Archives of Gynecology and Obstetrics

https://doi.org/10.1007/s00404-018-4848-8

MATERNAL-FETAL MEDICINE

Neonatal outcome in gestational‑diabetic mothers treated

with antenatal corticosteroids delivering at the late preterm and term
Eyal Krispin1,2   · Alyssa Hochberg1,2 · Rony Chen1,2 · Arnon Wiznitzer1,2 · Eran Hadar1,2 · Adi Borovich1,2

Received: 29 March 2018 / Accepted: 29 June 2018

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Abstract
Objective  To determine the association between antenatal corticosteroid treatment and neonatal complications in diabetic
mothers delivering after 34 weeks of gestation.
Methods  A retrospective cohort study of women with singleton pregnancies diagnosed with gestational diabetes who deliv-
ered after 34 weeks of gestation in a university-affiliated medical center (2012–2016). Mothers treated with corticosteroids
prior to 34 + 0 weeks of gestation were divided according to gestational age at delivery: late-preterm (34 + 0 to 36 + 6) and
term (37 + 0 to 41 + 6). Each group was compared to women delivering at the same gestational age who were not treated
with corticosteroids. Primary outcome was defined as a neonatal adverse composite outcome. Birth weight was amongst
secondary outcomes measured. Logistic regression analysis was utilized to adjust results to potential confounders.
Results  During the study period, 161 diabetic mothers delivered at late-preterm. Amongst them, 47 (30%) were treated
with corticosteroids. 2101 diabetic mothers delivered at term, amongst them 82 (4%) were treated with corticosteroids.
Primary outcome did not differ between groups. Multivariate analysis demonstrated that corticosteroid treatment was not
associated with neonatal adverse composite outcome when delivery occurred at the late preterm, nor at term (adjusted odds
ratio (aOR) = 0.708, 95% CI 0.2–2.3, p = 0.572, and aOR = 1.6, 95% CI 0.2–12.7, p = 0.635, respectively). Birth weight was
significantly lower in women treated with corticosteroids (2486 vs. 2675 g, p = 0.02 at late-preterm, and 3160 vs. 3319 g,
p < 0.001 at term).
Conclusion  Corticosteroid treatment for diabetic mothers was not associated with neonatal adverse outcomes, but was found
associated with a lower birth weight, when delivery occurs after 34 weeks of gestation.

Keywords  Antenatal corticosteroids · Gestational diabetes mellitus · Late preterm · Term

Abbreviations Introduction
ACS Antenatal corticosteroid
RDS Respiratory distress syndrome Antenatal corticosteroid (ACS) treatment has long been rec-
TTN Transient tachypnea of the newborn ommended for pregnant women at risk for preterm delivery
GDM Gestational diabetes mellitus between 24 + 0 and 33 + 6 weeks of gestation. It is con-
NICU Neonatal intensive care unit sidered one of the most important treatments to improve
GCT​ Glucose challenge test neonatal outcome [1–5]. Neonates delivered preterm whose
OGTT​ Oral glucose tolerance test mothers are treated with ACS have a significantly lower fre-
quency and severity of respiratory distress syndrome (RDS),
intracranial hemorrhage, necrotizing enterocolitis and death
compared with neonates born prematurely whose mothers
were not treated with corticosteroids [6, 7].
* Eyal Krispin
eyalkrispin@gmail.com Steroid treatment may have even more significance for the
prevention of respiratory complications in diabetic moth-
1
Department of Obstetrics and Gynecology, Helen ers, regardless of gestational age at delivery. It is debatable
Schneider Hospital for Women, Rabin Medical Center, whether neonates to diabetic mothers (both pre-gestational
49100 Petach Tikva, Israel
and gestational) are at increased risk for mortality and mor-
2
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, bidity when compared to neonates of non-diabetic mothers,
Israel

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even when delivery occurs after 34 weeks of gestation [8].
Furthermore, at any given gestational age, neonates to dia-
betic mothers are subjected to develop RDS and transient
tachypnea of the newborn (TTN). These complications pre-
sumably occur due to delayed surfactant synthesis, a result
of maternal hyperglycemia [9, 10], and reduced fluid clear-
ance in the fetal lungs, augmented by increased cesarean
delivery rates [11–13]. Whether ACS treatment is associated
with a reduction in respiratory complications in this more
prone population of neonates to diabetic mothers is yet to
be determined.
The aim of our study, therefore, was to investigate
whether ACS treatment prior to 34 weeks of gestation in dia-
betic mothers is associated with different rates of neonatal
morbidities when delivery occurs after 34 weeks, compared
to no such treatment.
Materials and methods
We conducted a retrospective cohort study of all women
carrying a singleton viable fetus that were diagnosed with
gestational diabetes mellitus (GDM) and delivered after
34 weeks of gestation in a single, university-affiliated, ter-
tiary medical center, between 2012 and 2016. The study was
approved by our local institutional review board (0232-16-
RMC), with waiver of informed consent due to the retro-
spective, observational design of the study.
Study population
The cohort was divided according to gestational age at
delivery: late preterm (34 + 0 to 36 + 6) and term (37 + 0 to
41 + 6). We compared maternal and neonatal outcomes in
women treated with antenatal glucocorticoids (study group),
to the remaining cohort to whom such treatment was not
administered (control group). Exclusion criteria included
preterm premature rupture of membranes, multiple gesta-
tions, pre-gestational diabetes, major fetal anomaly and fetal
chromosomal abnormalities.
Definitions
Diagnosis of GDM was based on abnormal 50 g glucose
challenge test (GCT > 140 mg/dl) followed by an abnor-
mal 100 g oral glucose tolerance test (OGTT). Screen-
ing and diagnosis of GDM is universally performed at
24–28 weeks of gestation, and diagnosis was established
according to Carpenter and Coustan’s criteria [14]. Once
the diagnosis of GDM was made, women were referred
to a multidisciplinary specialized clinic, and were treated
with appropriate diet and lifestyle modification. Daily
glucose is recommended to be monitored during fasting,
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Archives of Gynecology and Obstetrics
before each meal and either 1 or 2-h post-prandial. Treat-
ment is tailored according to glycemic control by either:
diet, oral anti-diabetic medications or insulin. Birth weight
percentile was calculated using gender-specific local popu-
lation-based birth weight curves [15]. Large for gestational
age babies were defined as newborns with birth weight
above the 90th percentile for gestational age. Small for
gestational age babies were defined as newborns with birth
weight below the 10th percentile for gestational age.
ACS therapy is recommended in cases of anticipated
preterm birth to improve newborn outcomes [16]. In this
study, we included women who were treated with a course
of corticosteroids once, at risk for preterm birth at 24 + 0
to 33 + 6 weeks of gestation. Indication for treatment was
cervical dynamics, defined as either transvaginal ultra-
sound measurement of a cervical length below 25 mm; or
digital vaginal examination demonstrating a cervical dila-
tion of more than 1.5 cm and 60% effacement. Premature
contractions were not an obligatory finding for treatment.
All women were treated with two 12-mg doses of beta-
methasone given intramuscularly 24 h apart.
Data collection
Data were retrieved from our delivery ward’s compre-
hensive computerized perinatal database. Data from the
neonatal unit and the neonatal intensive care unit (NICU)
was integrated into the delivery ward database using a
unique admission number assigned to each woman and
her offspring.
The following demographic and obstetrical vari-
ables were recorded: maternal age, gravidity, parity,
BMI, hypertensive disorders, gestational age at delivery,
mode of delivery and meconium-stained amniotic fluid.
Recorded neonatal outcomes included: birth weight, 5-min
Apgar score, hyperbilirubinemia, TTN, RDS, the need for
mechanical ventilation, meconium aspiration syndrome
(MAS), umbilical arterial pH < 7.1, seizures, sepsis, intra-
ventricular hemorrhage (IVH), necrotizing enterocolitis
(NEC), and NICU admission. Missing data were com-
pleted by careful manual chart review performed by the
study personnel.
The primary outcome was defined as a neonatal adverse
composite outcome including any one of the following:
Apgar at 5 min < 7, umbilical arterial pH < 7.1, neonatal
intensive care unit admission, respiratory composite out-
come (as elaborated below), hypoglycemia, sepsis, acidosis,
hypoxic ischemic encephalopathy, intra-ventricular hemor-
rhage, and necrotizing entero-colitis. Secondary outcomes
were neonatal birth weight and neonatal respiratory compos-
ite, including any of the following: TTN, RDS, mechanical
ventilation and meconium aspiration syndrome.
Archives of Gynecology and Obstetrics

Statistical analysis Late‑preterm birth

Data analysis was performed with the SPSS v21.0 pack-
age (Chicago, IL, USA). Continuous variables were com-
pared using Student’s t test and Mann–Whitney U test. The
Chi-square and Fisher’s exact tests were used for categori-
cal variables, as appropriate. Differences were considered
significant when p value was less than 0.05. Following the
bivariate analysis, logistic regression analysis was utilized
to adjust outcomes for potential confounders. Variables
with clinical impact or variables that were found different
between the groups (p < 0.05) in the bivariate analysis were
included in the regression model: birth weight, gestational
age at delivery, gravidity, parity, hypertensive disorders,
BMI and ACS treatment.
Results
Baseline characteristics of women in both groups—treat-
ment and control—are presented in Table 1. Women who
were treated with corticosteroids presented higher rates
of nulliparity compared to those not treated (55 vs. 34%,
respectively, p = 0.001), with no other significant differences
between groups.
Bivariate analysis of individual and composite neona-
tal outcomes is presented in Table 2. Regarding primary
outcome as defined in the “Materials and methods” sec-
tion, no significant difference was demonstrated between
groups. Multivariate analysis adjusting for gravidity, parity,
Table 1  Baseline characteristics for the late-preterm delivery sub-
groups
Treated with Not treated with p value
ACS (N = 47) ACS (N = 114)

Overall, during the study period 2262 women were diag- Maternal age (years) 34 (23–45) 34 (21–50) 0.970
nosed with GDM and delivered after 34 weeks of gestation. Maternal age > 35 years 22 (47) 52 (46) 0.620
One hundred and sixty-one delivered at the late preterm Gravidity 2 (1–7) 2 (1–9) 0.88
(34 + 0 to 36 + 6 weeks of gestation). Of them, 47 (29%) Parity 0 (0–5) 1 (0–8) 0.02
were treated with ACS prior to 34 + 0 weeks of gestation. Nulliparity 45 (55) 686 (34) 0.001
Two thousand one hundred and one delivered at term (37 + 0 Body mass index (kg/m2) 25 (16–38) 28 (20–55) 0.47
to 41 + 6). Of them, 82 (4%) were treated with ACS prior to Hypertensive ­disordersa 4 (5) 121 (6) 0.557
34 + 0 weeks of gestation (Fig. 1). Values are presented as median (range) for continuous variables and
as N (%) for categorical variables
ACS antenatal corticosteroids
a
 Hypertensive disorders—any of the following: chronic hypertension,
gestational hypertension, preeclampsia or eclampsia

Fig. 1  The study groups

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 Archives of Gynecology and Obstetrics

Table 2  Neonatal outcomes for Treated with ACS (N = 47) Not treated with ACS p value
the late-preterm delivery study (N = 114)
groups
Gestational age at delivery (weeks) 35.57 (34–36.85) 36.14 (34–36.85) 0.057
Meconium-stained amniotic fluid 10 (21) 39 (35) 0.648
Cesarean delivery 22 (47) 50 (44) 0.73
Birth weight (g) 2486 (1532–3870) 2675 (1730–4250) 0.02
Birth weight percentile 51 (6–98) 61 (1–99) 0.05
Large for gestational age 3 (7) 18 (16) 0.08
Small for gestational age 5 (11) 4 (4) 0.13
Neonatal intensive care unit admission 41 (19) 32 (36) 0.32
5-min Apgar score < 7 0 (0) 1 (1) 0.52
Hyperbilirubinemia 13 (28) 38 (33) 0.06
Transient tachypnea of the newborn 1 (2) 7 (6) 0.2
Respiratory distress syndrome 6 (13) 8 (7) 0.3
Hypoglycemia 3 (6) 13 (11) 0.29
Respiratory composite ­outcomea 11 (23) 25 (22) 0.84
Neonatal composite ­outcomeb 14 (32) 33 (30) 0.8

Values are presented as median (range) for continuous variables, and as N (%) for categorical variables
ACS antenatal corticosteroids
a
 Respiratory composite outcome—one of the following: transient tachypnea of the newborn, respiratory
distress syndrome, mechanical ventilation, meconium aspiration syndrome
b
 Neonatal composite outcome—one of the following: Apgar at 5  min < 7, umbilical arterial pH < 7.1,
neonatal intensive care unit admission, respiratory composite outcome, hypoglycemia, sepsis, acidosis,
hypoxic ischemic encephalopathy, intra-ventricular hemorrhage, and necrotizing entero-colitis

primiparity, hypertensive disorders, BMI, birth weight and Table 3  Baseline characteristics of the term delivery subgroups
gestational age at delivery, demonstrated that ACS treatment Treated with Not treated with p value
was not associated with adverse composite neonatal out- ACS (N = 82) ACS (N = 2019)
come (adjusted odds ratio (aOR) = 0.708, 95% CI 0.2–2.3,
p = 0.572). Maternal age (years) 32 (22–44) 34 (19–50) 0.004
Maternal age > 35 years 24 (30) 909 (45) 0.012
Birth weight was significantly lower in the treatment
Gravidity 2 (1–10) 3 (1–14) 0.55
group with a median reduction of 189 g compared to con-
Parity 0 (0–6) 1 (0–12) 0.001
trols (p = 0.02). Further analysis of birth weight demon-
Nulliparity 45 (55) 686 (34) 0.001
strated significantly lower median birth weight percentile, as
Body mass index (kg/m2) 23.3 (17–37) 25.9 (19–58) 0.21
calculated according to local reference values [15], adjusted
Hypertensive ­disordersa 4 (5) 121 (6) 0.557
for neonatal gender and gestational age at delivery (51 per-
centile in the treatment group vs. 61 in controls, p = 0.05). Values are presented as median (range) for continuous variables, and
Cesarean delivery rates were relatively high (45%), but did as N (%) for categorical variables
not differ significantly between groups. Respiratory com- ACS antenatal corticosteroids
plications, both individually and as a composite, were not a
 Hypertensive disorders—any of the following: chronic hypertension,
significantly different between groups. gestational hypertension, preeclampsia or eclampsia

Term birth

Baseline characteristics of women in both groups—treat-
ment and control—are presented in Table 3. Women who
were treated with corticosteroids were slightly younger
compared to controls (median 32 vs. 34 years, respectively,
p = 0.004). Nulliparity rates were also higher in the treatment
compared to the control group (55 vs. 34%, respectively,
p = 0.001). No other significant differences were demon-
strated between groups.
Bivariate analysis of individual and composite neona-
tal outcomes is presented in Table 4. A non-significant
trend towards a higher rate of neonatal adverse compos-
ite outcome was found in the treatment group (11 vs. 3%
in controls, p = 0.17). Multivariate analysis adjusting for
gravidity, parity, nulliparity, hypertensive disorders, BMI,
birth weight and gestational age at delivery, demonstrated
that ACS treatment was not significantly associated with

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Archives of Gynecology and Obstetrics

Table 4  Neonatal outcome of Treated with ACS (N = 82) Not treated with ACS p value
the term delivery subgroups (N = 2019)

Gestational age at delivery (weeks) 38.42 (37–41.42) 38.71 (37–41.85) 0.057

Meconium-stained amniotic fluid 4 (5) 121 (6) 0.676
Cesarean delivery 7 (9) 369 (18) 0.003
Birth weight (g) 3160 (1740–4275) 3319 (1960–6200) 0.001
Birth weight percentile 63 (1–99) 72 (1–98) 0.037
Large for gestational age 12 (15) 498 (25) 0.014
Small for gestational age 5 (6) 72 (4) 0.353
Neonatal intensive care unit admission 13 (10) 7 (141) 0.098
5-min Apgar score < 7 1 (1) 1 (20) 0.492
Hyperbilirubinemia 12 (15) 255 (13) 0.207
Transient tachypnea of the newborn 2 (2) 20 (1) 0.503
Respiratory distress syndrome 0 (0) 11 (1) 0.912
Hypoglycemia 2 (2) 36 (2) 0.662
Respiratory composite ­outcomea 9 (11) 123 (6) 0.763
Neonatal composite ­outcomeb 9 62 (3) 0.17

Values are presented as median (range) for continuous variables, and as N (%) for categorical variables
ACS antenatal corticosteroids
a
 Respiratory composite outcome—one of the following: transient tachypnea of the newborn, respiratory
distress syndrome, mechanical ventilation, meconium aspiration syndrome
b
 Neonatal composite outcome—one of the following: Apgar at 5  min < 7, umbilical arterial pH < 7.1,
neonatal intensive care unit admission, respiratory composite outcome, hypoglycemia, sepsis, acidosis,
hypoxic ischemic encephalopathy, intra-ventricular hemorrhage, and necrotizing entero-colitis

adverse composite neonatal outcomes (aOR = 1.6, 95% CI
0.07–5.1, p = 0.661).
Birth weight was significantly lower in the treatment
group with a median reduction of 159  g in controls vs.
those treated with ACS (p = 0.001). Further analysis of
birth weight demonstrated significantly lower median birth
weight percentile (63 percentile in the treatment group vs. 72
in controls, p = 0.05). Cesarean delivery rates were signifi-
cantly lower in the treatment group compared to controls (9
vs. 18%, respectively, p = 0.003). Respiratory complications,
both individually and as a composite, were rare and were not
significantly different between groups.
Discussion
The aim of our study was to investigate the association
between ACS treatment for suspected imminent preterm
labor and neonatal outcome in women with GDM deliver-
ing after 34 weeks of gestation. The key findings were: (1)
ACS treatment, given prior to 34 weeks of gestation, was
not significantly associated with a reduction in adverse com-
posite neonatal outcomes, nor with individual or composite
respiratory complications, in women with GDM eventually
delivering at late-preterm or term; (2) neonatal birth weight
was significantly lower in the treatment group in both the
late-preterm delivery group and the term delivery group; (3)
cesarean delivery frequencies were significantly lower in the
treatment group compared to controls in the term delivery
group.
ACS treatment was shown to reduce neonatal compli-
cations (mainly RDS and TTN) when delivery occurs fol-
lowing 34 weeks of gestation [17], nevertheless it may dis-
rupt glycemic control in diabetic mothers. The relationship
between maternal hyperglycemia and fetal macrosomia has
been well demonstrated, along with other related adverse
outcomes, such as: neonatal hypoglycemia, hyperbilirubine-
mia and operative delivery [18]. We found no significant
difference between the treatment and control groups, both
in the late-preterm and term delivery groups, regarding neo-
natal adverse composite outcome. This finding is reassur-
ing in the context of diabetic mothers, whose elevated post-
corticosteroid treatment glucose levels could predispose
to the above-mentioned complications. It is possible that
the hyperglycemia expected after steroid treatment is tran-
sient and exerts only a minimal effect on long-term glucose
maintenance, thus having little or no effect on fetal weight.
Refuerzo et al. [19] examined the timing, duration, and
severity of corticosteroid-associated hyperglycemia in preg-
nant women with and without GDM. They demonstrated that
several, but yet relatively short episodes of glucose elevation
occur in response to corticosteroids. It is possible that our
study did not show a difference in adverse composite neo-
natal outcomes between the control and treatment groups

13

because of the time elapsed from steroid treatment to deliv-
ery, or possibly because of a less than adequate sample size
to detect such a difference. It is also possible that ACS treat-
ment indeed does not improve specific or overall composite
adverse neonatal outcome in this specific population.
Regarding lower neonatal birth weight in the treatment
group in the late-preterm and term delivery groups, such an
effect might actually seem surprising considering the hyper-
glycemia affected after steroid treatment, with subsequent
possible disruption in glucose levels, predisposing to larger
fetuses. As stated earlier, this increase may be transient [19],
thus having a less significant effect on overall fetal weight
and glycemic control disruption. Our finding of smaller neo-
nates in the treatment group coincides with previous animal
studies and studies on multiple courses of corticosteroids,
where a higher rate of small for gestational age neonates
and an overall lower birth weight in the treatment group
was demonstrated [20–22]. An alternative explanation for
this finding could be found by the indication for ACS in
our study groups. The treatment was given due to concern
for preterm birth in the context of premature contractions
or cervical dynamics. A study by Espinoza et al. [23] dem-
onstrated that an episode of increased uterine contractility
may put the fetus at increased risk for additional pregnancy
complications, including growth restriction [23]. Be that
as it may, the precise etiology of lower birth weight in our
results is not fully understood. Further studies are necessary
to investigate whether treatment with corticosteroids could
impact fetal growth, even at a single dose and among women
with GDM.
Another finding in our study was that corticosteroid treat-
ment was associated with a significantly lower rate of cesar-
ean deliveries, when delivery occurs at term. It has been
demonstrated in various studies that macrosomia is associ-
ated with an increased risk of cesarean delivery [24–27],
and that almost all of the increased risk is attributable to
labor abnormalities [24, 28]. Our finding of a reduced rate
of cesarean deliveries in the treatment group at term may
be explained by lower frequency of LGA in the treatment
group, although data on specific indications for cesarean
delivery were lacking. Assuming this as a possible expla-
nation, we did not find cesarean delivery rates to be sig-
nificantly different between treatment and control groups
in the late preterm, despite lower frequency of LGA in the
treatment group. This may be due to overall smaller infants,
reducing LGA consequences.
This study has several limitations. Adverse neonatal out-
comes and cesarean delivery rates may differ between ges-
tational-diabetic women treated by diet or with medication,
and according to adequacy of glucose control [29–31]. We
did not have access to these variables during data analysis,
and therefore could not adjust the results for them accord-
ingly. Lack of control for the exact time period elapsed
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Archives of Gynecology and Obstetrics
between ACS treatment and delivery may also affect results,
and was not accounted for in our analysis. Lastly, data were
not available regarding the type of tocolysis given, and
although not expected to affect results, was not controlled
for during multivariate analysis. The strength of our study
lies in the opportunity to analyze a specific and unique popu-
lation not thoroughly investigated previously. Moreover, the
study was conducted in a single large tertiary medical center
with consistent management protocols for GDM follow-up
and treatment.
In conclusion, our findings suggest that ACS treatment for
gestational-diabetic mothers is not associated with improved
neonatal outcome when delivery occurs after 34 weeks of
gestation. Moreover, it was associated with lower birth
weight both in the late preterm and term. Further studies
are needed to better delineate the effects of corticosteroid
treatment in this population, as well as in women with pre-
gestational diabetes.
Author contributions  EK: protocol development, data analysis and
manuscript writing. AH: manuscript writing, data analysis. RC: pro-
tocol development and manuscript editing. AW: protocol development
and manuscript editing. EH: protocol development and manuscript edit-
ing. AB: protocol development, data analysis and manuscript editing.
Compliance with ethical standards 
Conflict of interest  The authors declare that they have no conflict of
interest.
Ethical approval  All procedures performed in studies involving human
participants were in accordance with the ethical standards of the insti-
tutional and/or national research committee and with the 1964 Helsinki
declaration and its later amendments or comparable ethical standards.
For this type of study formal consent is not required.
Human and animal rights statement  This article does not contain any
studies with animals performed by any of the authors.
References
1. American College of Obstetricians and Gynecologists (2016)
Periviable birth. Obstetric Care Consensus No. 4. Obstet Gynecol
127:157–169
2. Carlo WA, McDonald SA, Fanaroff AA, Vohr BR, Stoll BJ, Ehren-
kranz RA et al (2011) Association of antenatal corticosteroids
with mortality and neurodevelopmental outcomes among infants
born at 22 to 5 weeks’ gestation. Eunice Kennedy Shriver National
Institute of Child Health and Human Development Neonatal
Research Network. JAMA 306:234858
3. Mori R, Kusuda S, Fujimura M (2011) Antenatal corticoster-
oids promote survival of extremely preterm infants born at 22
to 23 weeks of gestation. Neonatal Research Network Japan. J
Pediatr 159:110–114
4. Chawla S, Natarajan G, Rane S, Thomas R, Cortez J, Lua J (2010)
Outcomes of extremely low birth weight infants with varying
doses and intervals of antenatal steroid exposure. J Perinat Med
38:419–423
Archives of Gynecology and Obstetrics
5. Chawla S, Bapat R, Pappas A, Bara R, Zidan M, Natarajan G
(2013) Neurodevelopmental outcome of extremely premature
infants exposed to incomplete, no or complete antenatal steroids.
J Matern Fetal Neonatal Med 26:1542–1547
6. American College of Obstetricians and Gynecologists (2016)
Management of preterm labor. Practice Bulletin No. 171. Obstet
Gynecol 128:155–164
7. Roberts D, Dalziel SR. Antenatal corticosteroids for accelerating
fetal lung maturation for women at risk of preterm birth. Cochrane
database of Systematic Reviews 2006, 3
8. Aviram A, Guy L, Ashwal E, Hiersch L, Yogev Y, Hadar E (2016)
Pregnancy outcome in pregnancies complicated with gestational
diabetes mellitus and late preterm birth. Diabetes Res Clin Pract
113:198–203
9. Gewolb IH, O’Brien J (1997) Surfactant secretion by type II pneu-
mocytes is inhibited by high glucose concentrations. Exp Lung
Res 23:245–255
10. Gewolb IH (1996) Effect of high glucose on fetal lung maturation
at different times in gestation. Exp Lung Res 22:201
11. Cordero L, Treuer SH, Landon MB, Gabbe SG (1998) Manage-
ment of infants of diabetic mothers. Arch Pediatr Adolesc Med
152:249–254
12. Persson B, Hanson U (1998) Neonatal morbidities in gestational
diabetes mellitus. Diabetes Care 21:79–84
13. Pinter E, Peyman JA, Snow K et al (1991) Effects of maternal
diabetes on fetal rat lung ion transport. Contribution of alveolar
and bronchiolar epithelial cells to Na+, K(+)-ATPase expression.
J Clin Investig 87:821
14. Carpenter MW, Coustan DR (1988) Criteria for screening tests
for gestational diabetes. Am J Obstet Gynecol 144:768–773
15. Dollberg S, Haklai Z, Mimouni FB, Gorfein I, Gordon ES (2005)
Birth weight standards in the live-born population in Israel. Isr
Med Assoc J 7:311–314
16. American College of Obstetricians and Gynecologists (2017)
Antenatal corticosteroid therapy for fetal maturation. Committee
Opinion No. 713. Obstet Gynecol 130:102–109
17. Gyamfi Bannerman C, Thom EA, Blackwell SC, Tita TN, Reddy
UM, Saade GR et al (2016) Antenatal betamethasone for women
at risk for late preterm delivery. N Engl J Med 374:1311–1320
18. Metzger BE, Lowe LP, Dyer AR, Trimble ER, Chaovarindr U,
Coustan DR et al (2008) Hyperglycemia and adverse pregnancy
outcomes. HAPO Study Cooperative Research Group. N Engl J
Med 358:1991–2002
19. Refuerzo JS, Garg A, Rech B, Ramin SM, Vidaeff A, Blackwell
SC (2012) Continuous glucose monitoring in diabetic women
following antenatal corticosteroid therapy: a pilot study. Am J
Perinatol 29:335–338
20. Wapner RJ, Sorokin Y, Thom EA, Johnson F, Dudley DJ, Spong
CY et  al (2006) Single versus weekly courses of antenatal
corticosteroids: evaluation of safety and efficacy. National Insti-
tute of Child Health and Human Development Maternal Fetal
Medicine Units Network. Am J Obstet Gynecol 195:633–642
21. Crowther CA, Haslam RR, Hiller JE, Doyle LW, Robinson JS
(2006) Neonatal respiratory distress syndrome after repeat expo-
sure to antenatal corticosteroids: a randomised controlled trial.
Australasian Collaborative Trial of Repeat Doses of Steroids
(ACTORDS) Study Group. Lancet 367:1913–1919
22. Battin M, Bevan C, Harding J (2012) Growth in the neonatal
period after repeat courses of antenatal corticosteroids: data from
the ACTORDS randomized trial. Arch Dis Child Fetal Neonatal
Ed 97:99–105
23. Espinoza J, Kusanovic JP, Kim CJ, Kim YM, Kim JS, Hassan SS
et al (2007) An episode of preterm labor is a risk factor for the
birth of a small-for-gestational-age neonate. Am J Obstet Gynecol
196:574
24. Modanlou HD, Dorchester WL, Thorosian A, Freeman RK (1980)
Macrosomia—maternal, fetal and neonatal implications. Obstet
Gynecol 55:420–424
25. Spellacy WN, Miller S, Winegar A, Peterson PQ (1985) Macroso-
mia—maternal characteristics and infant complications. Obstet
Gynecol 66:158–161
26. Bérard J, Dufour P, Vinatier D, Subtil D, Vanderstichèle S, Mon-
nier JC et al (1998) Fetal macrosomia: risk factors and outcome. A
study of the outcome concerning 100 cases > 4500 g. Eur J Obstet
Gynecol Reprod Biol 77:51–59
27. Lazer S, Biale Y, Mazor M, Lewenthal H, Insler V (1986) Com-
plications associated with the macrosomic fetus. J Repro Med
31:501–505
28. Menticoglou SM, Manning FA, Morrison I, Harman CR (1992)
Must macrosomic fetuses be delivered by a cesarean section? A
review of outcome for 786 babies ≥ 4,500 g. Aust N Z J Obstet
Gynaecol 32:100–103
29. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Rob-
inson JS (2005) Effect of treatment of gestational diabetes mel-
litus on pregnancy outcomes. Australian Carbohydrate Intolerance
Study in Pregnant Women (ACHOIS) Trial Group. N Engl J Med
352:2477–2486
30. Landon MB, Spong CY, Thom E, Carpenter MW, Ramin SM,
Casey B et al (2009) A multicenter, randomized trial of treatment
for mild gestational diabetes. Eunice Kennedy Shriver National
Institute of Child Health and Human Development Maternal-Fetal
Medicine Units Network. N Engl J Med 361:1339–1348
31. Hartling L, Dryden DM, Guthrie A, Muise M, Vandermeer B,
Donovan L (2013) Benefits and harms of treating gestational
diabetes mellitus: a systematic review and meta-analysis for the
U.S. Preventive Services Task Force and the National Institutes
of Health Office of Medical Applications of Research. Ann Intern
Med 159:123–129
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