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Gestational diabetes mellitus (GDM) is defined as carbohydrate
intolerance of variable severity with onset or first recognition
during pregnancy.1 The first recorded case was
described in Berlin in 1823,2 but the term gestational
diabetes did not appear in the medical literature until
1961.3 The initial studies in the
1960s developed diagnostic criteria which identified mothers
likely to develop type 2 diabetes later in life. However, as late as the
mid-1990s, GDM was not widely accepted as a risk factor for type 2
diabetes in Australia.
That situation has now changed, and the Federal Government has
established a committee to advise on the significance of GDM. This is
particularly relevant given that preliminary results from the
Australian Diabetes, Obesity and Lifestyle Study indicate that 7.2%
of Australians over the age of 25 years have diabetes, with 50% being
undiagnosed.4 The individual, societal
and healthcare costs of this diabetes epidemic are significant,
particularly as many individuals have complications such as
retinopathy by the time of diagnosis.5 As intervention in
high-risk groups, with advice on diet, exercise and weight control,
may delay the onset of type 2 diabetes and its
complications,6 any opportunities for such
intervention should not be missed.
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The initial diagnostic criteria for GDM were subsequently used to
identify risks of complications during the index pregnancy, such as
macrosomia and associated birth trauma. Nevertheless, whether
these diagnostic criteria can be used for predicting both later
diabetes and pregnancy outcome is contentious. These issues will be
largely settled by the Hyperglycaemia and Adverse Pregnancy Outcome
(HAPO) study, which is now under way. This study, funded by the United
States National Institutes of Health, will test 25 000 women in 16
field centres around the world. Two centres are in Australia — at the
John Hunter Hospital, Newcastle, and the Mater Mothers' Hospital,
Brisbane. Results are expected to become public in June 2004 and, it is
hoped, will answer current questions about the association between
various levels of glucose intolerance during pregnancy and adverse
outcomes. Evidence-based criteria for GDM to prevent or minimise
adverse pregnancy outcomes can then be developed. The longer-term
outcomes for the baby also need to be remembered, as evidence is
accumulating that raised glucose levels in utero are a risk
factor for later development of obesity and diabetes.7
Given these considerations, and given that GDM is mostly
asymptomatic and that it is not practical to perform glucose
tolerance tests on all pregnant women, a systematic screening
program is a necessary first step for detecting GDM. This raises three
obvious questions: whom to screen, how to screen and when to screen?
When to screen? There is general agreement on this issue, as
abnormal carbohydrate tolerance is likely to be seen from the
beginning of the third trimester. Screening should be carried out
between 24 and 28 weeks' gestation, or earlier in women from high-risk
ethnic groups or with a previous history of GDM.
How to screen? This question remains controversial. The most
validated method is plasma glucose measurement one hour after a
random 50 g glucose load.1 Many other suggested
methods have not gained wide acceptance.
Whom to screen? This question is also controversial and is
addressed by Davey and Hamblin8 in this issue of the Journal. They investigated 6032 Melbourne women who had
undergone universal screening for GDM, concluding that selective
screening on the basis of risk factors for GDM is practicable.
Selecting out women aged under 25 years who had a body mass index less
than 27 kg/m2 and no family history of
diabetes, and who did not belong to a high-risk ethnic group (eg,
Indigenous Australian, Pacific Islander, Asian or Middle Eastern
background), would have missed only two of 313 women diagnosed with
GDM (0.6%) and could have avoided up to 17% of screening tests.
The concept of selective screening is not new. It has been suggested by
both the American Diabetes Association and, in circumstances of
limited workforce resources, by the Australasian Diabetes in
Pregnancy Society.9 Davey and Hamblin point out
that their proposed form of selective screening requires rigorous
questioning about racial and family history and accurate
measurement of weight and height. Whether this would be done in
routine clinical practice is questionable. At least their proposal
is less onerous than that of Naylor and colleagues, who developed a
complicated scheme to exclude women from screening that reduces
screening tests by a third, but which most agree is not
practical.10
The other important issue is how many women with GDM would be missed by
this selective screening. Davey and Hamblin claim only 0.6% of
potential cases would be missed. This is at variance with the studies
of Moses and colleagues in
another Australian population,11 which found that
prevalence of GDM in a similar low-risk group of women was 2.8%.
Excluding this low-risk group from screening would still leave 80% of
women requiring tests, but would miss nearly 10% of all cases of GDM.
Both these estimates of the number who would be missed by selective
screening are based on current criteria for diagnosis of GDM, which,
as indicated earlier, are not based on studies of pregnancy outcome.
It is perhaps wise at this time to wait for the development of
evidence-based criteria for pregnancy outcome before making
further recommendations on screening for GDM. If possible,
universal screening should continue for the present. To fail to
diagnose this condition denies the opportunity for intervention to
improve pregnancy outcome and the long-term health prospects of both
the baby and the mother.
J Dennis Wilson
Clinical Associate Professor
Endocrinology Department, Canberra Hospital Canberra, ACT
dennis.wilsonATact.gov.au
- Metzger BE, editor. Proceedings of the Third International
Workshop-Conference on Gestational Diabetes Mellitus.
Diabetes 1991; 40 Suppl 2: 1-201.
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Williams JW. The clinical significance of glycosuria in pregnant
women. Am J Med Sci 1909; 137: 1-26.
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O'Sullivan JB. Gestational diabetes. Unsuspected, asymptomatic
diabetes in pregnancy. N Engl J Med 1961; 264: 1082-1085.
-
Dunstan D, deCourten M, Welbourn T, et al. The Australian Diabetes,
Obesity and Lifestyle study (AUSDIAB) B preliminary results.
Abstracts of the Annual Scientific Meeting of the Australian
Diabetes Society and Australian Diabetes Educators Association.
Cairns, QLD; 2000. Abstr OR601.
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UK Prospective Diabetes Study V1. Complications in newly
diagnosed type 2 diabetic patients and their association with
different clinical and biochemical risk factors. Diabetes Res
1990; 13: 1-11.
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Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing
NIDDM in people with impaired glucose tolerance. The Da Qing IGT and
Diabetes Study. Diabetes Care 1997; 20: 537-544.
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Silverman BL, Metzger BE, Cho CH, Loeb CA. Impaired glucose
tolerance in adolescent offspring of diabetes mothers:
relationship to fetal hyperinsulinism. Diabetes Care 1995;
18: 611-617.
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Davey RX, Hamblin PS. Selective versus universal screening for
gestational diabetes mellitus: an evaluation of predictive risk
factors, Med J Aust 2001; 174: 118-121.
-
Hoffman L, Nolan C, Wilson JD, et al, for the Australasian Diabetes
in Pregnancy Society. Gestational diabetes mellitus — management
guidelines. Med J Aust 1998; 169: 93-97.
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Greene MF. Screening for gestational diabetes mellitus
[editorial]. N Engl J Med 1997; 337: 1625-1626.
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Moses RG, Moses J, Davis WS. Gestational diabetes: do lean young
Caucasian women need to be tested? Diabetes Care 1998; 21:
1803-1806.
©MJA 2001
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