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BMC Pregnancy and Childbirth
Open Access
Research article
Borderline gestational diabetes mellitus and pregnancy outcomes
Hong Ju1, Alice R Rumbold2, Kristyn J Willson3 and Caroline A Crowther*1
Address: 1Discipline of Obstetrics and Gynaecology, The University of Adelaide, Women's and Children's Hospital, King William Road, North
Adelaide, South Australia, 5006, Australia, 2Menzies School of Health Research & Institute of Advanced Studies, Charles Darwin University, PO
BOX 41096, Casuarina, Northern Territory, 0811, Australia and 3Discipline of Public Health, The University of Adelai de, Adelaide, South Australia,
5005, Australia
Email: Hong Ju - hong.ju@adelaide.edu.au; Alice R Rumbold - alice.rumbold@menzies.edu.au;
Kristyn J Willson - kristyn.willson@adelaide.edu.au; Caroline A Crowther* - caroline.crowther@adelaide.edu.au
* Corresponding author
Abstract
Background: The impact of borderline gestational diabetes mellitus (BGDM), defined as a positive
oral glucose challenge test (OGCT) and normal oral glucose tolerance test (OGTT), on maternal
and infant health is unclear. We assessed maternal and infant health outcomes in women with
BGDM and compared these to women who had a normal OGCT screen for gestational diabetes.
Methods: We compared demographic, obstetric and neonatal outcomes between women
participating in the Australian Collaborative Trial of Supplements with antioxidants Vitamin C and
Vitamin E to pregnant women for the prevention of pre-eclampsia (ACTS) who had BGDM and
who screened negative on OGCT.
Results: Women who had BGDM were older (mean difference 1.3 years, [95% confidence interval
(CI) 0.3, 2.2], p = 0.01) and more likely to be obese (27.1% vs 14.1%, relative risk (RR) 1.92, [95%
CI 1.41, 2.62], p < 0.0001) than women who screened negative on OGCT. The risk of adverse
maternal outcome overall was higher (12.9% vs 8.1%, RR 1.59, [95% CI 1.00, 2.52], p = 0.05) in
women with BGDM compared with women with a normal OGCT. Women with BGDM were
more likely to develop pregnancy induced hypertension (17.9% vs 11.8%, RR 1.51, [95% CI 1.03,
2.20], p = 0.03), have a caesarean for fetal distress (17.1% vs 10.5%, RR 1.63, [95% CI 1.10, 2.41],
p = 0.01), and require a longer postnatal hospital stay (mean difference 0.4 day, [95% CI 0.1, 0.7],
p = 0.01) than those with a normal glucose tolerance.
Infants born to BGDM mothers were more likely to be born preterm (10.7% vs 6.4%, RR 1.68, [95%
CI 1.00, 2.80], p = 0.05), have macrosomia (birthweight ≥4.5 kg) (4.3% vs 1.7%, RR 2.53, [95% CI
1.06, 6.03], p = 0.04), be admitted to the neonatal intensive care unit (NICU) (6.5% vs 3.0%, RR
2.18, [95% CI 1.09, 4.36], p = 0.03) or the neonatal nursery (40.3% vs 28.4%, RR 1.42, [95% CI 1.14,
1.76], p = 0.002), and have a longer hospital stay (p = 0.001). More infants in the BGDM group had
Sarnat stage 2 or 3 neonatal encephalopathy (12.9% vs 7.8%, RR 1.65, [95% CI 1.04, 2.63], p = 0.03).
Conclusion: Women with BGDM and their infants had an increased risk of adverse health
outcomes compared with women with a negative OGCT. Intervention strategies to reduce the
risks for these women and their infants need evaluation.
Trial registration: Current Controlled Trials ISRCTN00416244
Published: 30 July 2008
BMC Pregnancy and Childbirth 2008, 8:31 doi:10.1186/1471-2393-8-31
Received: 27 February 2008
Accepted: 30 July 2008
This article is available from: http://www.biomedcentral.com/1471-2393/8/31
© 2008 Ju et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
BMC Pregnancy and Childbirth 2008, 8:31 http://www.biomedcentral.com/1471-2393/8/31
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Background
The prevalence of gestational diabetes mellitus (GDM) is
increasing all over the world [1,2]. In Australia the recent
prevalence estimates for GDM ranged from 5.2% to 8.8%
[3]. The risks for both mothers with GDM and their infants
are well-documented. For the infants, these include an
increased risk of macrosomia, birth injuries such as shoul-
der dystocia, bone fracture and nerve palsies, hypoglycae-
mia, and hyperbilirubinaemia [4-7]. Women with GDM
are at increased risk of developing pre-eclampsia and have
an increased chance of need for induction of labour and
caesarean section. Gestational diabetes is also a strong risk
factor for later development of type 2 diabetes [8].
Although the risks associated with GDM are well recog-
nised, the impact on maternal and infant health outcomes
is less clear for borderline gestational diabetes mellitus
(BGDM), which is characterised by values of glucose tol-
erance intermediate between normal and gestational dia-
betes. A recent 10 year audit examining the influence of
different levels of glucose tolerance on pregnancy compli-
cations, [9] revealed a significantly increased risk of pre-
eclampsia, caesarean section, neonatal hypoglycaemia
and hyperbilirubinaemia for women with BGDM com-
pared with women with normal glucose tolerance. The
results are consistent with other literature reports, which
identified an increasing risk of adverse maternal and
infant outcomes with increasing plasma glucose values
[10-12].
It is estimated that 6.6% of pregnant women or approxi-
mately 16,500 women have BGDM each year in Australia
[9]. Given the uncertainty surrounding BGDM, we
assessed data from participants in the Australian Collabo-
rative Trial of Supplements with antioxidants Vitamin C
and Vitamin E to pregnant women for the prevention of
pre-eclampsia (ACTS) [13] to compare the maternal
demographic, pregnancy and infant health outcomes of
women who had BGDM (screened positive for GDM on
oral glucose challenge test (OGCT) but their subsequent
oral glucose tolerance test (OGTT) was normal) with
women who screened negative on OGCT for GDM.
Methods
The study population included women participating in
the ACTS trial [13], a multi-centre randomised placebo
controlled trial of antioxidant (vitamins C and E) supple-
ments for the prevention of perinatal complications, who
had an OGCT as screening for gestational diabetes. The
methods and results of this trial have been reported previ-
ously [13]. Briefly, eligible women were: nulliparous, with
a singleton pregnancy between 14 and 22 weeks of gesta-
tion with a normal blood pressure at the time of recruit-
ment and who gave informed consent. Women with any
of the following were ineligible: known multiple preg-
nancy, known lethal fetal anomaly, known throm-
bophilia, chronic renal failure, antihypertensive therapy
or contraindication to vitamin C or E therapy including
haemochromatosis or anticoagulant therapy. Randomisa-
tion was performed through a central telephone randomi-
sation service. Women assigned to the vitamin group were
provided a daily dose of 1000 mg vitamin C and 400 IU
vitamin E until birth, and women in the control group
were provided a matching placebo. An OGTT was offered
between 24–30 weeks gestation, for those women who
screened positive on OGCT test. The study protocol was
approved by the research and ethics committees at the
nine collaboration hospitals around Australia.
We compared demographic, obstetric and neonatal out-
comes between women with BGDM and those who
screened normal on OGCT. As the ACTS found no signif-
icant differences between the antioxidant and placebo
groups for the risk of pre-eclampsia, intrauterine growth
restriction or other serious outcomes for the infant, the
analyses include the combined populations of women
who received either antioxidant or placebo supplements.
Data collection
Pregnancy outcome data including OGCT and OGTT
results were collected prospectively from women's medi-
cal records. Sociodemographic variables were collected
either from women's medical records or self-completed
questionnaires at trial entry and included: maternal age,
ethnicity, body mass index (BMI), social-economic status
as measured by socio-economic index for area (SEIFA)
score [14], maternal education, smoking status, blood
pressure at trial entry, and family history of pre-eclampsia.
Complete outcome data were available for all 1877
women randomised.
Outcome variables
BGDM was defined as a positive OGCT (blood glucose
≥7.8 mmol/L 1 hour after a 50 g glucose load) and normal
75 g OGTT (fasting blood glucose <5.5 mmol/L and 2
hour blood glucose <7.8 mmol/L). Pregnancy outcomes
assessed included: maternal adverse outcomes (a compos-
ite outcome defined as any of the following until six
weeks postpartum: death, pulmonary oedema, eclampsia,
stroke, thrombocytopenia, renal insufficiency, respiratory
arrest, placental abruption, abnormal liver function, pre-
term prelabour rupture of membranes, major postpartum
haemorrhage, postpartum pyrexia, pneumonia, deep-vein
thrombosis, or pulmonary embolus requiring anticoagu-
lant therapy) [13]; pregnancy induced hypertension
(PIH); pre-eclampsia (defined as systolic blood pressure
≥140 mmHg or diastolic blood pressure [Korokoff V] ≥90
mmHg on at least two occasions four or more hours apart,
or both arising after 20 weeks' gestation and one or more
of the following: proteinuria, renal insufficiency, liver dis-
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ease, neurological problems, haematologic disturbances,
or fetal growth restriction) [15]; antenatal hospitalisation;
preterm prelabour rupture of the membranes; induction
of labour; mode of birth; postnatal complications such as
postpartum haemorrhage and infection; and length of
hospital stay.
Neonatal outcomes included a composite outcome of
death or infant adverse outcome defined as: stillbirth or
death of a liveborn infant before hospital discharge, birth-
weight <3rd centile for gestational age, severe respiratory
distress syndrome, chronic lung disease, intraventricular
haemorrhage grade 3 or 4, cystic periventricular leukoma-
lacia, retinopathy of prematurity grade 3 or 4, necrotizing
enterocolitis, 5 minute Apgar score <4, seizures before 24
hours of age or requiring 2 or more drugs to control,
hypotonia for ≥2 hours, stupor, decreased response to
pain or coma, tube feeding for ≥4 days, care in the neona-
tal intensive care unit (NICU) >4 days, or use of ventila-
tion for ≥24 hours [13]; gestational age at birth; preterm
birth (<37 weeks); 5 minute Apgar score <7, infant body
size at birth (weight, length and head circumference),
small and large-for-gestational age (defined as a birth
weight below the 10th percentile or above 90th percentile
for gestation according to fetal sex on standardized birth-
weight charts, respectively), macrosomia (defined as
birthweight ≥4.5 kg), admission to NICU or neonatal
nursery, respiratory distress syndrome, mechanical venti-
lation, antibiotics use after birth, encephalopathy (Sarnat
2 or 3 score) and length of hospital stay.
Statistical analysis
Statistical analysis was carried out using SAS software, ver-
sion 9.1. Dichotomous variables were analysed using log-
binomial regression and presented as relative risks, with
95% confidence intervals; and continuous variables, if
normally distributed, were analysed using Student's t-test
and presented as mean differences, with 95% confidence
intervals; non-parametric tests were used for skewed data.
Analyses were then adjusted for maternal age and BMI
given the strong association of these factors with GDM. A
p value of 0.05 or less was considered to indicate statistical
significance.
Results
Of the 1877 women enrolled in the ACTS trial, 1804
(96%) did not have a fetal loss and underwent screening
using a 50 g oral glucose challenge test for gestational dia-
betes. Of the women screened 1596 (88%) had a normal
OGCT screening result, 68 (4%) had an abnormal OGTT
Table 1: Demographics of women with borderline GDM compared with women with a normal OGCT
Characteristics Borderline GDM
n = 140 (%)
Normal OGCT
n = 1596 (%)
Relative risk
[95% CI]
p value
Agea (years) 27.5 ± 5.4 26.3 ± 5.8 1.3 [0.3, 2.2] 0.01
Race
Caucasian 129 (92.1) 1517 (95.1) 0.97 [0.92, 1.02] 0.22
Asian 5 (3.6) 47 (2.9) 1.21 [0.49, 3.00] 0.68
Other 6 (4.3) 32 (2.0) 2.14 [0.91, 5.02] 0.08
BMI
Underweight (<18.5) 3 (2.3) 59 (4.0) 0.59 [0.19, 1.80] 0.34
Normal (18.5 – <25) 59 (45.7) 818 (55.9) 0.82 [0.67, 0.99] 0.04
Overweight (25 – <30) 32 (24.8) 380 (26.0) 0.96 [0.70, 1.31] 0.78
Obese (≥30) 35 (27.1) 207 (14.1) 1.92 [1.41, 2.62] <0.0001
SEIFAb
Low 40 (28.6) 429 (26.9) 1.06 [0.81, 1.40] 0.66
Low-Mid 25 (17.9) 288 (17.9) 1.00 [0.69, 1.44] 0.99
Mid-High 37 (26.4) 391 (24.5) 1.08 [0.81, 1.44] 0.61
High 38 (27.1) 490 (30.7) 0.88 [0.67, 1.17] 0.39
Education
Secondary or lower 54 (39.7) 704 (45.0) 0.88 [0.71, 1.09] 0.25
TAFE or equivalent 38 (27.9) 361 (23.1) 1.21 [0.91, 1.61] 0.19
University 44 (32.4) 498 (31.9) 1.02 [0.79, 1.31] 0.91
Smoking 37 (26.4) 340 (21.3) 1.24 [0.93, 1.66] 0.15
BP at trial entrya (mmHg)
Systolic BP 110.7 ± 11.2 110.1 ± 10.5 0.6 [-1.3, 2.4] 0.55
Diastolic BP 66.4 ± 9.0 65.3 ± 8.0 1.1 [-0.3, 2.5] 0.12
a Values are mean ± standard deviation, and the comparisons are mean difference (95% CI)
b Lower scores indicate lower socioeconomic status
BMI, Body mass index; BP, Blood pressure; SEIFA, Socio-economic index for area
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and 140 (8%) had BGDM (screened positive on OGCT,
normal OGTT).
Overall, women with BGDM and women with a normal
OGCT had similar characteristics at entry to the study
including ethnicity, socio-economic status and educa-
tional attainment (Table 1). Compared with women with
a normal OGCT, women with BGDM were older (mean
difference 1.3 years, [95%CI 0.3, 2.2], p = 0.01), less likely
to have a normal BMI (RR 0.82, [95%CI 0.67, 0.99], p =
0.04) and almost twice as likely to be obese (RR 1.92,
[95%CI 1.41, 2.62], p < 0.0001) (Table 1). There was no
statistically significant difference found between these
groups in the number of women who smoked or in their
mean systolic or diastolic blood pressure at study entry.
In unadjusted analyses women with BGDM were more
likely to experience a maternal adverse outcome (RR 1.59,
[95%CI 1.00, 2.52], p = 0.05) and to develop pregnancy
induced hypertension (RR 1.51, [95%CI 1.03, 2.20], p =
0.03) compared with women with a normal OGCT. These
differences were not seen when adjustment was made for
maternal age and BMI. There was no significant difference
in the rate of pre-eclampsia between the two comparison
groups (Table 2).
The rate of induction of labour was similar and the overall
caesarean section rate did not differ between groups. In
the unadjusted analyses significantly more women with
BGDM gave birth by caesarean section for fetal distress
(RR 1.63, [95%CI 1.10, 2.41], p = 0.01) compared with
women with a normal OGCT although this was not signif-
icant in the adjusted analyses. The length of postnatal hos-
pital stay was significantly longer (mean difference 0.4
days, [95%CI 0.1, 0.7], p = 0.01) for women with BGDM
compared to women with normal OGCT in the unad-
justed analyses but not when adjusted for maternal age
and BMI (Table 2).
Overall there was no difference in the risk of death or
infant adverse outcome between the two groups (Table 3).
In unadjusted analyses infants born to women with
BGDM were at increased risk of being born preterm (RR
1.68, [95%CI 1.00, 2.80], p = 0.05) and were also signifi-
cantly more likely to be macrosomic (birthweight ≥4.5 kg)
(RR 2.53, [95%CI 1.06, 6.03], p = 0.04) compared with
infants born to women with a normal OGCT. When
adjusted for maternal age and BMI the association with an
earlier gestational age at birth and the risk of being mac-
rosomic remained for infants born to women with BGDM
compared with infants born to women with a normal
OGCT (Table 3).
The hospital stay was significantly longer (unadjusted p =
0.001, adjusted p = 0.01) for infants born to BGDM moth-
ers compared with infants born to mothers with a normal
Table 2: Clinical outcomes among women with borderline GDM compared with women with a normal OGCT
Outcome Borderline GDM
n = 140 (%)
Normal OGCT
n = 1596 (%)
Unadjusted relative
risk
[95% CI]
p value Adjusted relative risk
[95% CI]
p value
Maternal adverse
outcome
18 (12.9) 129 (8.1) 1.59 [1.00, 2.52] 0.05 1.47 [0.92, 2.34] 0.11
Pregnancy induced
hypertension
25 (17.9) 189 (11.8) 1.51 [1.03, 2.20] 0.03 1.31 [0.90, 1.90] 0.16
Pre-eclampsia 9 (6.4) 86 (5.4) 1.19 [0.61, 2.32] 0.60 1.08 [0.56. 2.10] 0.82
Antenatal
hospitalisation
29 (20.7) 287 (18.0) 1.15 [0.82, 1.62] 0.42 1.17 [0.83, 1.65] 0.36
PPROM 6 (4.3) 41 (2.6) 1.67 [0.72, 3.86] 0.23 1.54 [0.66, 3.57] 0.32
Induction of labour 49 (35.0) 498 (31.2) 1.12 [0.88, 1.42] 0.34 1.06 [0.84. 1.34] 0.62
Vaginal birth 94 (67.1) 1184 (74.2) 0.90 [0.80, 1.02] 0.10 0.96 [0.86, 1.08] 0.48
Normal vaginal birth 70 (50.0) 865 (54.2) 0.92 [0.78, 1.10] 0.36 1.00 [0.85. 1.17] 1.00
Instrumental vaginal
birth
24 (17.1) 319 (20.0) 0.86 [0.59, 1.25] 0.42 0.87 [0.60, 1.27] 0.48
Caesarean section 46 (32.9) 412 (25.8) 1.27 [0.99, 1.64] 0.06 1.13 [0.89. 1.43] 0.33
Elective 10 (7.1) 101 (6.3) 1.13 [0.60, 2.11] 0.70 1.01 [0.54, 1.88] 0.98
Emergency 36 (25.7) 311 (19.5) 1.32 [0.98, 1.78] 0.07 1.17 [0.87, 1.56] 0.30
Caesarean section for
fetal distress
24 (17.1) 168 (10.5) 1.63 [1.10, 2.41] 0.01 1.43 [0.97, 2.11] 0.07
Major postpartum
haemorrhage
4 (2.9) 42 (2.6) 1.09 [0.40, 2.98] 0.87 0.96 [0.35, 2.66] 0.94
Postpartum pyrexia 3 (2.1) 13 (0.8) 2.63 [0.76, 9.12] 0.13 2.33 [0.66, 8.17] 0.19
Maternal length of
staya (days)
3.5 ± 2.0 3.1 ± 1.7 0.4 [0.1, 0.7] 0.01 0.3 [-0.0. 0.6] 0.06
a Value is mean ± standard deviation, and the comparison is mean difference (95% CI).
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OGCT (Table 3). Infants born to BGDM mothers were
more than twice as likely to be admitted to NICU (unad-
justed p = 0.03, adjusted p = 0.04) and more likely to be
admitted to the neonatal nursery (unadjusted p = 0.002,
adjusted p = 0.01). Antibiotic use less than 48 hours after
birth was significantly greater among infants born to
BGDM mothers (unadjusted and adjusted p = 0.01) and
more infants born to the BGDM women had Sarnat stage
2 or 3 encephalopathy (unadjusted and adjusted p = 0.03)
compared with infants born to women with a normal
OGCT (Table 3).
Discussion
In this cohort of primiparous women in Australia, 8%
were found to have BGDM. In this study, associations
with BGDM were identified for maternal obesity and
increasing maternal age, similar to those identified for
gestational diabetes in other literature [16-18].
In our study, women with BGDM had a higher risk of
adverse health outcomes overall, and were more likely to
develop pregnancy induced hypertension, require a cae-
sarean section for fetal distress and have a longer postna-
tal hospital stay. However, we did not detect a statistically
significant increase in the risk of pre-eclampsia or caesar-
ean section overall among women with BGDM, which has
been reported by previous studies [9-11]. Increasing
maternal age and BMI are strongly associated with adverse
maternal health outcomes. When these factors were
adjusted for, no differences were seen for health outcomes
between women with BGDM and normal women.
We identified an increased risk of preterm birth amongst
BGDM mothers. The reason for this is not readily appar-
ent, given that there is no difference in the rate of induc-
tion of labour between the two groups. Infants of BGDM
mothers were more likely to require a NICU and/or nurs-
Table 3: Clinical outcomes among babies born to women with borderline GDM compared with women with a normal OGCT
Outcome Borderline GDM Normal OGCT Unadjusted relative
risk
[95% CI]
p value Adjusted relative risk
[95% CI]
p value
Births n = 140 (%) n = 1596 (%)
Infant death or adverse
outcome
18 (12.9) 162 (10.2) 1.27 [0.80, 2.00] 0.31 1.25 [0.79. 1.98] 0.34
Stillbirth 1 (0.7) 13 (0.8) 0.88 [0.12, 6.65] 0.90 0.79 [0.10, 6.08] 0.82
Neonatal death 0 5 (0.3) -- -- -- --
Perinatal death 1 (0.7) 18 (1.1) 0.63 [0.09, 4.71] 0.66 0.56 [0.07, 4.21] 0.57
GA at birtha (weeks) 39.7 (38.5–40.9) 40.1 (39.0–41.0) -- 0.004 -- 0.003
Preterm birth
(GA <37 weeks)
15 (10.7) 102 (6.4) 1.68 [1.00, 2.80] 0.05 1.64 [0.97, 2.75] 0.06
Very preterm birth
(GA <34 weeks)
4 (2.9) 33 (2.1) 1.38 [0.50, 3.84] 0.54 1.40 [0.50, 3.91] 0.53
Extremely preterm
birth (GA <28 weeks)
0 12 (0.8) -- -- -- --
Apgar 5 minute <7 3 (2.1) 33 (2.1) 1.04 [0.32, 3.33] 0.95 1.05 [0.32, 3.40] 0.94
Birthweightb (g) 3375 ± 626.3 3388 ± 593.4 -13.0 [-116, 89.5] 0.80 -28.8 [-132, 73.9] 0.58
Birth lengthb (cm) 50.2 ± 2.5 50.3 ± 3.3 -0.06 [-0.6, 0.5] 0.82 -0.09 [-0.7, 0.5] 0.75
Birth head
circumferenceb (cm)
34.3 ± 1.8 34.4 ± 1.9 -0.10 [-0.4, 0.2] 0.55 -0.17 [-0.5, 0.2] 0.34
Liveborns n = 139 (%) n = 1583 (%)
SFGA (Birthweight <10th
percentile)
10 (7.2) 153 (9.7) 0.74 [0.40, 1.38] 0.35 0.76 [0.41. 1.42] 0.39
LFGA (Birthweight ≥90th
percentile)
19 (13.7) 153 (9.7) 1.41 [0.91, 2.20] 0.13 1.29 [0.83, 2.00] 0.27
Macrosomia (Birthweight
≥4.5 kg)
6 (4.3) 27 (1.7) 2.53 [1.06, 6.03] 0.04 2.27 [0.97, 5.34] 0.06
Length of staya (days) 3 (3–5) 3 (2–4) -- 0.001 -- 0.01
Admission to nursery 56 (40.3) 450 (28.4) 1.42 [1.14, 1.76] 0.002 1.35 [1.09, 1.68] 0.01
Admission to NICU 9 (6.5) 47 (3.0) 2.18 [1.09, 4.36] 0.03 2.05 [1.02, 4.13] 0.04
RDS 0 14 (0.9) -- -- -- --
Mechanical ventilation 2 (1.4) 33 (2.1) 0.69 [0.17, 2.85] 0.61 0.65 [0.16, 2.71] 0.56
Antibiotics <48 hours 14 (10.1) 78 (4.9) 2.04 [1.19, 3.51] 0.01 2.14 [1.24, 3.68] 0.01
Sarnat stage 2 or 3
encephalopathy
18 (12.9) 124 (7.8) 1.65 [1.04, 2.63] 0.03 1.69 [1.06, 2.69] 0.03
a Values are median (IR range). b Value is mean ± standard deviation, and the comparison is mean difference (95% CI). GA, gestational age; SFGA,
small for gestational age; LFGA, large for gestational age; NICU, neonatal intensive care unit; RDS, respiratory distress syndrome
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ery admission and longer hospital stays. This may be
explained by the higher rate of pregnancy induced hyper-
tension, caesarean section for fetal distress, preterm birth
and encephalopathy (Sarnat stage 2 or 3) in this group.
Infants born to BGDM mothers in both unadjusted anal-
yses and when adjusted for maternal age and maternal
BMI were also at higher risk of macrosomia, which is con-
sistent with previous studies [10,11].
Our study has identified increased risks of maternal
adverse health outcomes overall and a range of infant
adverse health outcomes associated with BGDM. In Aus-
tralia, there are over 250,000 births annually [19]. Our
data suggest that a substantial number of Australian preg-
nant women, over 20,000 each year, will have BGDM and
therefore maternal and infant adverse health outcomes
that are directly or indirectly attributable to BGDM. Evi-
dence from the Australian Carbohydrate Study in Preg-
nant Women (ACHOIS) trial [20] confirmed that
untreated mild GDM is associated with relatively rare but
nonetheless significant adverse perinatal outcomes. The
trial demonstrated that the risk of these outcomes can be
reduced with standard treatment consisting of individual
dietary and lifestyle advice during pregnancy. There is,
however, insufficient evidence regarding the benefits and
harms of similar intervention for women with BGDM,
with only one small clinical trial identifying a significantly
reduced risk of large-for-gestational age infants with die-
tary advice and regular blood glucose monitoring for
women with borderline glucose intolerance [21]. Data
from our analysis highlight the need for well-designed
large randomised clinical trials to investigate the benefits
and harms of such treatment for women with BGDM.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
All authors contributed to the study design, interpretation
of the data and preparation of the drafts of the manu-
script. In addition CAC and ARR coordinated the study
and the collection of data. KJW performed the data analy-
ses. All authors read and approved the final manuscript.
Acknowledgements
We are indebted to the women and their children who participated in the
ACTS study, the ACTS Study Group [13], Helena Oakey for statistical sup-
port and Melissa Ewens for administration in support for this paper.
The ACTS trial was funded by grants from the National Health and Medical
Research Council, Australia and the Channel 7 Research Foundation, South
Australia.
Ethics
Children, Youth and Women's Health Service (CYWHS) Human Research
and Ethics Committee (HREC)
References
1. Dabelea D, Snell-Bergeon JK, Hartsfield CL, Bischoff KJ, Hamman RF,
McDuffie RS: Increasing prevalence of gestational diabetes
mellitus (GDM) over time and by birth cohort: Kaiser Per-
manente of Colorado GDM Screening Program. Diabetes Care
2005, 28(3):579-84.
2. ACOG Committee on Practice Bulletins-Obstetrics: ACOG Prac-
tice Bulletin. Clinical management guidelines for obstetri-
cians-gynecologists. Number 55, September 2004 (replaces
practice pattern number 6, October 1997). Management of
Postterm Pregnancy. Obstet Gynecol 2004, 104(3):639-646.
3. Cheung NW, Byth K: The population health significance of ges-
tational diabetes. Diabetes Care 2003, 26:2005-9.
4. Acker DB, Sachs BP, Friedman EA: Risk factors for shoulder dys-
tocia. Obstet Gynecol 1985, 66(6):762-8.
5. Langer O, Yogev Y, Most O, Xenakis EM: Gestational diabetes:
the consequences of not treating. Am J Obstet Gynecol 2005,
192:989-997.
6. Langer O, Rodriguez DA, Xenakis EM, McFarland MB, Berkus MD,
Arrendondo F: Intensified versus conventional management of
gestational diabetes. Am J Obstet Gynecol 1994, 170:1036-1047.
7. Soler N, Soler S, Malins J: Neonatal morbidity among infants of
diabetic mothers. Diabetes Care 1978, 1:340.
8. Kim C, Newton KM, Knopp RH: Gestational diabetes and the
incidence of type 2 diabetes: a systematic review. Diabetes
Care 2002, 25:1862-68.
9. Dodd JM, Crowther CA, Antoniou G, Baghurst P, Robinson JS:
Screening for gestational diabetes: the effect of varying
blood glucose definitions in the prediction of adverse mater-
nal and infant health outcomes. Aust N Z J Obstet Gynaecol 2007,
47(4):307-312.
10. Sermer M, Naylor CD, Gare DJ, Kenshole AB, Ritchie JW, Farine D,
Cohen HR, McArthur K, Holzapfel S, Biringer A, et al.: Impact of
increasing carbohydrate intolerance on maternal-fetal out-
comes in 3637 women without gestational diabetes. The
Toronto Tri-Hospital Gestational Diabetes Project. Am J
Obstet Gynecol 1995, 173(1):146-156.
11. Sermer M, Naylor CD, Farine D, Kenshole AB, Ritchie JW, Gare DJ,
Cohen HR, McArthur K, Holzapfel S, Biringer A: The Toronto Tri-
Hospital Gestational Diabetes Project: A preliminary
review. Diabetes Care 1998, 21(Suppl 2):B33-42.
12. Yogev Y, Xenakis EM, Langer O: The association between preec-
lampsia and the severity of gestational diabetes: the impact
of glycemic control. Am J Obstet Gynecol 2004, 191(5):1655-1660.
13. Rumbold AR, Crowther CA, Haslam RR, Dekker GA, Robinson JS:
Vitamin C and E and the risks of preeclampsia and perinatal
complications. New England Journal of Medicine 2006,
354(17):1796-806.
14. ABS: Census of Population and Housing: Socio-economic
Indexes for Areas (SEFIA). In Cat. no. 2033.0.55.001 Canberra:
ABS; 2001.
15. Brown MA, Hague WM, Higgins J, Lowe S, McCowan L, Oats J, Peek
MJ, Rowan JA, Walters BN, Austalasian Society of the Study of Hyper-
tension in Pregnancy: The detection, investigation and manage-
ment of hypertension in pregnancy: full consensus
statement. Aust N Z J Obstet Gynaecol 2000, 40:139-155.
16. Innes KE, Byers TE, Marshall JA, Baron A, Orleans M, Hamman RF:
Association of a woman's own weight with subsequent risk of
gestational diabetes. Journal of the American Medical Association
2002, 287:2534-41.
17. Pettitt DJ, Bennett PH, Knowler WC, Baird HR, Aleck KA: Gesta-
tional diabetes mellitus and impaired glucose tolerance dur-
ing pregnancy. Long-term effects on obesity and glucose
tolerance in the offspring. Diabetes 1985, 34 Suppl 2:119-122.
18. Robson S, Chan A, Keane RJ, Luke CG: Subsequent birth out-
comes after an unexplained stillbirth: preliminary popula-
tion-based retrospective cohort study. Aust N Z J Obstet
Gynaecol 2001, 41:29-35.
19. Laws PJ, Abeywardana S, Walker J, Sullivan EA: Australia's mothers
and babies 2005. Perinatal statistics series no. 20. Cat. No. PER 40
2007 [http://www.npsu.unsw.edu.au/NPSUweb.nsf/page/ps20]. Syd-
ney: AIHW National Perinatal Statistics Unit
20. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson
JS: Australian Carbohydrate Intolerance Study in Pregnant
Women (ACHOIS) Trial Group. Effect of treatment of ges-
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tational diabetes mellitus on pregnancy outcomes. New Eng-
land Journal of Medicine 2005, 352:2477-86.
21. Bonomo M, Corica D, Mion E, Goncalves D, Motta G, Merati R,
Ragusa A, Morabito A: Evaluating the therapeutic approach in
pregnancies complicated by borderline glucose intolerance:
a randomized clinical trial. Diabetic Medicine 2005, 22:1536-41.
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