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Ges ta tional dia betes me lli tus:

Past p resent and f ut ur e


Definition
GDM is defined as carbohydrate intolerance of
variable severity that is first diagnosed during pregnancy,
regardless of the need for insulin or persistence of the diabetic
state after delivery.

It is considered the most common metabolic


complication of pregnancy.

Despite the decline in maternal and perinatal morbidity/


mortality in recent years, the care of pregnant women with
GDM is still unclear, particularly regarding diagnosis.
Pathophysi ol ogy of GD M

The growth and development of the human


conceptus take place within the metabolic milieu
provided by the mother, where circulating maternal
glucose, amino acids and lipids provide the building
blocks for fetal development.

Abnormal maternal mixture of metabolites gain


access to the developing fetus in-utero, modifying the
phenotypic gene expression in newly forming cells,
which in turn may lead to short and long-term effects in
the offspring.

The fetal tissues most likely to be affected are neural


cells, adipocytes, muscle cells and pancreatic β-cells.
Pa thophysi ology of
GDM
Pathophysi ol ogy of GDM
contd
Screenin g and Di agnosi s: G DM-
Ri sk Assessment
Rationale

 If diagnosed and treated early and appropriately, the risk


of in-utero fetal death is no higher than for the general
population of pregnant women.

 Among women with GDM, fetal morbidity is lower in


those who achieve optimal glucose concentration than in
those who do not.

 Identification of those women early in pregnancy with


previously undiagnosed type 2 diabetes.

 Maternal hyperglycaemia influences the future health of


the child.
Screening and
Di agnos is
Low risk
GCT is unnecessary in patients meeting the following criteria:
 Belonging to an ethnic group that is not at risk of diabetes (ethnic groups at risk are Hispanics,
Africans, South or South-East Asians)
 No history of diabetes in first –degree relatives
 Age < 25 years
 Normal body weight before pregnancy
 No personal history of metabolic imbalance
 No history of adverse pregnancy outcome
Average risk
GCT should be performed in weeks 24-28 using one of the following two methods:
 Two stage testing: GCT with 50 g glucose, followed, if the results warrant, by an OGTT (75g or
100g, according to accepted criteria)
 One-stage testing: OGTT only (75g or 100g)
High risk
Testing should be performed as soon as feasible in women who meet the following criteria:
 Obese
 Family history of type 2 diabetes
 Personal history of GDM
 Glucose intolerance or glycosuria
If findings are negative, testing should be repeated in weeks 24-28 of pregnancy or at the first signs
of diabetes .
ALUES FOR DIAGNOSIS OF DIABETES AND OTHER CATEGORIES OF HYPERGLYCAEM

PARAMETER DM IGT IFG GDM


FASTING ≥7.0 <7.0 mmol/L ≥6.1 ≥7.0 mmol/L (126 mg/dl)
mmol/L mmol/L
and <7.0
mmol/L
2HPP ≥11.1 >7.8 & <11.1 11.1 mmol/L (200 mg/dl)
mmol/L mmol/L
OGTT-75g
FASTING 5.3 mmol/L (95 mg/dl)
1-HR 10.0 mmol/L (180 mg/dl)
2-HR 8.6 mmol/L (155 mg/dl)
OGTT-100g
FASTING 5.3 mmol/L (95 mg/dl)
1-HR 10.0 mmol/L (180 mg/dl)
2-HR 8.6 mmol/L (155 mg/dl)
3-HR 7.8 mmol/L (140mg/dl)

Note:
abetes can only be diagnosed in an asymptomatic individual when these diagnostic values are confirmed on another da
he classic symptoms of diabetes are polyuria, polydipsia and unexplained weight loss.
wo or more of the venous plasma concentrations in OGTT must be met or exceeded for GDM. The test should
e done in the morning after at least 3 days of unrestricted diet (>150g carbohydrate per day) and unlimited physical act
he subject should remain seated and should not smoke throughout the test.
Re cla ssific atio n

Fasting glucose level 75g OGTT


Normal <110(6.1) <140 after 2h (7.8)

Glucose intolerance 110-25(6.1-6.9) 140-199 after 2h(7.8-11.1)

Diabetes >126(7.0) >200 after 2 h (11.1)

All values are in mg/dl.(mmol/L


Treatme nt
A. Glycaemic Targets (? Optimal levels)
 FBG ≤ 95mg/dl (5.3mmo/l)

 1-Hr Postprandial<140mg/dl (7.8)

 2-Hr Postprandial <120mg/dl (6.7)

 Glucose and insulin levels in the fetus need to be measured.

 Glucose self monitoring better than laboratory monitoring.

 No place in management of GDM for urine glucose monitoring.

 During delivery
-plasma glucose 80-120mg/dl (4.4-6.7mm/L)
-Whole blood glucose 70-110mg/dl (ie 3.9-6.1mm/L)
? Glycated Haemoglobin
Tre atm ent c ontd
B. Diet
 Cornerstone of treatment
 Individualized depending
 Personal needs
 Weight status (BMI)
 Level of daily physical activity
? Daily minimum caloric allowance (25kcals/kg body wt)
_ Carbohydrate composition 35-55%
_ Complex carbohydrates are recommended.
Weight gain
- 7kg in women who were overweight before
pregnancy (BMI ≥ 29kg/m2)
- up to 18kg in women who were underweight BMI
≤19.9kg/m2).
Tr eatme nt contd

C. Pharmacological Treatment
 If diet alone fails to maintain:

 FBG < 5.5 mmo/L

 1hr post meal < 8.0mmo/L

 2hr post meal < 7.0mmo/L

Then insulin should be given


Long-term Eff ects a nd
Po st -n atal Care
 GDM women are at a high risk of acquiring type 2
diabetes mellitus after delivery.

 Reassess 2-6 wks after delivery.

 Those with negative findings should undergo repeat


testing 1year later.

 After delivery should maintain regular physical activity


and appropriate weight.

 Counseling before next pregnancy

 Recommend folic Acid to reduce possibility of fetal


nervous system abnormalities (neural tube defects).
Th e future (The HAP O ST UD Y)

Rationale

 Need to develop uniform international measures for the detection of


pregnancies at risk of poor outcome due to maternal hyperglycaemia.

Design and Time-line

 This is a 5year investigator-initiated prospective, observational study.

 Recruited 25,000 pregnant women of different ethnic-racial backgrounds


undergoing treatment in 16 leading obstetric centres in different geographic
areas worldwide (10 Countries).

 Primary outcome indicators:


- Caeserian delivery
- Increased fetal size
- Neonatal morbidity (hypoglycaemia)
- Fetal hyperinsulinaemia
-
Findings will be published in 2005,
Concl usi on
GDM definitely merits our attention as a distinct disease with
significant prevalence by all standards of diagnostic criteria.

It is associated with a defined set of maternal and perinatal


complications that adversely affect pregnancy outcome and also
have long-term implications e.g. an increased risk of future diabetes
for both mother and offspring.

However the following remain unresolved:-


- what degree of maternal hyperglycaemia is
associated, with a measurable risk to the fetus?
- At what level of maternal hyperglycaemia should we
intervene to prevent the known maternal and perinatal morbidity and
mortality?

The HAPO study will hopefully answer these questions and


more and establish an international consensus on the controversial
issue of Diagnosis and management of GDM.

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