12:1-4. 17. Kösters JP, Gøtzsche PC. Regular self-examination or
2. Malaysian Cancer Statistics - Data and figure Peninsular clinical examination for early detection of breast cancer.
Malaysia 2006 [Internet]. 1st ed. National Cancer Cochrane Database Syst Rev 2003;Issue 2.
Registry, Ministry of Health Malaysia; 2006 [cited 4 May 18. US Preventive Services Task Force. Recommendation
2015]. Available from: http://www.moh.gov.my/images/ Summary - US Preventive Services Task Force [Internet].
gallery/Report/Cancer/MalaysiaCancerStatistics2006. 2009 [cited 5 May 2015]. Available from: http://
pdf www.uspreventiveservicestaskforce.org/Page/Topic/
3. Youlden DR, Cramb SM, Yip CH, Baade PD. Incidence recommendation-summary/breast-cancer-screening
and mortality of female breast cancer in the Asia-Pacific 19. Miller AB, Baines CJ. The role of clinical breast
region. Cancer Biol Med 2014;11(2) examination and breast self-examination. Prev Med
4. Jemal A, Siegel R, Ward E, et al. Cancer Statistic 2008. 2011;53:118-20.
CA Cancer J Clin 2008;58:71-96. 20. Suzuki A, Ishida T and Ohuchi N. Controversies in
5. Yip CH, Taib NA, Ibrahim M. Epidemiology of breast breast cancer screening for women. Jpn J Clin Oncol
cancer in Malaysia. Asian Pacific J Cancer Prev 2014;44(7):613-18
2006;7:369-74 21. Jørgensen KJ, Gøtzsche PC. Over-diagnosis in publicly
6. Leong BDK, Chuah JA, Kumar VM, et al. Trends of breast organised mammography screening programmes:
cancer treatment in Sabah, Malaysia: a problem with systematic review of incidence trends. BMJ
lack of awareness. Singapore Med J 2009;50(8):772-6. 2009;339:2587
7. Taib NA, Yip CH, Ibrahim M, et al. Breast cancer in 22. Brodersen J, Siersma VD. Long-term psychosocial
Malaysia: Are our women getting the right message? A consequences of false-positive screening
10 year experience in a single institution in Malaysia. mammography. Ann Fam Med 2013;11(2):106-15.
Asian Pac J Cancer Prev 2007;8(1):141-5. 23. Armstrong K, Moye E, William S, Berlin JA and Reynolds
8. Clinical Practice Guidelines (CPG); Management of Breast EE. Screening mammography in women 40 to 49 years
Cancer [Internet]. 2nd ed. Malaysia: Ministry of Health of age: A systematic review for the American College of
(MOH), Malaysia; 2010 [cited 5 May 2015]. Available Physicians. Ann Intern Med. 2007;146:516-26
from: http://www.moh.gov.my/attachments/6915.pdf 24. Ring A, Reed M, Leonard R, et al. The treatment of early
9. Pace LE and Keating NL. A systematic assessment of breast cancer in women over the age of 70. Br J Cancer
benefits and risks to guide breast cancer screening 2011; 105, 189 -193.
decisions. JAMA 2014;311(13):1327-35 25. Kalager M, Adami HO, Bretthauer M, and Tamimi
10. Breast Cancer Screening [Internet]. 1st ed. Canada: RM. Over-diagnosis of invasive breast cancer due to
Canadian Task Force on Preventive Health Care mammography screening: results from the Norwegian
(CTFPHC); 2011 [cited 5 May 2015]. Available from: screening program. Ann Intern Med. 2012;156:491-9.
http://canadiantaskforce.ca/files/guidelines/2011-
breast-cancer-systematic-review-en.pdf
11. Gøtzsche PC, Jørgensen KJ. Screening for breast cancer
with mammography. Cochrane Database Syst Rev
2013;Issue 6.
12. Miller AB, Wall C, Baine, Ping Sun, To T, Narod SA.
Twenty five year follow-up for breast cancer incidence
and mortality of the Canadian National Breast Screening
Study: randomised screening trial. BMJ 2014;348
13. Jørgensen K. Is the tide turning against breast
screening?. Breast Cancer Research 2012;14(4):107.
14. Early Breast Cancer Trialists’ Collaborative Group
(EBCTCG). Effects of chemotherapy and hormonal
therapy for early breast cancer on recurrence and 15-
year survival: an overview of the randomised trials. The
Lancet, 2005;365(9472):1687-717.
15. Jørgensen KJ, Zahl P, Gøtzsche PC. Breast cancer
mortality in organised mammography screening in
Denmark: comparative study. BMJ 2010:340;1241
16. The Canadian Task Force on Preventive Health Care
(CTFPHC). Recommendations on screening for breast
48 References
07 Colorectal Cancer
SUMMARY
In Peninsular Malaysia, colorectal cancer (CRC) is the most common cancer in

males and the second most common, after breast cancer, in females.
CRC is a slow growing disease for approximately 10 years from adenomatous
polyps to invasive cancer, thus, providing an opportunity for screening.
A few modalities of screening tests are available with varying degrees of sensitivity
and specificity.
Faecal occult blood tests (FOBT), followed by colonoscopy, after positive test
results has been shown to reduce CRC mortality by 13-21% after 8-13 years of
screening, and 25% after adjusting for attendance to screening.
Harm associated with screening procedures including colonoscopy is small <1%
(10/1,000 procedures).
RECOMMENDATIONS
In average-risk individuals aged 50 to 75 years old, yearly screening Grade A

using gFOBT or iFOBT is indicated.
Alternative screening strategies for average risk individuals are Grade A
colonoscopy every 10 years or sigmoidoscopy every 5 yearly plus
FOBT every 3 years.
In increased-risk individuals, colonoscopy is indicated every 5 Grade A
years from age 40 years or at an age 10 years younger than the
age of first diagnosis of CRC in family.
7.1 Introduction
Colorectal cancer (CRC) is a worldwide problem with an annual incidence of

approximately one million cases and an annual mortality of more than 500,000
worldwide (1). In Malaysia, the published incidence of cancer in 2007 showed
CRC is the second most common cancer in males after trachea, bronchus and
lung cancer and the second most common in females after breast cancer (2).
In 2007, there were 2,246 cases of CRC, which represents 12.3% of all cases
registered with the National Cancer Registry. The incidence was slightly higher
Introduction 49
among males (ASR 13.4/100,000) compared to females (ASR 10.2/100,000 population).
The incidence was highest among Chinese Malaysians with ASR of 19.4/100,000 and
14.6/100,000 for male and female respectively, and lower among Malays and Indians with
ASR of 10.1/100,000 (male) and 7.5/100,000 (female), 10.2/100,000 (male) and 6.9/100,000
(female) respectively (2).
In Malaysia, the incidence of the CRC is shown to increase exponentially with age then
plateaus in the sixth decade. More than 80% of CRC occurred above 50 years of age and
peaked at the age of 60 years. Only 5%-8% of cases reported were below 40 years of age
(2, 3). The incidence peaked at a younger age group in males compared to females - 60-69
years in male (29.1%) and above 70 years in females (30.5%), respectively (4).
CRC is a slow growing disease that may present without symptoms for several years. In
most cases, up to 70-90% of CRC arise from the formation of small, non-cancerous or
adenomatous polyps (5, 6). The average time from onset of a polyp (<1cm) to onset of
carcinoma –the dwell time –is about 10-15 years (7, 8). However, the dwell time appears
to vary with the location of the cancer. It is longer in the distal colon than in the proximal
colon and it is shortest in the recto-sigmoid segment (5). Given that adenomatous polyps
are precursors to cancer and that polyps and early cancers are usually asymptomatic, there
is strong rationale to support screening asymptomatic individuals for early cancer detection
and prevention.
Three categories of risk for colorectal cancer are suggested: (9, 10)
Low Risk Average risk Increased risk
Asymptomatic individuals Asymptomatic individuals aged Asymptomatic individuals at any

aged < 50 years with ≥ 50 years age with
negative family history • with negative family • 1 first degree relative
history, diagnosed with CRC < 60
Or years
• with 1 first degree relative Or
diagnosed with CRC aged • 2 first or second degree
≥ 60 years* relatives diagnosed with CRC
Or at any age
• with non-first degree relative
with CRC
* an individual with one first degree relative diagnosed with CRC at the age of 60 has a similar risk of CRC 10 years earlier then general population (11)
The following individuals are at higher risk of CRC than general population and require
disease specific surveillance:
• Individual with suspected or genetically diagnosed familial adenomatous

polyposis (FAP) or hereditary non-polyposis colorectal cancer (HNPCC)
50 Introduction
• Patients with Inflammatory bowel disease, chronic ulcerative colitis and Crohn’s
colitis
The surveillance should be undertaken in secondary or tertiary care settings.
7.2 Benefit of screening and treating colorectal cancer
The main treatment modality for CRC is surgery with adjuvant chemotherapy or radiotherapy.
The prognosis after CRC treatment is very good. The 5-year survival rate for early-stage
cancers is greater than 90%, whereas the 5-year survival rate for those diagnosed with
widespread cancer is less than 10% (12). Screening program for CRC has been shown
to reduce the incidence of CRC and improve CRC mortality. Two large RCTs using FOBT
as the screening test showed a reduction of CRC mortality by 13-21% after 8-13 years
of screening. The benefit in mortality can be delayed as the other two RCTs did not show
mortality benefit until after 15-18 years of screening. Combined results from these four RCTs
showed a 16% reduction in CRC mortality (RR 0.84; CI: 0.78-0.90) and three of the studies
that used biennial screening interval showed a 15% reduction (RR 0.85, CI: 0.78-0.92). The
non-compliance rate, however, for those RCTs ranged from 33-46% for the first screen
and between 22-40% for at least one round of screening. After adjusting for attendance at
screening, the relative risk mortality reduction was 25% (RR 0.75, CI: 0.66 - 0.84) for those
screened (13) Level I. No study has evaluated whether screening colonoscopy alone reduces
the incidence of or mortality from CRC in people at average risk (14-17) but polypectomy
colonoscopy has been shown to reduce the incidence of CRC by 76-90% (18-20) Level II-2.
Case-control studies of sigmoidoscopy have also reported a 59-80% reduction in mortality
with a screening frequency of 5 and 10 years (21-24) Level II-2. The benefit of colorectal cancer
screening for individuals with a life expectancy less than 10 years, however, was noted to
be small (27).
Starting age for screening
The percentage of CRC among males is highest in the 60-69 years age group (29.1%)
and among females, in ≥70 years age group (30.5%) (2). Due to the estimated 10-year
timescale for the adenoma-carcinoma sequence, experts agree that screening should target
those over 50 years (25). Moreover, screening colonoscopy in people aged 40–49 years
confirms that CRC are uncommon in this age group and supports the recommendation that
screening of average-risk individuals should begin at age 50 years (26). Routine screening
in asymptomatic individuals aged above 75 years is not recommended due to small benefit
and potential increased harms.
Benefit of screening and treating colorectal cancer 51

Screening interval
Yearly screening is more effective than biennial screening and individuals who follow through
with screening will have a greater benefit. Although the sensitivity of a single gFOBT is low
(30-50%), a programme of repeated annual testing can detect as many as 92% of cancers
(27). After 18 years of follow-up, yearly FOBT resulted in a cumulative reduction of CRC
deaths by 33% compared to 21% reduction from biennial testing (28). For individuals who
have undergone polyp excision, a cohort study showed that development of advanced
neoplasia was rare up to 5 years after a negative colonoscopy (18).
In summary, average risk individuals should benefit from any of the following: (29-31)
1. FOBT annually between 50 to 75 years old

2. Colonoscopy every 10 years
3. Sigmoidoscopy every 5 years and FOBT every 3 years
Among increased risk individuals, e.g., with family history in a first degree relative, the risk of
CRC parallels the risk in persons with no family history but precedes it by about 10 years (11).
Hence, they would benefit from starting screening at younger age and at shorter intervals
of screening. Generally, it is recommended to have colonoscopy every five years from age
40 years or at an age 10 years younger than the age of first diagnosis of CRC in the family.
7.3 Screening Tests
Screening tests for CRC broadly fall into two categories. In one category are the faecal
tests, i.e., guaiac-based faecal occult blood test (gFOBT), immunochemical faecal occult
bleeding test (iFOBT), and stool DNA test (sDNA), which are primarily effective in identifying
CRC. In the second category are the partial or full structural examinations, i.e., flexible
sigmoidoscopy, colonoscopy, double-contrast barium enema (DCBE), and computed
tomography colonography (CT colonography), which are effective at detecting cancer and
premalignant adenomatous polyps. These tests differ in complexity and accuracy for the
detection of CRC and advanced neoplasia (33) (Appendix 1). Generally, the sensitivity of
the tests in the order of the least to the most sensitive test are gFOBT < iFOBT < flexible <
sigmoidoscopy < colonoscopy. The specificity for tests are also varied. In order from the
least to the most specific tests are iFOBT≈ gFOBT < flexible sigmoidoscopy ≈ colonoscopy
(32). Operator dependent tests such as flexible sigmoidoscopy, CT colonography and
colonoscopy may have variations in the validity of the test from one setting to another.
DCBE is not preferred because of poor sensitivity despite the hassle of bowel preparation.
CT colonography is also not recommended because of the variability in reporting standard
outside research settings (30). Up to now, only FOBT screening has been evaluated directly
in RCTs for the mortality benefit of CRC cancer.
52 Screening Tests
Choices of FOBT
Special consideration is needed for FOBT. Three consecutive stools testing for the presence
of occult blood is needed because identifying two positive test results has been shown to
reduce the risk of CRC mortality (28, 29, 34, 35). Rehydration of gFOBT is not recommended.
Although rehydration of the guaiac-based slides increases sensitivity, the readability of the
test is unpredictable, and rehydration substantially increases the false-positive rate (36, 37).
Newer guaiac-based and immunochemical tests are available with improved sensitivity and
acceptable specificity. Dietary restrictions during testing are recommended to reduce the
false-positive rate for the more sensitive guaiac-based tests but are not necessary for the
immunochemical and less sensitive guaiac-based tests. gFOBT requires three repeated
samples while iFOBT requires only one sample. Single sample iFOBT was shown to have
comparable specificity but better sensitivity than gFOBT (38). The participation rate for iFOBT
and detection rate was also shown to be higher than with gFOBT, (38, 39) presumably
because iFOBT is more convenient as it does not require dietary restriction and only a single
sample.
7.4 Harm of Screening
Harms from colorectal cancer screening are related to false positive results and further testing
with colonoscopy (31). Anxiety with false positive results has been documented but relief and
assurance appeared to outweigh the initial negative emotion after the diagnostic workout
(40). From a review for the US Preventive Service Task force, the estimated rate of serious
harm from colonoscopy in the general population was 2.8/1,000 procedures. The serious
outcomes included perforation, haemorrhage, diverticulitis, cardiovascular complications,
abdominal pain and death (31). The risk of similar serious complications was almost 10
times lower in flexible sigmoidoscopy at 0.34/1,000 procedures (31). The estimates of harm
from the reviews were lower than observed in several cohorts of colorectal cancer screening
programmes outside controlled trial settings. The risks of adverse events associated with
colonoscopy from screening programmes were 4.7-7.5/1,000 procedures for major events
(41, 42) Level III and 100/1,000 for minor events (41). The main major adverse events reported
include perforation or haemorrhage (41, 42). However, the majority of adverse events were
associated with therapeutic procedures during colonoscopy (41, 42). Older individuals over
65 years old had a higher risk of complications (42).
Based on a questionnaire survey among 10,078 individuals from Hong Kong, about half
had reported bodily discomfort and physical harms from the screening (43) Level III. The survey
findings were observational and based on a self-reported questionnaire from participants in
a CRC screening programme. The bodily discomfort and physical harms were not defined.
Although CT colonoscopy may overcome the challenges related to endoscopic procedure
and has an advantage over examining extracolonic anatomy, the risk of radiation has
been noted, and uncertainty in the benefit of discovering extracolonic abnormalities. The
radiation risk is small but could be significant at population level where widespread CT-based
screening is undertaken. Extracolonic abnormalities findings are common (up to 1 in every 4
procedures) with 7-16% of patients with these abnormalities requiring further evaluation (31).
In summary, there is lack of published literature on benefits and harms of colorectal cancer
screening locally. From the review of evidence from developed countries, the benefit of
colorectal cancer screening was estimated to outweigh the harm (44). Although harms were
commonly reported in the study based in Hong Kong, the degree of harm was not defined.
Appendix CRC1
Test Validity Potential advantages and disadvantages

FOBT gFOBT • Simple, non-invasive, inexpensive, high
Sensitivity: 25–50% (28, 31) acceptance
Specificity: 98–99% (37) • Not diagnostic
iFOBT
Sensitivity: 61-91% (31)
Specific: 91-98% (31)
sDNA Sensitivity: 52% (45) Level II-2 • Improved sensitivity over gFOBT, but with
no difference in specificity
Specificity 95% (45) Level II-2 • No dietary modifications are needed,
improved patient acceptance
Flexible Sensitivity ranges from 73.3% for small polyps • More expensive than gFOBT
sigmoidoscopy to 96.7% for cancer and large polyps (46) Level I • Peri-procedural discomfort.
• Serious complications, e.g., death, perforation,
major bleeding, severe abdominal symptoms,
and syncope have been reported.
Colonoscopy Specificity ranges from 92% for small polyps • Enable complete visualization of the entire
to 94% for cancer and large polyps (46) Level I colon, detection and removal of polyps and
diagnostic sampling of cancers
Relative sensitivity of colonoscopy for • Inconvenience of bowel preparation
colorectal cancer (95%) was greater than that Operator dependent result,
for barium enema (82.9%) (47) Level II-2 • Complications of procedure include
sedation, perforation,
• Availability of the services may be limited
DCBE Sensitivity is 53% for polyps 6-10 mm in size • Enables evaluation of the entire colon
and 48% for those >1 cm in size compared to • Perforation rate is lower than that of colonoscopy
colonoscopy (48) Level I • Complete bowel prep is required
• Diagnostic sensitivity is inferior to colonoscopy
• Lacks therapeutic capability
CT colonography Sensitivity was 94% for polyps of at least 10 • Higher patient acceptance
mm in diameter and 94% for polyps of at least • Better imaging of the colon
8 mm and 89% for polyps at least 6 mm in • Enable visualization of extra-colonic findings,
diameter and specificity was 96%, 92% and • Risk of radiation exposure
80% respectively (49) Level II • Availability of the services may belimited
Guaiac-based faecal occult blood test (gFOBT), immunochemical faecal occult bleeding test (iFOBT), and stool DNA test (sDNA].
Appendix CRC1 55
REFERENCES
1. World Health Organisation (WHO). Global cancer rate. 18. Winawer SJ, Zauber AG, Ho MN, et al. Prevention of
Geneva 2003. colorectal cancer by colonoscopic polypectomy. N Engl
2. Zainal Ariffin O, Nor Saleha IT. NCR Report 2007. Kuala J Med 1993;329(27):1977-81.
Lumpur: National Cancer Registry, Ministry of Health, 19. Citarda F, Tomaselli G, Capocaccia R, et al. The Italian
Malaysia, 2011 Multicentre Study group. Efficacy in standard clinical
3. Reis L, Eisner MR, Kosary CL. SEER Cancer statistic practice of colonoscopic polypectomy in reducing
review 1975-2002. National Cancer Institute, Bethesda, colorectal cancer incidence. Gut 2001;48(6):812-5.
USA 2007. 20. Thiis-Evensen E, Hoff GS, Sauar J, et al. Population-
4. MR Hassan, W Lim (eds). The first annual report of the based surveillance by colonoscopy: effect on the
National Cancer Patient Registry-Colorectal Cancer, incidence of colorectal cancer. Telemark Polyp Study I.
2007-2008. Kuala Lumpur, Malaysia 2010. Scand J Gastroenterol 1999;34(4):414-20.
5. Launoy G, Smith TC, Duffy SW, et al. Colorectal cancer 21. Selby JV, Friedman GD, Quesenberry CP, Weiss NS.
mass-screening: Estimation of faecal occult blood test A case-control study of screening sigmoidoscopy
sensitivity, taking into account cancer mean sojourn and mortality from colorectal cancer. N Engl J Med
time. Int J Cancer 1997;73(2):220-4. 1992;326(10):653-7.
6. Peipins LA, Sandler RS. Epidemiology of colorectal 22. Muller AD, Sonnenberg A. Protection by endoscopy
adenomas. Epidemiol Rev 1994;16(2):273-97. against death from colorectal cancer: A case-
7. Stryker S, Wolff B, Culp C, et al. Natural history of untreated control study among veterans. Arch Intern Med
colonic polyps. gastroenterol 1987;93(5):1009-13. 1995;155(16):1741-8.
8. Morson BC. The evolution of colorectal carcinoma. 23. Newcomb PA, Storer BE, Morimoto LM, et al. Long-term
Clinical Radiology 1984;35(6):425-31. efficacy of sigmoidoscopy in the reduction of colorectal
9. Tejpar S. Risk stratification for colorectal cancer and cancer incidence. J Natl Cancer Inst 2003;95(8):622-5.
implications for screening. Acta gastro-enterologica 24. Kavanagh AM, Fuchs CS, Giovannucci EL, Colditz
Belgica 2005;68(2):241. GA. Screening endoscopy and risk of colorectal
10. Winawer S, Fletcher R, Rex D, Bond J, Burt R, Ferrucci cancer in United States men. Cancer Causes Control
J, et al. Colorectal cancer screening and surveillance: 1998;9(4):455-62.
clinical guidelines and rationale—update based on new 25. Radzi M, Lim W, Khamizar W, et al. The first annual report
evidence. Gastroenterology 2003;124(2):544-60. of the National Cancer Patient Registry - colorectal
11. Fuchs CS, Giovannucci EL, Colditz GA, et al. A prospective cancer 2007-2008. Med J Malaysia 2009;64 (Supp B
study of family history and the risk of colorectal cancer. 61).
N Engl J Med 1994;331(25):1669-74. 26. Imperiale TF, Wagner DR, Lin CY, et al. Results of
12. O’Connell JB, Maggard MA, Ko CY. Colon cancer screening colonoscopy among persons 40 to 49 years
survival rates with the new American Joint Committee of age. N Engl J Med 2002;346(23):1781-5.
on cancer sixth edition staging. J Natl Cancer Inst 27. Lee SJ, Boscardin WJ, Stijacic-Cenzer I, Conell-Price J,
2004;96(19):1420-5. O’Brien S, Walter LC. Time lag to benefit after screening
13. Hewitson P, Glasziou P, Irwig L, et al. Screening for for breast and colorectal cancer: meta-analysis of
colorectal cancer using the faecal occult blood test, survival data from the United States, Sweden, United
Hemoccult. Cochrane Database Syst Rev 2011(2): Kingdom, and Denmark. BMJ 2013; 346:e8441.
CD001216. 28. Mandel JS, Bond JH, Church TR, et al. Reducing
14. Winawer SJ, Fletcher RH, Miller L, et al. Colorectal mortality from colorectal cancer by screening for fecal
cancer screening: Clinical guidelines and rationale. occult blood. N Engl J Med 1993;328(19):1365-71.
Gastroenterol 1997;112(2):594-642. 29. Mandel JS, Church TR, Ederer F, Bond JH. Colorectal
15. Smith RA, von Eschenbach AC, Wender R, et al. cancer mortality: Effectiveness Of biennial screening for
American Cancer Society guidelines for the early fecal occult blood. J Natl Cancer Inst 1999;91(5):434-7.
detection of cancer: Update of early detection guidelines 30. Sung JJ, Lau JY, Young GP, Sano Y, Chiu H, Byeon J,
for prostate, colorectal and endometrial cancers. CA et al. Asia Pacific consensus recommendations for
Cancer J Clin 2001;51(1):38-75. colorectal cancer screening. Gut 2008;57(8):1166-76.
16. U.S. Preventive Services Task Force. Screening for 31. Whitlock EP, Lin JS, Liles E, Beil TL, Fu R. Screening
colorectal cancer: Recommendation and rationale. Ann for colorectal cancer: a targeted, updated systematic
Inter Med 2002;137(2):129-31. review for the US Preventive Services Task Force. Ann
17. Rex DK, Johnson DA, Lieberman DA, et al. Colorectal Intern Med 2008; 149(9):638-58.
cancer prevention 2000: screening recommendations 32. Pignone M, Sox HC. Screening for colorectal cancer:
of the American College of Gastroenterology. Am J US Preventive Services Task Force recommendation
Gastroenterol 2000;95(4):868-77. statement. Ann Intern Med 2008;149(9):627-37.
56 References
33. Levin B, Lieberman DA, McFarland B, et al. Screening 46. Markowitz A, Winawer S. Screening and surveillance for
and surveillance for the early detection of colorectal colorectal cancer. Semin Oncol 1999;26:485-98.
cancer and adenomatous polyps, 2008: A joint guideline 47. Rex DK, Rahmani EY, Haseman JH, et al. Relative
from the American Cancer Society, The US Multi-Society sensitivity of colonoscopy and barium enema for
Task Force on colorectal cancer, and the American detection of colorectal cancer in clinical practice.
College Of Radiology. Gastroenterol 2008;134(5):1570- Gastroenterol 1997;112(1):17-23.
95. 48. Winawer SJ, Stewart ET, Zauber AG, et al. A comparison
34. Hardcastle JD, Chamberlain JO, Robinson MHE, of colonoscopy and double-contrast barium enema
et al. Randomised controlled trial of faecal-occult- for surveillance after polypectomy. N Engl J Med
blood screening for colorectal cancer. Lancet 2000;342(24): 1766-72.
1996;348(9040):1472-7. 49. Pickhardt PJ, Choi JR, Hwang I, et al. Computed
35. Kronborg O, Fenger C, Olsen J, et al. Randomised study tomographic virtual colonoscopy to screen for colorectal
of screening for colorectal cancer with faecal-occult- neoplasia in asymptomatic adults. N Engl J Med
blood test. Lancet 1996;348(9040):1467-71. 2003;349(23):2191-200.
36. Young GP, St John JB, Winawer SJ, Rozen P. Choice
of fecal occult blood tests for colorectal cancer
screening: Recommendations based on performance
characteristics in population studies. Am J Gastroenterol
2002;97(10):2499-507.
37. Allison JE, Tekawa IS, Ransom LJ, Adrain AL. A
comparison of fecal occult blood tests for colorectal-
cancer screening. N Engl J Med 1996;334(3):155-60.
38. Van Rossum LG, van Rijn AF, Laheij RJ, et al: Random
comparison of guaiac and immunochemical faecal
occult blood tests for colorectal cancer in a screening
population. Gastroenterology 2008;135:82-90.
39. Hol L, van Leerdam ME, van Ballegooijen M, et al:
Screening for colorectal cancer: randomised trial
comparing guaiac-based and immunochemical faecal
occult blood testing and flexible sigmoidoscopy. Gut
2010;59:62-8.
40. McGovern PM, Gross CR, Krueger RA, Engelhard
DA, Cordes JE, Church TR. False-positive cancer
screens and health-related quality of life. Cancer Nurs.
2004;27(5):347-52.
41. Denis B, Gendre I, Sauleau EA, Lacroute J, Perrin P.
Harms of colonoscopy in a colorectal cancer screening
programme with faecal occult blood test: a population-
based cohort study. Dig Liver Dis 2013;45(6):474-80.
42. Rutter CM, Johnson E, Miglioretti DL, Mandelson MT,
Inadomi J, Buist DS. Adverse events after screening
and follow-up colonoscopy. Cancer Causes Control.
2012;23(2):289-96.
43. Wong M, Ching J, Hirai H, Lam T, Griffiths S, Chan F et
al. Perceived obstacles of colorectal cancer screening
and their associated factors among 10,078 Chinese
participants. PLoS ONE 2013;8(7):e70209.
44. Richardson AK, Potter JD. Screening for colorectal
cancer and prostate cancer: challenges for New
Zealand. N Z Med J 2014;127(1395):23-30.
45. Imperiale TF, Ransohoff DF, Itzkowitz SH, et al. Fecal
DNA versus fecal occult blood for colorectal-cancer
screening in an average-risk population. N Engl J Med
2004;351(26):2704-14.
References 57
08 Prostate Cancer
SUMMARY
Prostate cancer is common in aging men.

Screen-detected cancer often has an indolent clinical course.
There is conflicting evidence on whether prostate cancer screening using PSA
Level for the general population reduces mortality effectively.
A large number of men need to be screened and treated to prevent one death from
prostate cancer.
The sensitivity and specificity of PSA test vary with different cut-off values. A cut-
off value of 4ng/ml has a high false positive rate.
Prostate cancer screening is associated with a high number of false positive and
significant complications from prostate biopsy and treatment of screen detected
prostate cancer.
RECOMMENDATIONS
Screening prostate cancer with PSA test is not indicated for the Grade D
general population.
8.1 Introduction
Prostate cancer is the second most common cancer among men worldwide with
an age-standardized rate (ASR) of 28.5 cases per 100,000 persons in 2008 (1).
In the United States of America (US), it is the most commonly diagnosed cancer
with ASR of 66.2 per 100,000 persons per year, and the second leading cause
of cancer death among American men (1, 2). In Malaysia, from the National
Cancer Registry 2007, prostate cancer was the fourth most common cancer
among men at 6.2% with men of Chinese ethnicity having the highest rate at
8.7 per 100,000 men followed by Indian (5.8) and Malay (4.8) (3). Comparatively,
the incidence among men in the United States (US) or European countries is
higher than in Asia. However, deaths from prostate cancer among the latter
group are projected to increase compared to declining mortality rate in the US
(2, 4). The increasing incidence and declining mortality rate among Americans
and Europeans can be attributed to the higher screening pattern or improved
58 Introduction
treatment options (4, 5).
The prevalence of undiagnosed prostate cancer at autopsy is estimated to be as high as

70% at the age of 70 – 79 years old (5). The estimated lifetime risk of prostate cancer is
15.9%, but the lifetime risk of dying from prostate cancer is only 2.8% (6). Only a small
proportion of men with prostate cancer presents with symptoms and dies from the disease.
Most cases of prostate cancer progress slowly and are not life-threatening (5). In Sweden,
where a high number of men undertake screening, most of the tumours diagnosed are
localised with intermediate risk and an indolent clinical course (7).

The risk factors for prostate cancer include:
• Increasing age (8) Level II-3, (9) Level III, (10) Level II-3
• Ethnicity - In Malaysia, Chinese men have the highest risk of developing prostate
cancer followed by Indians and Malays (2, 10) Level II-3
• Positive family history of prostate cancer (OR: 2.5, 1.1-2.9)(8, 12) Level II-2; higher
risk with a positive family history involving first degree relative, brother or more than
two family members (13) Level I
• Current smokers, especially heavy smoker (14) Level I
In Malaysia, according to the 2007 National Cancer Registry, most of the prostate cancers in
Malaysia were diagnosed at stage 3 or higher (15) The economic burden of prostate cancer
treatment is high (4, 16) and even higher with advanced disease. Although late diagnosis
and the high cost of treatment in late disease, determining the net benefit of screening for
prostate cancer in developing Asian countries is challenging (5) because benefit of early
detection from prostate cancer screening is controversial.
8.2 The benefit of screening and treating prostate cancer
There is conflicting evidence on whether PSA, used as a prostate cancer screening modality
for the general population, can reduce mortality effectively. Screening for prostate cancer
detects more localised disease (17) Level I. In a report from the Prostate, Lung, Colorectal and
Ovarian (PLCO) Cancer Screening Trial, among patients aged 55 to 74 years, the incidence
of death from prostate cancer was low and did not differ between the group assigned to
prostate specific antigen (PSA) and digital rectal examination (DRE) screening (2.0/10,000
person-years), and the control group (1.7/10,000 person-years) (18) Level I. In another
randomised controlled trial with 20 years of follow-up in Sweden, among men aged 50-69
years, it was noted that there was no difference in the prostate cancer mortality rate between
men assigned to screening with PSA and DRE (81%) and those not assigned to screening
(86%) (19) Level I. On the contrary, the European Randomised Study of Screening and Prostate
Cancer (ERSPC) mortality conducted among men aged 50-74 years old showed that, after
The benefit of screening and treating prostate cancer 59

11 years of follow-up, the death rate from prostate cancer was reduced by 21% with PSA
based screening (relative risk ratio 0.79, 95% CI: 0.68-0.91). However, in order to prevent
one death from prostate cancer, 1,055 men needed to be screened and an additional 37
men needed to be treated. (20) A meta-analysis of 5 randomised controlled trials on the use
of PSA as a screening for prostate cancer after more than 10 years initiating screening did
not show convincing evidence of benefit in using PSA as an effective screening tool (21) Level I.
Given the various disease progressions of screened detected prostate cancer, the
management of early prostate cancer is debatable. Management options include watchful
waiting, active surveillance, surgery and radiation. No consensus has been made so far on
the optimal management (6).
8.3 Screening tests
Prostate Specific Antigen (PSA)
PSA test has high sensitivity but poor specificity and positive predictive value in diagnosing
prostate cancer. The sensitivity and specificity vary with different cut off values. One study
reported sensitivity of 73.9% and specificity of 51.9% for prostate cancer prediction when
using a value less than 4ng/mL but lower sensitivity and higher specificity with a higher cut
off value (22) Level III. Another study found that prostate cancer among men with PSA Level
less than 0.5 and up to 4ng/mL was not unusual (6.6% with PSA at 0.5ng/mL to 26.9% with
PSA 4ng/mL) (23) Level I. In other words, no Level of PSA can exclude prostate cancer (5). In
the Prostate Cancer Prevention Trial (PCPT), PSA values at 1.1, 2.1, 3.1, 4.1 ng/mL yielded
sensitivities of 83.4%, 52.6%, 32.2%, and 20.5%, and specificities of 38.9%, 72.5%, 86.7%,
and 93.8%, respectively, in detecting prostate cancer (24) Level I. There is no specific cut-off
point of PSA for monitoring healthy men for their risk of prostate cancer and for suggesting
biopsy. It is more of a continuum of risks at all values (24) Level I. Prediction of cancer by PSA
is slightly better in men less than 70 years old compared to older men (Area Under the ROC
0.669±0.013, compare to 0.663±0.13, p=0.03) (24) Level III. Overall, the predictive value of
PSA is not optimal.
Digital Rectal Examination (DRE)
DRE has lower sensitivity than PSA in detecting prostate cancer. The sensitivity and specificity
of DRE was 37% and 91%, respectively. The sensitivity was lower when the PSA is less than
3ng/mL but increased with higher PSA Levels. The positive predictive value of DRE when
used in men with PSA less than 3ng/mL ranged from 4-11% but increased to 33-83% when
the PSA exceeds 3ng/mL (25) Level I. Abnormal DRE findings may be useful in a selected
population with abnormal PSA to avoid unnecessary biopsies and over-diagnosis.
• The positive predictive value of an abnormal DRE (48.6%) done as an adjunct to
PSA test for prostate cancer is higher in than when the DRE is normal (22.4%) (26)
Level I
.
• High percentages of abnormal DRE (71.0%-85.7%) done as an adjunct to PSA test
detects prostate cancer with poorer staging; Gleason score >7 (26) Level I
• The detection rate of prostate cancer using DRE alone was 2.5%. It helped to
detect 17% of the prostate cases that may not be detected when screened with
PSA alone (25) Level I.
In summary, the predictive value of PSA and DRE, either alone or in combination, may
predict prostate cancer to a certain degree, but prediction is improved at higher PSA Levels.
Despite the ability of prostate biopsy to confirm the diagnosis of prostate cancer, it is difficult
to differentiate between indolent and aggressive cancer (6).
False positive results are common and vary with different Levels of PSA. One study estimated
false positive rates of 11.3% and 19.8% for a threshold of 4.0 and 3.0 ng/mL, respectively
(5). In addition, men with false positive results were noted to suffer from persistent worry (6).
About one third of men who went through prostate biopsy experienced pain, fever, bleeding,
infection and transient urinary difficulty, while serious complications requiring hospitalization
were estimated to occur in 1% (27) to 2.1% (28) of cases. Death from biopsy was estimated
to be 0.2% (28).
Over-diagnosis of cancer, which is clinically insignificant in most cases, was estimated to

be up to 50% in the group of men from the Rotterdam section of the ERSPC trial invited
for PSA test (16) Level I. Despite the fact that most screen-detected cancers would remain
asymptomatic, most patients and treating doctors will choose active treatment strategies
which have a high rate of complications, such as urinary incontinence and erectile dysfunction
(up to 40%). The death rate associated with treatment was noted to be as high as 0.5% (6).
With non-demonstrable benefit of screening, and high proportions of harm from screening
and early treatment of screen-detected prostate cancer, it is concluded that the harms
outweigh the benefit of prostate cancer screening (5, 6).
REFERENCES
1. Ferlay J, Shin HR, Bray F, et al. Estimates of worldwide screening for prostate cancer. J Natl Cancer Inst
burden of cancer in 2008: GLOBOCAN 2008. Int J 2003;95:868-78.
Cancer 2010;127: 2893-917. 18. Andriole GL, Crawford ED, Grubb III RL, et al. Mortality
2. Jemal A, Siegel R, Ward E, Murray T. Cancer statistics, results from a randomised prostate-cancer screening
2007. CA Cancer J Clin 2007;57:43-66. trial. N Engl J Med 2009;360: 1310-9.
3. Zainal Afriffin, I.T Nor Saleha. National Cancer Registry 19. Sandblom G, Varenhorst E, Rosell J, et al. Randomised
Report 2007. Ministry of Health Malaysia 2011. prostate cancer screening trial: 20 year follow up. BMJ
4. Namiki M, Akaza H, Lee SE, et al. The prostate 2011;342:d1539.
cancer working group report. Jap J Clin Oncol 2010; 20. Schroder FH, Hugosson J, Roobol MJ et al. Prostate-
40(1):i70-i75. cancer mortality at 11 years of follow-up.N Engl J Med
5. Bell N, Gorber S, Shane A, Joffres M, Singh H, Dickinson 2012; 366: 981–90
J, Shaw E, Dunfield L and Tonelli M. Recommendations 21. Ilic D, Neuberger MM, Djulbegovic M, Dahm P. Screening
on screening for prostate cancer with the prostate- for prostate cancer. Cochrane Database of Syst Rev
specific antigen test. CMAJ 2014; 186(16): 1225-34. 2013: 1.
6. Moyer V. (2012). Screening for prostate cancer: U.S. 22. de Abreu DS. Bio-impedence and chronoamperometry
Preventive Services Task Force Recommendation as an adjunct to prostate specific antigen screening for
Statement. Ann Intern Med 2012; 157(2):120. prostate cancer. Cancer Manag Res 2011;3:109-16.
7. Bratt O, Berglund A, Adolfsson J, et al. Prostate cancer 23. Thompson IM, Pauler DK, Goodman PJ, et al.
diagnosed after prostate specific antigen testing of men Prevalence of prostate cancer among men with a
without clinical signs of the disease: A population based prostate specific antigen Level ≤4.0ng/Ml. N Engl J Med
study from the National Prostate Cancer Register of 2004;350(22):2239-46.
Sweden. Scand J Urol Nephrol 2010;44:384-90. 24. Thompson IM, Ankerst DP, Chen Chi, et al. Operating
8. Mazdak H, Mazdak M, Jamali L, Keshteli AH. characteristics of prostate specific antigen in men
Determination of prostate cancer risk factors in Isfahan, with an initial PSA Level of 3.0 ng/mL or lower. JAMA
Iran: a case - control study. Med Arh 2012;66(1):45-8. 2005;291(1):66-71.
9. American Cancer Society. Cancer facts and figures 25. Schroder FH, Hugosson J, Roobol MJ, et al. Screening
2012. Atlanta 2012. and prostate-cancer mortality in a Randomised
10. Lim GCC, Rampal S, Halimah Y. Cancer incidence in European Study. N Engl J Med 2009:360;1320-8.
Peninsular Malaysia, 2003 - 2005. National Cancer 26. Gosselaar C, Roobol MJ, Roemeling S, Schroder FH.
Registry. Kuala Lumpur 2008. The role of the digital rectal examination in subsequent
11. Yanke BV, Carver BS, Bianco FJ Jr, et al. African- screening visits in the european randomized study of
American race is a predictor of prostate cancer screening for prostate cancer (ERSPC). Eur Urology
detection: incorporation into a pre-biopsy nomogram. 2008;54:581-8.
BJU Int 2006 Oct;98(4):783-7. 27. Rosario DJ, Lane JA, Metcalfe C, Donovan JL, Doble
12. Mohd Nizam S, Shamsul AS, Zulkifli MZ. Risk factors A, Goodwin L, et al. Short term outcomes of prostate
for prostate cancer in Universiti Kebangsaan Malaysia biopsy in men tested for cancer by prostate specific
Medical Centre: a case-control study. Asian Pacific J antigen: prospective evaluation within ProtecT study.
Cancer Prev 2009;10:1015-20. BMJ 2012;344:d7894.
13. Kiciński M, Vangronsveld J, Nawrot TS. An 28. Screening for prostate cancer with prostate specific
epidemiological reappraisal of the familial aggregation antigen and treatment of early-stage or screen-detected
of prostate cancer: a meta-analysis. PLoS One prostate cancer: a systematic review of the clinical
2011;6(10):e27130. benefits and harms [Internet]. 1st ed. Canada: Canadian
14. Huncharek M, Haddoc KS, Reid R, Kupelnick B. Smoking Task Force on Preventive Health Care (CTFPHC);
as a risk factor for prostate cancer: a meta-analysis 2014 [cited 18 May 2015]. Available from: http://
of 24 prospective cohort studies. Am J Public Health canadiantaskforce.ca/files/guidelines/2014-prostate-
2010;100693-701. cancer-systematic-review-en.pdf
15. Zainal Ariffin O, Nor Saleha IT. NCR Report 2007. Kuala
Lumpur: National Cancer Registry, Ministry of Health,
Malaysia, 2011
16. Stokes ME,Ishak J, Proskorovsky I, et al. Lifetime
economy burden of prostate cancer. BMC Health
Services Research 2011;11:349.
17. Draisma G, Boer R, Otto SJ, et al. Lead time and over
detection due to prostate specific antigen screening;
estimates from the European Randomised Study of
62 References
09 Tobacco
SUMMARY
Tobacco usage (including smoking) is prevalent in Malaysia.

Smoking cessation and abstinence result in substantial morbidity and mortality
benefit.
Recording smoking status as part of vital sign assessment in the clinic improves
the intervention and abstinence rate.
The 5A strategy (Ask, Advise, Assess, Assist, and Arrange) is an effective
intervention to improve the rate of smoking abstinence.
RECOMMENDATIONS
Screening for tobacco abuse by recording smoking status as part Grade A

of vital sign assessment in the clinic is indicated annually.
9.1 Introduction
The Global Adult Tobacco Survey (GATS) 2011 reported a 22% prevalence of
current smokers in Malaysia (1). The World Health Organisation has identified
tobacco, alcohol and illicit drugs among the top 20 risk factors for ill-health which
are responsible for 8.8% of all deaths (2). It is estimated that 10,000 deaths due
to smoking-related illnesses are reported in Malaysia every year, making it the
primary cause of death in this country since the 1980s. Furthermore, if the trend
continues, there will be 30,000 deaths due to smoking-related diseases by the
year 2020 (3).
9.2 Benefit of screening and treating tobacco

addiction
Screening for tobacco smoking has been shown to increase rates of clinician
intervention resulting in significant reductions in morbidity and mortality (4 -7) Level
I
. Recording smoking status as part of vital signs in medical records significantly
Introduction 63
results in a higher rate of brief intervention by primary care doctors. In one study on the effect
of screening for smoking, 61.9% of smokers reported receiving any counselling on smoking
cessation in intervention practices, compared with 53.4% of smokers at control practices,
i.e., a difference of 8.5% (P = .04) (8) Level I. In another study, the effect of recording smoking
status routinely resulted in a higher rate of physician interventions for smoking cessation (OR
2.6; 95% CI 1.3-5.2) (9) Level I.
Counselling by paramedics has also proven to reduce rates of tobacco abstinence (RR 1.29;
95% CI 1.20 to 1.39) (10). Routine physician screening and counselling may increase quit
rates at 6-12 months from 3% (usual care) to 8-11% (11) Level I.
9.3 Screening tests
The 5A strategy (Ask, Advise, Assess, Assist, and Arrange) as a screening tool has been
shown to improve the rate of smoking abstinence (12) Level I.
The 5A strategies are:
• ASK - all patients about smoking

• ADVISE - brief, non-judgmental advice about smoking cessation
• ASSESS - readiness to stop smoking
• ASSIST - offer intervention to help smoking cessation (counselling, nicotine
replacement treatment)
• ARRANGE –follow-ups and referrals as appropriate.
Therefore, routine recoding of smoking status should be part of the vital sign assessment in
primary care.
The published literature on harm of tobacco screening is scarce (13). Harm from the screening
test and brief intervention, e.g., 5A strategy, was shown to be minimal (8). Harm from
treatment for tobacco dependence is mainly from the side-effects of nicotine replacement
therapy and nicotine receptor partial agonist, which are temporary during treatment.
Screening for tobacco addiction may strain the resources for counselling services. However,
these constraints are small compared to the benefit of tobacco smoking cessation.
REFERENCES
1. Tee, GH. Epidemiology of tobacco consumption: The

Malaysian Perspective. 2012; Malaysia.
2. World Health Organization International (WHO) | The
World Health Report 2002 -Reducing risks, promoting
healthy life [Internet]. 2002 [cited 22 April 2015].
Available from: http://www.who.int/whr/2002/en/
3. Disease Control Division, Ministry of Health Malaysia
2003, Clinical practice guidelines on treatment of
tobacco use and dependence 2003.
4. Fiore MC, Jorenby DE, Schensky AE, et al. Smoking
status as the new vital sign: effect on assessment and
intervention in patients who smoke. Mayo Clin Proc
1995; 70(3): 209-13.
5. Katz DA, Muehlenbruch DR, Brown RL, et al.
Effectiveness of implementing the agency for healthcare
research and quality smoking cessation clinical practice
guideline: a randomized control trial. J Natl Cancer Inst
2004; 96(8): 594-603.
6. Ahluwalia JS, Gibson CA, Kenney RE, et al. Smoking
status as a vital sign. J Gen Intern Med 1999; 14
(7):402-8.
7. Critchley J, Capewell S. Smoking cessation for the
secondary prevention of coronary heart disease.
Cochrane Database Syst Rev 2004; (1): CD003041.
8. Rothemich SF, Woolf SH, Johnson RE, Burgett AE, Flores
SK, Marsland DW, Ahluwalia JS. Effect on cessation
counseling of documenting smoking status as a routine
vital sign: an ACORN study. Ann Fam Med 2008; 6(1):
60-8
9. Seale JP. Shellenberger S. Velasquez MM. Boltri JM.
Okosun I. Guyinn M. Vinson D. Cornelius M. Johnson JA.
Impact of vital signs screening & clinician prompting on
alcohol and tobacco screening and intervention rates: a
pre-post intervention comparison. BMC Family Practice
2010. 11:18
10. Rice VH, Hartmann-Boyce J, Stead LF. Nursing
interventions for smoking cessation. Cochrane Database
Syst Rev 2013, Issue 8.
11. Bernstein S. Preventive Care in the Emergency
Department: Diagnosis and management of smoking and
smoking-related illness in the emergency department: a
systematic review. Acad Emerg Med 2002;9(7):720-9.
12. Bentz CJ, Bayley KB, Bonin KE, et al. Provider feedback
to improve 5a’s tobacco cessation in primary care: a
cluster randomized control trial. Nicotine Tob Res 2007;
9(3):341-9.
13. Uspreventiveservicestaskforce.org. Home - US
Preventive Services Task Force [Internet]. 2009
[cited 23 April 2015]. Available from: http://www.
uspreventiveservicestaskforce.org/
References 65
10 Alcohol
SUMMARY
Although the prevalence of alcohol drinking is increasing, the majority are low risk
drinkers.
There is evidence of benefit in screening and brief intervention for communities in
which the majority of drinkers are mild to moderate consumers.
RECOMMENDATIONS
Screening for alcohol consumption should be done among those at Grade B

risk groups using AUDIT-C.
10.1 Introduction
Alcohol consumption in Malaysia has shown a small increase over time. The
National Health Morbidity Survey (NHMS) reported increasing prevalence of
ever-consumed and current drinkers among those aged 13 years and above in
the past five years (ever-drinker: 16.1% in 2006 versus 17.8% in 2011, current
drinker: 11.1% in 2006 versus 11.6% in 2011) (1, 2). It was estimated that 76.3
million people worldwide (2004 data) suffer from alcohol use disorders (3). In
comparison to global data, Malaysia showed a higher prevalence of low-risk
drinkers (49.2%). On the other hand, the other drinkers’ profiles, notably, ex-
drinker (35.6%), risky (14%) and high-risk drinkers (1.2%) were lower than the
global prevalence (2).
At-risk groups of problematic alcohol consumption among patients attending

primary care clinics are (4, 5) Level III:
• middle-aged males
• adolescents
• certain occupational groups, such as, business executives, entertainers,
sex workers, workers in pubs, and seamen.
In Malaysia, a higher prevalence of current drinkers was reported in Kuala

Lumpur followed by Sarawak and Sabah, in urban areas, among males, and
those in 20-24 years age group. By ethnicity, the highest prevalence of current
66 Introduction
drinkers was among Chinese followed by other Bumiputera and Indians (2).
10.2 Benefit of screening and treating alcohol use
For people with a mild to moderate alcohol drinking pattern, brief intervention has proven to
be effective at primary care settings (6 -8) Level I A Cochrane review on brief interventions in
primary care found a significant reduction in men’s alcohol consumption (mean difference -57
grams/week, 95% CI: -89 to -25, I2 = 56%), but not women’s. (Mean difference: -10 grams/
week, 95% CI: -48 to 29, I2 = 45%) (7). The brief interventions included in the review were
carried out either by a general physician, a nurse or a psychologist. Training is needed to do
brief interventions for alcohol use (7). In Malaysia, training for brief intervention is available
and can be implemented by doctors and paramedics. However, there is insufficient evidence
to support alcohol screening and brief intervention for primary-care patients with very heavy
drinking or alcohol dependence, especially if this pattern of drinking is prevalent (9) Level I.
They require referral to a specialised unit for management.
10.3 Screening tests
There are several tools to screen for alcohol abuse, such as CAGE, AUDIT and the Brief
Michigan Alcohol Screening Test. These tests have almost similar sensitivity (75% -84%)
and specificity (87%-90%) (10). The AUDIT was developed by the World Health Organization
(WHO). It is a simple method of screening for excessive drinking and to assist in brief
assessment. It also comes in a simplified form, AUDIT-C (3 item questionnaire), that mainly
asks about consumption and it has almost similar validity to AUDIT (10 item questionnaire)
(11). The AUDIT questionnaire, developed together with an intervention programme, has
shown to be effective in reducing alcohol problem drinking (12 -16).
A score of ≥ 4 for males and ≥ 3 for females from the total scores is considered positive for
hazardous drinkers (17, 18) - refer to appendix for AUDIC-C screening questionnaire.
Although the evidence of harm from screening is scarce (19), alcohol use may be associated
with stigma in certain cultures. Hence, labelling of alcohol misuse may cause anxiety and
have a negative social impact. However, the benefit of treatment outweighs the harm.
Appendix Alcohol 1
AUDIT-C Questionnaire
Patient Name: Date of Visit:
1. How often do you have a drink containing alcohol?

(Score)
a. Never 0
b. Monthly or less
1
c. 2-4 times a month 2
d. 2-3 times a week 3 3
e. 4 or more times a week 4
2. How many standard drinks containing alcohol do you have on a typical day?
(Score)
a. 1 or 2 0
b. 3 or 4 1
c. 5 or 6 2
d. 7 to 9 3
e. 10 or more 4
3. How often do you have six or more drinks on one occasion?

(Score)
a. Never 0
b. Less than monthly 1
c. Monthly 2
d. Weekly 3
e. Daily or almost daily 4
Total score (sum score of all responses):
68 Appendiox Alcohol 1
REFERENCES
1. Ministry of Health Malaysia. The National Health 17. Bush K, Kivlahan DR, McDonell MB, et al. The AUDIT
Morbidity Survey III Report. Malaysia; 2006. alcohol consumption questions (AUDIT-C): An effective
2. Ministry of Health Malaysia. The National Health brief screening test for problem drinking. Arch Internal
Morbidity Survey 2011. Malaysia; 2011. Med 1998; (3): 1789-95.
3. World Health Organization. Global Status Report On 18. Bradley KA, Bush KR, Epler AJ, et al. Two brief
Alcohol And Health. 2004. alcohol-screening tests from the Alcohol Use Disorder
4. Murray RM. Screening and early detection instruments Identification Test (AUDIT): Validation in a female
for disabilities related to alcohol consumption. Alcohol- veterans’ affairs patient population. Arch Internal Med
Related Disabilities. Geneva, World Health Organization 2003; Vol 163: 821-9.
1977; 2: 89-105. 19. Moyer V. Primary care interventions to prevent tobacco
5. World Health Organization. Problems related to alcohol use in children and adolescents: U.S. Preventive
consumption, Report of a WHO Expert Committee. Tech Services Task Force Recommendation Statement.
Report Series 650, Geneva, World Health Organization Pediatrics. 2013; 132(3):560-5.
1980.
6. Kypri K, Langley JD, Saunders JB, et al. Randomized
controlled trial of web-based alcohol screening and brief
intervention in primary care. Arch Intern Med 2008;
168(5): 530-6.
7. Kaner EF, Dickinson HO, Beyer F, et al. The Effectiveness
of brief alcohol interventions in primary care settings: a
systematic review. Drug Alcohol Rev 2009; 28(3): 301-
23.
8. Riper H, van Straten A, Keuken M, et al. Curbing problem
drinking with personalized-feedback interventions a
meta-analysis. Am J Prev Med 2009; 36(3): 247-55.
9. Saitz R. Alcohol screening and brief intervention in
primary care: absence of evidence for efficacy in people
with dependence or very heavy drinking. Drug Alcohol
Rev 2010; 29(6): 631-40.
10. Soderstrom CA, Smith GS, Kufera JA, et al. The accuracy
of the CAGE, the brief Michigan alcoholism screening
test and alcohol use disorder identification test in
screening trauma centre patients for alcoholism. J
Trauma 1997; 43(6): 962-9.
11. Bradley KA, DeBenedetti AF, Volk RJ, et al. AUDIT-C As a
brief screen for alcohol misuse in primary care. Alcohol
Clin Exp Res 2007; 31(7): 1208-17.
12. Kelly TM, Donovan JE, Chung T, et al. Alcohol use
disorders among emergency department-treated older
adolescents: a new brief screen using AUDIT, CAGE,
CRAFT And RAPS-QF. Alcohol Clin Exp Res 2004; 28(5):
746-53.
13. Bien TH, Miller WR, Tonigan S. Brief intervention for
alcohol problems: a review. Addiction 1993; 88: 315-
36.
14. Kahan M, Wilson L. Becker L. Effectiveness of physician-
based interventions with problem drinkers: A review.
Canadian Med Assoc J 1995; 152(6):851-9.
15. Wilk AI, Jensen NM, Havighurst TC. Meta-analysis of
randomized control trials addressing brief interventions
in heavy alcohol drinkers. J General Internal Me 1997;
12:274-87.
16. Lee JD, Delbanco B, Wu E, Gourevitch MN. Substance
use prevalence and screening instrument comparisons
in urban primary care. Subst Abus 2011; 32(3): 128-34.
References 69
11 Illicit Drugs
SUMMARY
Malaysia has a low prevalence of illicit drug use. With strict drug laws, screening
for illicit drugs may have legal implications.
There is insufficient evidence to support screening for illicit drug use in adults in
primary care.
RECOMMENDATIONS
Routine screening for illicit drug use is not indicated. Grade I
11.1 Introduction
The 2010 National Anti-Drug Agency Report (1) reported a prevalence of 0.08%
of illicit drug users in Malaysia. The screening of adolescents in the National
Service (PLKN) found that the prevalence of illicit substance use was 1.3% (2).
Illicit drugs were responsible for 0.4% of deaths. Although illicit drug use can
lead to serious health problems, the prevalence is low in general population.
Consequently, screening will have a low detection rate.
11.2 Benefit of screening and treating illicit drug

use
The United States Agency for Healthcare Research and Quality states that
screening for drug misuse is not useful in populations with a low prevalence of
drug use/ misuse (3) Level II-3 (counselling for drug misuse).
Although important, screening for illicit drug use among general population
adults in a country that has strict drug laws may have potential legal implications.
70 Introduction
REFERENCES
1. National Anti-Drug Agency (AADK). The national anti-

drug agency drug report. Malaysia; 2010.
2. Norizzati BIB, Noor Ani A, Noraida MK, et al. Mental
health problem among youth in Malaysia. Abstract Book
National Public Health Conference 2011.
3. Lanier D, Ko S. Screening in primary care settings for
illicit drug use: Assessment of screening instruments - a
supplemental evidence update for the U.S. Preventive
Services Task Force. Evidence Synthesis No. 58, Part
2. AHRQ Publication No. 08-05108-EF-2. Rockville,
Maryland: Agency for Healthcare Research and Quality.
2008.
References 71
12 Human Immunodeficiency Virus
Infection
SUMMARY
In Malaysia, HIV is concentrated among intravenous drug users, commercial sex

workers, men who have sex with men (MSM), and transgender persons.
Early detection and treatment have individual and public health benefits.
Sequential rapid testing and serum antibody testing strategies are highly accurate.
RECOMMENDATIONS
HIV screening is indicated for individuals with high risk of infection. Grade B
12.1 Introduction
The overall growth of the global AIDS epidemic appears to have stabilized,
with declining incidence each year. In 2009, 2.6 million people were infected,
nearly 19% lower than the number in 1999. The success of therapy has reduced
annual AIDS-related deaths, from a peak of 2.1 million in 2004 to 1.9 million in
2009. However, the number of new infections is still substantial. This has led to
the increasing total number of people living with HIV worldwide; reaching 33.3
million in 2009 (1) Level III.
In Malaysia, a similar trend is observed. The annual number of newly reported

HIV cases has been steadily decreasing from almost 7,000 in 2002 to 3,479 in
2011. The HIV prevalence among adults (15-49 years) in Malaysia is 0.5% (2)
Level III. 26% of reported infections are amongst young people between the
ages 13-29 years, 2.4% aged less than 19 years and 1.0% aged less than 13
from 1986 to December 2011 (2) Level III. The percentage of HIV-positive pregnant
women detected has been maintained at below 0.04% since the introduction
of the National Prevention of Maternal to Child Transmission of HIV Program
(PMTCT) in 1998 (3) Level III.
Malaysia is classified by the World Health Organisation (WHO) as a country with

a concentrated low-level HIV epidemic where the four most-at-risk populations
include injecting drug users, female sex workers, men who have sex with men,
72 Introduction
(MSM), and transgender persons. The 2012 prevalence rates by the risk groups was 18.9%,
4.2%, 12.6% and 5.7%, respectively (5) Level III.
Numerous studies show that patients with HIV are still presenting at a late stage of the
disease. In the United Kingdom, national surveillance data showed that approximately one-
third of all HIV infections in adults remain undiagnosed and that approximately 33% of newly
diagnosed individuals have a CD4 cell count of less than 200 (an accepted marker of ‘late’
diagnosis) (6) Level III. Similar findings are also seen in other countries such as those in sub-
Saharan Africa (7) Level II-2, India (8) Level II-2, the United States and Canada (9) Level II-2, and France
and Belgium (10) Level II-2. Studies also show that patients who present with advanced HIV
disease had missed opportunities for diagnosis in the years prior to being diagnosed (11,
12) Level II-2.
12.2 Benefit of screening and treating HIV infection
Early detection and treatment result in significant benefit in HIV morbidity and mortality. Early
treatment of HIV infection slows its progression to AIDS (13). Early initiation of antiretroviral
therapy has been shown to reduce the rate of sexual transmission of HIV-1 by 96% and
clinical events (which were defined as occurrence of pulmonary tuberculosis, severe bacterial
infection or death) by 41%, indicating both personal and public health benefits from such
therapy (14) Level II-1. With early detection of HIV infection, there is also an opportunity to initiate
chemoprophylaxis for the spouse of HIV patients (13).
Conversely, late diagnosis of HIV infection has been associated with increased mortality and
morbidity, and impaired response to antiretroviral therapy (15) Level II-3. A national audit by the
British HIV Association (BHIVA) showed that 24% of deaths occurring amongst HIV-positive
adults in the UK in 2006 were directly attributable to the diagnosis of HIV being made too
late for effective treatment (16) Level III. Persons with HIV infection who present late, as defined
by an initial CD4 count of < 200 cell / mm3, incur a higher cumulative direct HIV treatment
expenditure than those who present earlier in the disease process (17, 18) Level II-2.
Screening tests for HIV infection include Enzyme Immunoassay (EIA) and antibody rapid
test. EIA test has a sensitivity of >99.5%, and specificity of >99.5% (19). The highly sensitive
Rapid Test is a feasible, accurate and quick screening test (20) Level I (21) Level III. Local
data have demonstrated that the Rapid Test (Hemo-Strip®) has a sensitivity of 100% and a
specificity of 100% (22) Level III. However, a reactive Rapid Test result should be confirmed with
another EIA, Particle Agglutination (PA) or the Western Blot (23) Level III.
Screening tests 73
Two strategies can be adopted for screening HIV infection: 1) HIV Antibody Testing Using
Single Rapid Test (1RTK Strategy) (Appendix HIV -1) and 2) HIV Antibody Testing (24)
(Appendix HIV-2). In both strategies, a first screening test is performed using either the
Rapid Test or HIV antibody test. A positive result is followed by a second test using a different
method. This sequential rapid testing algorithm has been shown to have high accuracy and
cost-effectiveness (25, 26).
As Malaysia is a concentrated low-level epidemic country WHO does not recommend routine
screening for patients attending health facilities. (27). Screening should be prioritized as
provider-initiated testing and counselling for patients with signs and symptoms suggestive
of HIV infection. Special consideration should be also be given to (28):
1. Patients with sexually transmitted infection

2. Men who have sex with men
3. Sex worker
4. Patients with tuberculosis
5. Injecting drug users
6. Spouse with the above risk factors
Rapid testing and initial antibody screening may result in anxiety, social stigma and depression
if the results are reactive. However, no study has systematically compared the psychological
impact of rapid testing and conventional antibody testing (19). Although early diagnosis of
HIV infection may expose patients to the side effects of treatment earlier compared to late
diagnosis, the benefits of treatment at the optimal time outweigh the risk of medication side-
effects.
Appendix HIV-1
HIV Antibody Testing Using Single Rapid Test (1RTK strategy)
Request for screening
RTK Screening site
Simple
REACTIVE Rapid Test using finger prick NON–REACTIVE
Blood / venous blood
(regard as 1st sample)
Report as: Anti– Report as: Anti– HIV

HIV Rapid Test REACTIVE Rapid Test NON–
Name of Rapid Test Kit REACTIVE
End
Results Obtain venous
reported in blood sample 3ml
documented in plain tube Fill up
form: Fax, Request Form and
postal, provide Rapid Test
telephone Result on form
Send to Nearest Hospital

Screening centre with
EIA/Combo & PA facilities
Follow adult confirmation

test (next algorithm)
Appendix HIV1 75
HIV Antibody Testing strategy
Screening requested
(Venous blood sample)
Test 1: EIA HIV 1/2

Reactive (R) Non-Reactive (N)
Antibody test
*Test 2: anti-HIV test using

Repeat as necessary
Notify to nearest different Ab test from 1st test
District Health such as PA
Note:
EIA : Reactive + EIA : Reactive + EIA : Reactive + *2nd test can be
PA : Detected + **PA: Not Detected **PA : Inconclusive + another EIA or PA.
**Exclude Prozone
reaction in PA.
Dotted arrow
indicates that
Report reactive. Make Immunoblot maybe
Send blood sample to
request for fresh sample required in special
Regional HIV Testing
for patient verification: circumstances.
Do EIA & PA
Test 3: Immunoblot
Reactive Immunoblot Negative Immunoblot

Indeterminate
Obtain fresh blood from patient

for verification. Obtain another
blood sample for
EIA : Reactive EIA : Reactive EIA : Non-Reactive

PA : Detected PA : Not Detected PA : Not Detected
Patient Investigate for: Patient mix up / Sample mix up
76 Appendix HIV1
REFERENCES
1. Joint United Nations Programme on HIV/AIDS of antiretroviral therapy. Clin Infect Dis 2009;49(10):
(UNAIDS). UNAIDS Report On The Global Aids 1570-8.
Epidemic 2010 [Internet]. 2010. (cited 29 April 2015). 16. British HIV Association (BHIVA). 2005-6 Full results of
Available from: http://www.unaids.org/globalreport/ mortality audit [Internet]. 2005. (cited 29 April 2015).
documents/20101123_GlobalReport_full_en.pdf. Available from: http://www.bhiva.org/documents/
2. HIV/STI Section, Ministry of Health Malaysia. The Global ClinicalAudit/FindingsandReports/MortalityAudit.ppt
AIDS Response 2012, Country Progress Response. 17. Krentz HB, Auld MC, Gill MJ. The high cost of medical
Malaysia 2012. care for patients who present late (CD4<200 cells/μl)
3. AIDS/STD Section, Disease Control Division, Ministry with HIV infection. HIV Medicine 2004;5:93-8.
of Health Malaysia. Summary of HIV/AIDS cases 2006. 18. Fleishman JA, Yehia BR. The Economic Burden of Late
Malaysia 2006. Entry Into Medical Care for Patients With HIV Infection.
4. AIDS/STD Section, Disease Control Division, Ministry Med Care 2010;48 (12):10719.
of Health Malaysia. Summary findings of behavioural 19. Uspreventiveservicestaskforce.org. Recommendation
surveillance survey (BSS) in Malaysia 2006. Commercial Summary - US Preventive Services Task Force [Internet].
Sex Workers, IDUs. Malaysia 2006. 2013 [cited 23 April 2015]. Available from: http://
5. Ministry of Health. International behavioural surveillance www.uspreventiveservicestaskforce.org/Page/Topic/
survey. Malaysia 2012. recommendation-summary/human-immunodeficiency-
6. Sullivan AK, Curtis H, Sabin CA, et al. Newly diagnosed virus-hiv-infection-screening?ds=1&s=HIV
HIV infections: review in UK and Ireland. BMJ 20. Moyer V. Screening for HIV: U.S. Preventive Services
2005;330:1301-2 Task Force Recommendation Statement. Ann Intern
7. Kigozi I, Dobkin L, Martin JN. Late disease stage Med. 2013;159(1):51-60.
at presentation to an HIV clinic in the era of free 21. Lyamuya EF, Aboud S, Urassa WK. Evaluation of simple
antiretroviral therapy in Sub-Saharan Africa. J Acquir rapid HIV assays and development of national rapid
Immune Defic Syndr 2009;52(2):280 HIV test algorithms in Dar es Salaam, Tanzania. BMC
8. Alvarez-Uria G, Midde M, Pakam R, et al. Factors Infectious Dis 2009;9:19.
associated with late presentation of HIV and estimation 22. Ng K, Saw T, Baki A, Singh N, Lyles C. SHORT REPORT
of antiretroviral treatment need according to CD4 Evaluation of a rapid test for the detection of antibodies
lymphocyte count in a resource-Limited Setting: Data to human immunodeficiency virus type 1 and 2. Int J
from an HIV Cohort Study in India. Interdiscip Perspect STD AIDS. 1999;10(6):401-4.
Infect Dis 2012; 2012:293795. 23. Centers for Disease Control and Prevention (CDC).
9. Althoff KN, Gange SJ, Klein MB, et al. Late presentation Revised recommendations for HIV testing of
for HIV Care in United States and Canada. Clin Infect Dis adults,adolescents, and pregnant women in health-care
2010;50(11):1512-20. settings. MMWR 2006; 55/(RR14):1-17.
10. Ndiaye B, Salleron J, Vincent A. Factors associated 24. Ministry of Health (Moh.gov.my). Official Portal for
with presentation to care with advanced HIV disease Ministry of Health Malaysia. View Listing Circulars, HIV
in Brussels and Northern France: 1997-2007. BMC screening test and validation flowchart [Internet]. 2011
Infectious Dis 2011;11:11 [cited 24 April 2015]. Available from: http://www.moh.
11. Lyons MS, Lindsell CJ, Wayne BD. Comparison of gov.my/english.php/database_stores/store_view_
missed opportunities for earlier HIV diagnosis in 3 page/10/199
geographically proximate emergency departments. Ann 25. Ménard D, Maïro A, Mandeng M, Doyemet P, Koyazegbe
Emerg Med 2011; 58(1 Suppl 1):S17-22.e1. T, Rochigneux C et al. Evaluation of rapid HIV testing
12. Fetene NW, Feleke A. Missed opportunities for earlier strategies in under equipped laboratories in the Central
HIV testing and diagnosis at the health facilities of African Republic. J. Virol. Methods 2005;126(1-2):75-
Dessie Town, North East Ethiopia. BMC Public Health 80.
2010, 10:. 26. Farnham PG, Hutchinson AB, Sansom SL, Branson BM.
13. Ministry of Health (Moh.gov.my). Official Portal for Comparing the costs of HIV screening strategies and
Ministry of Health Malaysia; CPG-Infectious Disease technologies in health-care settings. Public Health Rep
[Internet]. 2014 [cited 24 April 2015]. Available from: 2008;123:Suppl 351–62.
http://www.moh.gov.my/english.php/pages/view/214 27. WHO Guidance On Provider. Initiated HIV testing and
14. Cohen MS, Chen YQ, McCauley M, et al. Prevention of counselling in health facilities. WHO Library Cataloguing-
HIV-1 infection by early antiretroviral therapy. N Eng J in-Publication Data 2007.
Med 2011;365(6):493-505. 28. Palfreeman A, Fisher M, Ong E. Testing for HIV: concise
15. Losina E, Schackman BR, Sadownik SN. Racial and guidance. Clin Med. 2009;9(5):471-6.
gender disparities in life expectancy losses among
HIV-infected persons in the United States: impact of
risk behavior, late initiation and early discontinuation
References 77
13 Domestic violence
SUMMARY
Screening women for domestic violence increases the identification of victims,

particularly among pregnant mothers.
Risks for domestic violence include female gender, young age, low income,
depression, partner with substance abuse and terminating a relationship.
Screening for domestic violence, followed by interventions, improves health
outcomes.
Issues about domestic violence should be explored in a non-judgmental manner
and in the absence of the abuser.
RECOMMENDATIONS
Screening for domestic violence may be indicated for women of Grade C

childbearing age.
Screening for domestic violence during obstetric care should occur Grade C
at the first antenatal visit, at least once per trimester, and at the
postpartum check-up.
13.1 Introduction
Domestic violence is defined by the World Health Organization as any behaviour
within an intimate relationship that causes physical, psychological or sexual
harm to those in the relationship (1). In Malaysia, the Domestic Violence Act (Act
521) 1994 provides legal protection for victims of domestic violence (2). Victims
are reported to be mainly women although the opposite can also occur (3).
Studies have shown that up to 41% of women attending primary care

consultations have experienced some form of domestic violence in their life (3-8).
The risks for domestic violence include female gender, young age, low income,
depression, partner with substance abuse and termination of a relationship (9-
13). A review of prevalence of domestic violence in Peninsular Malaysia noted
39% of women older than age 15 years in 1990 suffered some form of violence
and 68% of battered women were beaten while pregnant. The rate of abuse can
increase during pregnancy with 32% of pregnant women reporting to have been
abused in developing countries (14).
78 Introduction
Domestic violence can result in physical injuries and death to the victims (15-17).
Notwithstanding, the biggest burden of domestic violence comes from its psychological
implications. Mental health problems contribute to 60% of domestic violence health
outcomes (18) including post-traumatic stress disorder (PTSD), depression, panic attacks,
insomnia, suicide, substance abuse and alcoholism (15, 19-22). The abusive relationship is
also associated with exacerbating chronic diseases, such as hypertension, diabetes mellitus
and ischaemic heart disease (23), unwanted and unplanned pregnancy, anaemia, first and
second trimester bleeding, poor weight gain, low birth weight and late prenatal care booking
(14-24).
Furthermore, domestic violence often co-exists with child abuse (25). Children living in homes
with domestic violence are likely to have increased risks of behavioural problems and social
incompetence (27, 28), as well as experience domestic violence in their adult relationships,
(26, 27).
13.2 Benefit of screening and managing domestic

violence
Identifying domestic violence is the first step in intervention. It can be approached via
universal screening or case finding. Systematic reviews have found inadequate evidence
to support one approach over another (29, 30) Level I. Current evidence suggests that the
likelihood of identifying abused women increases when screening for domestic violence is
conducted (31, 32) Level I.
A recent systematic review reported that screening women for domestic violence, with an
intervention, can reduce the recurrence of domestic violence and improve health outcomes
(31) Level I. An intervention involving intensive advocacy for abused women who were
already in refuges has been shown to reduce physical violence after one to two years of
intervention (33) Level I. Among pregnant women, screening for domestic violence followed
by a brief intervention has been shown to reduce re-victimizations, improve birth outcomes,
reduce pregnancy coercion and to motivate the abused women to discontinue their abusive
relationship (34-37) Level I. This brief intervention consists of the following:
i. Validation of domestic violence experience. This is done by listening non-

judgmentally and providing appropriate responses such as ‘No one deserves to be
abused’, ‘You are not alone and help is available’
ii. Review the safety issues
iii.
Offer relevant domestic violence information. This includes the nature of an
abusive relationship and domestic violence resources, such as the One-Stop-Crisis-
Centre (OSCC)
Benefit of screening and managing domestic violence 79

There are many tools for screening domestic violence. Seven screening tools are reported
to have high diagnostic accuracy in detecting past, current, or recent domestic violence
or predicting the likelihood of future domestic violence (31) Level I. These are: Hurt, Insult,
Threatened, Scream (HITS); Ongoing Violence Assessment Tool (OVAT); Slapped, Threatened,
and Throw (STaT); Humiliation, Afraid, Rape, Kicks (HARK); Woman Abuse Screening Tool
(WAST); Partner Violence Screen (PVS); Childhood Trauma Questionnaire-Short Form (CTQ).
These screening instruments have sensitivity and specificity ranging from 80-100%. However,
none of the above has been validated in Malaysia. A 20 item questionnaire which forms
parts of the WHO Women’s Health and Life Experiences Questionnaire, has been translated
and pyshometrically validated in Malaysia.(38) However, its sensitivity and specificity has not
been established.
Sample domestic violence screening questions (39)
Framing Statement
A framing statement in the beginning of the assessment to show that screening is done universally and
not only when domestic violence is suspected:
“Because violence is common in many women’s lives and because there is available help, I now ask every
patient about domestic violence”
Sample Questions
The following questions could be incorporated into the routine medical history-taking:
“Within the past one year (or since you have been pregnant), have you been hit, slapped, kicked or
otherwise physically hurt by someone?”
“Are you in a relationship with a person who threatens or physically hurts you?”
“Has anyone forced you to have sexual activities that make you feel uncomfortable?”
Questions regarding domestic violence should only be asked (40, 41):
• in the absence of the patient’s partner

• in a non-judgmental manner
• with clinicians reaffirming the confidentiality of the information given
Clinicians are strongly advised against couple counselling without the victim’s permission.
80 Screening tests
The potential harm of screening includes shame, guilt feeling, fears of revenge and/
or abandonment by the spouse. Nevertheless, direct evidence of harm has not been
demonstrated. A review by the USPSTF on three clinical trials and 11 observational studies
did not reveal any significant harm from screening and interventions associated with intimate
partner violence (42).
REFERENCES
1. Krug EG, Mercy JA, Dahlberg LL, Zwi AB. The world report 12. Tollestrup K, Sklar D, Frost FJ, Olson L, Weybright J,
on violence and health. Lancet 2002;360(9339):1083- Sandvig J, et al. Health indicators and intimate partner
8. violence among women who are members of a managed
2. Attorney-General’s Chambers (AGC) Malaysia. Domestic care organization. Prev Med 1999;29:431-40.
Violence Act 1994, Malaysia. 13. Vest JR, Catlin TK, Chen JJ, Brownson RC. Multivariate
3. Sassetti MR. Domestic violence. Prim Care analysis of factors associated with intimate partner
1993;20(2):289-305. violence. Am J Prev Med 2002;22(3):156-64.
4. Bradley F, Smith M, Long J, O’Dowd T. Reported frequency 14. Campbell JC, Garcia-Moreno C, Sharps P. Abuse during
of domestic violence: cross-sectional survey of women pregnancy in industrialized and developing countries.
attending general practice. BMJ 2002;324:271. Violence Against Women 2004;10(7):770-89.
5. Brown JB, Lent B, Schmidt G, Sas G. Application of 15. Coker AL, Smith PH, Bethea L, King MR, McKeown
the Woman Abuse Screening Tool (WAST) and WAST- RE. Physical health consequences of physical and
Short in the family practice setting. J Fam Pract psychological intimate partner violence. Arch Fam Med
2000;49(10):896-903. 2000;9(5):451-7.
6. Hegarty KL, Taft AT. Overcoming the barriers to 16. Campbell JC. Health consequences of intimate partner
disclosure and inquiry of partner abuse for women violence. The Lancet 2002;359(9314):1331-6.
attending general practice. Aust N Z J Public Health 17. Kyriacou DN, Anglin D, Taliaferro E, Stone S, Toni T,
2001;25:433-7. Linden JA, et al. Risk factors for injury to women from
7. McCauley J, Kern D, Kolodner K, Dill L, Schroeder A, domestic violence. N Eng J Med 1999;341:1892-8.
DeChant H, et al. The “Battering Syndrome”: prevalence 18. Vichealth.vic.gov.au. The Health Costs of Violence:
and clinical characteristics of domestic violence in Measuring the burden of disease caused by intimate
primary care internal medicine practices. Ann Intern partner violence [Internet]. 2004 [cited 5 May 2015].
Med 1995;123(10):737-46. Available from: https://www.vichealth.vic.gov.au/
8. Richardson J, Jeremy C, Petruckevitch A, Chung WS, media-and-resources/publications/the-health-costs-of-
Moorey S, Feder G. Identifying domestic violence: cross- violence
sectional study in primary care. BMJ 2002;324:274. 19. Pico-Alfonso MA. Psychological intimate partner
9. Wong YL, Othman S. Early detection and prevention of violence: the major predictor of posttraumatic stress
domestic violence using the Women Abuse Screening disorder in abused women. Neurosci Biobehav Rev
Tool (WAST) in primary health care clinics in Malaysia. 2005;29:181-93.
Asia Pac J Public Health 2008;20(2):102-16. 20. Dienemann J, Boyle E, Baker D, Wiederhorn N, Campbell
10. Coker AL, Smith PH, McKeown RE, King MJ. Frequency JC. Intimate partner abuse among women diagnosed
and correlates of intimate partner violence by type: with depression. Issues Ment Health Nurs 2000;21:400-
Physical, sexual, and psychological battering. Am J 513.
Public Health 2000;90(4):553-9. 21. Jones L, Hughes M, Unterstaller U. Post-traumatic stress
11. Hegarty K, Hindmarsh ED, Gilles MT. Domestic violence disorder (PTSD) in victims of domestic violence: A review
in Australia: definition, prevalence and nature of of the research. Trauma Violence Abuse 2001;2(2):99-
presentation in clinical practice. MJA 2000;173:363-7. 119.
REFERENCES
22. Golding JM. Intimate partner violence as a risk factor improve postpartum outcomes in African-American
for mental disorders: a meta-analysis. J Fam Violence mothers: a randomized controlled trial. Obstet Gynecol
1999;14(2):99-132. 2008;112(3):611-20.
23. Ruiz-Pérez I, Plazaola-Castaño J, del Río-Lozano M. 36. Miller E, Decker MR, McCauley HL, Tancredi DJ,
Physical health consequences of intimate partner Levenson RR, Waldman J, et al. A family planning
violence in Spanish women. Eur J Public Health clinic partner violence intervention to reduce risk
2007;17(5):437-43. associated with reproductive coercion. Contraception
24. Hegarty KL, Gunn J, Chondros P, Small R. Association 2011;83(3):274-80.
between depression and abuse by partners of women 37. Kiely M, El-Mohandes AA, El-Khorazaty MN, Blake SM,
attending general practice: descriptive, cross sectional Gantz MG. An integrated intervention to reduce intimate
survey. BMJ 2004;328:621-4. partner violence in pregnancy: a randomized controlled
25. Appel AE, Holden GW. The co-occurrence of spouse and trial. Obstet Gynecol 2010;115(2 Pt 1):273-83.
physical child abuse: A review and appraisal. J Fam 38. Norkhafizah S, Zaharah S, Siti Hawa A, et al. Validity and
Psychol 1998;12(4):578-99. reliability of the Malay version of WHO Women’s Health
26. Kitzmann KM, Gaylord NK, Holt AR, Kenny ED. Child and Life Experiences Questionnaire. J Interpers Violence
witnesses to domestic violence: a meta-analytic review. 2013;28(12):2557-80
J Consult Clin Psychol 2003;71(2):339-52. 39. American College of Obstetricians and Gynecologists.
27. Stiles MM. Witnessing domestic violence: the effect on Intimate partner violence: Committee opinion No. 518.
children. Am Fam Physician 2002;66(11):2052-66. Obstet Gynecol 2012;119:412-7.
28. Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz 40. Taket A, Nurse J, Smith K, Watson J, Shakespeare J,
AM, Edwards V. Relationship of childhood abuse and Lavis V, et al. Routinely asking women about domestic
household dysfunction to many of the leading causes violence in health settings. BMJ 2003;327:673-6.
of death in adults: The Adverse Childhood Experiences 41. Taft AJ, Hegarty KL, Feder GS. Tackling partner violence
(ACE) Study. Am J Prev Med 1998;14(4):245-58. in families. Med J Aust 2006;185(10):535-6.
29. Feder G, Ramsay J, Dunne D, Rose M, Arsene C, Norman 42. Moyer V. Screening for Intimate Partner Violence and
R, et al. How far does screening women for domestic Abuse of Elderly and Vulnerable Adults: U.S. Preventive
(partner) violence in different health-care settings meet Services Task Force Recommendation Statement.
criteria for a screening programme? Systematic reviews Annals of Internal Medicine. 2013; 58(6):478.
of nine UK National Screening Committee criteria. Health
Technol Assess 2009;13(16):iii-iv, xi-xiii, 1-113, 37-
347.
30. U.S. Preventive Services Task Force. Screening for
family and intimate partner violence: Recommendation
Statement. Am Fam Physician 2004;70(4):747-51.
31. Nelson HD, Bougatsos C, Blazina I. Screening women for
intimate partner violence: a systematic review to update
the U.S. Preventive services task force recommendation.
Ann Intern Med 2012;156(11):796-808.
32. Taft A, O’Doherty L, Hegarty K, Ramsay J, Davidson L,
Feder G. Screening women for intimate partner violence
in healthcare settings. Cochrane Database Syst Rev
2013, Issue 4.
33. Ramsay J, Carter Y, Davidson L, Dunne D, Eldridge
S, Feder G, et al. Advocacy interventions to reduce
or eliminate violence and promote the physical and
psychosocial well-being of women who experience
intimate partner abuse. Cochrane Database Syst Rev
2009(3):CD005043.
34. El-Mohandes AA, Kiely M, Gantz MG, El-Khorazaty
MN. Very preterm birth is reduced in women receiving
an integrated behavioral intervention: a randomized
controlled trial. Matern Child Health J 2011;15(1):19-
28.
35. El-Mohandes AA, Kiely M, Joseph JG, Subramanian
S, Johnson AA, Blake SM, et al. An intervention to
82 References
14 Depression
SUMMARY
Although prevalent, the detection and treatment of depression in primary care

settings remain low.
Routine screening using questionnaires for depression, without staff assistance
in depression care, has minimal short-term impact on detection and beneficial
outcome.
Screening can improve outcomes if it is coupled with adequate depression care
support.
RECOMMENDATIONS
Screening for depression may be indicated for high-risk patients Grade C

in primary care settings if staff-assisted depression care support
is available.
14.1 Introduction
Depression is a global public-health issue (1-5) with considerable consequences

(6-12). The estimated one-year and lifetime prevalence of major depression
in the general population worldwide have been reported to range from 3.2 to
6.7 % (1, 2). In the United States (US), 20.1% of adults reported significant
depressive symptoms in national health surveys (3). However, the prevalence
of major depression in the primary care setting ranged from 2.2 to 36.1% (2,
4). In the Asia Pacific region, the prevalence of major depression in the general
population was reported to range from 1.3 to 5.5% (5). In Malaysia, a recent
review on depression prevalence found comparable rates of 6.3% to 13.9% in
the community and 6.7% to 14.4% in the primary care setting (6).
The Global Burden of Disease Study ranked depression as the fourth leading
cause of disease burden in the year 2000, accounting for 4.4% of total disability-
adjusted life years (DALYs) (7). By 2020, depression is projected to rank second
in the leading causes of disease burden (8). Depression increases the risk of
morbidity (1, 4, 9, 10) and mortality (12-15). In the US, a 2013 report cites major
depression as the most common cause of suicide (15). Moreover, from 1990 to
Introduction 83
2000, the economic burden of depression rose by 7% while its treatment rate increased by
over 50% (12).
The risk groups for depression include those with (16-23):
• physical health problems causing disability

• past history of depression
• family history of depression
• other mental health problems such as substance abuse or dementia
• adverse psychosocial factors
Other risk factors that have been identified include genetic predisposition, female gender,
lower education and poor self-perception of health.
14.1 Benefit of screening and treating depression
Although depression remains under-recognized and under-treated (3, 24), routine

screening by clinicians using questionnaires for depression have proven to have minimal
and short term impact on its detection and management or outcome (25-27). According
to a Cochrane review, screening and feedback to clinicians of the screening scores do not
increase the detection of depression (relative risk 1.00; 95% confidence interval 0.89 to 1.13)
(25). Although a higher intervention rate on screen-detected cases (relative risk 1.35; 95%
confidence interval 0.98 to 1.85) was noted in small studies (25), the benefit of screening
programmes was not evident without staff assistance in depression care (25, 27). However,
screening coupled with adequate staff-assisted and organisational depression care support
(28-30) showed improved outcomes, although it was associated with increased cost (31).
An established treatment for major depression is available and is effective (32). The majority
of patients with depression attending primary care have mild symptoms. The benefit of
treatment for mild major depression is smaller compared to the benefit of treatment for
moderate and severe major depression (33). After 10 to 16 weeks of treatment, a study
reported that patients on antidepressants, psychotherapy and in the control group had a
remission rate of 46%, 48% and 24.4%, respectively (34). In older adults, treatment with
anti-depressants was associated with a higher remission rate compared to the placebo (OR,
2.13 [CI, 1.61 to 2.86]) (35). A meta analysis also found that psychotherapy is effective in
achieving remission compared to no treatment (OR, 2.47 [CI, 1.76 to 3.47]) (36).
84 Benefit of screening and treating depression

Although many screening tools for depression exist, they have different validities in
detecting depression (37). Screening for depression should be done using the simplest
tool or questionnaire without substantially compromising validity (33). A few studies have
looked at the validity of various screening instruments appropriate for primary care settings
(Table 1). PHQ-9 (39-43) and PHQ-2 (43, 44) have demonstrated high sensitivity. Other
questionnaires, such as GDS-15, GDS-30, BDI, BDI-SF, CES-D, HADS and DASS-21, have
also been reviewed (37, 45-52). The construct validity of the translated versions of DASS-21
(BM DASS-21) (53 -55), DASS-24 (BM DASS-24) (56) and PHQ-9 (57) has been tested in
Malaysia. They have demonstrated similar validity but with a higher number of items.
On the other hand, the adapted PHQ-2, a brief Two Questions With Help Questions (TQWHQ)
(42, 58), including the translated TQWHQ (Malay version) (59), has been shown to have good
validity. The two questions asked in the TQWHQ are similar in content to the PHQ-2 (44) and
Two Whooley Questions (60, 61), with an addition of a help question, Q3 (Appendix). The
addition of the help question has improved the tool’s specificity in diagnosing depression in
primary care (42, 58, 59). Therefore, if screening is indicated, the TQWHQ (Malay version)
can be considered as the screening tool for local settings provided that referrals for further
evaluation and management for patients who are detected to have depression is in place
(57).
Table 1: Validity of commonly available screening instruments for depression
Assessment tool Sensitivity (%) Specificity (%)

1. PHQ-2 (43, 44) 83 83 -92
2. TQWHQ (42, 60) - adapted PHQ 2 86 – 96 78 – 89
3. TQWHQ (Malay version) (59) 87 95
4. Whooley questions (60, 61) 96 – 97 57-67
5. PHQ-9 (39-43) 74-85 89 -94
6. GDS-15 (46, 47) 78 –81 74 –78
7. GDS-30 (46, 47) 77 -83 65-70
Screening for depression may impose potential harm, such as false-positive results, the
inconvenience of confirmatory assessments, stigmatization, the expenses and adverse
effects of treatment in case of misdiagnosis (32). Other potential harms may also comprise
treatment avoidance, deterioration in patient-provider relationship and over treatment (62).
So far, no evidence of harms from screening for depression in adults has been reported
(32, 63). Nevertheless, there is some evidence on the harm from treatment which includes
increased suicidal behaviours in younger adults who were on paroxetine for major depressive
disorder (MDD) and increased risk for upper gastrointestinal bleeding with SSRI use among
older adults (32).
Appendix – Depression 1
TWO QUESTIONS ON DEPRESION AND ONE QUESTION ON HELP (TQWHQ) MALAY VERSION (52).
Question Content Response Score

Q1 Dalam tempoh sebulan yang lalu, adakah anda sering
diganggui dengan perasaan murung, sedih atau Tidak / No 0
tiada harapan?
Ya / Yes 1
During the past month, have you often been bothered by
feeling down, depressed or hopeless?
Q2 Dalam tempoh sebulan yang lalu, adakah anda sering

kehilangan minat atau keseronokan dalam melakukan kerja- Tidak / No 0
kerja?
Ya / Yes 1
During the past month, have you often been bothered by
having little interest or pleasure in doing things?
Q3 Jika YA kepada satu ataupun kedua-dua soalan ini, adakah Tidak / No 0

anda memerlukan bantuan dengan masalah anda ini?
Ya, tetapi bukan 1
If YES to either or both of these 2 questions, do you want hari ini / Yes, but
help with this? not today
Ya / Yes 2
Patients with a positive score (score of 2 or more) on TQWHQ, should then complete the PHQ-9 (37, 53) or be evaluated
further (54).
Appendix - Depression 1 87
REFERENCES
1. Moussavi S, Chatterji S, Verdes E, Tandon A, Patel V, from: http://www.afsp.org/understanding-suicide/facts-

Ustun B. Depression, chronic diseases, and decrements and-figures
in health: results from the World Health Surveys. The 16. Hirschfeld RMA, Weissman MM. Risk factors for major
Lancet 2007; 370(9590):851-8. depression and bipolar disorder. In Davies KL, Charney
2. Waraich P, Goldner EM, Somers JM, Hsu L. Prevalence D, Coyle JT, Nemeroff C. (Eds) Neuropsychopharma-
and incidence studies of mood disorders: a systematic cology: Philadelphia: Lippincot Williams and Wilkins, The
review of the literature. Can J Psychiatry 2004; Fifth Generation of Progress 2002;1017-26.
49(2):124-38. 17. Martin GC, Nandini D. Risk factors for depression among
3. Shim RS, Baltrus P, Ye J, Rust G. Prevalence, treatment, elderly community subjects: a systematic review and
and control of depressive symptoms in the United meta-analysis. Am J Psychiatry 2003;160:1147-56.
States: results from the National Health and Nutrition 18. Osama AA, Nabilla AS, Elawad NAM. Gender and risk
Examination Survey (NHANES), 2005 - 2008. J Am of depression in Saudi Arabia, a systematic review and
Board Fam Pract 2011; 24(1):33-8. meta-analysis. J Public Health Africa 2010;1(1)
4. Herrman H, Patrick DL, Diehr P, et al. Longitudinal 19. Djernes JK. Prevalence and predictors of depression in
investigation of depression outcomes in primary care in populations of elderly: a review. Acta Psychiatr. Scand
six countries: the LIDO study. Functional status, health 2006;113(5):372-87.
service use and treatment of people with depressive 20. Riemann D, Voderholzer U. Primary insomnia: a
symptoms. Psychol Med 2002;32(2002):889–902 risk factor to develop depression? J Affect Disord
5. Chiu E. Epidemiology of depression in the Asia Pacific 2003;76(1-3):255-9.
region. Australas Psychiatry 2004; 12:4-10. 21. Nouwen A, Winkley K, Twisk J, Lloyd CE, Peyrot M,
6. Firdaus M, Tian PSO. A review on the prevalence of Ismail K, Pouwer F, and for the European Depression in
depression in Malaysia. Curr Psychiatry Rev 2011:7(3); Diabetes (EDID) Research Consortium. Type 2 diabetes
234-8 mellitus as a risk factor for the onset of depression:
7. Ustun TB, Ayuso–Mateos JL, Chatterji S, Mathers C, a systematic review and meta-analysis. Diabetologia
Murray CJ. Global burden of depressive disorders in the 2010;53(12):2480–6.
year 2000. Br J Psychiatry 2004;184:386–92 22. Chang QH, Zheng RW, Yong HL, Yi ZX, Qing XL.
8. Murray CJ, Lopez AD. Alternative projections of mortality Education and risk for late life depression: a meta-
and disability by cause 1990-2020: Global Burden of analysis of published literature. Int J Psychiatry Med
Disease Study. Lancet 1997;349:1498-504. 2010;40 (1):109-24.
9. Spijker J, de Graaf R, Bijl RV, Beekman AT, Ormel J, 23. Bonde JPE. Psychosocial factors at work and risk of
Nolen WA. Duration of major depressive episodes in depression: a systematic review of the epidemiological
the general population: results from The Netherlands evidence: Review Occup Environ Med 2008;65:438-45
Mental Health Survey and Incidence Study (NEMESIS). 24. Cepoiu M, McCusker J, Cole MG, Sewitch M, Belzile E,
Br J Psychiatry 2002;181:208-13. Ciampi A. Recognition of depression by non-psychiatric
10. William WE, Huibo S, Gerald N, Ben HL, Bienvenu physicians: a systematic literature review and meta-
OJ, Peter Z. Population-based study of first onset analysis (Structured abstract). J Gen Intern Med
and chronicity in major depressive disorder. Arch Gen 2008;23(1):25-36
Psychiatry. 2008;65(5):513-20. 25. Gilbody S, House A, Sheldon T. Screening and case
11. Berto P, D’Ilario D, Ruffo P, Di Virgilio R, Rizzo F. finding instruments for depression. Cochrane Database
Depression: cost-of-illness studies in the international of Sys Rev 2009(1).
literature, a review. J Ment. Health Policy Econ 26. Gilbody S, Sheldon T, Wessely S. Should we screen for
2000;3(1):3-10 depression? BMJ 2006;332:1027
12. Paul E, Kessler RC, Birnbaum HG, Leong SA, Lowe 27. O’Connor EA, Whitlock EP, Beil TL, Gaynes BN.
SW, Berglund PA, Corey-Lisle PKG. The economic Screening for depression in adult patients in primary
burden of depression in the United States: How did it care settings: a systematic evidence review. Ann Intern
change between 1990 and 2000? J Clin Psychiatry Med. 2009;151(11):793-803.
2003;64(12):1465-75. 28. Palmer SC, Coyne JC. Screening for depression in
13. Lawson RW, George EV, Victoria EW. A systematic medical care: Pitfalls, alternatives, and revised priorities.
review of the mortality of depression. Psychosom Med J Psychosom Res 2003;54(4):179-287
1997; 61:6-17. 29. Pignone MP, Gaynes BN, Rushton JL, Burchell CM,
14. Amanda BJ, Andrew P, Harvey WA. Factors influencing Orleans CT, Mulrow CD, Lohr KN. Screening for
risk of premature mortality in community cases of depression in adults: a summary of the evidence for the
depression: a meta-analytic review. Epidemiol Res Int U.S. Preventive Services Task Force. Ann Intern Med.
2011;2011:12 2002;136(10):765-76
15. American Foundation for Suicide Prevention. Facts and 30. Bijl D, van Marwijk HW, de Haan M, van Tilburg W,
Figures [Internet]. 2013 [cited 29 April 2015]. Available Beekman AJ. Effectiveness of disease management
88 References
programmes for recognition, diagnosis and treatment M, Friedrich F. The criterion validity of the Geriatric
of depression in primary care. Eur J Gen Pract Depression Scale: a systematic review. Acta Psychiatr
2004;10(1):6-12. Scand 2006;114:398–410
31. Gilbody S, Bower P, Whitty P. Costs and consequences 46. Mitchell AJ, Bird V, Rizzo M, Meader N. Diagnostic
of enhanced primary care for depression. Systematic validity and added value of the geriatric depression
review of randomised economic evaluations. Br J scale for depression in primary care: A meta-analysis of
Psychiatry 2006;189:297-308 GDS 30 and GDS 15 . J Affect Disord 2010;125(1):10-7
32. U.S. Preventive Services Task Force. Screening for 47. Furlanetto LM, Mendlowicz MV, Bueno J. The validity
depression in adults: U.S. Preventive Services Task of the Beck Depression Inventory—Short Form as a
Force Recommendation Statement. Ann Intern Med. screening and diagnostic instrument for moderate and
2009;151:784-92. severe depression in medical inpatients. J Affect Disord
33. Ministry of Health. Management of Major Depressive 2005;86:87–91.
Disorder 2007 [Internet]. 1st ed. Malaysia: 2007 [cited 48. Lasaa L, Ayuso-Mateosa JL, Va´zquez-Barqueroa JL,
29 April 2015]. Available from: http://www.moh.gov.my/ D´ıez-Manriquea FJ, Dowrick CF. The use of the Beck
attachments/3897.pdf Depression Inventory to screen for depression in the
34. Casacalenda N, Perry JC, Looper K. Remission in major general population: a preliminary analysis. J Affect
depressive disorder: a comparison of pharmacotherapy, Disord 1999;57(2000):261–5
psychotherapy, and control conditions. Am J Psychiatry 49. Bjellanda I, Dahlb AA, Haugc TT, Neckelmann D. The
2002;159:1354-60 validity of the hospital anxiety and depression scale.
35. Wilson K, Mottram P, Sivanranthan A, Nightingale A. An updated literature review. J Psychosom Res 2001;
Antidepressant versus placebo for depressed elderly. 52(2002):69–77
Cochrane Database Syst Rev. 2001:CD000561 50. Brennan C, Worrall-Davies A, McMillan D, Gilbody S,
36. Pinquart M, Duberstein PR, Lyness JM. Treatments House A. The hospital anxiety and depression scale:
for later-life depressive conditions: a meta-analytic A diagnostic meta-analysis of case-finding ability. J
comparison of pharmacotherapy and psychotherapy. Psychosom Res 2010;69(2010):371–8.
Am J Psychiatry 2006;163:1493-501 51. Henry JD, Crawford JR. The short-form version of the
37. Williams JW, Noel PH, Cordes JA, Ramirez G, Depression Anxiety Stress Scales (DASS-21): Construct
Pignone M. Is this patient clinically depressed? JAMA validity and normative data in a large non-clinical
2002;287:1160–70. sample. Br J Clin Psychol 2005;44:227–39
38. Douglas MM, Screening for depression. Am Fam 52. Gloster AT, Rhoades HM, Novy D, Jens Klotsche, Senior A,
Physician 2012;85(2):139-44. Kunik M, Wilson N, Stanley MA. Psychometric properties
39. Kroenke K, Spitzer RL, Williams JBW, Löwe B. The of the Depression Anxiety and Stress Scale-21 in older
patient health questionnaire somatic, anxiety, and primary care patients. J Affect Disord 2008;110:248–
depressive symptom scales: a systematic review. Gen 59
Hosp Psychiatry 2010;32(2010);345–59 53. Ramli M, Ariff MF, Zaini Z. Translation, validation and
40. Manea L, Gilbody S, McMillan D. Optimal cut-off psychometric properties of Bahasa Malaysia version of
score for diagnosing depression with the Patient the Depression, Anxiety and Stress Scales (DASS-21).
Health Questionnaire (PHQ-9): a meta-analysis. CMAJ ASEAN Journal of Psychiatry 2007;8(2):82-9.
2012;184(3):E191–6 54. Ramli M., Salmiah MA, Nurul Ain M. Validation and
41. Wittkampf KA, Naeije L, Schene AH, Huyser J, van Weert psychometric properties of Bahasa Malaysia version of
HC. Diagnostic accuracy of the mood module of the the Depression Anxiety and Stress Scales (DASS) among
Patient Health Questionnaire: a systematic review. Gen diabetic patients. Malaysian Journal of Psychiatry
Hosp Psychiatry 2007;29(2007):388–95 2010;18(2):40-5.
42. Arroll B, Goodyear-Smith F, Crengle S, Gunn J, Kerse 55. Ramli M, Roszaman R, Kartini A, Rosnani S. Concurrent
N, Fishman T, Falloon K, Hatcher S. Validation of PHQ- validity of the depression and anxiety components in
2 and PHQ-9 to screen for major depression in the the Bahasa Malaysia version of the Depression Anxiety
primary care population. Ann Fam Med 2010;8(4):348- and Stress Scales (DASS). ASEAN Journal of Psychiatry
53 2011;12(1)
43. Gilbody S, Richards D, Brealey S, Hewitt C. Screening for 56. Ramli M, Rosnani S, Aidil Faszrul AR. Psychometric
depression in medical settings with the Patient Health profile of Malaysian version of the Depressive, Anxiety
Questionnaire (PHQ): a diagnostic meta-analysis. J Gen and Stress Scale 42-item (DASS-42). Malaysian Journal
Intern Med 2007;22:1596–602. of Psychiatry 2012;20(1);3-9.
44. Kroenke K, Spitzer RL, Williams JBW. The Patient Health 57. Sherina MS, Arroll B, Goodyear-Smith F. Criterion validity
Questionnaire-2. Validity of a two-item depression of the PHQ-9 (Malay version) in a primary care clinic in
screener. Med Care 2003;41(11):1284–92 Malaysia. Med J Malaysia 2012;67(3):309-15.
45. Wancata J, Alexandrowicz R, Marquart B, Weiss 58. Arroll B, Goodyear-Smith F, Kerse N, Fishman T, Gunn
References 89
REFERENCES
J. Effect of the addition of a “help” question to two

screening questions on specificity for diagnosis of
depression in general practice: diagnostic validity study.
BMJ 2005;331(7521):884.
59. Sherina MS, Arroll B, Goodyear-Smith F, Azhar MDZ.
Screening for depression with a brief questionnaire in
a primary care setting: validation of the two questions
with help question (Malay Version). The Int J.Psychiatry
in Medicine 2011;41(2):143-54
60. Whooley MA, Avins AL, Miranda J, Browner WS. Case
finding instruments for depression: Two questions are
as good as many. J Gen Int Med 1997;12(7):439-45
61. Arroll B, Khin N, Kerse N. Screening for depression in
primary care with two verbally asked questions: cross
sectional study. BMJ 2003;327:1144–6
62. Uspreventiveservicestaskforce.org. Final Research
Plan: Depression in Adults: Screening - US
Preventive Services Task Force [Internet]. 2014
[cited 29 April 2015]. Available from: http://www.
uspreventiveservicestaskforce.org/Page/Document/
ResearchPlanFinal/depression-in-adults-screening1
63. Care C. Depression—Systematic Review [Internet].
Canadian Task Force on Preventive Health Care.
2012 [cited 29 April 2015]. Available from: http://
canadiantaskforce.ca/ctfphc-guidelines/2013-
depression/systematic-review/
90 References
15 Scoliosis in Adolescents
SUMMARY
Scoliosis is not rare among adolescents, especially girls.

Early detection with non-surgical intervention improves disease outcome and
reduces surgical intervention.
Regional data demonstrate the cost benefit of a school-based screening programme
for idiopathic scoliosis.
RECOMMENDATIONS
A school-based screening programme for scoliosis using a Grade B

scoliometer to measure angle of trunk rotation is indicated for girls
aged 12 years.
15.1 Introduction
Scoliosis is defined as a lateral curvature of the spine greater than 10 degrees

as measured using the Cobb method on a standing radiograph, and idiopathic
scoliosis is the most common type (1) Level III. The reported prevalence of
adolescent idiopathic scoliosis (AIS) varies depending on the degree of curvature
used in its definition.
In general, the prevalence of AIS is relatively low (2) Level II-3, e.g., a review
article reported prevalence rates in the USA of 2 to 4% among children and
adolescents (3) Level III. A study in one urban area in Malaysia reported a prevalence
of 1.36% and 4.14% among children aged 11 and 15 years, respectively (4) Level
II-3
and a study on schoolchildren in Singapore found an increasing prevalence of
AIS among females between age 9 to 13 years old (5) Level II-3.
Scoliosis is more common, and progresses faster, in girls than boys, thus,
requiring treatment earlier compared to scoliosis in boys (4) Level II-3. Scoliosis
has a significant impact on the physical and psychosocial health of affected
individuals.
Thoracic curves are more likely to cause pulmonary complications whereas
Introduction 91
lumbar curves are more likely to produce postural problems. A lower marriage rate among
patients with scoliosis and their lack of participation in social functions infer that they have
poor self-image and are socially isolated (6) Level II-3.
15.2 Benefit of screening and treating adolescent

idiopathic scoliosis
In Malaysia, one study on untreated idiopathic scoliosis found that most patients present late
in adolescence and need surgical intervention (7) Level II-3. The mean age at presentation was
o
15 years and the median rate of curve progression was 7.03 per year. The mean curve size
at presentation was 41.6 degrees (7) Level II-3. Surgical intervention can be avoided if mild to
moderate scoliosis is detected early. Progressive Action Short Brace (PASB) and Milwaukee
brace are effective in improving thoraco-lumbar curves (8, 9) Level II-3. Countries with screening
programmes have noted a reduction in the need to have corrective surgery (10). However,
a more recent meta-analysis reported the evidence supporting bracing as an early effective
intervention is weak. (11)
Scoliosis can be assessed by measuring the angle of trunk rotation (ATR). ATR is measured
by a scoliometer placed on the spine of the adolescent in an Adam forward bent position
(Figure 15.1). Asymmetry noted by ATR should cast suspicion on the presence of AIS.
(a) (b)
Figure 15.1 Adam forward bent position (a), positioning a scoliometer (b)
92 Screening tests
o
An ATR of ≥7 needs further radiological evaluation (12) Level III. In a study on 150 children
referred to hospitals for evaluation of scoliosis, a comparison of the ATR from scoliometer
readings with Cobb angle measurements of lateral deviation of the spine found that an ATR
o
of 7o was significantly correlated with Cobb angle and scoliosis of ≥25 (13) Level III. This is
lower than the level to start bracing treatment - 300. The International Society on Scoliosis
Orthopaedic and Rehabilitation Treatment (SOSORT) recommends using the screening
o
referral criterion of ATR≥7 at any level of the spine for further assessment. Using this criterion
reduces the need for referral, spinal radiography and follow-up, thus, maintaining the cost
effectiveness of spinal screening programs (12 -16, 19) Level III (18) Level II-3.
Although The US Preventive Screening Task Force recommendations in 2010 - 2011 (20)
Level III
do not include screening scoliosis in adolescents, screening is recommended in local,
regional guidelines (5) Level II-3 (10, 16) Level III, the American Academy of Scoliosis Research,
Scoliosis Research Society, the Pediatric Orthopedic Society of North America and the
American Academy of Pediatrics (1) Level II-3. Some societies have recommended screening
twice for girls aged 10 and 12 years and males at the age of 13 or 14 (1) Level II-3. Singapore
has recommended yearly screening for adolescent girls (5) Level II-3. The Health Technology
Assessment (HTA) Ministry of Health Malaysia has recommended screening among high
risk adolescents especially 12 year-old girls using a combination of Adams forward-bending
test and scoliometer (10, 17) Level III because of the late presentation of AIS in the majority
of Malaysian patients. A study from Singapore has demonstrated the cost-effectiveness of
screening scoliosis among high-risk groups (21) Level III.
A review of evidence by HTA in 2009 noted that there was no progression of the curvature
in a majority of patients detected through screening, but there was progression in a greater
proportion of girls than boys (10). Screening may result in unnecessary brace wear and referral
for specialty, thus, the USPSTF has concluded that the harms of screening adolescents for
AIS exceed the potential benefits (20). However, the awareness of AIS is probably higher in
developed countries compared to developing countries, and screening may not add benefit
compared to the natural presentation of patients with AIS. In Malaysia, on the other hand,
many of the patients with AIS may not be aware of the early presentation of scoliosis. Hence,
although more patients will be unnecessarily followed-up with a screening programme, the
benefit of screening likely outweighs the harm.
REFERENCES
1. Richards BS, Vitale MG. Screening for idiopathic 16. Forman SF, Emans SJ. Current goals for adolescent
scoliosis in adolescents. an information statement. The healthcare. Hosp Physician 2000;36(1), 27-48
Orthopaedic Forum. J Bone Joint Surg Am 2008; 90(1): 17. Sabirin J, Bakri R, Buang SN, et al. School scoliosis
195-8. screening programme? A systematic review. Med J
2. Nery LS, Halpern R, Nery PC, et al. Prevalence of Malaysia 2010; 65(4): 261-7.
scoliosis among school students in a town in Southern 18. Bunge EM, Juttmann RE, van Blezen FC et al. Estimating
Brazil. Sao Paulo Med J 2010; 128(2): 69-73. the cost effectiveness of screening for scoliosis: a case
3. Reamy BV, Slakey JB. Adolescent idiopathic scoliosis: control study. Pediatrics 2008; 121 (1): 9-14.
review and current concepts. Am Fam Physician 2001; 19. Yawn BP, Yawn RA. The estimated cost of school
64(1): 111-6. screening. Spine 2000; 25 (18): 2387-91.
4. Azlin A. Screening for scoliosis among students age 20. U.S. Preventive Services Task Force. The guide to clinical
11 and 15 years old at Kuala Terengganu, Terengganu. preventive services 2010 - 2011: Recommendations of
Thesis submitted in partial fulfilment for the degree of the U.S. Preventive Services Task Force. Rockville (MD):
Masters of Medicine (family medicine) 2005. Agency for Healthcare Research and Quality (US); 2010
5. Yong F, Wong HK, Chow KY. Prevalence of adolescent 21. Thilagaratnam S. School-based screening for scoliosis:
idiopathic scoliosis among female school children in is it cost effective? Singapore Med J 2007; 48(11):
Singapore. Ann Acad Med Singapore 2009; 38(12): 1012.
1056-63.
6. McCarthy RE. Prevention of the complications of
scoliosis by early detection. Clin Orthop Relat Res
1987; (222): 73-8.
7. Chuah SI, Kareem BA, Selvakumar K et al. The natural
history of scoliosis curve progression of untreated
curves of different aetiology with early (mean 2 years)
follow up in surgically treated curves. Med J Malaysia
2001; 56 Suppl C: 37-40.
8. Aulisa AG, Guzzanti V, Galli M, et al. Treatment of
thoraco-lumbar curves in adolescent females affected
by idiopathic scoliosis with a progressive action short
brace (PASB): assessment results according to the SRS
committee on bracing and non-operative management
standardization criteria. Scoliosis 2009; 4: 21.
9. Jiang J, Qiu Y, Mao S, et al. The influence of elastic
orthotic belt and sagittal profile in adolescent idiopathic
thoracic scoliosis: a comparative radiographic study
with Milwaukee. BMC Musculoskelet Disord 2010; 11:
219.
10. Ministry of Health (MOH). Health Technology
Assessment Report [Internet]. Malaysia: Ministry of
Health; 2009. Available from: http://www.moh.gov.my/
attachments/7508.pdf.
11. Negrini S, Minozzi S, Bettany Saltikov j, et al. Braces for
idiopathic scoliosis in adolescents. Cochrane Database
Syst Rev 2010: 1
12. Samuelsson L, Norén L. Trunk Rotation In Scoliosis. The
influence of curve type and direction in 150 children.
Acta Orthop Scand 1997; 68(3): 273-6.
13. Grivas TB, Wade MH, Negrini S, et al. SOSORT
consensus paper: school screening for scoliosis. Where
are we today? Scoliosis 2007; 2: 17.
14. Huang SC. Cut-off point of the scoliometer in school
scoliosis screening. Spine (Phila Pa 1976) 1997;
22(17): 1985-9.
15. Bunnell WP. Outcome of spinal screening. Spine 1993;
18(12): 1572-1580.
94 References
16 Hearing Loss in Older People
SUMMARY
Hearing loss due to presbycusis is common among older people.

Hearing loss is associated with impaired quality of life but most cases are treatable.
Screening and treatments are non-invasive and generally are safe.
There is a high rate of non-use of hearing aids after hearing impairment is detected
by screening.
Current evidence primarily reports the benefit of using hearing aids for symptomatic
people.
The evidence is insufficient to assess the balance of benefits and harms of
screening for hearing loss in asymptomatic adults aged 60 years or older.
RECOMMENDATIONS
Routine screening for hearing impairment in asymptomatic adults Grade I

aged 60 years or older is not indicated.
Evaluation of hearing impairment should be as indicated clinically.
16.1 Introduction
Hearing loss is common in older adults with increasing prevalence and severity
with age (1 - 4) Level III. In the United States, national data showed that hearing
impairment affects 25% to 40% of those 65 years or older (3) Level III. In Malaysia,
a study in a primary care clinic reported that 24.3% of adults 60 years and
above felt they had hearing loss while 36.9% were detected to have hearing
loss by pure tone audiometry (5) Level III. Of the adults with hearing loss, majority
has mild hearing loss; 26.1% of adults above 60 years had mild hearing loss,
3.6% had moderate hearing loss, 6 (5.4%) had severe hearing loss and 1.8%
had profound hearing loss. Severity of hearing loss is defined as mild hearing
loss at 26-40 dBHL, moderate hearing loss at 41-60 dBHL, severe hearing loss
as 61-80 dBHL and profound hearing loss at 81 dBHL and above by pure tone
audiometry (PTA) measurement.(6)
Hearing loss can impact quality of life, ability to function and emotional wellbeing
Introduction 95
in older adults (7-10) Level I & III Studies have found that hearing loss is associated with increased
emotional dysfunction, depression, and social isolation (8 -11) Level III.
Hearing impairment is often missed and under-diagnosed for various reasons. The older
person with a hearing impairment may not be aware of their problem. The most common
cause of hearing loss in older persons is age-related hearing loss (presbycusis), a problem
which progresses with advancing age. The symptoms may be relatively mild or slowly
progressive. In addition, a study has revealed that some people may perceive hearing loss
but do not seek medical attention (1) Level III. Other than presbycusis, cerumen impaction and
chronic otitis media, which are treatable if detected early, may be present in up to 30% of
elderly patients with hearing loss (12) Level III.
16.2 Benefit of screening and treating hearing impairment
The benefits of a hearing aid were well demonstrated in adult patients with sensory neural
hearing loss (13) Level I. However, as this high quality review noted, the benefits were less clear
among screen-detected patients with presbycusis. Although one RCT showed benefits of
better communication ability, social function, life satisfaction, and emotional balance (8),
other RCTs (14, 15) were not able to show similar results with certainty (16). The review
commented that the RCT, which showed the benefits of hearing aids, recruited patients
not typically seen in the community (16) Level II. The findings are supported by a review
which showed self-reported hearing disability was the only significant factor affecting all
four outcome measures of hearing aid usage: help-seeking, hearing-aid uptake, use, and
satisfaction. (17)
There is direct evidence from randomized controlled trials evaluating the effect of screening
among adults aged 50 years and above to show that screening is associated with only a
small increase in hearing aid used (18). Many cohort studies following up patients after
screening and detecting hearing loss also demonstrated low hearing aid use, (19 -22) Level II
unless hearing impairment is significant (> 35dB hearing loss) (23) Level III. The small increase
in hearing aid usage was not found to have a discernible effect on hearing-related quality of
life in secondary analysis (16). Hence, hearing aid benefits only a small group of people with
mild hearing lost (> 26-40 dB hearing loss).
A cost analysis study in the United Kingdom found that a simple systematic screen, using two
questions concerning hearing problems and audiometric screening instrument, is justifiable
and may be cost-effective. The costs of screening and intervention were in the range of £800
-1000 (RM 4000 -5500) per quality-adjusted life-year using the Health Utilities Index (23) Level
III
. A later study on the cost-effectiveness of screening noted that patients screened with
audioscope have a higher hearing aid use after one year, rendering it more cost-effective (24)
Level II
. However, similar cost-effectiveness study is not available in Malaysia.
96 Benefit of screening and treating hearing impairment

Screening tests that can be used in an office setting include:
a) The Single Global Screening Question: “Do you or your family think that you may
have hearing loss?”
b) The Hearing Handicap Inventory for the Elderly-Screening (HHIES)
c) The AudioScope (a handheld otoscope with a built-in function of an audiometer)
d) The whispered voice test- if carried out meticulously.
As a screen for mild hearing loss (>25 dB), the Single Global Screening Question and HHIES
have almost similar sensitivity (58 -67%) (24). Although the whisper voice test has higher
sensitivity (95%), (25) Level II-2 it is difficult to standardise, and has high inter-observer variability
and poor test-retest reliability (26). All four methods have similar specificity (82-89%) (25) Level
II-2
.
As a screen for moderate hearing loss (>40 dB), the Single Global Screening Question
and HHIES also have comparable sensitivity (72-81%) while the AudioScope has higher
sensitivity (96%) (25) Level II-2. Both methods and the AudioScope have similar specificity
(72-76%) (25) Level II-2.
No randomized trial or controlled observational study has evaluated harms associated with
screening for hearing loss in older adults. A few case series have reported the potential
harms of hearing aids which include dermatitis, accidental retention of mould, cerumen
impaction, otitis externa and middle ear problems (27 -29) Level III. However, hearing aids are
non-invasive and are generally believed to be safe.
REFERENCES
1. Cruickshanks KJ, Wiley TL, Tweed TS, et al. Prevalence 16. Chou R, Dana T, Bougatsos C, Fleming C, Beil T.
of hearing loss in older adults in Beaver Dam, Wisconsin. Screening adults aged 50 years or older for hearing
The epidemiology of hearing loss study. Am J Epidemiol loss: a review of the evidence for the U.S. preventive
1998; 148(9):879-86. services task force. Ann Int Med 2011;154(5):347-55.
2. Gates GA, Cooper JC Jr, Kannel WB, Miller NJ. Hearing 17. Knudsen LV, Oberg M, Nielsen C, Naylor G, Kramer SE.
in the elderly: the Framingham cohort, 1983–1985, Factors influencing help seeking, hearing aid uptake,
part I: basic audiometric test results. Ear Hear 1990; hearing aid use and satisfaction with hearing aids: a
11(4):247-56. review of the literature. Trends Amplif 2010; 14(3):127-
3. Reuben DB, Walsh K, Moore AA, Damesyn M, Greendale 54
GA. Hearing loss in community-dwelling older persons: 18. Yueh B, Collins MP, Souza PE, Boyko EJ, Loovis
national prevalence data and identification using simple CF, Heagerty PJ, et al. Long-term effectiveness of
questions. J Am Geriatr Soc 1998; 46(8):1008-11. screening for hearing loss: the Screening for Auditory
4. Wallhagen MI, Strawbridge WJ, Cohen RD, Kaplan Impairment—Which Hearing Assessment-Test (SAI-
GA. An increasing prevalence of hearing impairment WHAT) randomized trial. J Am Geriatr Soc 2010;58:427-
and associated risk factors over three decades 34.
of the Alameda County Study. Am J Public Health 19. Meyer C, Hickson L, Khan A, Hartley D, Dillon H,
1997;87(3):440-42. Seymour J. Investigation of the actions taken by adults
5. Rosdina AK, Leelavathi M, Zaitun A, Lee VKM, Azimah who failed a telephone-based hearing screen. Ear Hear
MN, Majmin SH, Mohd KA. Self-reported hearing loss 2011;32(6):720-31.
among elderly Malaysians. Malaysian Family Physician 20. Thodi C, Parazzini M, Kramer SE, Davis A, Stenfelt S,
2010;5(2):91-4. Janssen T, et al. Adult hearing screening: follow-up and
6. World Health Organization fact sheet. Deafness and outcomes. Am J Audiol 2013;22(1):183-5.
hearing impairment. In: Organization W.H, editor. World 21. van den Berg PJ, Prins A, Verschuure H, Hoes AW.
Health Fact Sheet (#300 ed.) Geneva: World Health Effectiveness of a single and a repeated screen for
Organization; 2006. hearing loss in the elderly. Audiology 1999;38(6):339-
7. Gates GA, Mills JH. Presbycusis. Lancet 2005; 40.
366(9491): 1111-20. 22. Yasuda K, Furukawa M. [Hearing examination program
8. Mulrow CD, Aguilar C, Endicott JE, et al. Quality-of-life status in those aged 65 to 74--Knazawa hearing
changes and hearing impairment: a randomized trial. examination program findings]. Nihon Jibiinkoka Gakkai
Ann Intern Med 1990; 113(3): 188-94. kaiho. 2009;112(2):73-81.
9. Weinstein BE, Ventry IM. Hearing impairment and social 23. Davis A, Smith P, Ferguson M, Stephens D, Gianopoulos
isolation in the elderly. J Speech Hear Res 1982; 25(4): I. Acceptability, benefit and costs of early screening for
593-9. hearing disability: a study of potential screening tests
10. Carabellese C, Appollonio I, Rozzini R, et al. Sensory and models. Health technology assessment (Winchester,
impairment and quality of life in a community elderly England) 2007;11(42):1-294.
population. J Am Geriatr Soc 1993; 41(4): 401-7. 24. Liu CF, Collins MP, Souza PE, Yueh B. Long-term cost-
11. Appollonio I, Carabellese C, Magni E, Frattola L, effectiveness of screening strategies for hearing loss. J
Trabucchi M. Sensory impairments and mortality in Rehabil Res Dev 2011;48(3):235-43.
an elderly community population: a six-year follow-up 25. Roger Chou, Tracy Dana, Christina Bougatsos, et al.
study. Age and ageing 1995;24(1):30-6. Screening for hearing loss in adults ages 50 years
12. Yueh B, Shapiro N, MacLean CH, Shekelle PG . Screening and older : a review of the evidence for the U.S.
and management of adult hearing loss in primary care. Preventive Services Task Force. Evidence Syntheses,
JAMA 2003;289:1976-85 No. 83. Oregon Evidence-based Practice Center and
13. Chisolm T H JCE, Danhauer J L, Portz L J, Abrams H Kaiser Permanente Center for Health Research. AHRQ
B, Lesner S, McCarthy P A, Newman C W. A systematic Publication No. 11-05153-EF-1. March 2011.
review of health-related quality of life hearing aids: 26. Boatman DF, Miglioretti DL, Eberwein C, et al. How
final report of the American Academy of Audiology Task accurate are bedside hearing tests? Neurology 2007;
Force on the Health-Related Quality of Life Benefits of 68(16): 1311-4.
Amplication in Adults 2007;18(2):151-83 27. Kohan D, Sorin A, Marra S, Gottlieb M, Hoffman R.
14. Yueh B, Souza PE, McDowell JA, Collins MP, Loovis Surgical management of complications after hearing aid
CF, Hedrick SC,et al. Randomized trial of amplification fitting. Laryngoscope 2004;114(2):317-22.
strategies. Arch Otolaryngol Head NeckSurg 28. Sood A, Taylor JS. Allergic contact dermatitis from
2001;127:1197-204. hearing aid materials. Dermatitis 2004;15(1):48-50.
15. Jerger J, Chmiel R, Florin E, Pirozzolo F, Wilson N. 29. Lear JT, Sandhu G, English JS. Hearing aid dermatitis:
Comparison of conventional amplification and an a study in 20 consecutive patients. Contact Dermatitis
assistive listening device in elderly persons. Ear Hear 1998;38(4):212.
1996;17:490-504.
98 References
17 Visual Impairment in Older Persons
SUMMARY
Visual impairment in older persons is common.

Although most of the common causes of visual impairment in older persons can
be treated, the overall outcome through screening has not proven beneficial,
possibly due to poor adherence to treatment advice. There is insufficient evidence
to support routine screening for visual impairment.
Visual acuity chart and pinhole test are the usual screening tests easily done in
primary care settings.
RECOMMENDATIONS
Routine screening for visual impairment is not indicated. Grade I

Evaluation of visual impairment should be as indicated clinically.
17.1 Introduction
Visual impairment is defined as a presenting visual acuity of worse than 6/18 but
equal or better than 3/60; whereas blindness is diagnosed when visual acuity
is worse than 3/60 (1) Level III. The prevalence of visual impairment among older
persons in Malaysia was 12.3% (2) Level III. An unpublished finding from National
Eye Survey II in 2014 reported a prevalence of low vision (presenting with visual
acuity of less than 6/18 to 3/60) of 5.4%. The prevalence worldwide varies from
7 to 34% (3). Visual impairment in older Malaysians is associated with increased
risk of falls and low fragility hip fracture (4) Level II-2, as well as reduced visual
related quality of life (5) Level III. The common causes of visual impairment include
uncorrected refractive error, cataract, and age-related macular degeneration
(2, 6) Level III. These conditions can be effectively treated, hence, may result in
improved health-related quality of life (7, 8) Level II-2.
Introduction 99
17.2 Benefit of screening visual impairment and treating
common causes of visual impairment
Corrective lenses (9) and cataract surgeries have been shown to be beneficial interventions
for refractive errors and aged-related cataract (9, 10). In addition, a lower rate of progression
of vision loss has also been demonstrated in patients who undertook treatment for age-
related macular degeneration (9).
The aim of screening for visual impairment is to improve visual function. Cluster and
randomised controlled trials have showed that vision screening using visual acuity testing
followed by the necessary intervention does not improve visual acuity, other clinical or
functional outcomes, and vision-related quality of life when compared to no or delayed
screening (11 - 14) Level I.
In a meta-analysis, three to five years after screening, the risk ratio for visual acuity less than
6/18 in the universal screening group compared to a targeted screening group with health-
related problems was 1.07 (95% CI 0.84 to 1.36, p = 0.58). The visual function difference
of 0.4 (95% CI -1.7 to 2.5, p = 0.69) between the universal and targeted screening groups
was also not significant (15) level I. Adherence to treatment advice after identification of visual
impairment in many trials was noted to be poor (9). The common reasons for poor adherence
were disbelief in the test results, not having financial support and not knowing the need to
see an eye care provider (16).
In primary care, the screening tests for measuring visual acuity of both distance and reading
acuity in older persons include the visual acuity chart and pinhole test (17) Level III. The visual
acuity chart has higher sensitivity in detecting reading acuity (sensitivity: 98%; specificity:
3%) than the distance visual acuity (sensitivity: 47%; specificity: 84%). The pinhole test has a
sensitivity of 34% and specificity of 86% in detecting refractive error (18) Level III.
Screening questions have weak validity (9) as patients may overestimate the adequacy of
their vision (19).
There is no evidence on serious harm from vision screening of asymptomatic older persons (9)
besides the potential general harm caused by screening, such as anxiety and complications
of treatment following screen-detected visual impairment. Posterior capsule opacification of
100 Benefit of screening visual impairment and treating common causes of visual impairment
intra-ocular lenses, which is reported and can be treated easily, is uncommon after cataract
surgery. Other complications of cataract surgery are also uncommon (1% or less) (9). Notably,
a small increased risk of falls is associated with the use of multifocal lenses in older adults (9)
and after screening by optometrists (12).
Some guidelines have recommended vision screening of community-dwelling older persons

annually because treatment is available for most causes of visual impairment (20) Level III.
However, this recommendation is based on the clinical experience of the guidelines group.
Vision screening in older persons as part of a periodic health examination in the primary
care setting is not recommended because of insufficient direct evidence on the benefit of
screening (9, 21) Level III. Nevertheless, physicians should individualise the decision to screen
patients with subjective decrease in vision.

REFERENCES
1. World Health Organization. ICD update and revision of follow-up and factors associated with follow-up
platform: Change the definition of blindness. Geneva, of participants with abnormal frequency doubling
WHO, 2010. perimetry technology results. Ophthalmic Epidemiol
2. Zainal M, Ismail SM, Ropilah AR, et al. Prevalence of 2007;14(3):134-40.
blindness and low vision in Malaysian population: 17. Chu-Ai Teh R, Lim WS, Basri R, Ismail NH. Utility of
Results from the national eye survey 1996. Br J a patient-response screening question for visual
Ophthalmol 2002;86(9):951-6. impairment. J Am Geriatr Soc 2006;54(2):370-2.
3. Evans BJ, Rowlands G. Correctable visual impairment in 18. Ivers RQ, Macaskill P, Cumming RG, Mitchell P. Sensitivity
older people: a major unmet need. Ophthalmic Physiol and specificity of tests to detect eye disease in an older
Opt 2004;24(3):161-80. population. Ophthalmol 2001;108:968-75
4. Chew FLM, Yong C-K, Ayu SM, Tajunisah I. The 19. Long CA, Holden R, Mulkerrin E, Sykes D. Opportunistic
association between various visual function tests and screening of visual acuity of elderly patients attending
low fragility hip fractures among the elderly: a Malaysian outpatient clinics. Age ageing 1991;20(6):392-5.
experience. Age Ageing 2010;39(2):239-45. 20. Ministry of Health, Singapore. Functional screening
5. Omar R, Knight VF, Sazlina K, Syarifah N SA. Effect of for older adults in the community. Ministry of Health,
visual disturbances on daily activities and quality of life Singapore: Chung Printing; 2010.
among elderly in the Klang Valley. No date (Assessed 21. American Academy of Family Physicians. Visual- clinical
2015 Apr 27). Available from: http://ukm.academia. preventive services: Recommendations, Resources &
edu/RokiahOmar/Papers/247039/Effect_of_Visual_ Policies [Internet]. No date (Assessed 2015 Apr 27).
Disturbances_on_a daily_activities_and_quality_of_ Available from: http://www.aafp.org/online/en/home/
life_among_elderly_in_the_Klang_Valley. clinical/exam/visual.html.
6. Jessa Z, Evans B, Thomson D, Rowlands G. Vision
screening of older people. Ophthalmic Physiol Opt
2007;27(6):527-46.
7. Owsley C, McGwin G, Scilley K, et al. Effect of refractive
error correction on health-related quality of life and
depression in older nursing home residents. Arch
Ophthalmol 2007;125(11):1471-7.
8. Owsley C, McGwin G, Scilley K, et al. Impact of cataract
surgery on health related quality of life in nursing home
residents. Arch Ophthalmol 2007;91:1359-63.
9. Chou R, Dana T, Bougatsos C. Screening older adults
for impaired visual acuity: a review of evidence for the
U.S Preventive Services Task Force. Ann Intern Med
2009;151:44-58.
10. Riaz Y, Mehta J, Wormald R, Evans J, Foster A, Ravilla T
et al. Surgical interventions for age-related cataract. Am
J Ophthalmol 2007;143(4):733-4.
11. Swamy B, Cumming RG, Ivers R et al. Vision screening
for frail older people: a randomised trial. Br J Ophthalmol
2009;93(6):736 -41.
12. Cumming RG, Ivers R, Clemson L, et al. Improving vision
to prevent falls in frail older people: a randomized trial. J
Am Geriatric Society 2007;55:175-81.
13. Smeeth L, Fletcher AE, Hanciles S, et al. Screening
older people for impaired vision in primary care: cluster
randomised trial. BMJ 2003;327(7422):1027.
14. Eekhof J, De Bock G, Schaapveld K, Springer M.
Effects of screening for disorders among the elderly:
an intervention study in general practice. Fam Pract
2000;17(4):329 -33.
15. Smeeth L, Iliffe S. Community screening for visual
impairment in the elderly. Cochrane Database Syst Rev
2006(3):Cd001054.
16. Mansberger SL, Edmunds B, Johnson CA, Kent KJ,
Cioffi GA. Community visual field screening: prevalence
102 References
18 Risk of fall in older people
SUMMARY
Falls are common among older people and are associated with a substantial risk
of morbidity and mortality.
There are many risk factors associated with falls especially history of previous falls.
However, there is no single reliable screening test to adequately predict the risk
of falls.
Structured exercise and Vitamin D supplementation are noted to reduce the risk
of falls.
In the local context, there is no evidence to support the effectiveness of falls
prevention intervention. Moreover, there are limited resources in the primary care
setting to conduct multi-factorial fall risk assessment and intervention.
RECOMMENDATIONS
Identification of intrinsic and extrinsic risk factors, followed by Grade C

subsequent interventions to reduce the risk is indicated for high-
risk patients with relevant medical co-morbidities.
Screening, followed by a comprehensive fall risk assessment and Grade I
structured intervention (balance and strengthening exercise), is
indicated if facilities are available.
18.1 Introduction
Falls are common among the older people (1). In the United States, up to
40% of older persons aged 65 years and above in the community had one or
more falls in the previous 12 months (2, 3 Level III). A tenth of the older people in
the community and a fifth of institutionalised older people sustained an injury
secondary to their falls (4). In Malaysia, a study on the prevalence of falls among
older people attending an urban primary care clinic was reported to be 47% (5
Level III
). Most of them had experienced recurrent falls with the majority occurring
in their homes.
From various studies, it can be summarized that the risks of falls are related
to both intrinsic and extrinsic factors (4, 6, 7, 8) Level III, the majority of which are
Introduction 103
preventable (9, 10) Level III.
Intrinsic risk factors include medical co-morbidities of (4, 9, 11, 12, 13):
i. vision impairment
ii. muscular-skeletal and gait imbalance
iii. cognitive impairment
iv. polypharmacy
v. a history of fall
Extrinsic factors, which are related to environmental hazards, include rugs, slippery flours,
inadequate handrails and unsuitable footwear (4, 8).
Falls could lead to significant morbidity, and mortality, as well as affect the quality of life of
the older persons (1 Level III). Fall in older people is the main risk factor for fragility fracture and
hence the morbidity and mortality associated with it (4). It is also a risk factor for intracranial
haemorrhage, functional limitations, soft tissue injuries and dislocation. Hence, the healthcare
cost after falls and mortality are substantial (6).
18.2 Benefit of screening and intervention for fall

prevention
A few effective primary care interventions to prevent falls and recurrent falls among
community dwelling older persons have been shown. (9, 14 -17 Level I). Exercise in the form
of strength training and balance, gait, and coordination training, either carried out as a single
intervention or as part of a multi-component, has proven beneficial in preventing falls (16)
Level III
. Specifically, the systematic review found the benefit of physical therapy or exercise
intervention (OR 0.87 (0.81–0.94) to be moderate (16) Level I. Similarly, a moderate benefit with
vitamin D supplementation (0.83 (0.77–0.89) (16) Level I. In a multi-factorial clinical assessment
with comprehensive management of identified risk factors, however, there was only a small
reduction in the risk of falls (RR 0.89, CI 95%, 0.76 -1.00) (16) Level I. The USPSTF has defined
multi-factorial assessment and management as “a clinical assessment of ≥2 domains of
functioning, generally supplemented by assessment of falls-related or general geriatric risk
factors or conditions, with assessment results used as a basis for remedial management
(16, 18).
The benefits of other single intervention strategies, such as visual correction, medication
assessment and withdrawal and home-hazard modification, have not been demonstrated
(16).
104 Benefit of screening and intervention for fall prevention

Many of the trials on fall risk intervention involved older people with high risk identified through
clinical assessment (16). In summary, stronger evidence of benefit was seen in single specific
intervention than comprehensive multi-factorial intervention (18). Treating risk factors for
falling can reduce falls by 30 to 40% (15) Level I. However, the benefit of falls intervention
can be subject to cultural variations because it is related to customary activities by the
community (19). Given that the participants in trials have a high risk of falls and there is no
consistency in selecting trial participants, direct evidence to support the benefit of screening
compared to non-screening cannot be concluded (16).
While the risks of falls have been identified and many screening tools to assess these risks
have been developed, no single tool can adequately predict falls (20, 21) Level III. Most tools
discriminate poorly between fallers and non-fallers. The common tests used, such as Timed
Up and Go Test, and Functional Reach Test, are based on clinical judgment and have cut-
off values for the standardized times that have not been validated locally (17, 18, 21) Level III.
Therefore, screening by asking if the individual has fallen in the past year is suggested (9, 17,
22) Level III. This questioning has a sensitivity of 93% to 95% and specificity of 20% to 21% in
predicting a single fall in the subsequent year (21) Level III. A history of ever-fall has a sensitivity
of 77% and specificity of 55% to predict recurrent falls (21) Level III. The American Geriatrics
Society/British Geriatrics Society guideline for falls prevention also recommends enquiring
about gait or balance problems (9) Level III.
A positive answer to any of the above questions improves falls prediction and warrants
a multi-factorial fall assessment, where available (16) Level III. Multi-factorial assessment
includes medication review, gait and balance, visual acuity, heart rate and rhythm, postural
hypotension, feet and footwear, and environmental hazards assessment (9) Level III. The
treatment of individual risk factors can be undertaken by trained clinicians. The optimal
benefit of screening is seen if multi-factorial assessments and interventions are undertaken.
The reported harms arising from physical therapy and exercise intervention, such as a
paradoxical increase in falls and increased physician visits, are small (18) Level III. According to
the USPSTF, there are no reports on the side effects of vitamin D supplementation. However,
concomitant administration of calcium and vitamin D supplementation has a small increased
risk of renal calculi (HR 1.17, 95% CI 1.02 to 1.34). There is also no evidence of serious
harms associated with multi-factorial clinical assessment with comprehensive management
of identified risk factors (18) Level III.

REFERENCES
1. Ozcan A, Donat H, Gelecek N, et al. The relationship a systematic evidence review for the U.S. Preventive
between risk factors for falling and the quality of life in Services Task Force. Ann Intern Med 2010;153:815-25.
older adults. BMC Public Health 2005;5:90. 17. The Royal Australian College of General Practitioners.
2. Centers for Disease Control and Prevention (CDC). Self- Guidelines for preventive activities in general practice.
reported falls and falls at home among person more 7th edn. Melbourne: The Royal Australian College of
or equal 65 years - United States 2006. MMWR Morb General Practitioners 2009.
Mortal Wkly Rep 2008;57:225-9. 18. Moyer VA. Prevention of falls in community-dwelling
3. Rubenstein LZ, Josephson KR. The epidemiology of falls older adults: U.S. Preventive Services Task Force
and syncope. Cli Geriatric Med 2002;18:141-58. Recommendation Statement. Ann Intern Med
4. Karlsson MK, Magnusson H, von Schewelov T, 2012;157:197-204.
Rosengren BE. Prevention of falls in the elderly -a 19. Tan P, Khoo E, Chinna K, Hill K, Poi P, Tan M. An
review. Osteoporos Int 2013;24:747–62 individually-tailored multifactorial intervention program
5. Sazlina SG, Krishnan R, Samsul AS, et al. Prevalence for older fallers in a middle-income developing country:
of falls among older people attending a primary care Malaysian Falls Assessment and Intervention Trial
clinic in Kuala Lumpur Malaysia. Malaysian Journal of (MyFAIT). BMC Geriatr. 2014;14(1):78.
Community Health 2008;14(1):11-5. 20. Scott V, Votova K, Scanlan A, Close J. Multifactor and
6. Kannus P, Saevanen H, Palavanen M, et al. Prevention mobility assessment tools for falls risk among older
of falls and consequent injuries in elderly people. Lancet adults in community, home support long term patient
2005;366:1885-93. care setting. Age Ageing 2007;36:130-9.
7. Tinetti ME. Clinical Practice. Preventing falls in elderly. N 21. Simon Gates, Lesley A Smith, Joanne A Fisher, et al.
Engl J Med 2003;348:42-9. Systematic review of accuracy of screening instrument
8. Connelv BR, Wolf SL. Environmental and behavioural for predicting falls among independent older adults. J
circumstances associated with falls at home among Rehabil Res Dev 2001;45:1105-16.
healthy elderly individuals. Atlanta FICSIT Group. Arch 22. Ganz DA, Bao Y, Shekelle PG, Rubenstein LZ. Will my
Phys Med Rehabil 1997;78:179-86. patient fall? JAMA 2007;297(1):77-86.
9. Panel for Prevention of Falls in Older Persons, American
Geriatrics Society and British Geriatrics Society.
Summary of the updated American Geriatrics Society/
British Geriatrics Society Clinical practice guideline for
prevention of falls in older persons. J Am Geriatr Soc
2011;59(1):148-57.
10. National Institute for Health and Clinical Excellence.
The assessment and prevention of falls in older people.
London: National Institute for Health and Clinical
Excellence 2004.
11. Tromp AM, Pluijm SMF, Smit JH, Deeg DJH, Bouter LM,
Lips PTAM. Fall-risk screening test: a prospective study
on predictors for falls in community-dwelling elderly. J
Clin Epidemiol 2001;54(8):837-44.
12. Chu LW, Chi I, Chiu AY. Incidence and predictors of
falls in the Chinese elderly. Ann Acad Med Singapore
2005;34(1):60-72.
13. Deandrea S, Lucenteforte E, Bravi F, Foschi R, La Vecchia
C, Negri E. Risk factors for falls in community-dwelling
older people: a systematic review and meta-analysis.
Epidemiology. 2010;21(5):658-68
14. Gillespie LD, Gillespie WJ, Robertson MC, et al.
Interventions for preventing falls in older people living
in the commmunity. Cochrane Database Syst Rev
2012;9:CD007146.
15. Chang JT, Morton SC, Rubenstein LZ, et al. Interventions
for the prevention of falls in older adults: systematic
review and metaanalysis of randomised clinical trials.
BMJ 2004;328:680.
16. Michael YL, Whitlick EP, Lin JS, et al. Primary Care -
Relevant interventions to prevent falling in older adults:
106 References
19 Dementia in Older People
SUMMARY
Dementia is common among older persons.

The burden of dementia is high, especially those with behavioural and psychological
symptoms of dementia.
Evidence is lacking on the benefit of screening asymptomatic older person.
There are potential psychological, social and ethical impacts on persons with
a positive screening test but who do not meet the criteria for dementia after
evaluation.
There is insufficient evidence to recommend screening for dementia in
asymptomatic people aged 60 and above at primary care.
RECOMMENDATIONS
Routine screening for dementia in individuals aged 60 and above Grade I

is not indicated. Evaluation of dementia should be as indicated
clinically.
19.1 Introduction
Dementia is defined as an acquired syndrome of decline in memory and at
least one other cognitive domain, such as language, visual-spatial or executive
function, sufficient to interfere with social or occupational functioning in an alert
person (1) Level III. Alzheimer’s disease and vascular dementia are the two most
common causes of dementia. In Malaysia, the NMHS-III study showed that
11.2% of the adult population has some form of psychiatric morbidity (2) Level III.
The prevalence of dementia in Malaysia (3) Level III was found to be 9.5% (in 60-69
age group), which is similar to a study in Thailand (9.88%) (4) Level III but higher than
the prevalence in Singapore (5.2%) (5) Level III. Our estimate of the prevalence of
dementia is higher than the age-standardized prevalence of 5-7% in most world
regions (6). The variation in the estimates is likely due to different tools used in
the studies. Dementia affects individuals functioning in various stages depending
on the degree of ailment. In the early stages, instrumental activities of daily living
and organizational ability are affected, while in later stages, activities of daily
Introduction 107
living are also affected and, ultimately, are dependent on caregivers for almost all aspects
of living. In one study, patients with dementia living at home were noted to have a high level
of unmet needs in care for their daytime activities and psychological distress (7). Therefore,
the caregivers’ burden is significant. In middle and low income countries, the caregivers of
patients with dementia experience substantial strains and adverse economic impact similar
to those in high income countries (6).Level III Mild cognitive impairment (MCI) is a clinical entity
that may predict later development of dementia. Hence, detecting MCI is argued to result in
early detection of risk of dementia, which allows for early intervention to improve prognosis,
and facilitate decision-making while patients still retain their decision-making capacity (8).
19.2 Benefit of screening and treating dementia
There is some evidence to suggest that early detection and active treatment at the point
of sharp decline in cognitive function delays the subsequent need for nursing home care
and reduces the risk of misdiagnosis and inappropriate management (9) Level III. However,
the established modalities for treatment, i.e., cholinesterase inhibitors, confer only modest
benefits in terms of clinicians’ global impression of change in cognition, function, and
behaviour in mild to moderate Alzheimer’s disease (10) Level I. Current evidence does not
support the use of cholinesterase inhibitors in the treatment of mild cognitive impairment
(11) Level I. Although diagnosing dementia provides an opportunity for non-pharmacological
interventions, such as caregiver support, the evidence for any benefit in early detection is
lacking.

The Mini-Mental State Examination (MMSE) is the best-studied screening instrument for
primary care settings with a sensitivity of 88.3% (95% CI, 81.3% to 92.9%) and specificity
of 86.2% (CI, 81.8% to 89.7%) using the most commonly reported MMSE cut-off scores of
23/24 or 24/25 (12) Level III, (13) Level II for detecting dementia. A drawback of the MMSE is that
its accuracy depends upon the age, education, and ethnicity of the individual. In this regard,
it is most accurate for Caucasians with at least a high school education (14) Level III, (15) Level IIII.

Other instruments with adequate test performance to detect dementia include the Clock
Drawing Test, Mini-Cog, Memory Impairment Screen, Abbreviated Mental Test, 7-Minute
Screen and Informant Questionnaire on Cognitive Decline in the Elderly. These tests are
promising but need further testing in primary care populations (13) Level III.
108 Screening tests

Concerns have been raised about the potential psychological, social and ethical impact
on persons with a positive screening test but who do not meet the criteria for dementia
after evaluation. Stress-inducing practical, social and psychological difficulties have been
reported among patients coping with an uncertain diagnostic label (16) Level III, (17) Level III.
There are ethical concerns of exposing, otherwise well, screen-positive individuals to

possible morbidity from current pharmacological modalities of treatment (18) Level II-2, (19) Level
III
. A recent study reported that new users of cholinesterase inhibitors are associated with
increased rates of hospital visits for syncope and bradycardia, pacemaker insertion, and hip
fracture among community-dwelling older people with dementia (18) Level II-2. The risk of these
previously under-recognised serious adverse events must be weighed carefully against the
drugs’ high costs and the generally modest benefits.
Thus, current evidence does not support routine screening of dementia in asymptomatic
older people in primary care setting due to lack of evidence on positive health outcomes
with screening (20) Level II-2.

REFERENCES
1. American Psychiatric Association, ed. Diagnostic and 14. Gauthier S, Reisberg B, Zaudig M, et al. Mild cognitive
statistical manual of mental disorders. Washington D.C impairment. Lancet 2006;367(9518):1262-70.
1994. 15. Banningh L, Vernooij-Dassen M, Rikkert MO, et al. Mild
2. Institute of Public Health. Psychiatric Morbidity, a report cognitive impairment: coping with an uncertain label. Int
of the Third National Health and Morbidity Survey. J Geriatr Psychiatry 2008;23(2):148-54.
Ministry of Health Malaysia 2006. 16. Birks J. Cholinesterase inhibitors for Alzheimer’s
3. Hamid TA, Krishnaswamy S, Abdullah SS, Momtaz disease. Cochrane Database Syst Rev 2006.
YA. Socio-demographic risk factors and correlates of 17. Doody RS, Ferris SH, Salloway S, et al. Donepezil
dementia in older Malaysians. Dement Geriatr Cogn treatment of patients with MCI: 48-week randomized,
Disord 2010;30(6):533-9. placebo-controlled trial. Neurology 2009;72:1555-61.
4. Chiam PC, Ng TP, Tan LL, et al. Prevalence of dementia 18. Gill SS, Anderson GM, Fischer HD, et al. Syncope and
in Singapore--results of the national mental health its consequences in patients with dementia receiving
survey of the elderly 2003. Ann Acad Med Singapore cholinesterase inhibitors: a population-based cohort
2004;33(5 Suppl):S14-5. study. Arch Intern Med 2009;169(9): 867-73.
5. Senanarong V, Poungvarin N, Sukhatunga K, et al. 19. Whitehouse PJ, Juengst ET. Anti-aging medicine and
Cognitive status in the community dwelling Thai elderly. mild cognitive impairment: practice and policy issues for
J Med Assoc Thai 2001;84(3):408-16. geriatrics. J Am Geriatr Soc 2005 Aug;53(8):1417-22.
6. Prince M, Brodaty H, Uwakwe R, Acosta D, Ferri C, 20. Borson S, Scanlan J, Hummel J, et al. Implementing
Guerra M et al. Strain and its correlates among carers routine cognitive screening of older adults in primary
of people with dementia in low-income and middle- care: process and impact on physician behavior. J Gen
income countries. A 10/66 Dementia Research Group Intern Med 2007;22(6):811-7.
population-based survey. Int J Geriatr Psychiatry
2012;27(7):670-82.
7. Miranda-Castillo C, Woods B, Galboda K, Oomman S,
Olojugba C, Orrell M. Unmet needs, quality of life and
support networks of people with dementia living at
home. Health Qual Life Outcomes 2010;8(1):132.
8. Lin JS, O’Connor E, Rossom R, Perdue LA, Burda BU,
Thompson M, Eckstrom E. Screening for cognitive
impairment in older adults: An evidence update for
the U.S. Preventive Services Task Force. Evidence
Report No. 107. AHRQ Publication No. 14-05198-EF-
1. Rockville, MD: Agency for Healthcare Research and
Quality; 2013.
9. Dementia: a NICE-SCIE guideline on supporting people
with dementia and their careers in health and social
care. Social Care Institute for Excellence (2006) National
Institute for Health and Clinical Excellence. The British
Psychological Society and Gaskell. National Clinical
Practice Guideline 2006.
10. McDowell I, Kristjansson B, Hill GB, Hebert R. Community
screening for dementia: the Mini Mental State Exam
(MMSE) and Modified Mini-Mental State Exam (3MS)
compared. J Clin Epidemiol 1997;50(4):377-83.
11. Jennifer S, Elizabeth O, Rebecca C, Leslie A, Elizabeth
E. Screening for cognitive impairment in older adults: a
systematic review for the U.S. Preventive Services Task
Force. Ann Intern Med 2013;159:601-12.
12. Sahadevan S, Lim PP, Tan NJ, Chan SP. Diagnostic
performance of two mental status tests in the older
Chinese: influence of education and age on cut-off
values. Int J Geriatr Psychiatry 2000;15(3):234-41.
13. Ng TP, Niti M, Chiam PC, Kua EH. Ethnic and educational
differences in cognitive test performance on mini-mental
state examination in Asians. Am J Geriatr Psychiatry
2007 Feb;15(2):130-9.
110 References
20 Urinary Incontinence in Older People
SUMMARY
Urinary incontinence is common among older persons in the community.

The causes of urinary incontinence can be potentially treated, but the evidence for
quality of life improvements following treatment is limited.
Simple validated screening questions are available for use on selected patients.
The evidence is insufficient to assess the balance of benefits and harms of
screening for urinary incontinence in asymptomatic adults aged 60 years or older.
RECOMMENDATIONS
Routine screening for urinary incontinence for adults aged 60 years Grade I
or older is not indicated. Evaluation of urinary incontinence should
be as indicated clinically.
20.1 Introduction
The International Continence Society defines urinary incontinence as a condition

where there is any involuntary loss or leakage of urine which is a social or
hygienic problem (1). Urinary incontinence can be classified as urge, stress,
overflow, functional, or mixed incontinence. Reversible causes of incontinence
should be ruled out. These include delirium, infection (UTI), atrophic vaginitis,
pharmaceuticals, psychological causes such as depression, excess urinary
output due to, e.g., hyperglycaemia, restricted mobility and stool impaction (2)
Level III
. The prevalence of urinary incontinence ranges from 4.6 to 42% in the
community (3 -6) Level III and is higher in institutions (6) Level III. In a rural community
in Selangor, the prevalence was noted to be 9.9% (7) Level III. A high rate of urinary
incontinence in the general population suggests that screening for this condition
should be increased in general practice (8, 9) Level III. Urinary incontinence is
associated with the development of decubitus ulcers, sepsis, renal failure and
increased mortality (9) Level III. Psychosocial implications include loss of self-
esteem, restriction of social and sexual activities and depression (9) Level III. It is a
key factor in deciding on nursing home placement (10) Level III.
Introduction 111
20.2 Benefit of screening urinary incontinence and
treating urinary incontinence
Behavioural therapy has been shown to reduce incontinence episodes and reduced quantity
of urine loss in patients with stress and urge urinary incontinence (11) Level III. However, the
role of medications in urge urinary incontinence has shown only a small effect in improving
symptoms (12) Level I. There is limited evidence on quality of life improvements among patients
treated for urinary incontinence.
The following questions have been validated for use as a screening tool for urinary
incontinence as they are simple and efficient.
“In the last one year, have you ever lost urine and gotten wet?”
“If yes, have you lost urine on six separate days?”
The sensitivity of these questions is reported to be 65.5%, specificity 96%, positive predictive
value 93.7%, and negative predictive value 81.7% (13) Level III. Urinary incontinence can also
be screened using the International Consultation on Incontinence Questionnaire Urinary
Incontinence -Short Form (ICIQ-UI-SF) (14) Level III. This has a sensitivity and specificity of
92.1% and 55.6%, respectively, and positive predictive value and negative predictive value of
88.3% and 65.9%, respectively. This questionnaire represents a good compromise between
scientific expectations and practicality (14). However, using a screening questionnaire like
the ICIQ-UI-SF would be time consuming because older adults may not be fluent in English
(13) level III which could lead to misinterpretation of the results/findings by the assessors if they
are untrained (13) Level III. Furthermore, using ICIQ-UI-SF requires permission from ICIQ group.
There is no randomised trial or controlled observational study evaluating harms associated

with screening for incontinence among older adults. Some guidelines recommend screening
for urinary incontinence because it causes considerable impairment leading to a reduced
quality of life (9, 14) Level III. This recommendation was based on the clinical experience
of the guideline group. Urinary incontinence screening in the primary care setting is not
recommended because of insufficient direct evidence on its benefit. However, physicians
should individualise the decision-making process to screen for urinary incontinence among
older persons.

REFERENCES
1. Foldspang A, Mommens S. The International Continence

Society (ICS) Incontinence definition: Is the social and
hygienic aspect appropriate for etiologic research? J
Clin Epidemio 1997; 50(9): 1055-60.
2. The Royal Australian College of General Practice.
Clinical practice guidelines on managing incontinence
in general practice. 1st Edition 2002.
3. Homma Y, Imajo C, Takahashi S, et al. Urinary symptoms
and urodynamics in a normal elderly population. Scand
J Urol Nephrol Suppl 1994; 157: 27-30.
4. Andrews G, Cheok F. The Australian longitudinal study
of aging: key findings of a multidimensional pilot survey
study. Adelaide: Center for Aging Studies; 1990:1- 25.
5. Kok AL, Voorhorst FJ, Burger CW, et al. Urinary and
faecal incontinence in community-residing elderly
women. Age & Ageing 1992; 21(3): 211-5.
6. Chan CJ, Lee KS, Anne M, et al. Urinary incontinence
among the elderly people of Singapore. Age & Ageing
1991; 20(4): 262-6.
7. Sherina Mohd Sidik. The prevalence of urinary
incontinence among the elderly in a rural community in
Selangor. Malays J Med Sci 2010; 17(2): 18-23.
8. Scottish Intercollegiate Guidelines Network (SIGN).
Clinical Guidelines - Numerical List: Management of
urinary incontinence in primary care [Internet]. 2015
[cited 27 April 2015]. Available from: http://www.sign.
ac.uk/guidelines/published/numlist.html
9. Weiss BD. Diagnostic evaluation of urinary incontinence
in geriatric patients. Am Fam Physician 1998; 57(11):
2675-84
10. Johnson TM II, Bernard SL, Kincade JE, et al. Urinary
incontinence and risk of death among community-living
elderly people: results from the National Survey on Self-
Care and Aging. J Aging Health 2000;12:25-46
11. Fantl J. Efficacy of bladder training in older women with
urinary incontinence. JAMA 1991;265(5):609-13.
12. Shamliyan T, Wyman J, Ramakrishnan R, Sainfort F,
Kane R. Benefits and harms of pharmacologic treatment
for urinary incontinence in women. Ann Intern Med
2012;156(12):861.
13. Ministry of Health, Singapore. Clinical practice
guidelines on functional screening for older adults in
the community. Singapore 2010.
14. Avery K, Donovan J, Peters TJ, Shaw c, Gotoh M, Abrams
P. ICIQ: a brief and robust measure for evaluating the
symptoms and impact of urinary incontinence. Neurourol
Urodyn 2004;23(4):322-30
References 113
115

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First Edition 2015

The decision to screen for diseases must be made on a sound

DATUK DR NOOR HISHAM BIN ABDULLAH

In a broader sense, health screening is one of the components

PROFESSOR DR TONG SENG FAH

Cardiovascular Dr Ambigga Devi A/P S. Krishnapillai

Dr Mazapuspavina Md. Yasin

Osteoporosis Dr Adibah Hanim Ismail

Dr Tong Seng Fah

Chronic obstructive Dr Ching Siew Mooi

vi Consensus Working Group

Cervical cancer Dr Fuziah Paimin

Dr Harmy bin Mohamed Yusoff

Dr Irmi Zarina Ismail

Dr Norhayati Mohd Noor

Depression Dr Baizury Bashah

Dr Sherina Mohd Sidik

Human immuno Dr Vickneswari A/P Ayadurai

Consensus Working Group vii

Domestic violence Dr Inderjit Singh Ludher

Dr Sajaratulnisah Binti Othman,

Scoliosis in Dr Sri Wahyu Taher

Older age group: Dr Ambigga Devi A/P S. Krishnapillai

Dr Lee Ping Yein

Dr Noorlaili Mohd Tohit @ Mohd Tauhid

Dr Sazlina Shariff Ghazali

Dr Zaiton Ahmad (Late)

viii Consensus Working Group

Internal reviewers Dr Harmy bin Mohamed Yusoff

Dr Teng Cheong Lieng

Dr Tong Seng Fah

External Reviewers Professor James Dickinson

Professor Mark Harris,

External Reviewers Dr Asma Abdullah

Dr Feisul Idzwan Mustapha

Dr Lee Fatt Soon

Dr Lee Tong Weng

External Reviewers Dr Lee Wai Khew

Dr. Marhani Midin

Dr. Mohamad Aziz Salowi

Dr Nor Azmi Kamarudin

Dr Ong Teng Aik

Dr Pang Yong Kek

Dr Sabarul Afian Mokhtar

Dr Shaiful Bahari Ismail

Dr Sheila A/P Marimuthu

Dr Suresh Kumar A/L Chidambaram

Dr Tan Chow Wei

Dr. Feisul Idzwan Mustapha

Dr Mohd Aminuddin Mohd Yusof

Dr. Noridah bt. Mohd Saleh

1. Screening for asymptomatic conditions such as hypertension, diabetes,

2. Screening for symptomatic conditions that are under-reported by patients

3. Assessing health risk behaviours such as smoking and nutritional status.

Determining the evidence for health screening

By evidence-based practice, health screening should only be recommended if

xii Define Health Screening

1. Review of primary literature from MEDLINE and Cochrane database

2. Review of screening guidelines from the United States Preventive Service

Determining the benefits of health screening

Fig 1: Process of screening and factors diluting the benefit of screening

Referral for Referral for Morbidity and