Research
Selective versus universal screening for gestational diabetes
mellitus: an evaluation of predictive risk factors
Richard X Davey and P Shane Hamblin
MJA 2001; 174: 118-121
For editorial comment, see Wilson
Abstract -
Methods -
Results -
Discussion -
Acknowledgements -
References -
Authors' details
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More articles on Obstetrics & gynaecology and women's health
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Objective: To assess whether selective screening
for gestational diabetes mellitus (GDM) on the basis of risk-factor
assessment is a practicable alternative to universal
screening. Design: Case-control study. Setting: A 212-bed regional specialist hospital in
Melbourne, providing services in obstetrics and gynaecology,
paediatrics, geriatrics and rehabilitation. Subjects: 6032 women who gave birth at the hospital, May 1996 to
August 1997 and November 1997 to August 1998; all were screened for
GDM, and 313 were diagnosed with the condition. Main outcome measures: Odds ratios (ORs) for risk factors
(age, obesity, family history of diabetes mellitus and high-risk
racial heritage) in women with GDM compared to those without GDM;
proportion of women with GDM whose diagnosis would have been missed by
selective screening. Results: ORs were 1.9 for age ≥25 years (95% CI, 1.3-2.7),
2.3 for body mass index ≥27 kg/m2 (95% CI, 1.6-3.3), 2.5 for
high-risk racial heritage (95% CI, 2.0-3.2), and 7.1 for family
history of diabetes mellitus (95% CI, 5.6-8.9). Other proposed
criteria (previous GDM and glycosuria) added no further diagnostic
power. Selective screening using the above four criteria would have
missed two of 313 cases (0.6%) and could have saved screening up to
1025 women without GDM (17% of all women). Conclusions: Selective screening for GDM based on prior risk
assessment can reduce the need for testing, with negligible loss of
diagnostic efficiency.
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Gestational diabetes mellitus (GDM) is officially described as
carbohydrate intolerance with onset or first recognition during
pregnancy.1 It is associated with
increased incidence of maternal hypertension, pre-eclampsia and
obstetric intervention; a third of women with GDM develop diabetes
mellitus in later life. Babies of mothers with GDM may be either
macrosomic or small-for-gestational-age, and may suffer birth
trauma, hypoglycaemia and other metabolic disturbances. Potential
effects later in the child's life are still debated. In Australia, at
least 5% of pregnancies are affected by GDM. However, there is no
sharply defined maternal blood glucose level beyond which morbidity
invariably ensues in either mother or baby,2 and there is disagreement
about how to diagnose GDM and how aggressively to treat it.3 In 1998, both the American Diabetes Association (ADA) and the WHO
Consultation on diabetes published recommendations on diagnosis
and classification of diabetes mellitus that included comments on
GDM.4,5 The Australasian
Diabetes in Pregnancy Society (ADIPS) has also published GDM
guidelines.6
Both the ADA and ADIPS recommendations acknowledge that there are
variable levels of risk for GDM and, consequently, that selective
rather than universal screening can be considered. Selective
screening both reduces costs and, for women deemed not to need
screening, eliminates the minor physical inconvenience of the
procedure and any anxiety raised by the possibility of suffering
diabetes. Both ADA and ADIPS list risk factors for GDM (Box 1). The WHO
Consultation's delineation of risk factors for GDM was less
clear.5
We tested the hypothesis that selective screening for GDM is a
practicable alternative to universal screening. We also
investigated the effect of using the different age criteria of ADIPS
and ADA as a basis for selective screening.
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| Methods |
We undertook a case-control study to compare the likelihood of
particular risk factors (defined in Box 2) among women with and
without GDM. We also determined the proportion of women with GDM whose
diagnosis would have been missed by selective screening, based on
different sets of risk factors.
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Study population | |
Sunshine Hospital is a 212-bed regional specialist hospital in
Melbourne, Victoria, which provides service in obstetrics and
gynaecology, paediatrics, geriatrics and rehabilitation. The
study population comprised all 6032 women who gave birth at the
hospital over the 26 months May 1996 to August 1997 and November 1997 to
August 1998. Women who gave birth in September and October 1997 were
excluded, as their laboratory data were incomplete.
All women were screened with a 50 g glucose challenge test, according
to the ADIPS protocol.6 Those with an abnormal
result (defined as plasma glucose level after one hour of ≥7.8
mmol/L) proceeded to a 2 h 75 g oral glucose tolerance test
(OGTT); GDM was diagnosed if the fasting plasma glucose level was
≥5.5 mmol/L, or the 2 h level was ≥8.0 mmol/L.
Nearly all patients diagnosed with GDM were managed by an
endocrinologist (P S H) in conjunction with one of the clinic
obstetricians and were offered review and ongoing care from a
dietitian and a diabetes nurse educator.
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Data retrieval |
Case group: We identified all post-delivery patient
separations coded for GDM by computer search of the hospital medical
information system, with cross-referencing to laboratory,
dietitian and diabetes nurse educator records. Women who gave birth
twice in the study period were included only once, using details from
their first GDM-affected pregnancy. There were 313 women diagnosed
with GDM.
Information on risk factors for these women was obtained from medical
records containing details of pregnancy management and delivery,
endocrinologist's and dietitian's notes and laboratory records (by
R X D). If racial heritage was unclear, patients were telephoned at
home to obtain more details. Body mass index (BMI) was available for
only 290 of the 313 women (93%), but other data were available for over
99%.
Control group: For the 5719 women without GDM,
information on age was also obtained from the hospital medical
records. However, it was impracticable to investigate racial
heritage as closely for this group as for the case group. Therefore, if
country of birth was recorded as being in Europe, Asia or Central and
South America, it was used for risk categorisation (45.5% of women).
All other women were allocated to risk groups in the same proportions
as found in the case group. While this biases the outcome in favour of
the null hypothesis, it is more accurate than making no such
allocation at all.
BMI and family history were not available for the 5719 women without
GDM. Therefore, the BMI comparison used BMI data obtained from 303
consecutive non-diabetic women presenting for a glucose challenge
test at about 28 weeks' gestation as part of a 1995 study at Sunshine
Hospital.8 As the patient catchment
area was unchanged between 1995 and 1998, this group should represent
an unbiased sample of women who presented between 1995 and 1998.
For the family history comparison, a recent estimate of prevalence of
diabetes mellitus in Australia9 was used for the non-GDM
patients. Background risk was corrected for the bias caused by the
tendency of patients with diabetes to visit their doctors twice as
often as non-diabetic patients.10 It was also doubled to give
a worst-case estimate, as each parent might pass on heritable risk
independently.
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Statistical analyses and ethics approval | |
Data were analysed using Stata statistical software.11 Odds ratios
were calculated from the comparative prevalence in affected and
control populations by Cornfield's method.
Ethics approval for this study was not required by the Victorian
Health Services Act 1988 and was not sought. Data were
permanently de-identified after analysis.
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Risk-factor comparison | |
Prevalence of risk factors among women with and without GDM is shown in
Box 3, along with odds ratios. Women with GDM were almost twice as
likely to be aged 25 years or over compared with those without GDM, more
than twice as likely to have a BMI ≥27 kg/m2 or to have a high-risk racial
heritage, and more than seven times as likely to have a family history
of diabetes mellitus.
To determine the value of racial heritage as a predictor of GDM in
isolation from family risk, we determined the OR for high-risk racial
heritage among women with no family history of diabetes mellitus.
This OR was not statistically different from the earlier OR for
high-risk racial heritage that included women with a family history.
Furthermore, birth in Australia, New Zealand or North America (of
non-Indigenous background) does not necessarily equate
with low heritable GDM risk. Of the 313 women with GDM, 94 were born in
these countries, but 19 of these had high-risk racial heritage.
Finally, we also assessed whether glycosuria in pregnancy or
previous GDM had any extra value as predictors of GDM. All women with
these risk factors qualified for screening on other grounds.
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Effect of selective screening | |
The numbers of women with GDM who would be screened on the basis of risk
factors, using different age thresholds, are shown in Box 4. Only the
290 women with complete data for all risk factors are included.
However, all 23 women with incomplete risk-factor data would have
undergone screening under these selective screening policies, as
all had at least one risk factor (10 had two factors and five had three).
Selective screening on the basis of at least one risk factor, using the
ADIPS age criterion (≥30 years), would have missed 12 women with
GDM (95% CI, 6-19; 4%). Using the ADA age criterion (≥25 years),
selective screening would have missed only two women with GDM (95% CI,
0-5; 0.6%). Furthermore, χ2 tests showed that the
proportions of women with GDM who had risk factors other than age did
not differ significantly between age groups (≥30 years, ≥25
years and all ages); all P values exceeded 0.67.
Among the women without GDM, 83% were aged 25 years or over and 48% were
aged 30 years or over. A selective screening policy could therefore
have saved testing up to 17%-52% of women without GDM, depending on the
age threshold used and the presence of risk factors other than age.
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| Discussion
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We found that selective screening for GDM using the four criteria
common to the ADA and ADIPS lists of risk factors -- older age, obesity,
family history of diabetes and high-risk racial heritage -- would
have missed few women with GDM in our study population. It is clear that
the age threshold for screening proposed by ADA (25 years) is
diagnostically safer than the ADIPS threshold of 30 years, missing
only 0.6% versus 4% of women with GDM.
However, our data also show that it is important to examine risk
factors other than age even when the lower age threshold is used, as the
other factors underlying susceptibility to GDM operate
irrespective of age. Family history and heredity are immutable, and
obesity may also be partly under genetic control. These observations
are also consonant with the theory that pregnancy unmasks diabetes
mellitus prematurely.12
We also found that previous GDM and glycosuria in pregnancy added
nothing to the above four criteria for screening. However, this does
not mean that GDM in a previous pregnancy should be ignored. It is often
regarded as a criterion for a full OGTT, without a prior glucose
challenge test, earlier than 28 weeks' gestation; the wisdom of this
practice is not doubted.
Not only are the ADA criteria for screening diagnostically safer than
the ADIPS criteria, they are also more precise in their definitions.
Australian women would benefit if ADIPS recommendations were
brought into line with ADA recommendations.
Our conclusions differ from those of Moses and colleagues, who found
no benefit from selective screening in their study in the Illawarra
region of New South Wales.13,14 Indeed, Moses has
championed universal screening.15 However, the Illawarra
protocol for GDM screening varied from contemporary practice, as it
did not measure fasting glucose level or stringently control the time
between the glucose load and blood sampling, making comparison
difficult. Its outcomes have been questioned.16,17
In North America, a recent, albeit small, retrospective study of GDM
screening in Michigan specifically assessed the ADA selective
screening recommendations and concluded that they can be used as they
miss "few" (4%) women with GDM.18
A larger study was reported by the Toronto Trihospital
Investigators.19 They proposed a scheme
that used among its criteria those later published by ADA to
differentiate risk levels for GDM, sparing 35% of pregnant women the
need for a glucose challenge test.
This is at least twice as efficient as using the ADA
criteria in our population, which potentially spared up to 17% of
women a glucose challenge test (depending on the presence of risk
factors other than age). However, an accompanying editorial
concluded that the Trihospital criteria were "so hard to discern"
that universal screening would continue as the only practicable
alternative.20 For busy clinicians,
simple systems are essential.
Our study differed from the Toronto study in that only women with
positive results on a glucose challenge test proceeded to an OGTT,
while, in Toronto, all women had a full OGTT. We will have missed the
small number of women who would have had positive results on an OGTT
despite their negative results on a challenge test -- perhaps 3%,
based on the Toronto data. Short of performing a full OGTT on all
pregnant women, which is impracticable, this group will
always escape detection.
The Toronto ORs for risk factors among those with GDM generally accord
with ours (1.6 for age ≥35 years [95% CI, 1.1-2.5], 3.2 for BMI
≥25.1 kg/m2 [95% CI, 2.1-4.8], 4.8 for
Asian race [95% CI, 3.0-7.6]), but our results differ in two ways.
Toronto race groupings, apart from "Asian", are difficult to
interpret and, by using "white" and "black", ignore the extreme
variation among "white" Europeans. Secondly, family history of
diabetes mellitus in Toronto did not correlate significantly with
higher risk of GDM, whereas our findings strongly support the
inclusion of family history among criteria for a glucose challenge
test.
Our study, along with the Michigan and Toronto studies, indicates
that a selective approach to GDM screening in pregnancy is
justifiable. Our simplified algorithm for selective screening is
shown in Box 5. In practice, the proportion of women spared a glucose
challenge test by selective screening will vary between
populations. Consequently, whether selective screening is locally
practicable will be a decision for individual groups of
obstetricians, endocrinologists and pathologists with local
knowledge. It is clear that consideration of a patient's age,
rigorous questioning about racial and family history and accurate
measurement of height and weight can reduce the need for screening
among suitable populations. Selective screening can reduce costs
and maternal anxiety, with negligible loss in diagnostic power.
Nevertheless, GDM poses still further challenges. Australia needs a
better-directed, more organised, totally inclusive approach to
follow-up of women who have had GDM. The third who will go on to develop
diabetes mellitus need to be tracked, monitored, and managed
prospectively into a healthier future.
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Acknowledgements | |
We thank dietitians Candy d'Menzie-Bunshaw and Ruth Cuttler,
specialist diabetes nurse consultant Elizabeth Borg, and health
information manager Sianne Banks and her staff at Sunshine Hospital
for their invaluable assistance with the study, and Lucy Inocencio
for her excellent technical assistance.
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| References
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- Metzger BE, editor. Summary and recommendations of the Third
International Workshop-Conference on Gestational Diabetes
Mellitus. Diabetes 1991; 40 Suppl 2: 197-201.
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Sacks DA, Greenspoon JS, Abu-Fadil S, et al. Towards universal
criteria for gestational diabetes: The 75-gram glucose tolerance
test in pregnancy. Am J Obstet Gynecol 1995; 172: 607-614.
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Jovanovic L. A tincture of time does not turn the tide [editorial].
Diabetes Care 2000; 23: 1219-1220.
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The Expert Committee on the Diagnosis and Classification of
Diabetes Mellitus. Report of the expert committee on the diagnosis
and classification of diabetes mellitus. Diabetes Care
1998; 21 (Suppl 1): S5-S19.
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Alberti KGMM, Zimmet PZ for the WHO Consultation. Definition,
diagnosis and classification of diabetes mellitus and its
complications. Part 1. Diagnosis and classification of diabetes
mellitus. Provisional report of a WHO consultation. Diabet Med
1998; 15: 539-553.
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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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Beischer NA, Oats JN, Henry OA, et al. Incidence and severity of
gestational diabetes mellitus according to country of birth in women
living in Australia. Diabetes 1991; 40: 35-38.
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Davey R. The glucose challenge test: different drink dilutions.
Diabet Med 1996; 13: 917-918.
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Welborn TA, Reid CM, Marriott G. Australian Diabetes Screening
Study: impaired glucose tolerance and non-insulin-dependent
diabetes mellitus. Metabolism 1997; 46 (12 Suppl 1): 35-39.
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Australian Bureau of Statistics. National health survey:
diabetes, Australia, 1995. Canberra: AGPS, 1997. (Catalogue No.
4371.0.)
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StataCorp. 1999. Stata Statistical Software: Release 6. College
Station. TX: Stata Corporation.
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Yue DK, Molyneaux LM, Ross GP, et al. Why does ethnicity affect
prevalence of gestational diabetes? The underwater volcano theory.
Diabet Med 1996; 13: 748-752.
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Moses R, Griffiths R, Davis W. Gestational diabetes: do all women
need to be tested? Aust N Z J Obstet Gynaecol 1995; 35: 387-389.
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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.
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Moses RG. Diabetes in pregnancy [editorial]. Med J Aust
1998; 169: 68-69.
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Davey R. Of gestational diabetes, finesse, and an antipodean
snark [letter]. Diabetes Care 1999; 22: 873-874.
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Moses RG, Moses J, Davis WS. Response to Davey [letter].
Diabetes Care 1999; 22: 874.
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Williams CB, Iqbal S, Zawacki CM, et al. Effect of selective
screening for gestational diabetes. Diabetes Care 1999; 22:
418-421.
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Naylor CD, Sermer M, Chen E, Farine D. Selective screening for
gestational diabetes mellitus. N Engl J Med 1997; 337:
1591-1596.
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Greene MF. Screening for gestational diabetes mellitus
[editorial]. N Engl J Med 1997; 337: 1625-1626.
(Received 15 May, accepted 21 Sep, 2000)
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Western Hospital, Melbourne, VIC.
Richard X Davey, FRCPA, FACB, Clinical Pathologist; P
Shane Hamblin, FRACP, Senior Endocrinologist.
Reprints will not be available from the authors. Correspondence: Dr R
X Davey, Western Hospital, Gordon Street, Footscray, VIC 3011.
richard.daveyATwh.org.au
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1: Risk factors for gestational
diabetes mellitus, listed by different sources |
Risk factor |
Australasian Diabetes
in Pregnancy Society6 |
American Diabetes
Association4 |
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Age
Obesity
Family history of diabetes mellitus
Previous GDM
High risk "ethnic" group
Glycosuria
Previous adverse pregnancy outcome |
Yes (>30 years)
Yes (not defined)
Yes
Yes
Yes (examples given)
Yes
Yes |
Yes (>25 years)
Yes (BMI >27kg/m2)
Yes (first-degree relative)
Not mentioned*
Yes (examples given)
Not mentioned
Not mentioned* |
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GDM=Gestational diabetes mellitus.
BMI=Body mass index. *While the ADA did not consider previous GDM or adverse
pregnancy outcome as sufficiently significant for women to be included in
the high-risk GDM group, it did report them as criteria for diabetes testing
in asymptomatic, undiagnosed individuals,4 thereby acknowledging them as
markers of early, silent diabetes mellitus. Including Australian Indigenous,
Polynesian, Asian and Middle Eastern women. Including Hispanic-American,
Native American, Asian-American, African-American and Pacific Islander women.
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2: Definitions of risk factors used in this study
Age: Age was not further defined by ADA or ADIPS; we used age at estimated time of conception — the most conservative calculation.
Obesity: As defined by the ADA — body mass index ≥27kg/m2, determined from pre-pregnancy mass and height.
Family history of diabetes mellitus: As defined by the ADA — diabetes mellitus affecting a first-degree relative.
Racial susceptibility: Termed "ethnic" risk by ADA and ADIPS. We classified a woman as having high-risk racial heritage if she or her parents were born in one
of the countries around the Mediterranean (including the Levant, but not the rest
of Europe), the Indian subcontinent or Asia, or belonged to the Indigenous populations of Australia, the Pacific or the Americas.7
ADA = American Diabetes Association. ADIPS=Australasian Diabetes in Pregnancy Society.
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3: Prevalence and odds ratios
of risk factors for gestational diabetes mellitus (GDM) |
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Prevalence |
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Risk factor |
Women with GDM
(n=313) |
Women without GDM (variable
n*) |
Odds ratio
(95% CI) |
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Age (years) >25 |
90.1% |
82.9% |
1.9 (1.3-2.7) |
>30 |
58.5% |
47.8% |
1.5 (1.2-1.9) |
Body mass index >27 kg/m2 |
36.2% |
19.8% |
2.3 (1.6-3.3) |
Family history of diabetes mellitus |
39.9% |
8.6% |
7.1 (5.6-8.9) |
High-risk racial heritage |
68.7% |
46.4% |
2.5 (2.0-3.2) |
Among women with no family history |
71.7%§ |
42.8%¶ |
2.9 (2.1-4.0) |
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*Sample size varied
between risk factors: 5719 (age), 303 (body mass index), 50371 (family history)
and 5719 (racial heritage). Data were available for 290 of the 313 women.
High-risk racial heritage: peri-Mediterranean (56 women), Indian subcontinent
(20), Asia (124), South America (12), Indigenous populations (3); low risk
racial heritage: United Kingdom (61), other European countries (35) and
other (2). §n=187. ¶n=5324.
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4: Effect
if selective screening were used among 290* women with gestational diabetes
mellitus |
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Number of women who would be
screened (% of women with GDM) |
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Risk factors |
ADIPS age threshold
(≥30 years) |
ADA age threshold
(≥25 years) |
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Age ≥ threshold
Only risk factor
Plus any one other factor
Plus any two other factors
Plus any three other factors
Total |
13 (4%)
78 (27%)
54 (19%)
20 (7%)
165 (57%) |
23 (8%)
120 (41%)
90 (31%)
27 (9%)
260 (90%) |
Age ≤ threshold
One risk factor
Two risk factors
Three risk factors
Total |
60 (21%)
42 (14%)
11 (4%)
113 (39%) |
18 (6%)
6 (2%)
4 (1%)
28 (10%) |
Any risk factor |
278 (96%) |
288 (99%) |
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*23 women with gestational diabetes mellitus
but incomplete data on risk factors are not included. Risk factors other
than age were body mass index ≥27kg/m2,
family history of diabetes mellitus and high-risk racial heritage. |
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