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DIABETES MELLITUS :

Classification and Diagnosis

Djoko Wahono Soeatmadji

Department of Internal Medicine


Medical Faculty, Brawijaya University
Dr. Saiful Anwar Hospital
Malang

1. Description of diabetes
2. Classification base on
etiopathogenesis
of the disease
3. Diagnostic criteria
4. Testing for diabetes

Diabetes Mellitus
A group of metabolic diseases
Characterized by hyperglycemia
Resulting from defects in insulin secretion ,
insulin action, or both

Classification of Diabetes and Allied


Categories of Glucose Intolerance
(WHO, 1985; PERKENI, 1993)

A. Clinical Classification
1. Diabetes Mellitus
IDDM
NIDDM Obese
Non-obese
Secondary Diabetes
MRDM
2. Gestational Diabetes
3. Impaired Glucose Tolerance

B. Statistical Risk Classification

ETIOLOGIC CLASSIFIACTION
I.

Type 1 (-cell destruction leading to absolut deficiency)


A. Immune mediated
B. Idiopathic

II. Type 2
Predominantly insulin resistance + relative insulin
deficiency
Predominantly secretory defect + insulin resistance
III. Other specific types
IV. Gestasional diabetes mellitus
Type 1 + Type 2 = 70 95% of diabetes
The Expert Committee,1997

Correlation between the therapeutic and etiological


classification of diabetes (Slama, 2003)
Therapeutic classification
Aetiological
classification

IDDM
Type 1a (autoimmune)
LADA (late stage)
Type 1b (idiopathic)
DM linked to acute or chronic
pancreatic diseases Cancer,
pancreatitis etc)
MODY 3
DM associated with
endocrinopathies (Cushing,
acromegaly)
Gestasional diabetes
Mitochondriopathy
Flatbush diabetes

NIDDM
Type 2 associated with metabolic
syndrome
Type 2 without insulin resistance
LADA (early phase)
DM linked to acute or chronic
pancreatic diseases Cancer,
pancreatitis etc)
MODY (including MODY3)
DM associated with
endocrinopathies (Cushing,
acromegaly)
Gestasional diabetes
Mitochondriopathy
Flatbush diabetes

Controversies in Classification
=
Controversies in Management
Type 1 diabetes = Insulin dependent DM
(Dependency on insulin for life)
Type 2 diabetes = Non Insulin Dependent DM
= Not requiring insulin ??

Clinical Features
Age at onset
Onset
Weight
Spontaneous ketosis
Chronic complication
Epidemiology
Prevalence
Sex
Insulin (C-petide) level
Genetics
Concordance in twins
HLA asoociation
Pathology
Islet cell mass
Insulitis at onset
Immunology
Associated with other endocrinopathy
Anti-islet ell immunity
Humoral
Cell mediatedl

Type 1

Type 2

Usually < 30
Acute
Non obese
Common
(++)

Usually > 40
Insidious
Obese
Rare
(++)

0,5%
Male prepdominancece
/ (-)

2%
Female predominance
/N/

40%
(+) (DR3/DR4)

70 90%
(-)

Severely reduced
Present

Moderately reduced
?

Frequent

Frequent

60 80% at onset
35 50% at onset

5 20%
< 5%

Many diabetic individuals do not


easily fit into a single class

10 20 % of subjects with NIDDM show (+)


ICA and/or anti GAD65Abs

Type 1 Diabetes
(-cell destruction leading to
absolut deficiency)

Hypothetical stages and loss of beta cells in an individual progressing to


type 1A diabetes (Eisenbarth, NEJM, 1986) (16)

Clinical Subtypes of Type 1 Diabetes

Slowly progressive Type 1 (SP type 1) diabetes (Diabetes


Care 16: 780 788, 1993)
1. ICA and/or GAD ab (+)
2. Non-insulin dependent at onset
3. Non-insulin requiring period more than 13 months
after the onset or diagnosis
Regular
Fulminant Type 1 diabetes ( N Eng J Med 342: 301, 2000)
1. Ketosis/ketoasidosis within a week after the onset of
hyperglycemic symptoms
2. Serum C-peptide < 0.3 ng/ml (fasting) and
< 0.5 ng/ml (after meal or iv. Glucagon)
3. AIC < 5.5% on first visit

The destruction of -cells and the appearance of type 1 diabetes according to


the age of onset and the putative pathogenetic mechanism (Paolo Pozzilli and
Umberto Di Mario : Diabetes Care 2001 24: 1460-1467)

Natural History of Type 1 DM


-cell function
100%

GAD65 antibodies
ICA antibodies
IAA antibodies
IA2 and IA-2
Abnormal -cell function test
Tolerance reestablished
T-cell tests (+)

T-cell tests ()

Clinical onset

5-10%

Time (months to years)

Type 2 Diabetes

Pathogenesis of Type 2 Diabetes

Insulin resistance
?

vs
-cell dysfunction

Natural History of Type 2


Diabetes
Glucose
350
300
mg/dL 250
200
150
100

Post-prandial glucose
Fasting glucose

Relative to normal

(%)

Insulin resistance
250
200
150
100
50 At risk for Beta-cell dysfunction
Insulin level
diabetes
0
30
0
5
10 15 20 25
-10 -5

Years
R.M. Bergenstal, International Diabetes Center

Insulin Resistance
Normal -cells

Abnormal -cells

Compensatory
Hyperinsulinemia

Inadequate Insulin
Response

Isulin Resistance
Syndrome

Type 2 Diabetes

Hypertension
Dyslipidemia Obesity

CVD

Retinopathy
Neuropathy
Nephropaty

Pathogenesis of Type 2 Diabetes


Impaired -Cell function
Enzymatic defects
Reduced mass
Premature aging

Sine qua none


(and sufficients )

Genetic

Insulin resistance
Obesity (Genetic ?)
Inactivity
Hyperglycemia
Hyperinsulinemia
Drugs

Secondary and
facilitative

Environmental

F
A
M
I
L
Y
S
T
U
D
Y

F
E
N
O
T
Y
P
E
VS
G
E
N
O
T
Y
P
E

DISORDERS OF GLYCAEMIA
Etiologic types and Stages
Hyperglycemia

Stages Normoglycemia
Types

Type 1
Type 2
Other
types
Gestational
diabetes

Normal glucose
regulation

Diabetes Mellitus

IGT or

Insulin requiring

IFG

No

For control

Insulin requirement

+++

For survival

+++++

Many diabetic individuals do not


easily fit into a single class

10 20 % of subjects with NIDDM show (+)


ICA and/or anti GAD65Abs

Hidden dangers of the


metabolic syndrome iceberg

Hyperglycemia
Hypertension
Atherogenic
dyslipidemia

Insulin resistance
+
Hyperinsulinaemia

Abdominal obesity

Impaired
fibrinolysis

Pro-inflammatory
profile

CASE
Female 56 y.o, diagnosed as NIDDM 7
years ago, BMI 22 kg/m2, addhere to diet,
routine exercise, Tx. Glibenclamide 15
mg/day + metformin 1500 kg, Blood
sugar : fasting 230 mg ; 2 h pp 324 mg%
Past medical history : good controlled
with 2 mg glibenclamide but gradually
needs higher dose and finally needs
combined oral hypoglycemic drugs

OTHER SPECIFIC TYPES


A. Genetic defects of -cell function
B. Genetic defects in insulin action
C. Diseases of the exocrine pancreas
D. Endocrinopathies
E. Drug or chemical induced
F. Infections
G. Uncommon forms of immune mediated-diabetes
H. Other genetic syndromes associated with diabetes

The Expert Committee,1997.

GENETIC DEFECTS OF -CELL


FUNCTION
1. Chromosome 12,HNF-1 (MODY3)
2. Chromosome 7,glucokinase (MODY2)
3. Chromosome 20,HNF-4 (MODY1)
4. Mitochondrial DNA
5. Others

The Expert Committee,1997

GENETIC DEFECTS IN INSULIN ACTION

1.Type A insulin resistance


2.Leprechaunism
3.Rabson-Mendenhall syndrome
3.Lipoatriphic diabetes
4.Others
The Expert Committee. Diabetes Care 1997; 20:1183-1196

DRUG OR CHEMICAL INDUCED


1. Vacor
2. Pentamidine
3. Nicotinic acid
4. Glucocorticoid
5. Thyroid hormone
6. Diazoxide

7. -adrenergic agonist
8. Thiazides
9. Dilantin
10. -interferon
11. Others

The Expert Committee,1997.

ENDOCRINOPATHIES
Acromegaly
Cushings syndrome
Glucagonoma
Pheochromocytoma
Hyperthyroidism
Somatostatinoma
Aldosteronoma
Others

The Expert Committee,1997

INFECTIONS
Congenital rubella
Cytomegalo virus
Others

The Expert Committee,1997

UNCOMMON FORMS
OF IMMUNE-MEDIATED DIABETES

Stiff-man syndrome
Anti-insulin receptor anribodies
Others

The Expert Committee,1997

OTHER GENETIC SYNDROME


SOMETIMES ASSOCIATED WIH DIABETES

Downs syndrome
Klinefelters syndrome
Tuners syndrome
Wolframs syndrome
Friedereichs ataxia
Huntungtons chorea
Laurence-Moon-Biedl syndrome
Myotonic dystrophya
Porphyria
Prader-Willy syndrome
Others
The Expert Committee,1997

DIAGNOSTIC CRITERIA

Criteria Diagnosis of Diabetes Mellitus


1.. Symptoms (+) & casual plasma glucose > 200 mg%
(11.1 mmol/L)
or
2. FPG 126 mg% (7.0 mmol/L)
or
3. 2hPG 200 mg/dl during OGTT
Casual is defined as any time of day without regard to time since last meal.
The classic symptoms of diabetes include polyuria, polydipsia, and
unexplained weight loss
Glucose load described by WHO (75 g anhydrous glucose dissolved in
water)
In the absence of unequivocal hyperglycema with acute metabolic
decompensation, these criteria should be confirmed by repeat testing on a
different day

(The Expoert Committee,1997)

Symptoms and signs of diabetes

Linked to osmotic diuresis


Polyuria
Increased thirst and polydipsia
Blurred vision
Drowsiness, dehydration
Linked to lacked of insulin
Hyperglyceaemia with massiveglucosuria
Extreme fatigue
Muscle wasting
Weight loss
Ketosis, ketoasidosis
Symtoms of decreased resistance to infections
Skin infection
Genital pruritus
Linked to caloric depletion
Increased appetite
Weight loss

Slama, 2003

CATEGORIES WHEN THE


OGTT IS USED
Glucose load described by WHO (75 g
anhydrous glucose dissolved in water)

Categories of 2 hours after glucose


loading (2 hPG) values
Normal: 2 hPG 140 mg%
IGT

: 2 hPG 140 mg% and 200 mg%

DM

: 2 hPG 200 mg%*

Provisional diagnosis of diabetes (the diagnosis must be confirmed, as


described above).

The Expert Committee,1997

Categories of FPG values


FPG <100 mg/dl (6.1 mmol/l) = normal
fasting glucose;
FPG 100 (6.1 mmol/l) - 125 mg/dl (7.0
mmol/l) = IFG;
FPG 126 mg/dl (7.0 mmol/l)*
Provisional diagnosis of diabetes (the diagnosis must be confirmed, as
described above)

ADA, 2004

Diagnostic Criteria for epidemiological


studies estimates of prevalence and
incidence should be based on FPG 126
mg%

The Expert Committee,1997

CRITERIA FOR TESTING FOR DIABETES


(SCREENING)
1. All individuals at age 45 - repeat every 3 years
2. Considered at a younger age or be carried more
frequently :
- Obese > 120% or BMI 27kg/m2
- First degree relative with diabetes (+)
- Members of a high-risk ethnic population
- Delivered a baby weighing 9 lb (Indonesia ?) or
have been diagnosed with GDM
- Hypertensive ( 140/90)
- HDL-chol < 35 mg% and/or TG > 250 mg%
- On previous testing had IGT or IFG

The Low-risk Group


Age < 25
Normal weight
No family history of diabetes
Not members of and ethnic/racial
group with a high prevalence of
diabetes

The Expert Committee,1997

GESTATIONAL DIABETES

SCREENING AND DIAGNOSTIC SCHEME


FOR GDM (24 28 week of gestation)
Plasma glucose 50-g
100-g
screening test diagnostic test
Fasting
1-h
2-h
3-h

140 mg/dl
-

105
190
165
145

mg/dl
mg/dl
mg/dl
mg/dl

The Expert Committee,1997

Diagnosis of GDM with a 100-g or 75-g glucose load


mg/dl

mmol/l

100-g Glucose load


Fasting
1-h
2-h
3-h

95
180
155
140

5.3
10.0
8.6
7.8

75-g Glucose load


Fasting
1-h
2-h

95
180
155

5.3
10.0
8.6

Two or more of the venous plasma concentrations must be met or exceeded


for a positive diagnosis

Hospital Admission Guidelines For


Diabetes Mellitus

Life-threatening acute metabolic complications of


diabetes
Newly diagnosis diabetes in children and adolescents
Substantial poor metabolic control (Etiology of control
problems ? Modification of therapy ?)
Severe chronic complications that require intensive
treatment
Severe condition unrelated to diabetes that
significantly affects its control or complicated by
diabetes
Uncontrolled or newly discovered insulin-requiring
diabetes during pregnancy
Institution of intensive insulin regimens

Thank You
For Your Attention !!

djoko w soeatmadji

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