CLINICAL OBSTETRICS AND GYNECOLOGY
Volume 56, Number 4, 774–787
Clinical Diagnosis of
Gestational Diabetes
EDMOND A. RYAN, MD
Division of Endocrinology and Metabolism, Heritage Medical
Research Centre, Alberta Diabetes Institute, University of Alberta,
Edmonton, Alberta, Canada
Abstract: Gestational diabetes mellitus (GDM) diag-
nosis remains controversial. ACOG criteria are based
on the long-term risk of maternal diabetes. ADA
recently suggested diagnosing GDM with 1 elevated
value on an oral glucose tolerance test based on a 1.75-
fold risk of large-for-gestational age infants resulting
in a 17.8% rate of GDM. Given the lack of neonatal-
based outcomes for the traditional position and prob-
lems of reproducibility and benefit/harm balance of
the ADA approach, an alternative is presented herein
based on a 2-fold risk of a large-for-gestational age
baby, requiring 2 separate abnormalities to reduce
false positives giving a more balanced benefit/harm
ratio (10% GDM rate).
Key words: gestational diabetes, diagnosis, screening,
pregnancy
Introduction
Any parent will do a lot for their children
and no one more so then the expectant
mother. Hence pregnant women will give
up coffee, forgo alcohol, and even those
addicted to smoking will try and stop—all
with the view of doing what is best for
their baby. However, there is an implicit
Correspondence: Edmond A. Ryan, MD, Division of
Endocrinology and Metabolism, Heritage Medical Re-
search Centre, Alberta Diabetes Institute, University of
Alberta, Edmonton, AB, Canada. E-mail: edmond.
ryan@ualberta.ca
The author declares that there is nothing to disclose.
CLINICAL OBSTETRICS AND GYNECOLOGY
774 | www.clinicalobgyn.com
r 2013, Lippincott Williams & Wilkins
societal contract within this arrange-
ment—‘‘If pregnant, I will do all in my
power for my child’s well-being but you
have to be sure what you ask of me is truly
worthwhile and best.’’ The proposed In-
ternational Association of Diabetes in
Pregnancy Study Groups (IADPSG) cri-
teria for gestational diabetes mellitus
(GDM) fail in this regard when subject
to careful clinical analysis. As we will see,
the proposed single abnormality on a
single oral glucose tolerance test (OGTT)
for diagnosing GDM is poorly reprodu-
cible, addresses the cause of only a minor-
ity of the cases of large-for-gestational age
infants (LGA), and, in terms of benefit/
harm analysis, does not succeed for the
near-fifth of the pregnant women it will
label as GDM. An interim proposal uti-
lizing a 2-step approach (a 50 g screening
test followed by a 75 g OGTT) using
criteria based on a 2-fold increase risk of
LGA is a more reasonable strategy pend-
ing better ways of identifying women with
risks for LGA.
Background
Even before the discovery of insulin, an
association of macrosomia with pre-
sumed diabetes1 and neonatal pancreatic
/ VOLUME 56 / NUMBER 4 / DECEMBER 2013

islet hyperplasia with maternal glycosuria
were reported.2 In 1924, it was noted that
glycosuria could occur due to ‘‘a type of
diabetes peculiar to pregnancy’’ distinct
from renal glycosuria and classic diabe-
tes.3 Allen4 from Chicago in 1939 found
that ‘‘benign glycosurics are more likely to
give birth to larger babies than do normal
women’’ and mentions that in reviewing
the obstetrical histories of women now
having diabetes that ‘‘they gave birth to
a high percentage of giant babies long
before their clinical diabetes had become
manifest.’’ In 1945, Miller5,6 published
that women who later developed diabetes
were likely to have larger infants with a
higher mortality and associated islet hy-
perplasia, findings supported by others.7,8
Pedersen9 in 1952 documented a link be-
tween higher maternal glucose during
pregnancy and neonatal hypoglycemia
hypothesizing the involvement of fetal
hyperinsulinemia. Jackson and Woolf10
also confirmed that women who later
went on to develop diabetes had a history
of larger babies with higher stillbirth rates
but more importantly made the observa-
tion that ‘‘prediabetes plus pregnancy
gives us the embryopathy’’ and the im-
portance of its recognition.11,12 Hoet also
recognized that increased maternal glu-
cose was harmful to the baby in the short
term and wondered if the exposure could
lead to long-term diabetes in the offspring
and with regard to the mother felt that
pregnancy was diabetogenic and could
lead to persisting diabetes, using the term
‘‘metagestational’’ diabetes for this occur-
ence.13 He suggested that therapy would
help both mother and offspring. Thus, by
the 1950s, the association of large babies
and/or stillbirth with the later develop-
ment of diabetes in the mother was estab-
lished together with the finding that these
infants had pancreatic islet hyperplasia
presumably related to fetal exposure to
higher glucose levels.
It was then that these 2 findings were
pulled together under the umbrella of
Diagnosing Gestational Diabetes 775
‘‘gestational diabetes’’ by Elsie Carrington
et al who first mentioned the term gesta-
tional diabetes when they performed
OGTTs in 621 women and labeled women
as ‘‘suspicious, prediabetes, or gestational
diabetes’’ proportional to the postload 2-
hour glucose value.14 She found that if
these identified women classified as suspi-
cious, prediabetes, or GDM (n = 37) were
treated they experienced no stillbirths/neo-
natal deaths compared with a similar
group of glucose-intolerant women
(n = 34) diagnosed within 5 days postpar-
tum and thus untreated in whom were seen
10 stillbirths/neonatal deaths.14 O’Sulli-
van15 in 1961 helped cement this link of
GDM and later maternal diabetes by per-
forming OGTT in 7061 higher risk women
[family history of diabetes, previous baby
over 4.1 kg (9 pounds), poor obstetrical
history, and a glucose Z130 mg/dL
(7.2 mmol/L) 1 hour after a 50 g glucose
load]. Of note, only 0.86% had diabetes
but by 5 years postpartum 28.5% of 137
studied had diabetes. In a subsequent
study, O’Sullivan and Mahan16 continued
to focus on the long-term risk of diabetes
developing in these women and using the
pregnancy OGTT proposed using an
upper cutoff of 2 SD above the mean, with
slight rounding of the numbers, to give a
subsequent long-term diabetes rate of
22.6% and a GDM rate of 1.99%. The
National Diabetes Data Group17 (NDDG)
subsequently modified these numbers for
venous plasma giving proposed thresholds
of fasting 105 mg/dL (5.8 mmol/L); 1 hour
of 190 mg/dL (10.6 mmol/L); 2 hours of
165 mgs/dL (9.2 mmol/L), and 3 hours of
145 mg/dL (8.1 mmol/L) and Carpenter
and Coustan18 provided their own modifi-
cation of the numbers to account for use of
plasma versus whole blood and using glu-
cose oxidase methodology for measure-
ment of glucose. Thus, the original
association of large babies and islet hyper-
plasia with a transient diabetes of preg-
nancy shifted to a focus of identifying a
prediabetic group at higher risk for
www.clinicalobgyn.com
776 Ryan
long-term diabetes in whom treatment dur-
ing pregnancy would benefit the baby.
Although the diagnosis of diabetes in
the nonpregnant state became uniform
based on the subsequent development of
microvascular disease, specifically eye
and kidney damage,17 the situation for
GDM remained in considerable flux. A
review in 2006 showed at least 9 different
criteria for diagnosing GDM among 12
sets of recommendations across the world
meaning that a person in one country with
a set of values could be diagnosed with
GDM and in another country with iden-
tical numbers would be told there is no
problem.19 It is against this background
of confusion that the large Hyperglycemia
Adverse Pregnancy Outcome (HAPO)
study set out to confirm not only the
relationship between glucose and speci-
fied outcomes, but also facilitate identifi-
cation of diagnostic criteria that could be
applied worldwide.20 HAPO was an ob-
servational study of 23,316 women who
had a 75 g OGTT with sampling at 0, 1,
and 2 hours and all of whom were fol-
lowed barring those with undisputed glu-
cose intolerance being present [fasting
plasma glucose >105 mg/dL (5.8 mmol/
L) or the 2 hours postload glucose
>200 mg/dL (11.1 mmol/L)]. The partic-
ipants were followed prospectively for
primary outcomes of birth weight above
the 90th percentile for gestational age
(LGA), clinical neonatal hypoglycemia,
cord blood C-peptide above the 90th per-
centile, and primary cesarean section de-
livery rate. The glucose levels were divided
into 7 categories such that equivalent
numbers of women for each of the glucose
measures (fasting, 1 and 2 h postload)
were in each group. There was a signifi-
cant association for all of these outcomes
with the glucose values at fasting and at 1
and 2 hours post load. However, the
slopes for the caesarean section delivery
rate and the clinical neonatal hypoglyce-
mia rates, though statistically significant,
showed only a slight rise over the glucose
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range. Of the secondary outcomes that
were also significantly related to maternal
glucose, the strongest relationship was for
preeclampsia but also held for shoulder
dystocia and birth injury.20 Although the
LGA rate and cord C-peptide were sig-
nificantly related to glucose, the slopes
were linear and the absence of an inflec-
tion point left the topic as to where the
criteria for GDM should be drawn open
to debate.
The IADPSG convened a meeting in
Pasadena in 2008 to find a common
ground for glucose thresholds for diag-
nosing GDM. The group consensus de-
cided that a level of Z the glucose levels
(either fasting, 1 and 2 h postload on the
OGTT) associated with a 1.75-fold in-
creased risk above the mean of >90th
percentile of birth weight, percent body
weight, and cord C-peptide would merit a
diagnosis of GDM.21 The thresholds were
fasting: 92 mg/dL (5.1 mmol/L), 1 hour:
180 mg/dL (10.0 mmol/L), and 2-hour
postload: 153 mg/dL (8.5 mmol/L). These
levels are equivalent to glucose category 5
in the HAPO study and would result in
17.8% of pregnant women being diag-
nosed as having GDM. Of these women
identified with GDM, 8.3% will be diag-
nosed based on fasting level, an additional
5.7% based on the 1-hour value, and a
further 2.1% on the 2-hour value with a
final 1.7% unblinded in the study from
the outset as having very high glucose
values. As each value in turn was associ-
ated with adverse outcomes it was felt that
1 abnormal value on the OGTT would
suffice for the diagnosis. Finally, the
IADPSG group felt that a single OGTT
would be adequate. The American Dia-
betes Association (ADA) subsequently
endorsed these findings and now recom-
mend that all pregnant women with no
known glucose intolerance receive a 75 g
OGTT between 24 and 28 weeks and if 1
value during the OGTT meets or exceeds
the levels of fasting [92 mg/dL (5.1 mmol/
L)], 1 hour [180 mg/dL (10.0 mmol/L)], and

2-hour postload [153 mg/dL (8.5 mmol/L)],
a diagnosis of GDM is warranted.22
These proposals have provoked debate
within the diabetes and obstetrical com-
munities.23–28 In response the National In-
stitute of Health organized a Consensus
Conference, which was held in March
2013 to review both the American College
of Obstetricians and Gynecology (ACOG)
position, the IADPSG/ADA position, and
to decide which of the 2 or if an alternative
option was the most appropriate way for-
ward. Although in an ideal world any
diagnostic criteria would be based on pro-
spective studies that look at various cut-
offs25 with defined endpoints relating to the
neonate, such work will take years and is
not readily feasible in the foreseeable fu-
ture. Thus I will now examine both the
ACOG and IADPSG position and argue
for an alternative set of glucose thresholds,
those associated with a 2-fold increased risk
of LGA in the HAPO study and are fasting:
95 mg/dL (5.3 mmol/L), 1 hour: 191 mg/dL
(10.6 mmol/L), and 2-hour postload:
162 mg/dL (9.0 mmol/L).
GDM Consequences
GDM is associated with adverse out-
comes for both the mother and the baby
and hence the rationale for detection and
treatment. In the short term there may be
LGA infants (frequency: 16%29,30) that
are difficult to deliver resulting in should-
er dystocia (frequency: 0.6% to 2.1%29,30)
and trauma to the baby, particularly clav-
icular fractures and of more concern cer-
vical nerve palsies (frequency: 0.7% to
1.0%29,31). Fortunately, only 6.7% of
these nerve palsies lead to permanent
damage.32 Other short-term risks for the
baby include the need for cesarean deliv-
ery (frequency: 21% to 34%29,33,34), per-
haps earlier delivery (frequency: 9%29)
with a need for neonatal-intensive care
(NICU), jaundice, and rarely respiratory
distress (frequency: 0.3%29). These large
babies may result in vaginal tears for the
Diagnosing Gestational Diabetes 777
mother during delivery but the mother’s
long-term risk of developing type 2 dia-
betes is substantial (frequency at 9 to 15 y
postpartum: 15% to 50%35–38). A system-
atic review has confirmed that the treat-
ment of GDM is beneficial in reducing
LGA and macrosomia and a trend for
lessening birth trauma33 with similar ben-
efits recently confirmed by a meta-anal-
ysis: less macrosomia, shoulder dystocia,
and preeclampsia.39 The long-term risk
for the mother developing diabetes can
be ameliorated by intervention as demon-
strated by the Diabetes Prevention Pro-
gram II, particularly in the form of diet or
exercise or with the use of metformin.40
The offspring of women with GDM may
have an increased risk of obesity41,42 and
glucose intolerance,43,44 but in the major-
ity of studies examining this issue have
found that the frequently present mater-
nal obesity greatly weakens any role as-
signed to glucose.45–49
Gestational Diabetes Screening
(GDS) and Diagnosis—
ACOG Position
The ACOG criteria for GDM stem from
O’Sullivan’s studies and so are based on
the historical criteria relationship of find-
ing GDM and a subsequent long-term
risk of diabetes in the mother,16,50 expos-
ing a fundamental flaw in the ACOG
position in that the criteria are not derived
from outcomes that focus on the baby
such as LGA or birth trauma. Given that
GDM has a direct consequence on the
fetus in the form of LGA and subsequent
increased risk of birth trauma, it would
seem provident to base criteria on out-
comes that pertain to the fetus. A further
problem with the ACOG position is that
for screening they have suggested that
either a 50 g GDS, clinical criteria, or
clinical history could be used. The best
evidence available indicates that a univer-
sal approach to screening is much more
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778 Ryan
appropriate—60% of women with GDM
in a universal screening program did not
have risk factors.51 Thus an evidenced-
based approach would at least involve
universal screening and not rely on clin-
ical risk factors. Finally, the ACOG posi-
tion utilizes 100 g OGTT but the criteria
to diagnose GDM can either be those of
the NDDG17 or the Carpenter Coustan
criteria.18 However, these criteria differ
by 10 mg/dL for 3 of the 4 values on the
OGTT—same test but different cutoffs to
determine normal or GDM,50 a situation
that is inherently ambiguous.
GDS and Diagnosis—
IADPSG Position
As described above, the IADPSG posi-
tion is based on criteria that relate to
outcomes in the neonate. The proposed
glucose levels with the 75 g OGTT of 92,
180, and 153 mg/dL (5.1, 10.0, and
8.5 mmol/L) for fasting, 1, and 2 hours,
respectively, are associated with a 1.75-
fold increased risk of LGA, fetal adipos-
ity, and elevated cord C-peptide. There
are problems with this approach in that
reproducibility is poor, the issue of
whether the glucose is the true culprit in
terms of LGA deserves examination, and
the benefit/harm analysis finds the posi-
tion wanting.
Reproducibility
The OGTT is very reliable when the sub-
ject is normal or has clear-cut diabetes;
however, in the more grey area of im-
paired glucose intolerance the situation
is more problematic. GDM falls into this
intermediate zone. In the largest GDM
study of 106 women who had an abnor-
mal 50 g screen and 1 value abnormal on
the initial OGTT, a repeat OGTT (mean,
4.6 wk later) showed 59.4% were still
abnormal with Z1 value raised.52 A
smaller study of screen-positive GDM
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women (n = 20, at least 1 value abnor-
mal) had 65% of women showing an
abnormal value on the second OGTT
performed within a week.53 To examine
reproducibility of the OGTT when a sin-
gle glucose value is abnormal, those stud-
ies with a diagnosis of impaired glucose
tolerance (IGT) have to be invoked. In the
largest study repeating an OGTT in sub-
jects with IGT, performed in 47- to 49-
year-old males (n = 353), the repeat
OGTT within a month showed that only
37.4% still had an abnormal OGTT.54 A
smaller study of IGT in 50- to 74-year-old
subjects (n = 198) showed better repro-
ducibility with 61% still abnormal on the
second OGTT within 2 to 6 weeks.55 A
systematic analysis of the reproducibility
of the OGTT found with impaired fasting
glucose or IGT, a diagnosis most akin to
GDM, that ‘‘caution should be exercised
when interpreting a single test result.’’56
Yet the IADPSG position is that a single
abnormality of a single glucose tolerance
test would suffice for the diagnosis of
GDM, a shaky foundation.
Evidence Base for the Role of
Glucose in the Complications of
GDM
Although the relationship of increasing
glucose to LGA was confirmed in the
HAPO study, it is clearly not the only
predictor. Subsequently the HAPO inves-
tigators published information on the role
of obesity.57 When both BMI and glucose
versus the odds ratio (OR) for LGA are
plotted, they confirm that in the majority
of women the BMI was a larger contrib-
utor to the OR for LGA than the glu-
cose.23 The original description of this
was critiqued for not matching the num-
bers in groups; subsequently this data was
published by the IADPSG group28 and
when the data is replotted it is apparent
that except for the highest glucose level
the maternal BMI gives a higher OR for a
 Diagnosing Gestational Diabetes 779

birth weight over the 90th percentile
(Fig. 1). Catalano et al58 also examined
this interplay and confirmed that both
GDM and BMI contribute to LGA. The
OR for LGA in the neonate from mater-
nal obesity versus normal weight women
was 2.07 and for GDM the OR was 2.58
yielding 174 or 164 g, respectively, in
terms of real-weight contributions to the
baby. In terms of preeclampsia, the OR
for the highest BMI group (>44.0 kg/m2)
was 14.1 and when fasting glucose was
included in the model the OR was 14.5, yet
the OR for the highest FPG group
(Z100 mg/dL, 5.6 mmol/L) was 4.7 but
this was attenuated to 2.13 when BMI
was included in the model.59 Catalano
and Hauguel-de-Mouzon60 in a review
points out the important background is-
sue that 60% of the pregnant population
are obese and hence is more important in
terms of LGA.
This is to be expected given Ricart’s
publications where he demonstrated that
obesity was more important in predicting
LGA than GDM in a prospective study of
9720 women by finding that only 3.8% of
macrosomia was attributable to GDM
but 23% was attributed to the upper
quartile of BMI>26.61 The respective
figures for LGA were 0.9% and 17.6%
and parenthetically the numbers for preg-
nancy-induced hypertension were 9.1%
and 50%. Obesity is more problematic
for the pregnancy than GDM and it is of
note that combined only 26% of LGA
was accounted for by both these factors. It
may be argued that the GDM women in
the Ricart study were treated but this
would be unlikely to drastically change
the result as only 9% of the study pop-
ulation had GDM (NDDG criteria). The
23% of women in this study who screened
positive for GDM but did not meet
NDDG criteria and so were untreated
for any GDM had a combined popula-
tion-attributable fraction for raised glu-
cose contributing to macrosomia of 7.7%,

FIGURE 1. Plot of odds ratio for infant with birth weight over the 90th percentile versus the
fasting glucose categories 1 to 7 (solid line, open triangles) or versus the BMI groups <23.3 to
>44.0 (dashed line, closed circles). Drawn from information from HAPO study28 and both sets
of data adjusted for multiple variables influencing LGA (model II) and matched for numbers in
groups. Adaptations are themselves works protected by copyright. So in order to publish this
adaptation, authorization must be obtained both from the owner of the copyright in the original
work and from the owner of copyright in the translation or adaptation.

www.clinicalobgyn.com
780 Ryan
well below the 23% of the fourth quartile
for BMI encompassing about the same
number of women.
Retnakaran prospectively looked at
women below the threshold for GDM as
defined by NDDG and so included those
who would be diagnosed by IADPSG
criteria. He found that prepregnancy
BMI (OR 1.16/1 kg/m2 increase) and
weight gain up to the time of the OGTT
(OR 1.12/1 kg increase) predicted LGA62
but glucose did not independently predict
LGA when considered in relation to other
risk factors. A large (N = 9835) retro-
spective study by Black et al63 recently
published indicates that both obesity and
glucose contribute to LGA with obesity
or overweight accounting for 20.6% of
the LGA occurring and GDM a further
12.2%. Given that obesity is more preva-
lent than GDM the population-attribut-
able fraction was similar for obesity
or both obesity and GDM combined:
21.6% for maternal overweight and obe-
sity and 23.3% if overweight or obese
combined with GDM.63 A retrospective
study of 186 women who had GDM by
IADPSG criteria but were untreated had
outcomes not significantly different to
controls and though there was a trend
for more LGA the rate was still only
9.1%.64 It is clear that both obesity and
GDM contribute to LGA and the effects
may be additive but between both of them
they do not account for the majority of
LGA. This latter point is highlighted by
the finding in HAPO that when the
IADPSG criteria are used only a minority
of women who have LGA babies will be
identified; 78% of women who deliver
LGA babies have glucose levels below
the threshold used by IADPSG.
Benefit-Harm Tradeoffs
An important issue is that in both of the
major studies showing benefit in treating
GDM, the Australian Carbohydrate In-
tolerance Study in Pregnant Women
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(ACHOIS) and the Maternal–Fetal Med-
icine Units Network (MFMU) studies, a
composite outcome was used as the pri-
mary endpoint.31,34 In these studies none
of the individual perinatal components of
these composite outcomes were signifi-
cantly altered by the therapeutic interven-
tion; for ACHOIS: death P = 0.07,
shoulder dystocia P = 0.08, bone fracture
P = 0.38, and nerve palsy P = 0.1131 and
in the MFMU study: perinatal mortality
P = 1.0, hypoglycemia P = 0.75, hyper-
bilirubinemia P = 0.12, elevated cord C-
peptide P = 0.07, and birth trauma
P = 0.33.34 The take-home message is
that it requires large numbers to show
the benefits of treating GDM so that
plans to increase the numbers diagnosed
with GDM by lowering the thresholds
as proposed by IADPSG struggle to
make sense in terms of a benefit/harm
balance.
The opportunity costs of treating so
many women with GDM are substantial.
The diagnosis of GDM usually leads to
referral to a diabetes care team of physi-
cian, diabetes nurse, and dietician. The
patient needs to monitor their glucose
perhaps use insulin and/or oral hypogly-
cemic agents. Aggressive treatment of
GDM may actually be associated with
increased risk of small-for-gestational–
aged infants.65,66 The obstetrician’s re-
sponse to the diagnosis will typically lead
to increased fetal monitoring, induction
of labor, or early delivery all of which may
result with more NICU baby admissions
and other long-term costs. Increased rates
of cesarean delivery and NICU admission
may well interfere with the immediate
postdelivery bonding of mother and
infant with unknown consequences.
Finally, the label of GDM for the woman
herself will have an influence in terms
of her own insurability for the future.
Each case of GDM costs 1152 to 1971
dollars extra to treat67,68 and when ex-
trapolated to the extra cases of GDM
which would be diagnosed based on

2009 birth rate figures for the United
States this comes to 300 to 591 million
dollars a year. All of this is occurring in
the setting that we are only identifying
about 25% of women who have large
babies.
Two studies have looked at the
IADPSG-proposed criteria and have
found that if special conditions are met
they may be cost effective. Werner et al67
demonstrated that when examined in the
light of immediate perinatal outcomes the
IADPSG were not cost effective; how-
ever, if one assumes the label of GDM
could be leveraged into prospective inter-
ventions that prevent type 2 diabetes then
using IADPSG criteria became cost effec-
tive. Such a presumption is unproven and
the extrapolation is based on Diabetes
Prevention Program data which used
the traditional criteria for diagnosing
GDM40; we have no information on meet-
ing the new criteria whether type 2 diabe-
tes can be prevented. Mission et al68 used
an extension of the finding in the MFMU
study that the C-section rate could be
lowered with the treatment of GDM and
if this was assumed then the IADPSG
criteria were cost effective. However,
the systematic analysis by Horvath
et al33 found no significant decrease in
the rate of caesarean deliveries with
the treatment of GDM and in fact, as
pointed out by the Toronto Tri-Hospital
study, the label of GDM can actually be
associated with an increased risk of
C-section.69
Given the situation that the current
ACOG criteria are not based on evidence
pertaining to the baby and the criteria are
ambivalent on the screening method and
actual thresholds for diagnosis; and that
the IADPSG criteria although based on
HAPO evidence are advocating a poorly
reproducible test with low thresholds that
exaggerate the importance of glucose for
neonatal outcomes and in diagnosing
nearly a fifth of pregnant women as
GDM are a poor bargain for pregnant
Diagnosing Gestational Diabetes 781
women and when scrutinized lacked suf-
ficient evidence to be accepted by the NIH
Consensus panel examining this issue,70 it
behooves us to look at alternatives.
Alternative
Use of a 50 g GDS followed by a 75 g
OGTT in select cases using cutoff criteria
equivalent to levels associated with an OR
of 2.0 for LGA in offspring.
Pending the identification of the true
cause of LGA, there is a better interim
approach that addresses the defects of the
ACOG position in that it can be based on
HAPO data but in using a 2 step process
and a 2-fold increased risk for LGA; it
addresses the issue of reproducibility
and the benefit/harm balance that the
IADPSG approach engenders. The
HAPO data showed that a 2-fold in-
creased risk of an LGA align with
category 6 glucose levels, that is: fasting
95 mg/dL (5.3 mmol/L), 1 hour 195 mg/dL
(10.6 mmol/L), and 2 hours post 75 g load
of 162 mg/dL (9.0 mmol/L). These fasting
and 1-hour levels are identical and the 2-
hour value just 2 mg/dL (0.1 mmol/L)
higher than what we have been using in
Canada for the diagnosis of GDM for 15
years.71 Thus we have knowledge of how
well these levels perform in a clinical
situation. The prevalence of GDM in
Canada is about 5% and the use of a
2-step approach helps reproducibility.
In most settings for the diagnosis of
diabetes, 2 abnormalities are required, an
initial abnormal value with a second con-
firmatory test. The 50 g GDS can provide
the first step of this diagnostic process and
its use has been found to be of value in a
systematic review.72 In addition, by hav-
ing an abnormal GDS there is a better
chance the abnormality is reproducible.
Cutoffs for the 50 g GDS Test
Traditionally the lower cutoff for this 50 g
screening test is 140 mg/dL (7.8 mmol/L)
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782 Ryan
to indicate the absence of any glucose
abnormality during pregnancy and this
level has a specificity and sensitivity of
82% to 87% and 77% to 79%, respec-
tively.73,74 In practice, population studies
show that 86% of women have values
<140 mg/dL (7.8 mmol/L) 1 hour after a
50 g glucose challenge and can be reas-
sured that they do not have GDM.75 In
the French study, an upper cutoff of
200 mg/dL (11.1 mmol/L) presumed that
GDM was present and with this they
could diagnose 1.3% as having GDM
based on the 50 g screen.75 In Canada we
have also been using an upper cutoff of
185 mg/dL (10.3 mmol/L) based on an
older study76 and this has proven cost
effective.77
Pending prospective studies it is rea-
sonable to set this upper cutoff at
Z200 mg/dL (11.1 mmol/L) after the
GDS to presume a diagnosis of GDM.
In principle there can be an upper cutoff.
A level of 400 mg/dL (22.2 mmol/L) after
a 50 g screen would convince all caregivers
that the pregnant woman has glucose
intolerance and they would not request a
confirmatory 75 g glucose tolerance test.
The IADPSG group proposed that after
75 g of glucose a level of Z180 mg/dL
(10 mmol/L) at 1 hour was diagnostic of
GDM so reaching a level of Z200 mg/dL
(11.1 mmol/L) after 50 g of glucose could
be reasonably assumed to diagnose
GDM. Carpenter and Coustan18 found
that when the level post 50 g screen was
Z185 mg/dL (10.3 mmol/L) (GDS test
performed after fasting) then 100% of
women had GDM. Ortego-Gonzalez
et al78 found that at a level of Z185 mg/
dL (10.3 mmol/L) that 96% had GDM.
Others have found that the post-
screen value had to be Z217 mg/dL
(12.1 mmol/L)79 or Z230 mg/dL (12.8
mmol/L)80 to have 100% probability of
having GDM on the OGTT. Other re-
ports indicate that setting the upper cutoff
to 200 mg/dL (11.1 mmol/L) did not per-
form as well with only 57%,81 62%,82 or
www.clinicalobgyn.com
69%83 having abnormal glucose toler-
ance. Although Lanni and Barrett84
found that of those with a GDS value
Z200 mg/dL (11.1 mmol/L) only 52%
had GDM, they do not specify how many
had any glucose intolerance. The princi-
ple that there is a level of cutoff that can be
diagnosed with GDM is there but perhaps
we do not know the exact number at the
moment and prospective studies will be
required to answer this. Finally Round
et al85 suggest that an approach of a
universal OGTT for screening used is
more cost effective but if acceptance of
the test by pregnant women is included in
the analysis then using the GDS before
proceeding to an OGTT is more prefera-
ble to pregnant women as long as the
prevalence of GDM is over 3.6%. Utiliz-
ing this approach which has been prac-
ticed in Canada, Meltzer et al77 showed
that using the glucose challenge test with
an upper cutoff to be the most cost-effec-
tive approach. This is clearly an area that
requires a prospective study to critically
analyze the upper and lower cutoffs that
allow the diagnosis and exclusion of
GDM based on the GDS test result. The
use of an upper cutoff to give a presump-
tive diagnosis of GDM will result in 1.4%
of women not having to bother with an
OGTT.
Benefit-Harm
A 2-fold increased risk of LGA associated
with these numbers gives a GDM rate of
10.5% in theory. The number of birth
traumas in the HAPO study was linearly
related to glucose over 7 categories at a
rate of increasing OR of 1.18/mmol. Giv-
en the numbers of women in these higher
glucose categories is decreasing it is clear
that the relative number of birth traumas
increased for the higher glucose catego-
ries. It is also evident from Figure 1 that it
was only in group 7 that the fasting glu-
cose level outweighed the highest BMI in
terms of increased OR for LGA.

Although it cannot be denied that most
LGA occurs in the absence of either obe-
sity or glucose, diagnosing GDM based
on category 6 and 7 will detect the most
egregious glucose intolerance at least and
give a more specific group of GDM to
work with. Finally, diagnosing GDM in
this smaller percentage inherently is a
better cost-benefit situation. Treating this
group will decrease the LGA rate and
shoulder dystocia rate and will be more
cost effective.
Suggested Alternative
Approach for Diagnosing
GDM
All pregnant women without known glu-
cose intolerance should be screened for
GDM at 24 to 28 weeks gestation with a
50 g glucose load given at any time of day
and a plasma glucose drawn 1 hour later. If
this value is <140 mg/dL (7.8 mmol/L) then
no glucose intolerance is evident. If the value
is Z200 mg/dL (11.1 mmol/L) the GDM
may be presumed present Figure 2. If the
value at 1 hour is 140 (7.8 mmol/L) to
199 mg/dL (11.0 mmol/L) then a 75 g
OGTT should be performed. The test
should be performed in carbohydrate-
replete individuals in the fasting state with
FIGURE 2. Outline of alternative proposed diagnostic approach to the pregnant women without
known glucose intolerance (as presented at the NIH Consensus Conference, see text for details).70
Diagnosing Gestational Diabetes 783
plasma venous blood drawn at fasting and 1
and 2 hours postglucose load. If Z1 values
meet or exceed the following then GDM is
present: fasting 95 mg/dL (5.3 mmol/L),
1 hour 195 mg/dL (10.6 mmol/L), and 2
hour 162 mg/dL (9.0 mmol/L). Once diag-
nosed GDM should be managed in a stand-
ard manner.
Future Directions
It is apparent that the alternative proposed
in this paper is truly only an interim ap-
proach. Some pressing issues that need to be
addressed are: (1) Is treating obesity a more
acceptable pragmatic approach?; (2) A pro-
spective study of appropriate cutoffs for 50 g
screen is required; (3) Is obesity or glucose
more important in setting the stage for
metabolic disease for next generation?; and
(4) Could a more selective filter be con-
structed from HAPO data using both glu-
cose and BMI to better selects group with
adverse outcomes? In the meantime the
alternative 2-step approach for diagnosing
GDM is the most reasonable way forward.
Conclusions
It is certain that other causes of LGA will be
identified so that a more targeted approach
www.clinicalobgyn.com
784 Ryan
to the prevention of LGA can be used in the
future. Perhaps a high level of fetal insulin
decreases IGF-binding protein-1 so that
more free IGF-1 may stimulate increased
growth. Alternatively there may be a novel
placental peptide that causes LGA that has
yet to be identified. In the meantime, the
alternative proposal presented herein is a
reasonable interim solution that address the
issue of reproducibility and identifies the
most severe glucose intolerance and is rea-
sonable use of resources.
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