DiabetesPregnancy FinalD 2013

Earn 2.
0 CME Credits
Endocrine Societys
Clinical
Guidelines
Diabetes and Pregnancy:

An Endocrine Society Clinical Practice Guideline
Authors: Ian Blumer, Eran Hadar, David R. Hadden, Lois Jovanovic, Jorge H. Mestman, M. Hassan Murad, and
Yariv Yogev
Affiliations: Charles H. Best Diabetes Centre (I.B.), Whitby, Ontario, Canada L1M 1Z5; Helen Schneider Hospital
for Women (E.H., Y.Y.), Petach Tikva 49100, Israel; Royal Victoria Hospital (D.R.H.), Belfast BT12 6BA, Northern
Ireland, United Kingdom; Sansum Diabetes Research Institute (L.J.), Santa Barbara, California 93105; University
of Southern California (J. H. M.), Los Angeles, California 90089; and Knowledge and Evaluation Research Unit,
Mayo Clinic (M. H. M.), Rochester, Minnesota 55905
Co-Sponsoring Associations: American Diabetes Association, European Association of Perinatal Medicine, and
European Society of Endocrinology.
Disclaimer: Clinical Practice Guidelines are developed to be of assistance to endocrinologists and other health
care professionals by providing guidance and recommendations for particular areas of practice. The Guidelines
should not be considered inclusive of all proper approaches or methods, or exclusive of others. The Guidelines
cannot guarantee any specific outcome, nor do they establish a standard of care. The Guidelines are not intended
to dictate the treatment of a particular patient. Treatment decisions must be made based on the independent
judgment of health care providers and each patients individual circumstances.
The Endocrine Society makes no warranty, express or implied, regarding the Guidelines and specifically
excludes any warranties of merchantability and fitness for a particular use or purpose. The Society shall not be
liable for direct, indirect, special, incidental, or consequential damages related to the use of the information
contained herein.
First published in Journal of Clinical Endocrinology & Metabolism, November 2013, 98: 42274249, 2013.
Endocrine Society, 2013
Endocrine Societys
Clinical
Guidelines

Table of Contents
Continuing Medical Education Information. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Summary of Recommendations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Method of Development of Evidence-Based Clinical Practice Guidelines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Introduction and Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13
Preconception Care of Women with Diabetes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Gestational Diabetes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Glucose Monitoring and Glycemic Targets. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
Nutrition Therapy and Weight Gain Targets for Women with Overt or Gestational Diabetes. . . . . . . . . . . . . . . 22
Blood Glucose-Lowering Pharmacological Therapy During Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
Labor, Delivery, Lactation, and Postpartum Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
CME Learning Objectives and Post-Test Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
CME Answers and Explanations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
Order Form. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Reprint Information, Questions & Correspondences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Inside Back Cover
Accreditation Statement
The Endocrine Society is accredited by the Accreditation Council for Continuing Medical Education to provide
continuing medical education for physicians.
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The Endocrine Society designates this enduring material for a maximum of 2 AMA PRA Category 1 Credits.
Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Learning Objectives
Upon completion of this educational activity, learners will be able to:
Recognize the appropriate target level of glycemic control (as reflected by the HbA1C) for a woman with
established diabetes before attempting to conceive.
Evaluate self-monitored blood glucose target levels for a woman with gestational diabetes and the appropriate therapeutic intervention if these targets are being exceeded.
Determine the appropriate frequency for ocular assessment for a pregnant woman with diabetes and
known retinopathy.
Select appropriate antihyperglycemic medication for a breastfeeding woman with type 2 diabetes.
Target Audience
This continuing medical education activity should be of substantial interest to endocrinologists and other health
care professionals that treat patients with diabetic patients during pregnancy and postpartum.
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As a provider of continuing medical education (CME) accredited by the Accreditation Council for Continuing
Medical Education, the Endocrine Society has a policy of ensuring that the content and quality of this educational
activity are balanced, independent, objective, and scientifically rigorous. The scientific content of this activity was
developed under the supervision of The Diabetes and Pregnancy Guidelines Task Force.
Disclosure Policy
Diabetes and Pregnancy
The faculty, committee members, and staff who are in position to control the content of this activity are required
to disclose to the Endocrine Society and to learners any relevant financial relationship(s) of the individual or
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The Endocrine Society has reviewed all disclosures and resolved or managed all identified conflicts of interest,
as applicable.
The following task force members who planned and/or reviewed content for this activity reported relevant financial relationships:
Ian Blumer, MD (chair) is a speaker for Astra-Zeneca, Bristol Myers Squibb, Eli Lilly, Medtronic, Novo Nordisk,
Roche and Sanofi-Aventis. He is also a member of advisory board for Bayer, Eli Lilly, GlaxoSmithKline, Novo
Nordisk, Janssen Pharmaceuticals, and Takeda.
David R. Hadden, MD is a member of the data monitoring committee for Novo Nordisk and a technical editor for
Wiley-Blackwell Publishing.
The following committee members who planned and/or reviewed content for this activity reported no relevant
financial relationships: M. Hassan Murad, MD; Lois Jovanovic, MD; Jorge H. Mestman, MD; Eran Hadar,
MD; Yariv Yogev, MD.
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D i a b e t es a n d P r eg n a n c y
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Abstract
Objective: Our objective was to formulate a clinical
practice guideline for the management of the pregnant woman with diabetes.
Participants: The Task Force was composed of a chair,
selected by the Clinical Guidelines Subcommittee of
the Endocrine Society, 5 additional experts, a methodologist, and a medical writer.
Evidence: This evidence-based guideline was developed using the Grading of Recommendations,
Assessment, Development, and Evaluation (GRADE)
system to describe both the strength of recommendations and the quality of evidence.
Conclusions: Using an evidence-based approach, this

Diabetes and Pregnancy Clinical Practice Guideline
addresses important clinical issues in the contemporary management of women with type 1 or type 2
diabetes preconceptionally, during pregnancy, and in
the postpartum setting and in the diagnosis and
management of women with gestational diabetes
during and after pregnancy.
J Clin Endocrinol Metab 98: 42274249, 2013
Consensus Process: One group meeting, several

conference calls, and innumerable e-mail communications enabled consensus for all recommendations
save one with a majority decision being employed for
this single exception.
Abbreviations: ACE, angiotensin-converting enzyme; BMI, body mass index; BP, blood pressure; CAD, coronary artery disease; GFR, glomerular filtration
rate; HbA1C, hemoglobin A1C; IADPSG, International Association of Diabetes and Pregnancy Study Groups; NPH, neutral protamine Hagedorn; OGTT,
oral glucose tolerance test.
Summary of
Recommendations
1.0. Preconception care of women with
diabetes
Preconception counseling
1.1. We recommend that preconception counseling
be provided to all women with diabetes who are

considering pregnancy. (1|
)
Preconception glycemic control
1.2. We suggest that women with diabetes seeking to
conceive strive to achieve blood glucose and hemoglobin A1C (HbA1C) levels as close to normal as
possible when they can be safely achieved without
undue hypoglycemia. (2|
) (See Recommendations 3.2ad.)
Insulin therapy
1.3a. We recommend that insulin-treated women
with diabetes seeking to conceive be treated with

multiple daily doses of insulin or continuous sc insulin
infusion in preference to split-dose, premixed insulin
therapy, because the former are more likely to allow
for the achievement and maintenance of target blood
glucose levels preconceptionally and, in the event of
pregnancy, are more likely to allow for sufficient
flexibility or precise adjustment of insulin therapy.
(1|
)
1.3c. We suggest that insulin-treated women with
diabetes seeking to conceive be treated with rapidacting insulin analog therapy (with insulin aspart or
insulin lispro) in preference to regular (soluble)
insulin. (2|
)
fully using the long-acting insulin analogs insulin

detemir or insulin glargine preconceptionally may
continue with this therapy before and then during
pregnancy. (2|
)
Folic acid supplementation
1.4. We recommend that beginning 3 months before
withdrawing contraceptive measures or otherwise

trying to conceive, a woman with diabetes take a daily
folic acid supplement to reduce the risk of neural tube
defects. (1|
) We suggest a daily dose of 5 mg
based on this doses theoretical benefits. (2|
)
Ocular care (preconception, during pregnancy,
and postpartum)
1.5a. We recommend that all women with diabetes
who are seeking pregnancy have a detailed ocular

assessment by a suitably trained and qualified eye care
professional in advance of withdrawing contraceptive
measures or otherwise trying to conceive (1|
),
and if retinopathy is documented, the patient should
be apprised of the specific risks to her of this worsening during pregnancy. If the degree of retinopathy
warrants therapy, we recommend deferring conception until the retinopathy has been treated and found
to have stabilized. (1|
)
1.5b. We recommend that women with established
retinopathy be seen by their eye specialist every

trimester, then within 3 months of delivering, and
then as needed. (1|
)
1.5c. We suggest that pregnant women with diabetes
not known to have retinopathy have ocular assessment performed soon after conception and then periodically as indicated during pregnancy. (2|
)
Renal function (preconception and during
pregnancy)
1.6a. We suggest that all women with diabetes
considering pregnancy have their renal function

assessed (by measuring their urine albumin to creatinine ratio, serum creatinine, and estimated glomerular filtration rate [GFR]) in advance of withdrawing
contraceptive measures or otherwise trying to
1.3b. We suggest that a change to a womans insulin

regimen, particularly when she starts continuous sc
insulin infusion, be undertaken well in advance of
trying to conceive to allow the patient to acquire
expertise in, and the optimization of, the chosen
insulin regimen. (Ungraded recommendation)
1.3d. We suggest that women with diabetes success-
conceive. (Ungraded recommendation) We suggest

that a woman with diabetes who has a significantly
reduced GFR be assessed by a nephrologist before
pregnancy, both for baseline renal assessment and to
review the womans specific risk of worsening renal
function in the event of pregnancy. (Ungraded
recommendation)
(particularly the duration of the womans diabetes and

her age), screening studies for coronary artery disease
(CAD) be undertaken in advance of withdrawing
conceive. (1|
)
1.8b. We recommend that if a woman with diabetes
preconceptional renal dysfunction have their renal

function monitored regularly during pregnancy.
(Ungraded recommendation)
is seeking pregnancy and has CAD, its severity should

be ascertained, treatment instituted, and counseling
provided as to the potential risks of pregnancy to the
woman and fetus before the woman withdraws contraception or otherwise tries to conceive. (1|
)
Management of hypertension
Management of dyslipidemia
1.7a. We recommend that satisfactory blood pressure

(BP) control (<130/80 mm Hg) be achieved and
maintained before withdrawing contraception or
otherwise trying to conceive. (1|
)
1.9a. We recommend against the use of statins in
1.6b. We suggest that all women with diabetes and
1.7b. We recommend that a woman with diabetes
who is seeking conception while taking an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker in almost all cases should
discontinue the medication before withdrawing
conceive. (1|
)
women with diabetes who are attempting to conceive.

(1|
)
1.9b. In view of their unproven safety during pregnancy, we suggest against the routine use of fibrates
and/or niacin for women with diabetes and hypertriglyceridemia attempting to conceive. (2|
)
1.9c. We suggest that bile acid-binding resins may
be used in women with diabetes to treat hypercholesterolemia; however, this is seldom warranted.
(2|
)
1.7c. We suggest that in the exceptional case where
the degree of renal dysfunction is severe and there is

uncertainty about when conception will occur, physicians and patients be engaged in shared decisionmaking about whether to continue ACE inhibitors or
angiotensin-receptor blockers. The patients should be
informed about the possible loss of the renal protective properties if the medication is discontinued and
the risk of teratogenesis if it is continued. (Ungraded
recommendation)
1.7d. We recommend when ACE inhibitors or angio-
tensin-receptor blockers have been continued up to

the time of conception that the medication should be
withdrawn immediately upon the confirmation of
pregnancy. (1|
)
Elevated vascular risk
1.8a. We recommend that if a woman with diabetes
has sufficient numbers of vascular risk factors
Thyroid function
1.10. For women with type 1 diabetes seeking concep-
tion, we recommend measurement of serum TSH and,

if their thyroid peroxidase status is unknown, measurement of thyroid peroxidase antibodies before withdrawing contraceptive measures or otherwise trying to
conceive. (1|
)
Overweight and obesity
1.11. We recommend weight reduction before preg-
nancy for overweight and obese women with diabetes.

(1|
)
2.0. Gestational diabetes

Testing for overt diabetes in early pregnancy
2.1. We recommend universal testing for diabetes
(see Table 1) with a fasting plasma glucose, HbA1C,

or an untimed random plasma glucose at the first
prenatal visit (before 13 weeks gestation or as soon as
possible thereafter) for those women not known to
already have diabetes. (1|
) In the case of
overt diabetes, but not gestational diabetes, a second
test (either a fasting plasma glucose, untimed random
plasma glucose, HbA1C, or OGTT) must be
performed in the absence of symptoms of hyperglycemia and found to be abnormal on another day to
confirm the diagnosis.
Testing for gestational diabetes at 24 to 28

weeks gestation
2.2. We recommend that pregnant women not previously identified (either during testing performed as per
recommendation 2.1 or at some other time before 24
weeks gestation) with overt diabetes or gestational
diabetes be tested for gestational diabetes (see Table
2) by having a 2-hour, 75-g OGTT performed at 24 to
28 weeks gestation. (1|
) We recommend that
gestational diabetes be diagnosed on this test using
the International Association of Diabetes and Pregnancy Study Groups (IADPSG) criteria (majority
opinion of this committee). (1|
)
The 75-g OGTT should be performed after an overnight fast of at least 8 hours (but not more than 14
hours) and without having reduced usual carbohydrate intake for the preceding several days. The test
should be performed with the patient seated, and the
TABLE 1. Diagnostic Criteria for Overt Diabetes and Gestational Diabetes at the First Prenatal Visit (Before 13 Weeks
Gestation or as Soon as Possible Thereafter) for Those Women Not Known to Already Have Diabetesa
Diagnosis
Fasting Plasma
Glucose,b
mg/dL (mmol/L)
Untimed (Random)
Plasma Glucose,b
mg/dL (mmol/L)
HbA1C,c %
Overt diabetes (type 1, type 2, or other)
126 (7.0)
200 (11.1)
6.5%
92125 (5.16.9)
NA
NA
Gestational diabetes
Abbreviation: NA, not applicable.
a These criteria for the diagnosis of overt diabetes in early pregnancy are congruent with those of the American Diabetes Association (57) and differ
somewhat from those of the IADPSG (70).
b Testing should use plasma glucose analyzed at a laboratory, not capillary blood glucose analyzed with a blood glucose meter.
c Performed using a method that is certified by the NGSP (National Glycohemoglobin Standardization Program) and standardized to the Diabetes Control
and Complications Trial (DCCT) (39) reference assay.
TABLE 2. Diagnostic Criteria for Overt Diabetes and Gestational Diabetes Using a 2-Hour 75-g OGTT at 24 to 28
Weeks Gestationa
Fasting Plasma
Glucose,b
mg/dL (mmol/L)
1-h Value,
mg/dL (mmol/L)
2-h Value,
mg/dL (mmol/L)
Overt diabetes (type 1, type 2, or other)
126 (7.0)
NA
200 (11.1)
92125 (5.16.9)
180 (10.0)
153199 (8.511.0)
Gestational diabetes
Abbreviation: NA, not applicable.
a These criteria for diagnosing overt diabetes based on the results of the 24- to 28-week glucose tolerance test differ somewhat from those of the American
Diabetes Association (57) and the IADPSG (70).
b Testing should use plasma glucose analyzed at a laboratory, not capillary blood glucose analyzed with a blood glucose meter.
Diagnosis
patient should not smoke during the test. One or more

abnormal values establishes the diagnosis, with the
exception that in the case of overt diabetes, but not
gestational diabetes, a second test (either a fasting
plasma glucose, untimed random plasma glucose,
HbA1C, or OGTT), in the absence of symptoms of
hyperglycemia, must be performed and found to be
abnormal on another day to confirm the diagnosis of
overt diabetes.
Management of elevated blood glucose
2.3a. We recommend that women with gestational
diabetes target blood glucose levels as close to normal

as possible. (1|
)
2.3b. We recommend that the initial treatment of
gestational diabetes should consist of medical nutrition therapy (see Section 4.0) and daily moderate
exercise for 30 minutes or more. (1|
)
2.3c. We recommend using blood glucose-lowering
pharmacological therapy if lifestyle therapy is insufficient to maintain normoglycemia in women with

gestational diabetes. (1|
)
Postpartum care
10
2.4a. We recommend that postpartum care for

women who have had gestational diabetes should
include measurement of fasting plasma glucose or
fasting self-monitored blood glucose for 24 to 72
hours after delivery to rule out ongoing hyperglycemia. (1|
)
2.4b. We recommend that a 2-hour, 75-g OGTT
should be undertaken 6 to 12 weeks after delivery in

women with gestational diabetes to rule out prediabetes or diabetes. (1|
) If results are normal,
we recommend this or other diagnostic tests for
diabetes should be repeated periodically as well as
before future pregnancies. (1|
)
2.4c. We suggest the childs birth weight and whether
or not the child was born to a mother with gestational

diabetes become part of the childs permanent medical
record. (Ungraded recommendation)
2.4d. We recommend that all women who have had

gestational diabetes receive counseling on lifestyle
measures to reduce the risk of type 2 diabetes, the
need for future pregnancies to be planned, and the
need for regular diabetes screening, especially before
any future pregnancies. (1|
)
2.4e. We suggest blood glucose-lowering medication
should be discontinued immediately after delivery for

women with gestational diabetes unless overt diabetes
is suspected, in which case the decision to continue
such medication should be made on a case-by-case
basis. (2|
)
3.0. Glucose monitoring and glycemic targets
Self-monitoring of blood glucose
3.1. We recommend self-monitoring of blood glucose
in all pregnant women with gestational or overt

diabetes (1|
) and suggest testing before and
either 1 or 2 hours after the start of each meal
(choosing the postmeal time when it is estimated that
peak postprandial blood glucose is most likely to
occur) and, as indicated, at bedtime and during the
night. (2|
)
Glycemic targets (Table 3)
3.2a. We recommend pregnant women with overt
or gestational diabetes strive to achieve a target
preprandial blood glucose <95 mg/dL (5.3 mmol/L).
Table 3. Glycemic Targets Preconceptionally for

Women with Overt Diabetes and During Pregnancy
for Women With Either Overt Diabetes or Gestational
Diabetesa
Target Value,
mg/dL (mmol/L)
Preprandial blood glucose
95 (5.3) b
1 h after the start of a meal
140 (7.8)
2 h after the start of a meal
120 (6.7)
a Note that blood glucose meters use capillary blood but display
corrected results equivalent to plasma glucose levels.
b Target fasting blood glucose is 90 (5.0 mmol/L) if this can be safely
achieved without undue hypoglycemia.
(1|
meals).
) for fasting target, 1|
4.0. Nutrition therapy and weight gain targets

for women with overt or gestational
diabetes
) for other
3.2b. We suggest that an even lower fasting blood
Nutrition therapy
glucose target of <90 mg/dL (5.0 mmol/L) be strived

for (2|
) if this can be safely achieved without
undue hypoglycemia.
4.1. We recommend medical nutrition therapy for
all pregnant women with overt or gestational diabetes

to help achieve and maintain desired glycemic control
while providing essential nutrient requirements.
(1|
)
3.2c. We suggest pregnant women with overt or
gestational diabetes strive to achieve target blood

glucose levels 1 hour after the start of a meal <140 mg/
dL (7.8 mmol/L) and 2 hours after the start of a meal
<120 mg/dL (6.7 mmol/L) (2|
) when these
targets can be safely achieved without undue
hypoglycemia.
Weight management
4.2a. We suggest that women with overt or gestational diabetes follow the Institute of Medicine
revised guidelines for weight gain during pregnancy
(1) (Table 4). (Ungraded recommendation)
3.2d. We suggest pregnant women with overt diabetes
strive to achieve a HbA1C <7% (ideally <6.5%).

(2|
)
4.2b. We suggest obese women with overt or gesta-
tional diabetes reduce their calorie intake by approximately one-third (compared with their usual intake
before pregnancy) while maintaining a minimum
intake of 1600 to 1800 kcal/d. (2|
)
Continuous glucose monitoring

3.3. We suggest that continuous glucose monitoring
be used during pregnancy in women with overt or

gestational diabetes when self-monitored blood
glucose levels (or, in the case of the woman with overt
diabetes, HbA1C values) are not sufficient to assess
glycemic control (including both hyperglycemia and
hypoglycemia). (2|
)
Carbohydrate intake
4.3. We suggest women with overt or gestational
diabetes limit carbohydrate intake to 35% to 45% of

total calories, distributed in 3 small- to moderate-sized
meals and 2 to 4 snacks including an evening snack.
(2|
)
TABLE 4. 2009 Institute of Medicine Recommendations for Total Weight Gain and Rate of Weight Gain During
Pregnancy, by Prepregnancy BMI (130)
Total Weight Gain
Prepregnancy BMI
Rates of Weight Gain in

Second and Third Trimester a
Range,
lb
Mean (Range),
kg/wk
Mean (Range),
lb/wk
Underweight (<18.5 kg/m2)
12.518
2840
0.51 (0.440.58)
1 (11.3)
Normal weight (18.524.9 kg/m2)
11.516
2535
0.42 (0.350.50)
1 (0.81)
711.5
1525
0.28 (0.230.33)
0.6 (0.50.7)
59
1120
0.22 (0.170.27)
0.5 (0.40.6)
Overweight (25.029.9 kg/m2)

Obese (30.0 kg/m2)
a Calculations assume a 0.5- to 2-kg (1.14.4 lb) weight gain in the first trimester.
Range,
kg
11
Nutritional supplements
Noninsulin antihyperglycemic agent therapy
4.4. We recommend pregnant women with overt or
5.2a. We suggest that glyburide (glibenclamide) is a
gestational diabetes should follow the same guidelines

for the intake of minerals and vitamins as for women
without diabetes (1|
), with the exception of
taking folic acid 5 mg daily beginning 3 months before
trying to conceive (see Recommendation 1.4). We
suggest that at 12 weeks gestation, the dose of folic
acid be reduced to 0.4 to 1.0 mg/d, which should
be continued until the completion of breastfeeding.
(2|
)
suitable alternative to insulin therapy for glycemic

control in women with gestational diabetes who fail
to achieve sufficient glycemic control after a 1-week
trial of medical nutrition therapy and exercise except
for those women with a diagnosis of gestational
diabetes before 25 weeks gestation and for those
women with fasting plasma glucose levels >110 mg/dL
(6.1 mmol/L), in which case insulin therapy is
preferred. (2|
)
5.0. Blood glucose-lowering pharmacological

therapy during pregnancy
Insulin therapy
5.1a. We suggest that the long-acting insulin analog

detemir may be initiated during pregnancy for those
women who require basal insulin and for whom
neutral protamine Hagedorn (NPH) insulin, in appropriate doses, has previously resulted in, or for whom it
is thought NPH insulin may result in, problematic
hypoglycemia; insulin detemir may be continued in
those women with diabetes already successfully taking
insulin detemir before pregnancy. (2|
)
12
5.2b. We suggest that metformin therapy be used for

glycemic control only for those women with gestational diabetes who do not have satisfactory glycemic
control despite medical nutrition therapy and who
refuse or cannot use insulin or glyburide and are not in
the first trimester. (2|
)
6.0. Labor, delivery, lactation, and

postpartum care
Blood glucose targets during labor and delivery
6.1. We suggest target blood glucose levels of 72 to
126 mg/dL (4.0 to 7.0 mmol/L) during labor and
delivery for pregnant women with overt or gestational
diabetes. (2|
)
5.1b. We suggest that those pregnant women successfully using insulin glargine before pregnancy may
continue it during pregnancy. (2|
)
Lactation
5.1c. We suggest that the rapid-acting insulin analogs
overt or gestational diabetes should breastfeed their

infant. (1|
)
lispro and aspart be used in preference to regular

(soluble) insulin in pregnant women with diabetes.
(2|
)
5.1d. We recommend the ongoing use of continuous
sc insulin infusion during pregnancy in women with

diabetes when this has been initiated before pregnancy (1|
), but suggest that continuous sc
insulin infusion not be initiated during pregnancy
unless other insulin strategies including multiple daily
doses of insulin have first been tried and proven
unsuccessful. (2|
)
6.2a. We recommend whenever possible women with
6.2b. We recommend that breastfeeding women with

overt diabetes successfully using metformin or
glyburide therapy during pregnancy should continue
to use these medications, when necessary, during
breastfeeding. (1|
)
Postpartum contraception
6.3. We recommend that the choice of a contracep-
tive method for a woman with overt diabetes or a

history of gestational diabetes should not be influenced by virtue of having overt diabetes or a history of
)
Screening for postpartum thyroiditis

6.4. We suggest that women with type 1 diabetes be
screened for postpartum thyroiditis with a TSH at 3

and 6 months postpartum. (2|
)
Method of Development
of Evidence-Based Clinical
Practice Guidelines
The Clinical Guidelines Subcommittee of the Endocrine Society deemed the diagnosis and treatment of
diabetes and pregnancy a priority area in need of a
clinical practice guideline and appointed a Task Force
to formulate evidence-based recommendations. The
Task Force commissioned two systematic reviews and
used the best available research evidence to develop
the recommendations.
The panelists on a few occasions left some recommendations ungraded (4). These are recommendations
that were supported only by indirect evidence or by
the unsystematic observations of the committee
members and resulted from their consensus and
discussion and have been included owing to their
clinical relevance and practicality. These recommendations should be considered suggestions (i.e., deviation from these recommendations is not unreasonable)
and are explicitly left ungraded due to the lack of
direct evidence.
Introduction and
background
In recent years, important new research has emerged
in the field of diabetes and pregnancy. This guideline
has been developed to address and distill this
burgeoning literature with the goal of assisting healthcare providers to best manage their pregnant patients
living with overt or gestational diabetes using contemporary, evidence-based strategies.
In this guideline, all references to diabetes specifically
and exclusively refer to diabetes mellitus. Also, unless
stated otherwise, the terms diabetes, overt diabetes,
and pregestational diabetes refer to either type 1 or
type 2 diabetes.
We use the traditional term gestational diabetes to
describe what has customarily been defined as any
degree of glucose intolerance with onset or first definition during pregnancy (5) while acknowledging that
the more contemporary term hyperglycemia in pregnancy has strong merit as a more appropriate term (6).
We have retained the longstanding term (gestational
diabetes) owing to its widespread familiarity and
traditional usage.
Select thyroid recommendations in this Diabetes and
Pregnancy Guideline are included as they relate
The Task Force followed the approach recommended

by the Grading of Recommendations, Assessment,
Development, and Evaluation (GRADE) group, an
international group with expertise in development
and implementation of evidence-based guidelines (2).
A detailed description of the grading scheme has been
published elsewhere (3). The Task Force also used
consistent language and graphical descriptions of both
the strength of a recommendation and the quality of
evidence. In terms of the strength of the recommendation, strong recommendations use the phrase we
recommend and the number 1, and less strong recommendations use the phrase we suggest and the
number 2. Cross-filled circles indicate the quality of
the evidence, such that
denotes very low
quality evidence;
, low quality;
,
moderate quality; and
, high quality. The Task
Force has confidence that persons who receive care
according to the strong recommendations will derive,
on average, more good than harm. Less strong recommendations require more careful consideration of the
persons circumstances, values, and preferences to
determine the best course of action. Linked to each
recommendation is a description of the evidence that
panelists considered in making the recommendation.
For some recommendations, remarks are present that

provide additional background information, commentary, or technical suggestions.
13
specifically to thyroid disease in pregnant women with

diabetes. See the 2012 Endocrine Society Clinical
Practice Guideline on pregnancy and thyroid disease
for a detailed discussion on this topic (7).
This guideline advocates for use of best practices based
on an analysis of the contemporary (and older)
medical literature. It is, however, recognized that cost
considerations and other practical realities may not
necessarily allow for implementation of certain of our
recommendations in some locales.
1.0. Preconception care of

women with diabetes
1.2. We suggest that women with diabetes seeking to
1.1. We recommend that preconception counseling
be provided to all women with diabetes who are

considering pregnancy. (1|
)
1.2. Evidence
1.1. Evidence
Preconception glycemic control

conceive strive to achieve blood glucose and HbA1C
levels as close to normal as possible when they can
be safely achieved without undue hypoglycemia.
(2|
) (See Recommendations 3.2ad.)
Preconception counseling
14
has had appropriate assessment and management of

comorbidities including hypertension and retinopathy, has discontinued potentially unsafe (during
pregnancy) medications, and has been taking appropriate folate supplementation beforehand (see the
recommendations and evidence that follow in this
section); 2) the importance of smoking cessation;
3) the major time commitment and effort required by
the patient in both self-management and engagement
with the healthcare team, both preconceptionally and
during pregnancy; and 4) the importance of notifying
the healthcare team without delay in the event of
conception.
Women with diabetes who receive preconception

counseling have better preconception glycemic
control (89) and are more likely to have favorable
pregnancy outcomes, including lower rates of congenital anomalies (910) and spontaneous abortions
(1112). By the time that a woman knows she is pregnant, much fetal organogenesis has typically been
completed (13).
1.1. Remarks
Preconception counseling can optimally be provided
by a multidisciplinary team that includes the diabetes
specialist, diabetes educator, dietitian, obstetrician,
and other healthcare providers, as indicated. If
possible, and with the patients consent, the womans
partner can be included as part of a supportive and
mentoring therapeutic relationship. Preconception
counseling should include a discussion regarding
1) the need for pregnancy to be planned and to occur
only when the woman has sufficient glycemic control,
Maternal hyperglycemia in the first few weeks of pregnancy increases the risk of fetal malformations, spontaneous abortions, and perinatal mortality (1418).
Ideal preconception blood glucose levels have not
been definitively established (19), and the exact
degree of risk of a congenital anomaly for a given
HbA1C is not precisely known. It has been reported
(16, 18) that the risk progressively rises in concert
with the degree of periconceptional HbA1C elevation, although an increased risk compared with the
general childbearing population has been observed
with an HbA1C as low as 6.4% (18). It has, however,
also been reported (20) that there is a stable degree of
anomaly risk of 3.9% to 5.0% with a periconceptional
HbA1C of up to 10.4%, with this risk then climbing
to 10.9% if the HbA1C is 10.4% or higher.
Insulin therapy
1.3a. We recommend that insulin-treated women
with diabetes seeking to conceive be treated with
multiple daily doses of insulin or continuous sc insulin
infusion in preference to split-dose, premixed insulin
therapy, because the former are more likely to allow
for the achievement and maintenance of target

blood glucose levels preconceptionally and, in the
event of pregnancy, are more likely to allow for sufficient flexibility or precise adjustment of insulin
therapy. (1|
)
1.3b. We suggest that a change to a womans insulin
regimen, particularly when she starts continuous sc

insulin infusion, be undertaken well in advance of
trying to conceive to allow the patient to acquire
expertise in, and the optimization of, the chosen
insulin regimen. (Ungraded recommendation)
1.3c. We suggest that insulin-treated women with
diabetes seeking to conceive be treated with rapidacting insulin analog therapy (with insulin aspart or
insulin lispro) in preference to regular (soluble)
insulin. (2|
)
1.3d. We suggest that women with diabetes success-
fully using the long-acting insulin analogs insulin

detemir or insulin glargine preconceptionally may
continue with this therapy before and then during
pregnancy. (2|
)
1.3ad. Evidence
1.3ad. Remarks
The issues of insulin glargine not being FDA-approved
for use during pregnancy and glargines theoretical
Folic acid supplementation

1.4. We recommend that beginning 3 months before
trying to conceive, a woman with diabetes take a daily
folic acid supplement to reduce the risk of neural tube
defects. (1|
) We suggest a daily dose of 5 mg
based on this doses theoretical benefits. (2|
)
1.4. Evidence
Taking a daily folic acid supplement preconceptionally reduces the risk of neural tube defects (38). The
optimal amount of folate that should be taken is
uncertain, but 5 mg/d has a good rationale (38).
Ocular care (preconception, during pregnancy,
and postpartum)
1.5a. We recommend that all women with diabetes
who are seeking pregnancy have a detailed ocular

assessment by a suitably trained and qualified eye care
professional in advance of withdrawing contraceptive
measures or otherwise trying to conceive (1|
),
and if retinopathy is documented, the patient should
be apprised of the specific risks to her of this worsening during pregnancy. If the degree of retinopathy
warrants therapy, we recommend deferring conception until the retinopathy has been treated and found
to have stabilized. (1|
)
1.5b. We recommend that women with established
retinopathy be seen by their eye specialist every

trimester, then within 3 months of delivering, and
then as needed. (1|
)
Rapid-acting insulin analogs are likely more able than

regular human insulin to help a woman achieve postprandial blood glucose targets and are less likely to
cause hypoglycemia; fetal outcomes, however, seem
comparable (2830). Compared with NPH insulin,
use of the long-acting insulin analogs insulin detemir
or insulin glargine is associated with lower rates of
nocturnal hypoglycemia (3132). Insulin detemir, but
not insulin glargine, is approved for use by the U.S.
Food and Drug Administration (FDA) during pregnancy. Both of these long-acting insulin analogs,
however, are widely used in pregnancy, with evidence
of safety in this setting (3337). Long-acting insulin
analogs are, however, more expensive than NPH
insulin.
mitogenicity should be discussed preconceptionally

with women with diabetes who are using insulin
glargine. When appropriate, insulin glargine may be
replaced by insulin detemir or NPH insulin. Glulisine
is not yet proven safe for use during pregnancy (studies
are ongoing) and is not currently FDA-approved for
this indication; as such, insulin aspart and lispro (both
of which have been found to be safe in pregnancy and
are FDA-approved) are preferred. For additional
remarks, please refer to Remarks 5.1ab.
15
1.5c. We suggest that pregnant women with diabetes
not known to have retinopathy have ocular assessment performed soon after conception and then periodically as indicated during pregnancy. (2|
)
1.5ac. Evidence
Established retinopathy can rapidly progress during,
and up to 1 year after, pregnancy and can lead to
sight-threatening deterioration (3842). The greater
the degree of preconceptional retinopathy, the greater
is the risk of retinopathy progressing during pregnancy
(40). The absence of retinopathy before conception
confers very small risk of development of significant
retinopathy during pregnancy; nonetheless, significant retinopathy can develop and progress during
pregnancy, even if not identified preconceptionally
(40). Additional risk factors for progression of retinopathy during pregnancy include preexisting hypertension (43), poorly controlled hypertension during
pregnancy (44), preeclampsia (45), and poor glycemic
control at the onset of and during pregnancy (41).
Renal function (preconception and during
pregnancy)
1.6a. We suggest that all women with diabetes
16
considering pregnancy have their renal function

assessed (by measuring their urine albumin to creatinine ratio, serum creatinine, and estimated GFR) in
advance of withdrawing contraceptive measures or
otherwise trying to conceive. (Ungraded recommendation) We suggest that a woman with diabetes who
has a significantly reduced GFR be assessed by a
nephrologist before pregnancy, both for baseline renal
assessment and to review the womans specific risk of
worsening renal function in the event of pregnancy.
1.6b. We suggest that all women with diabetes and
preconceptional renal dysfunction have their renal
function monitored regularly during pregnancy.
1.6ab. Evidence
Renal dysfunction in a pregnant woman with type 1
diabetes is associated with an increased risk of adverse
maternal and fetal outcomes, including an increased

risk of preeclampsia (4648). Mild preconceptional
renal dysfunction manifesting only as microalbuminuria may worsen during pregnancy with greater
amounts of proteinuria (47); however, the degree of
worsening is typically both modest and reversible
once pregnancy is completed so long as BP and blood
glucose remain well controlled during the pregnancy
(48). More severe preconceptional renal dysfunction,
as evidenced by a reduced GFR and elevated serum
creatinine, can significantly deteriorate during pregnancy and may not be reversible (42, 5051).
Management of hypertension
1.7a. We recommend that satisfactory BP control
(<130/80 mm Hg) be achieved and maintained before
withdrawing contraception or otherwise trying to
conceive. (1|
)
1.7b. We recommend that a woman with diabetes
who is seeking conception while taking an ACE

inhibitor or angiotensin-receptor blocker in almost all
cases should discontinue the medication before withdrawing contraceptive measures or otherwise trying to
conceive. (1|
)
1.7c. We suggest that in the exceptional case where
the degree of renal dysfunction is severe and there is

uncertainty about when conception will occur, physicians and patients be engaged in shared decisionmaking about whether to continue ACE inhibitors or
angiotensin-receptor blockers. The patients should be
informed about the possible loss of the renal protective properties if the medication is discontinued and
the risk of teratogenesis if it is continued. (Ungraded
recommendation)
1.7d. We recommend that when ACE inhibitors or
angiotensin-receptor blockers have been continued
up to the time of conception that the medication
should be withdrawn immediately upon the confirmation of pregnancy. (1|
)
1.7ad. Evidence
ACE inhibitors (5253) and angiotensin-receptor
blockers (5354) are teratogenic (55). This is most
proven for use of these drugs during the second and

third trimesters (55). Hypertension in a preconceptional woman increases the risk of adverse outcomes
during pregnancy, especially her risk of developing
preeclampsia (56).
1.7ad. Remarks
Safe and effective alternatives to ACE inhibitors and
angiotensin-receptor blockers for treating hypertension during pregnancy include methyldopa, labetalol,
diltiazem, clonidine, and prazosin (57).
Elevated vascular risk
1.8a. We recommend that if a woman with diabetes
has sufficient numbers of vascular risk factors (particularly the duration of the womans diabetes and her
age), screening studies for CAD be undertaken in
advance of withdrawing contraceptive measures or
otherwise trying to conceive. (1|
)
1.8b. We recommend that if a woman with diabetes
is seeking pregnancy and has CAD, its severity should

be ascertained, treatment instituted, and counseling
provided as to the potential risks of pregnancy to the
woman and fetus before the woman withdraws contraception or otherwise tries to conceive. (1|
)
1.8ab. Evidence
Myocardial infarction during pregnancy is associated
with adverse maternal and fetal outcomes including
maternal and fetal demise (5859). More recent
evidence indicates that the prognosis has improved
compared with older studies; however, high maternal
(11%) and fetal (9%) mortality rates continue to be
observed (60).
Management of dyslipidemia
women with diabetes who are attempting to conceive.
(1|
)
1.9b. In view of their unproven safety during
pregnancy, we suggest against the routine use of

fibrates and/or niacin for women with diabetes and
attempting
to
conceive.
1.9c. We suggest that bile acid-binding resins may

be used in women with diabetes to treat hypercholesterolemia; however, this is seldom warranted.
(2|
)
1.9ac. Evidence
Dyslipidemia, if not treated pharmacologically, seldom
poses a threat to the health of a woman with diabetes
during the comparatively short duration of pregnancy
and, typically, the relatively few months leading up to
conception. Also, there is uncertain safety of statins
during pregnancy (6162).
Thyroid function
1.10. For women with type 1 diabetes seeking conception, we recommend measurement of serum TSH and,
if their thyroid peroxidase status is unknown, measurement of thyroid peroxidase antibodies before withdrawing contraceptive measures or otherwise trying to
conceive. (1|
)
1.10. Evidence
Autoimmune thyroid disease is common among
women of childbearing age with type 1 diabetes with
prevalence rates as high as 44% (63). Hypothyroidism
is common among individuals with type 1 diabetes
(64). Untreated or insufficiently treated hypothyroidism reduces fertility and, in the event of pregnancy, increases the risk of miscarriage and impaired
fetal brain development (6569).
Overweight and obesity
1.11. We recommend weight reduction before preg-
nancy for overweight and obese women with diabetes.

(1|
)
1.11. Evidence
Women who are overweight or obese before pregnancy are at an increased risk for complications during
pregnancy (see Evidence 4.2ab).
1.9a. We recommend against the use of statins in
hypertriglyceridemia
(2|
)
17
2.0. Gestational diabetes

Testing for overt diabetes in early pregnancy
2.1. We recommend universal testing for diabetes
(see Table 1) with a fasting plasma glucose, HbA1C,

or an untimed random plasma glucose at the first
prenatal visit (before 13 weeks gestation, or as soon as
possible thereafter) for those women not known to
already have diabetes. (1|
) In the case of
overt diabetes, but not gestational diabetes, a second
test (either a fasting plasma glucose, untimed random
plasma glucose, HbA1C, or OGTT) must be
performed in the absence of symptoms of hyperglycemia and found to be abnormal on another day to
confirm the diagnosis.
2.1. Evidence
18
As discussed in Section 1.0, pregnant women with

overt diabetes and insufficient blood glucose control
in early pregnancy are at increased risk of having a
fetus with congenital anomalies and are at increased
personal risk of worsening of diabetic retinopathy and
nephropathy. Early diagnosis of previously undiscovered overt diabetes in a pregnant woman may allow
for the rapid institution of therapy to mitigate these
risks. A systematic review and meta-analysis (71)
demonstrated that abnormal screening test results
were associated with worse maternal and fetal
outcomes. The quality of supporting evidence for
screening, however, remains low because there are no
randomized trials that compare a screening vs.
no-screening strategy and measure patient-important
outcomes.
2.1. Remarks
We acknowledge that with universal testing for
diabetes in early pregnancy, there will be a high rate of
false-positive results (71) and that women with positive testing may have anxiety and will suffer the
burden of additional testing. Nevertheless, we recommended universal testing because we place the highest
value on preventing fetal complications. The Task
Force assumed that these values and preferences

would be consistent with those of most pregnant
women.
Testing for gestational diabetes at 24 to 28
weeks gestation
2.2. We recommend that pregnant women not previously identified (either during testing performed as per
recommendation 2.1 or at some other time before 24
weeks gestation) with overt diabetes or gestational
diabetes be tested for gestational diabetes (see Table
2) by having a 2-hour, 75-g OGTT performed at 24 to
28 weeks gestation. (1|
) We recommend that
gestational diabetes be diagnosed on this test using
the IADPSG criteria (majority opinion of this
committee [see 2.2. Remarks below]). (1|
)
The 75-g OGTT should be performed after an overnight fast of at least 8 hours (but not more than 14
hours) and without having reduced usual carbohydrate intake for the preceding several days. The test
should be performed with the patient seated, and the
patient should not smoke during the test. One or more
abnormal values establishes the diagnosis, with the
exception that in the case of overt diabetes, but not
gestational diabetes, a second test (either a fasting
plasma glucose, untimed random plasma glucose,
HbA1C, or OGTT), in the absence of symptoms of
hyperglycemia, must be performed and found to be
abnormal on another day to confirm the diagnosis of
overt diabetes.
2.2. Evidence
Pregnant women who develop gestational diabetes are
at risk of adverse pregnancy outcomes, which may be
prevented by adequate treatment (6, 72). The Hyperglycemia and Adverse Pregnancy Outcome study (6)
and other studies (7377) have confirmed continuous
graded relationships between higher maternal glucose
and increasing frequency of birth weight above the
90th percentile, primary cesarean section, neonatal
hypoglycemia, and elevated cord C-peptide level (a
surrogate marker for fetal hyperinsulinemia) as well as
an increased risk for preeclampsia, preterm delivery,
shoulder dystocia/birth injury, hyperbilirubinemia,
and neonatal intensive care admission.
The Task Force commissioned a systematic review

(71) to assess the yield, utility, and benefits of previously employed screening tests for gestational diabetes.
The review identified 39 original studies enrolling
87,830 women. None of the studies directly compared
the maternal and fetal outcomes of women who
received screening vs. women who did not receive
screening. The studies, however, described a statistically significant correlation between a positive
screening test and the development of macrosomia
and gestational hypertension. The yield and diagnostic accuracy of screening tests were, overall,
modest in predicting future development of gestational diabetes and clearly correlated with established
risk factors. The overall quality of this evidence was
considered low. Nevertheless, the Task Force made
several assumptions about patients values and preferences, including that patients will be more interested
in preventing pregnancy complications and would
likely place lower values on the burdens and costs of
screening.
Our recommendation, although in agreement with

the recommendations of the IADPSG and American
Diabetes Association (57, 70), differs materially from
the recommendation of other organizations including
the American College of Obstetricians and Gynecologists (78) and the National Institutes of Health (79).
It is acknowledged that this is an arguable and controversial recommendation; indeed, our committee failed
to establish unanimity on advocating for this recommendation. It is recognized that implementation of
the IADPSG criteria will lead to a substantial increase
in the numbers of pregnant women being diagnosed
with gestational diabetes with the attendant medicalization of pregnancies and with a concomitant
increase in healthcare costs both to individuals and to
society. Nonetheless, for those reasons as outlined
above, most of this committee has concluded that,
pending further evidence, adopting the IADPSG
criteria is warranted.
Management of elevated blood glucose
2.3a. We recommend that women with gestational
2.2. Remarks
The current definition of gestational diabetes (any
degree of glucose intolerance with onset or first definition during pregnancy) includes pregnant patients
who have a marked degree of hyperglycemia consistent with previously undiagnosed overt diabetes. To
exclude from the definition of gestational diabetes
those women with overt diabetes, most of our
committee supports redefining gestational diabetes as
defined in the Hyperglycemia and Adverse Pregnancy
Outcome study; that is, gestational diabetes is the
condition associated with degrees of maternal hyperglycemia less severe than those found in overt diabetes
but associated with an increased risk of adverse pregnancy outcomes (6).
2.3b. We recommend that the initial treatment of
gestational diabetes should consist of medical nutrition therapy (see Section 4.0) and daily moderate
exercise for 30 minutes or more. (1|
)
2.3c. We recommend using blood glucose-lowering
pharmacological therapy if lifestyle therapy is insufficient to maintain normoglycemia in women with

)
2.3ac. Evidence
Plasma glucose acts as a continuous variable in
exerting its effects on the fetus (6, 80). Even mild
hyperglycemia alters the normal metabolic adaptation
to pregnancy (8182), and correction of maternal
hyperglycemia reduces or prevents adverse outcomes
(83).
Lifestyle therapy for gestational diabetes results in a
lower incidence of reduced birth weight, large-forgestational-age births, and preeclampsia (72, 83).
Based on the preceding evidence (Evidence 2.2) and

the analysis thereof, this committee reached a majority
opinion recommending screening using the protocol
and threshold values as established by the consensus
panel of the IADPSG (70). The reader is referred to
the IADPSG recommendations on the diagnosis and
classification of hyperglycemia in pregnancy for
further reading on this subject (70).
diabetes target blood glucose levels as close to normal

as possible. (1|
)
19
Both aerobic exercise (8487) and non-weightbearing exercise (88) have been shown to lower blood
glucose levels in women with gestational diabetes.
Blood glucose-lowering pharmacological therapy is
effective at improving outcomes in women with gestational diabetes whose hyperglycemia does not respond
sufficiently to lifestyle therapy (72, 83, 8991). See
Section 5.0 for a discussion on blood glucose-lowering
pharmacological therapy during pregnancy.
Postpartum care
2.4a. We recommend that postpartum care for
women who have had gestational diabetes should

include measurement of fasting plasma glucose or
fasting self-monitored blood glucose for 24 to 72 hours
after delivery to rule out ongoing hyperglycemia.
(1|
)
2.4ae. Evidence
Women who have had gestational diabetes are at high
risk for the later development of impaired fasting
glucose, impaired glucose tolerance, overt diabetes
(9294), and the metabolic syndrome (92, 95107).
Infants born to mothers with gestational diabetes are
at increased risk of the later development of obesity or
type 2 diabetes (108).
2.4ae. Remarks
Blood glucose-lowering medication is not indicated
for women with gestational diabetes after delivery and
should be discontinued unless overt diabetes is
suspected with accompanying hyperglycemia of a
degree unlikely to respond sufficiently to lifestyle
therapy alone.
2.4b. We recommend that a 2-hour, 75-g OGTT
should be undertaken 6 to 12 weeks after delivery in

women with gestational diabetes to rule out prediabetes or diabetes. (1|
) If results are normal,
we recommend this or other diagnostic tests for
diabetes should be repeated periodically as well as
before future pregnancies. (1|
)
3.0. Glucose monitoring

and glycemic targets
2.4c. We suggest the childs birth weight and whether
3.1. We recommend self-monitoring of blood glucose
or not the child was born to a mother with gestational

diabetes become part of the childs permanent medical
record. (Ungraded recommendation)
20
2.4d. We recommend that all women who have had
gestational diabetes receive counseling on lifestyle

measures to reduce the risk of type 2 diabetes, the
need for future pregnancies to be planned, and the
need for regular diabetes screening, especially before
any future pregnancies. (1|
)
2.4e. We suggest blood glucose-lowering medication
should be discontinued immediately after delivery for

women with gestational diabetes unless overt diabetes
is suspected in which case the decision to continue
such medication should be made on a case-by-case
basis. (2|
)
Self-monitoring of blood glucose

in all pregnant women with gestational or overt
diabetes (1|
) and suggest testing before and
either 1 or 2 hours after the start of each meal
(choosing the postmeal time when it is estimated that
peak postprandial blood glucose is most likely to
occur) and, as indicated, at bedtime and during the
night. (2|
)
Glycemic targets
3.2a. We recommend pregnant women with overt or
gestational diabetes strive to achieve a target preprandial blood glucose 95 mg/dL (5.3 mmol/L) (Table 3).
(1|
) for fasting target, 1|
) for other
meals)
3.2b. We suggest that an even lower fasting blood
glucose target of 90 mg/dL (5.0 mmol/L) be strived

for (2|
) if this can be safely achieved without
undue hypoglycemia.
3.2c. We suggest pregnant women with overt or

gestational diabetes strive to achieve target blood
glucose levels 1 hour after the start of a meal 140 mg/
dL (7.8 mmol/L) and 2 hours after the start of a meal
120 mg/dL (6.7 mmol/L) (2|
) when these
targets can be safely achieved without undue
hypoglycemia.
3.2d. We suggest pregnant women with overt diabetes
strive to achieve an HbA1C 7% (ideally 6.5%).

(2|
)
Continuous glucose monitoring
3.3. We suggest that continuous glucose monitoring
be used during pregnancy in women with overt or

gestational diabetes when self-monitored blood
glucose levels (or, in the case of the woman with overt
diabetes, HbA1C values) are not sufficient to assess
glycemic control (including both hyperglycemia and
hypoglycemia). (2|
)
3.1.3.3. Evidence
Pregnant women with type 1 diabetes are at increased

risk of hypoglycemia including severe hypoglycemia,
especially during the first trimester (2125). There is
also an increased risk of hypoglycemia in pregnant
women with type 2 diabetes (26). Maternal hypoglycemia has not been proven to be deleterious to
the fetus and in particular has not been found to be
associated with an increased risk of congenital anomalies (27).
Although there is a paucity of literature on continuous glucose monitoring use during pregnancy, there
is evidence that in gestational diabetes, it will detect
clinically meaningful hypoglycemia and postprandial
hyperglycemia that may go unrecognized by selfmonitoring of blood glucose (110111). There is also
some evidence of improved HbA1C in women with
overt diabetes using continuous glucose monitoring
during pregnancy (112). The cost-effectiveness of
continuous glucose monitoring is not yet established.
3.1.3.3. Remarks
The recommendation regarding measuring blood
glucose at certain specific times after the start of a
meal allows for consistency in testing across different
cultural and personal eating preferences and also
takes into consideration the first phase of insulin
secretion. Routine testing for the presence of urine (or
blood) ketones is not warranted during pregnancy
except for those pregnant women with overt diabetes
The Task Force commissioned a systematic review

(109) to evaluate the association between different
blood glucose targets achieved during pregnancy and
maternal and fetal outcomes of women with gestational or overt diabetes. The review identified 34
original studies enrolling 9,433 women (15 randomized controlled trials, 18 cohort studies, and 1 casecontrol study). Meta-regression results demonstrated
that a cutoff point of 90 mg/dL (5.0 mmol/L) for
fasting plasma glucose was associated with the most
reduction in the risk of macrosomia (odds ratio =
0.53, 95% confidence interval = 0.310.90, P = .02).
This effect was mainly demonstrated in women with
gestational diabetes during the third trimester. A
cutoff point of <90 mg/dL (5.0 mmol/L) for preprandial value with other meals was associated with a
similar reduction in risk but it did not reach statistical
significance, likely due to the smaller sample size of
that subgroup (odds ratio = 0.69, 95% confidence
interval = 0.172.94, P = .58). Data in women with
type 1 and type 2 diabetes and for postprandial targets
were sparse. The analysis controlled for study intervention, diabetes type, and trimester but was unable
to control for maternal body mass index (BMI). The
analysis was associated with significant heterogeneity.

The overall quality of this evidence was low. The Task
Force considered the putative benefits of tight blood
glucose control and possible risk of hypoglycemia, as
well as patients values and preferences in that they
would likely be most averse to possible pregnancy
complications. Therefore, the Task Force recommended a target preprandial glucose of 95 mg/dL
(5.3 mmol/L) and suggested a lower preprandial
glucose of 90 mg/dL (5.0 mmol/L) when this can be
achieved without undue hypoglycemia. The Task
Force also suggested (rather than recommended) postprandial targets, considering that postprandial targets,
compared with preprandial targets, are supported by
relatively lower quality evidence.
21
(particularly those women with type 1 diabetes) in the

setting of suspected incipient or overt diabetic
ketoacidosis.
There are some data to suggest that increased fetal
abdominal circumference, as detected on ultrasound,
may be used to help determine whether insulin should
be introduced in women with gestational diabetes
(113114). We feel that at present, these data are
insufficient to warrant routine use of this parameter in
determining the optimal timing for, or need for, introducing insulin or other antihyperglycemic medication
in women with gestational diabetes.
nutrition program, adjusted as needed as pregnancy

progresses. It emphasizes healthy food choices, portion
control, and good cooking practices while taking into
account personal and cultural eating preferences,
prepregnancy BMI, desired body weight, physical
activity, and blood glucose levels and targets.
Weight management
4.2a. We suggest that women with overt or gestational diabetes follow the Institute of Medicine
revised guidelines for weight gain during pregnancy
(1) (Table 4). (Ungraded recommendation)
4.2b. We suggest obese women with overt or gesta-
4.0. Nutrition therapy and

weight gain targets

for women with overt
or gestational diabetes
Nutrition therapy
4.1. We recommend medical nutrition therapy for
all pregnant women with overt or gestational diabetes

to help achieve and maintain desired glycemic
control while providing essential nutrient requirements. (1|
)
4.1. Evidence
22
Although nutrition intervention for overt diabetes

and gestational diabetes is a fundamental treatment
modality (115119), there is a paucity of evidencebased data on this topic. Nevertheless, nutrition
therapy has been shown to improve glycemic control
for people living with overt diabetes (120121) and
for women with gestational diabetes (122).
4.1. Remarks
Medical nutrition therapy, defined as a carbohydratecontrolled meal plan that promotes adequate nutrition with appropriate weight gain, normoglycemia
and the absence of ketosis (123), is an individualized
tional diabetes reduce their calorie intake by approximately one-third (compared with their usual intake
before pregnancy) while maintaining a minimum
intake of 1600 to 1800 kcal/d. (2|
)
4.2ab. Evidence
In the absence of definitive evidence regarding optimal
weight gain for women with gestational or overt
diabetesand with evidence both that women who
gain excess weight during pregnancy may retain it after
childbirth (124) and that women who are overweight
or obese before pregnancy are at an increased risk for
complications during pregnancy (including hypertensive complications, stillbirth, and increased risk for
cesarean section) (125128)and with the reassurance that limiting maternal weight gain is not associated with a decrease in fetal birth weight (129), we
conclude that following the Institute of Medicine
recommendations for weight gain during pregnancy,
although not written specifically for women with overt
or gestational diabetes, is nonetheless appropriate for
women with these conditions (Table 4) (130).
Moderate energy restriction (16001800 kcal/d) in
pregnant women with overt diabetes improves mean
glycemia and fasting insulinemia without inhibiting
fetal growth or birth weight or inducing ketosis (129).
Energy intake of approximately 2050 kcal in all BMI
categories in women with gestational diabetes has
been reported to limit maternal weight gain, maintain
euglycemia, avoid ketonuria, and maintain an average
birth weight of 3542 g (131).
4.2ab. Remarks
Nutritional supplements
Successful pregnancy outcomes have been reported

within a wide range of calorie intakes ranging from
1500 to 2800 kcal/d (129, 131135); however, most
studies have been small and uncontrolled and relied
on self-reported dietary intake. Severe calorie restriction (<1500 kcal/d, or 50% reduction from prepregnancy), however, is to be avoided because there is
evidence, at least in pregnant women with type 1
diabetes, that this degree of calorie restriction
increases ketosis, which has been linked to impaired
fetal brain development (134). Moderate calorie
restriction (16001800 kcal/d, 33% reduction) does
not lead to significant ketosis (136137) and is appropriate for overweight or obese women with overt or
gestational diabetes. Calorie restriction is not
warranted for underweight or normal-weight women
with these conditions so long as fetal growth and
weight gain targets are being met.
4.4. We recommend pregnant women with overt or
Carbohydrate intake
4.3. We suggest women with overt or gestational
diabetes limit carbohydrate intake to 35% to 45% of

total calories, distributed in 3 small- to moderate-sized
meals and 2 to 4 snacks including an evening snack.
(2|
)
4.3. Evidence
4.4. Evidence
There is no indication that pregnant women with
overt or gestational diabetes should not follow the
same guidelines for nutrient intakes that are indicated
for all pregnant women, with the exception of folic
acid supplementation for which there is theoretical
benefit to be achieved by taking higher than usual
doses (see Evidence 1.4).
5.0. Blood glucose lowering pharmaco logical therapy during

pregnancy
Insulin therapy
5.1a. We suggest that the long-acting insulin analog
detemir may be initiated during pregnancy for those
women who require basal insulin and for whom NPH
insulin, in appropriate doses, has previously resulted
in, or for whom it is thought NPH insulin may result
in, problematic hypoglycemia; insulin detemir may be
continued in those women with diabetes already
successfully taking insulin detemir before pregnancy.
(2|
)
5.1b. We suggest that those pregnant women successfully using insulin glargine before pregnancy may
continue it during pregnancy. (2|
)
There is no definitive evidence for the optimal proportion of carbohydrate in the diet of women with overt
or gestational diabetes; values from 40% to 45% of
energy intake (138) to 60% (if the carbohydrate is
from complex sources) (139) have been recommended. Some authorities suggest that a minimum of
175 g/d carbohydrate should be provided, which is
higher than the 130 g/d recommended for nonpregnant women (1). Nonetheless, restricting the total
amount of carbohydrate ingested may assist with
glycemic control as may distributing carbohydrates
over several meals and snacks, manipulating the types
of carbohydrate consumed, and choosing lowglycemic-index foods (140141). No interventional
studies, however, have been conducted using the
glycemic index in pregnant women with diabetes.
gestational diabetes should follow the same guidelines

for the intake of minerals and vitamins as for women
without diabetes (1|
), with the exception of
taking folic acid 5 mg daily beginning 3 months before
trying to conceive (see Recommendation 1.4). We
suggest that at 12 weeks gestation, the dose of folic
acid be reduced to 0.4 to 1.0 mg/d, which should
be continued until the completion of breastfeeding
(2|
).
23
5.1c. We suggest that the rapid-acting insulin analogs
lispro and aspart be used in preference to regular

(soluble) insulin in pregnant women with diabetes.
(2|
)
5.1d. We recommend the ongoing use of continuous
sc insulin infusion during pregnancy in women with

diabetes when this has been initiated before pregnancy (1|
) but suggest that continuous sc
insulin infusion not be initiated during pregnancy
unless other insulin strategies including multiple daily
doses of insulin have first been tried and proven
unsuccessful. (2|
)
5.1ab. Evidence
In nonpregnant women, insulin detemir is associated
with less hypoglycemia than NPH insulin (142144).
Insulin detemir has not shown adverse maternal or
neonatal effects (34, 145). Glargine use during pregnancy was not associated with unexpected adverse
maternal or fetal outcomes in a large cohort study;
however, the lack of a control group and the restrospective nature of this study limit the interpretation of
the findings (33). Several retrospective cohort and
case-control studies of pregnant women found that
overall, the outcome with insulin glargine treatment
was no different from, or was superior to, NPH insulin
(35, 146150).
5.1ab. Remarks
24
Of the two available long-acting insulin analogs,

detemir has a theoretical advantage over glargine
during pregnancy because glargines much higher
affinity for the IGF-1 receptor (151) raises concerns
about increased mitogenic activity (151153). Nonetheless, glargine is unlikely to cross the placenta (36),
animal studies have not shown glargine to be embryotoxic (154), and women treated with insulin glargine
during the first trimester have a similar rate of congenital malformations as women treated with insulin
NPH (33, 155156). Insulin detemir is now approved
(Category B) by the FDA for use during pregnancy,
whereas insulin glargine does not currently have such
approval.
Before instituting insulin glargine or detemir in a

pregnant woman, the clinician should fully and
frankly discuss their advantages and possible disadvantages compared with NPH therapy and, in the
case of insulin glargine, its lack of FDA approval for
use in pregnancy.
5.1c. Evidence
Compared with human regular (soluble) insulin,
rapid-acting insulin used during pregnancy allows
greater lifestyle flexibility, greater patient satisfaction,
and improved quality of life (157) and may also
provide better postprandial blood glucose control
(158) and HbA1C reduction (159). Rapid-acting
insulin is, however, more expensive than regular
insulin. In most other respects, rapid-acting insulin
and regular insulin are comparable during pregnancy
(30, 159163). Moreover, both are associated with
similar rates of prematurity, cesarean delivery, worsening of retinopathy, hypertensive complications,
rates of shoulder dystocia, admission to a neonatal
intensive care unit, and neonatal hypoglycemia.
Rapid-acting insulin does not increase the risk of teratogenicity (30, 158159, 164166).
5.1c. Remarks
We suggest glulisine not be used during pregnancy
because it is not FDA-approved for use in pregnancy
and does not offer a proven advantage over lispro or
aspart.
5.1d. Evidence
Compared with multiple daily doses of insulin,
continuous sc insulin infusion used during pregnancy
in women with overt diabetes provides comparable or
better (167168) glycemic control and pregnancy
outcomes (169170) with no greater risk or possibly
lower risk (171) of maternal hypoglycemia (172).
Additionally, compared with multiple daily doses of
insulin, continuous sc insulin infusion provides greater
lifestyle flexibility, easier blood glucose management
in women experiencing morning nausea, less blood
glucose variability, and facilitates managing glucose
control in the peridelivery setting (171). An increased
risk of maternal ketoacidosis and neonatal hypoglycemia has, however, been reported (173).
5.1d. Remarks
Owing to the potential risk of temporarily worsened
blood glucose control, ketoacidosis, and hypoglycemia
when continuous sc insulin infusion is initiated, its
use during pregnancy should be limited to those
patients already successfully using this method of
insulin administration before pregnancy and to those
women who, during pregnancy, have not succeeded
with other insulin strategies including multiple daily
doses of insulin.
Noninsulin antihyperglycemic agent therapy
5.2a. We suggest that glyburide (glibenclamide) is a
suitable alternative to insulin therapy for glycemic

control in women with gestational diabetes who fail
to achieve sufficient glycemic control after a 1-week
trial of medical nutrition therapy and exercise except
for those women with a diagnosis of gestational
diabetes before 25 weeks gestation and for those
women with fasting plasma glucose levels >110 mg/dL
(6.1 mmol/L), in which case insulin therapy is
preferred. (2|
)
5.2b. We suggest that metformin therapy be used for
glycemic control only for those women with gestational diabetes who do not have satisfactory glycemic
control despite medical nutrition therapy and who
refuse or cannot use insulin or glyburide and are not in
the first trimester. (2|
)
5.2a. Evidence
5.2a. Remarks
Glyburide appears to be a safe and effective alternative to insulin in most women with gestational
diabetes. Compared with insulin, glyburide may be
more convenient, is less expensive (185), does not
require intensive educational instruction at initiation
of therapy, and is preferred by most patients (180,
184). Before instituting glyburide to treat gestational
diabetes, the clinician should have a full and frank
discussion with the pregnant woman regarding
glyburides possible advantages and disadvantages
compared with insulin therapy and its lack of FDA
approval for this indication. Unlike the case with
glyburide use during pregnancy complicated by gestational diabetes, there are no randomized clinical trials
regarding the use of noninsulin antihyperglycemic
medications in pregnant women with type 2 diabetes.
Most women with type 2 diabetes requiring blood
glucose-lowering medications are treated with insulin
in anticipation of, and then during, pregnancy.
In pregnant women taking glyburide, the umbilical

cord glyburide concentration is undetectable (91,
174177) or, at most, very low (178). Glyburide is
effective in controlling blood glucose in women
with gestational diabetes and has been associated
with favorable neonatal outcomes including the rate
of large-for-gestational-age infants, macrosomia,
neonatal intensive care unit admission, and neonatal
hypoglycemia (91). Although some evidence does
exist of higher rates of macrosomia and large-forgestational-age infants (177) in pregnant women
taking glyburide compared with women taking

insulin, neonates had similar body composition,
measures of glycemic control, and cord metabolic
biomarkers. The safety of glyburide in pregnancy is
also supported by a meta-analysis (179) of 6 randomized trials with overall good methodological quality,
which found no significant differences in glycemic
control, neonatal hypoglycemia, birth weight, or rate
of large-for-gestational-age infants born to mothers
taking oral agents (metformin or glyburide) vs.
mothers taking insulin. Glyburide, however, has been
found to be less likely to maintain satisfactory blood
glucose control in women with gestational diabetes
who have a fasting blood glucose >110 mg/dL (6.1
mmol/L) on a 100-g OGTT (180) or 50-g glucose
challenge (181, 182), have had their gestational
diabetes detected before 25 weeks gestation (183),
have glyburide initiated after 30 weeks, have fasting
plasma glucose 110 mg/dL (6.1 mmol/L) or 1-hour
postprandial glucose 140 mg/dL (7.8 mmol/L) (184),
or have pregnancy weight gain >12 kg (182).
25
5.2b. Evidence
Pregnancy outcomes in women exposed to metformin
at the time of conception and during early pregnancy
have been favorable (186193). Compared with
women with gestational diabetes taking insulin, those
taking metformin have no difference in maternal
glycemic control, significantly lower rates of neonatal
hypoglycemia, and no increased risk of congenital
anomalies or other serious maternal or neonatal
adverse events. Although not shown to be deleterious
to the fetus, metformin does cross freely through the
placenta, with similar metformin concentrations in
the fetal and maternal circulation (194195), and
long-term follow-up studies establishing safety are not
yet available. Also, nearly half of women with gestational diabetes treated with metformin monotherapy
have glycemic control failure rates requiring conversion to insulin therapy. Additionally, metformintreated women with gestational diabetes have
increased rates of preterm birth (90).
5.2b. Remarks
Compared with insulin therapy, metformin is typically

more convenient and less expensive and is not associated with the risk of hypoglycemia. Nonetheless,
certain concerns, as described, still preclude its routine
use in the treatment of gestational diabetes.
26
Because data on the safety and efficacy of the use of

other noninsulin antihyperglycemic medications
(apart from those discussed above) during pregnancy,
including the use of incretin-based therapies during
pregnancy, are not yet available, we do not recommend their use in this setting.
6.0. Labor, delivery,

lactation, and
postpartum care
Blood glucose targets during labor and delivery
6.1. We suggest target blood glucose levels of 72 to
126 mg/dL (4.07.0 mmol/L) during labor and delivery
for pregnant women with overt or gestational diabetes.
(2|
)
6.1. Evidence
Elevated maternal blood glucose during labor and
delivery increases the risk of neonatal hypoglycemia
and fetal distress (196201) as well as birth asphyxia
and abnormal fetal heart rate (201202), albeit with
these associations having been mainly demonstrated
in observational studies of women with type 1
diabetes.
6.1. Remarks
Because we did not determine there to be a single best
way of maintaining target blood glucose levels during
labor and delivery, we have not provided a recommendation regarding how this is to be achieved,
instead leaving it to the discretion of the individual
practitioner to implement their preferred management strategy.
Lactation
6.2a. We recommend whenever possible women with
overt or gestational diabetes should breastfeed their

infant. (1|
)
6.2b. We recommend that breastfeeding women with
overt diabetes successfully using metformin or
glyburide therapy during pregnancy should continue
to use these medications, when necessary, during
breastfeeding. (1|
)
6.2ab. Evidence
The increased risk of infants born to women with
diabetes for childhood obesity and the later development of impaired glucose intolerance and diabetes
(82) is reduced by breastfeeding (203212). Breastfeeding may also facilitate postpartum weight loss and
reduce maternal and neonatal risk for the later development of type 2 diabetes (213214).
The concentrations of metformin in breast milk are
generally low, and the mean infant exposure to
metformin has been reported in the range 0.28% to
1.08% of the weight-normalized maternal dose, well
below the level of concern for breastfeeding (215).
Metformin use by the breastfeeding woman vs. formula
feeding appears to have no adverse effects on infant
growth, motor-social development, and intercurrent
illness during the first 6 months of life (216). Glyburide
was not detected in breast milk, and hypoglycemia
was not observed in nursing infants of women using
glyburide (217). The exposure of infants to secondgeneration sulfonylureas (such as glipizide and
glyburide) through breast milk is expected to be
minimal, based on the limited data available. The
benefits of breastfeeding greatly outweigh the risks of
these medications, if any (218).
device (copper or levonorgestrel-releasing) are not at

increased risk of untoward effects (228232).
Progestin-only oral contraceptives do not affect
blood glucose values or BP in women with type 1
diabetes (233234); however, there is some limited
evidence that these medications increase the risk for
later developing type 2 diabetes in women who have
had gestational diabetes (224, 235).
Screening for postpartum thyroiditis
6.4. We suggest women with type 1 diabetes be
screened for postpartum thyroiditis with a TSH at 3
and 6 months postpartum. (2|
)
6.4. Evidence
Postpartum thyroiditis is common in women who
have type 1 diabetes (63, 236).
Postpartum contraception
6.3. We recommend that the choice of a contracep-
tive method for a woman with overt diabetes or a

history of gestational diabetes should not be influenced by virtue of having overt diabetes or a history of
)
6.3. Evidence
Combined oral contraceptive use by women with type

1 diabetes does not affect their glycemic control or
increase their risk of end-organ injury (219221).
Combined oral contraceptive use by women with a
history of gestational diabetes does not increase the
risk of later developing type 2 diabetes (222225).
Use of a contraceptive patch (226) or vaginal ring
(227) exerts a similar metabolic effect to that of oral
contraceptives. Compared with women without
diabetes, women with diabetes using an intrauterine
27
References
1.
Institute of Medicine Dietary Reference Intakes: Energy,

Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein,
and Amino Acids. Washington, DC: National Academies
Press; 2002.
2.
Atkins D, Best D, Briss PA, et al Grading quality of

evidence and strength of recommendations. BMJ. 2004;
328:1490.
3.
4.
5.
28
Swiglo BA, Murad MH, Schnemann HJ, et al. A case for

clarity, consistency, and helpfulness: state-of-the-art clinical
practice guidelines in endocrinology using the grading of
recommendations, assessment, development, and evaluation
system. J Clin Endocrinol Metab. 2008;93:666673.
Guyatt G, Oxman ED, Akl EA, et al. GRADE guidelines:
1. Introduction-GRADE evidence profiles and summary of
findings tables. J Clin Epidemiol. 2011;64:383394.
Classification and diagnosis of diabetes mellitus and other
categories of glucose intolerance. National Diabetes Data
Group. Diabetes. 1979;28:10391057.
6.
HAPO Study Cooperative Research Group. Hyperglycemia

and adverse pregnancy outcomes. N Engl J Med. 2008;
358:19912002.
7.
De Groot L, Abalovich M, Alexander EK, et al.

Management of thyroid dysfunction during pregnancy and
postpartum: An Endocrine Society clinical practice guideline.
J Clin Endocrinol Metab. 2012;97:25432565.
8.
Anwar A, Salih A, Masson E, Allen B, Wilkinson L,

Lindow SW. The effect of pre-pregnancy counselling for
women with pre-gestational diabetes on maternal health
status. Eur J Obstet Gynecol Reprod Biol. 2011;155:137139.
9.
Murphy HR, Roland JM, Skinner TC, et al. Effectiveness

of a regional prepregnancy care program in women with type
1 and type 2 diabetes: Benefits beyond glycemic control.
Diabetes Care. 2010;33:25142520.
10. Ray JG, OBrien TE, Chan WS. Preconception care

and the risk of congenital anomalies in the offspring of
women with diabetes mellitus: a meta-analysis. QJM.
2001;94:435444.
11. Dicker D, Feldberg D, Samuel N, Yeshaya A, Karp M,
Goldman JA. Spontaneous abortions in patients with
insulin-dependent diabetes mellitus: the effect of
preconceptional diabetic control. Am J Obstet Gynecol.
1988;158:11611164.
12. Rosenn B, Miodovnik M, Combs CA, Khoury J, Siddiqi
TA. Pre-conception management of insulin-dependent
diabetes: improvement of pregnancy outcome. Obstet
Gynecol. 1991;77:846849.
13. Holing EV. Preconception care of women with diabetes:
the unrevealed obstacles. J Matern Fetal Med. 2000;9:1013.
14. Inkster ME, Fahey TP, Donnan PT, Leese GP, Mires GJ,
Murphy DJ. Poor glycated haemoglobin control and adverse
pregnancy outcomes in type 1 and type 2 diabetes: systematic
review of observational studies. BMC Pregnancy Childbirth.
2006;6:30.
15. Nielsen GL, Mller M, Srensen HT. HbA1c in early
diabetic pregnancy and pregnancy outcomes: a Danish
population-based cohort study of 573 pregnancies in women
with type 1 diabetes. Diabetes Care. 2006;29:26122616.
16. Guerin A, Nisenbaum R, Ray JG. Use of maternal
GHb concentration to estimate the risk of congenital
anomalies in the offspring of women with prepregnancy
diabetes. Diabetes Care. 2007;30:19201925.
17. Suhonen L, Hiilesmaa V, Teramo K. Glycaemic control
during early pregnancy and fetal malformations in women
with type I diabetes. Diabetologia. 2000;43:7982.
18. Bell R, Glinianaia SV, Tennant PW, Bilous RW, Rankin J.
Peri-conception hyperglycaemia and nephropathy are
associated with risk of congenital anomaly in women with
pre-existing diabetes: a population-based cohort study.
[published online ahead of print April 1, 2012]. Diabetologia.
doi:10.1007/s00125-012-2455-y.
19. Langer O, Conway DL. Level of glycemia and perinatal
outcome in pregestational diabetes. J Matern Fetal Med.
2000;9:3541.
20. Jensen DM, Korsholm L, Ovesen P, et al. Peri-conceptional
A1C and risk of serious adverse pregnancy outcome in 933
women with type 1 diabetes. Diabetes Care. 2009;32:
10461048.
21. Persson B, Hansson U. Hypoglycaemia in pregnancy.
Baillieres Clin Endocrinol Metab. 1993;7:731739.
22. Rosenn BM, Miodovnik M, Holcberg G, Khoury JC,
Siddiqi TA. Hypoglycemia: the price of intensive insulin
therapy for pregnant women with insulin-dependent diabetes
mellitus. Obstet Gynecol. 1995;85:417422.
23. Evers IM, ter Braak EW, de Valk HW, van Der Schoot B,
Janssen N, Visser GH. Risk indicators predictive for severe
hypoglycemia during the first trimester of Type 1 diabetic
pregnancy. Diabetes Care. 2002;25:554559.
24. Nielsen LR, Pedersen-Bjergaard U, Thorsteinsson B,
Johansen M, Damm P, Mathiesen ER. Hypoglycemia in
pregnant women with type 1 diabetes: predictors and role of
metabolic control. Diabetes Care. 2008;31:914.
25. Robertson H, Pearson DW, Gold AE. Severe hypoglycaemia
during pregnancy in women with type 1 diabetes is common
and planning pregnancy does not decrease the risk. Diabet
Med. 2009;26:824826.
26. Confidential Enquiry into Maternal and Child Health
(CEMACH). Diabetes in Pregnancy: Are We Providing the
Best Care? Findings of a National Enquiry: England, Wales
and Northern Ireland. London, UK: CEMACH; 2007.
27. Pregnancy outcomes in the Diabetes Control and

Complications Trial. Am J Obstet Gynecol. 1996;174:
13431353.
28. Hod M, Damm P, Kaaja R, Visser GH, Dunne F, Demidova
I, Hansen AS, Mersebach H; Insulin Aspart Pregnancy
Study Group. Fetal and perinatal outcomes in type 1 diabetes
pregnancy: a randomized study comparing insulin aspart with
human insulin. Obstet Gynecol. 2008;198:186.e1e7.
29. Mathiesen ER, Kinsley B, Amiel SA, et al; Insulin Aspart
Pregnancy Study Group. Maternal glycemic control and
hypoglycemia in type 1 diabetic pregnancy: a randomized
trial of insulin aspart versus human insulin in 322 pregnant
women. Diabetes Care. 2007;30:771776.
30. Lapolla A, Dalfr MG, Spezia R, et al. Outcome of
pregnancy in type 1 diabetic patients treated with insulin
lispro or regular insulin: an Italian experience. Acta Diabetol.
2008;45:6166.
31. Ratner RE, Hirsch IB, Neifing JL, Garg SK, Mecca TE,
Wilson CA. Less hypoglycemia with insulin glargine in
intensive insulin therapy for type 1 diabetes. U.S. Study
Group of Insulin Glargine in Type 1 Diabetes. Diabetes Care.
2000;23:639643.
32. Vague P, Selam JL, Skeie S, et al. Insulin detemir is
associated with more predictable glycemic control and
reduced risk of hypoglycemia than NPH insulin in patients
with type 1 diabetes on a basal-bolus regimen with premeal
insulin aspart. Diabetes Care. 2003;26:590596.
33. Gallen IW, Jaap A, Roland JM, Chirayath HH. Survey
of glargine use in 115 pregnant women with type 1 diabetes.
Diabet Med. 2008;25:165169.
34. Lapolla A, Di Cianni G, Bruttomesso D, et al. Use of
insulin detemir in pregnancy: a report on 10 type 1 diabetic
women. Diabet Med. 2009;26:11811182.
35. Pyhnen-Alho M, Rnnemaa T, Saltevo J, Ekblad U,
Kaaja RJ. Use of insulin glargine during pregnancy. Acta
Obstet Gynecol Scand. 2007;86:11711174.
36. Pollex EK, Feig DS, Lubetsky A, Yip PM, Koren G. Insulin
glargine safety in pregnancy: a transplacental transfer
study. Diabetes Care. 2010;33:2933.
37. Mathiesen ER, Hod M, Ivanisevic M, et al; Detemir in
Pregnancy Study Group. Maternal efficacy and safety
outcomes in a randomized, controlled trial comparing insulin
detemir with NPH insulin in 310 pregnant women with
type 1 diabetes. Diabetes Care. 2012;35:20122017.
40. Chew EY, Mills JL, Metzger BE, et al. Metabolic control
and progression of retinopathy. The Diabetes in Early
Pregnancy Study. National Institute of Child Health and
Human Development Diabetes in Early Pregnancy Study.
Diabetes Care. 1995;18:631637.
41. Vestgaard M, Ringholm L, Laugesen CS, Rasmussen KL,
Damm P, Mathiesen ER. Pregnancy-induced sightthreatening diabetic retinopathy in women with type 1
diabetes. Diabet Med. 2010;27:431435.
42. Omori Y, Jovanovic L. Proposal for the reconsideration of
the definition of gestational diabetes. Diabetes Care.
2005;28:25922593.
43. Cundy T, Slee F, Gamble G, Neale L. Hypertensive
disorders of pregnancy in women with type 1 and type 2
44. Rosenn B, Miodovnik M, Kranias G, et al. Progression of
diabetic retinopathy in pregnancy: association with
hypertension in pregnancy. Am J Obstet Gynecol.
1992;166:12141218.
45. Lvestam-Adrian M, Agardh CD, Aberg A, Agardh E.
Pre-eclampsia is a potent risk factor for deterioration of
retinopathy during pregnancy in type 1 diabetic patients.
Diabet Med. 1997;14:10591065.
46. Sibai BM, Caritis S, Hauth J, et al. Risks of preeclampsia
and adverse neonatal outcomes among women with
pregestational diabetes mellitus. National Institute of Child
Health and Human Development Network of Maternal-Fetal
Medicine Units. Am J Obstet Gynecol. 2000;182:364369.
47. Ekbom P, Damm P, Feldt-Rasmussen B, Feldt-Rasmussen
U, Mlvig J, Mathiesen ER. Pregnancy outcome in type 1
diabetic women with microalbuminuria. Diabetes Care.
2001;24:17391744.
48. Dunne FP, Chowdhury TA, Hartland A, et al. Pregnancy
outcome in women with insulin-dependent diabetes mellitus
complicated by nephropathy. QJM. 1999;92:451-454.
49. Leguizamon G, Reece EA. Effect of medical therapy on
progressive nephropathy: influence of pregnancy, diabetes
and hypertension. J Matern Fetal Med. 2000;9:7078.
50. Biesenbach G, Grafinger P, Stger H, Zazgornik J. How
pregnancy influences renal function in nephropathic type 1
diabetic women depends on their pre-conceptional creatinine
clearance. J Nephrol. 1999;12:4146.
51. Gordon M, Landon MB, Samuels P, Hissrich S, Gabbe SG.
Perinatal outcome and long-term follow-up associated with
modern management of diabetic nephropathy. Obstet
Gynecol. 1996;87:401409.
52. Cooper WO, Hernandez-Diaz S, Arbogast PG, et al. Major
congenital malformations after first-trimester exposure to
ACE inhibitors. N Engl J Med. 2006;354:24432451.
38. Wilson RD, Johnson JA, Wyatt P, et al; Genetics

Committee of the Society of Obstetricians and
Gynaecologists of Canada and The Motherrisk Program.
Pre-conceptional vitamin/folic acid supplementation 2007:
the use of folic acid in combination with a multivitamin
supplement for the prevention of neural tube defects and
other congenital anomalies. J Obstet Gynaecol Can.
2007;29:10031026.
39. Diabetes Control and Complications Trial Research

Group. Effect of pregnancy on microvascular complications
in the Diabetes Control and Complications Trial. The
Diabetes Control and Complications Trial Research Group.
Diabetes Care. 2000;23:10841091.
29
53. Quan A. Fetopathy associated with exposure to angiotensin

converting enzyme inhibitors and angiotensin receptor
antagonists. Early Hum Dev. 2006;82:2328.
68. Leung AS, Millar LK, Koonings PP, Montoro M, Mestman

JH. Perinatal outcome in hypothyroid pregnancies. Obstet
Gynecol. 1993;81:349353.
54. Velzquez-Armenta EY. Angiotensin II receptor blockers in

pregnancy: a case report and systematic review of the
literature. Hypertens Pregnancy. 2007;26:5166.
69. Man EB, Brown JF, Serunian SA. Maternal

hypothyroxinemia: psychoneurological deficits of progeny.
Ann Clin Lab Sci. 1991;21:227239.
55. Bullo M, Tschumi S, Bucher B. Pregnancy outcome

following exposure to angiotensin-converting enzyme
inhibitors or angiotensin receptor antagonists: a systematic
review. Hypertension. 2012;60:444450.
70. International Association of Diabetes and Pregnancy

Study Groups Consensus Panel; Metzger BE, Gabbe SG,
Persson B, et al. International Association of Diabetes and
Pregnancy Study Groups recommendations on the diagnosis
and classification of hyperglycemia in pregnancy. Diabetes
Care. 2010;33:676682.
56. Magee LA, von Dadelszen P, Bohun CM, et al. Serious

perinatal complications of non-proteinuric hypertension:
an international, multicentre, retrospective cohort study.
J Obstet Gynaecol Can. 2003;25:372382.
57. American Diabetes Association. Standards of medical care
in diabetes2013. Diabetes Care. 2013;36(Suppl 1):S11
S66.
58. Silfen SL, Wapner RJ, Gabbe SG. Maternal outcome in
class H diabetes mellitus. Obstet Gynecol. 1980;55:749751.
59. Bagg W, Henley PG, Macpherson P, Cundy TF. Pregnancy
in women with diabetes and ischaemic heart disease. Aust N
Z J Obstet Gynaecol. 1999;39:99102.
60. Roth A, Elkayam U. Acute myocardial infarction associated
with pregnancy. J Am Coll Cardiol. 2008;52:171180.
61. Edison RJ, Muenke M. Mechanistic and epidemiologic
considerations in the evaluation of adverse birth outcomes
following gestational exposure to statins. Am J Med Genet A.
2004;131:287298.
62. Kazmin A, Garcia-Bournissen F, Koren G. Risks of statin
use during pregnancy: a systematic review. J Obstet Gynaecol
Can. 2007;29:906908.
63. Alvarez-Marfany M, Roman SH, Drexler AJ, Robertson

C, Stagnaro-Green A. Long term prospective study of
postpartum thyroid dysfunction in women with insulin
dependent diabetes mellitus. J Clin Endocrinol Metab.
1994;79:1016.
30
64. Umpierrez GE, Latif KA, Murphy MB, et al. Thyroid

dysfunction in patients with type 1 diabetes: a longitudinal
study. Diabetes Care. 2003;26:11811185.
65. Casey BM, Dashe JS, Wells CE, et al. Subclinical
hypothyroidism and pregnancy outcomes. Obstet Gynecol.
2005;105:239245.
66. Glinoer D, Soto MF, Bourdoux P, et al. Pregnancy in
patients with mild thyroid abnormalities: maternal and
neonatal repercussions. J Clin Endocrinol Metab.
1991;73:421427.
67. Haddow JE, Palomaki GE, Allan WC, et al. Maternal
thyroid deficiency during pregnancy and subsequent
neuropsychological development of the child. N Engl J Med.
1999;341:549555.
71. Prutsky G, Domecq, Elriayah T, et al. Screening of

gestational diabetes: a systematic review and meta-analysis.
J Clin Endocrinol Metab. 2013 Nov;98(11):43118.
72. Landon MB, Spong CY, Thom E, et al; Eunice Kennedy
Shriver National Institute of Child Health and Human
Development Maternal-Fetal Medicine Units Network. A
multicenter, randomized trial of treatment for mild gestational
diabetes. N Engl J Med. 2009;361:13391348.
73. Pettitt DJ, Knowler WC, Baird HR, Bennett PH.
Gestational diabetes: Infant and maternal complications of
pregnancy in relation to third-trimester glucose tolerance in
the Pima Indians. Diabetes Care. 1980;3:458464.
74. Jensen DM, Korsholm L, Ovesen P, Beck-Nielsen H,
Mlsted-Pedersen L, Damm P. Adverse pregnancy outcome
in women with mild glucose intolerance: is there a clinically
meaningful threshold value for glucose? Acta Obstet Gynecol
Scand. 2008;87:5962.
75. Sermer M, Naylor CD, Gare DJ, et al. Impact of increasing
carbohydrate intolerance on maternal-fetal outcomes in
3,637 women without gestational diabetes. The Toronto
Tri-Hospital Gestational Diabetes Project. Am J Obstet
Gynecol. 1995;173:146156.
76. Sacks DA, Greenspoon JS, Abu-Fadil S, Henry HM,
Wolde-Tsadik G, Yao JF. Toward universal criteria for
gestational diabetes: the 75-gram glucose tolerance test in
pregnancy. Am J Obstet Gynecol. 1995;172:607614.
77. Ferrara A, Weiss NS, Hedderson MM. Pregnancy plasma
glucose levels exceeding the American Diabetes Association
thresholds, but below the National Diabetes Data Group
thresholds for gestational diabetes mellitus, are related to
the risk of neonatal macrosomia, hypoglycaemia and
hyperbilirubinaemia. Diabetologia. 2007;50:298306.
78. Committee opinion no. 504: screening and diagnosis of
gestational diabetes mellitus. Obstet Gynecol. 2011;118:
751753.
79. National Institutes of Health Consensus Development
Conference Statement: National Institutes of Health Consensus
Development Conference Diagnosing Gestational Diabetes
Mellitus March 46 2013. Bethesda, MD: National Institutes
of Health; 2013.
80. HAPO Study Cooperative Research Group. Hyperglycemia

and Adverse Pregnancy Outcome (HAPO) Study:
associations with neonatal anthropometrics. Diabetes. 2009;
58:453459.
94. Lauenborg J, Hansen T, Jensen DM, et al. Increasing

incidence of diabetes after gestational diabetes: a long-term
follow-up in a Danish population. Diabetes Care.
2004;27:11941199.
81. Metzger BE, Rabinkar V, Vileisis RA, Freinkel N.

Accelerated starvation and the skipped breakfast in late
normal pregnancy. Lancet. 1982;i:588592.
95. Kousta E, Efstathiadou Z, Lawrence NJ, et al. The impact

of ethnicity on glucose regulation and the metabolic
syndrome following gestational diabetes. Diabetologia.
2006;49:3640.
82. Silverman BL, Rizzo TA, Cho NH, Metzger BE. Longterm effects of the intrauterine environment: the
Northwestern University Diabetes in Pregnancy Center.
Diabetes Care. 1998;21(Suppl 2):B142B149.
83. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries
WS, Robinson JS. Effect of treatment of gestational diabetes
mellitus on pregnancy outcomes. N Engl J Med.
2005;352:24772486.
84. Short KR, Pratt LV, Teague AM, Man CD, Cobelli C.
Postprandial improvement in insulin sensitivity after a single
exercise session in adolescents with low aerobic fitness and
physical activity. Pediatr Diabetes. 2013;14:129137.
85. Short KR, Pratt LV, Teague AM. The acute and residual
effect of a single exercise session on meal glucose tolerance in
sedentary young adults. J Nutr Metab. 2012;2012:278678.
86. Young JC, Treadway JL. The effect of prior exercise on oral
glucose tolerance in late gestational women. Eur J Appl
Physiol Occup Physiol. 1992;64:430433.
87. Avery MD, Walker AJ. Acute effect of exercise on blood
glucose and insulin levels in women with gestational diabetes.
J Matern Fetal Med. 2001;10:5258.
88. Jovanovic-Peterson L, Durak EP, Peterson CM.
Randomized trial of diet versus diet plus cardiovascular
conditioning on glucose levels in gestational diabetes. Am J
Obstet Gynecol. 1989;161:415419.
89. OSullivan JB, Gellis SS, Dandrow RV, Tenney BO. The
potential diabetic and her treatment in pregnancy. Obstet
Gynecol. 1966;27:683689.
90. Rowan JA, Hague WM, Gao W, Battin MR, Moore MP;
MiG Trial Investigators. Metformin versus insulin for the
treatment of gestational diabetes. N Engl J Med.
2008;358:20032015.
91. Langer O, Conway DL, Berkus MD, Xenakis EM,
Gonzales O. A comparison of glyburide and insulin in
women with gestational diabetes mellitus. N Engl J Med.
2000;343:11341138.
93. Pallardo F, Herranz L, Garcia-Ingelmo T, et al. Early

postpartum metabolic assessment in women with prior
gestational diabetes. Diabetes Care. 1999;22:10531058.
97. Lauenborg J, Mathiesen E, Hansen T, et al. The prevalence

of the metabolic syndrome in a Danish population of women
with previous gestational diabetes mellitus is three-fold
higher than in the general population. J Clin Endocrinol
Metab. 2005;90:40044010.
98. Schaefer-Graf UM, Buchanan TA, Xiang AH, Peters RK,
Kjos SL. Clinical predictors for a high risk for the
development of diabetes mellitus in the early puerperium in
women with recent gestational diabetes mellitus. Am J Obstet
Gynecol. 2002;186:751756.
99. Holt RI, Goddard JR, Clarke P, Coleman MA. A postnatal
fasting plasma glucose is useful in determining which women
with gestational diabetes should undergo a postnatal oral
glucose tolerance test. Diabet Med. 2003;20:594598.
100. Lbner K, Knopff A, Baumgarten A, et al. Predictors of
postpartum diabetes in women with gestational diabetes
mellitus. Diabetes. 2006;55:792797.
101. Wein P, Beischer NA, Sheedy MT. Studies of postnatal
diabetes mellitus in women who had gestational diabetes.
Part 2. Prevalence and predictors of diabetes mellitus after
delivery. Aust N Z J Obstet Gynaecol. 1997;37:420423.
102. Linn Y, Barkeling B, Rssner S. Natural course of
gestational diabetes mellitus: long term follow up of women
in the SPAWN study. BJOG. 2002;109:12271231.
103. Aberg AE, Jnsson EK, Eskilsson I, Eskilsson I, LandinOlsson M, Frid AH. Predictive factors of developing
diabetes mellitus in women with gestational diabetes. Acta
Obstet Gynecol Scand. 2002;81:1116.
104. Jrvel IY, Juutinen J, Koskela P, et al. Gestational diabetes
identifies women at risk for permanent type 1 and type 2
diabetes in fertile age: predictive role of autoantibodies.
Diabetes Care. 2006;29:607612.
105. OSullivan JB. Diabetes mellitus after GDM. Diabetes.
1991;40(Suppl 2):131135.
106. Stowers JM, Sutherland HW, Kerridge DF. Long range
implications for the mother. The Aberdeen experience.
Diabetes. 1985;34:106110.
107. Damm P. Gestational diabetes mellitus and subsequent
development of overt diabetes mellitus. Danish Med Bull.
1998;45:495509.
92. Kjos SL, Peters RK, Xiang A, Henry OA, Montoro M,

Buchanan TA. Predicting future diabetes in Latino women
with gestational diabetes. Utility of early postpartum glucose
tolerance testing. Diabetes. 1995;44:586591.
96. Bo S, Monge L, Macchetta C, et al. Prior gestational

hyperglycemia: a long-term predictor of the metabolic
syndrome. J Endocrinol Invest. 2004;27:629635.
31
108. Pettitt DJ, McKenna S, McLaughlin C, Patterson CC,

Hadden DR, McCance DR. Maternal glucose at 28 weeks of
gestation is not associated with obesity in 2-year-old offspring:
the Belfast Hyperglycemia and Adverse Pregnancy Outcome
(HAPO) family study. Diabetes Care. 2010;33:12191223.
121. Kulkarni K, Castle G, Gregory R, et al. Nutrition Practice

Guidelines for Type 1 Diabetes Mellitus positively affect
dietitian practices and patient outcomes. The Diabetes Care
and Education Dietetic Practice Group. J Am Diet Assoc.
1998;98:6270.
109. Prutsky GJ, Domecq JP, Zhen W, et al. Glucose targets in

pregnant women with diabetes: a systematic review and
meta-analysis. J Clin Endocrinol Metab. 2013 Nov;98(11):
431924.
122. Reader D, Splett P, Gunderson E. Impact of gestational

diabetes mellitus nutrition practice guidelines implemented
by registered dietitians on pregnancy outcomes. J Am Diet
Assoc. 2006;106:14261433.
110. Chen R, Yogev Y, Ben-Haroush A, Jovanovic L, Hod M,

Phillip M. Continuous glucose monitoring for the evaluation
and improved control of gestational diabetes mellitus.
J Matern Fetal Neonatal Med. 2003;14:256260.
123. American Dietetic Association. Nutrition Practice

Guidelines for Gestational Diabetes [CD-ROM]. Chicago,
IL: American Dietetic Association; 2002.
111. McLachlan K, Jenkins A, ONeal D. The role of continuous

glucose monitoring in clinical decision-making in diabetes in
pregnancy. Aust N Z J Obstet Gynaecol. 2007;47:186190.
112. Voelmle M, Gottlieb P, Ellis S, Wallace A, Gerard L. Fetal
outcomes and improved A1c values in pregnant women with
type 1 diabetes using real-time continuous glucose sensors.
Diabetes. 2007;56:A117.
113. Buchanan TA, Kjos SL, Montoro MN, et al. Use of fetal
ultrasound to select metabolic therapy for pregnancies
complicated by mild gestational diabetes. Diabetes Care.
1994;17:275283.
114. Kjos SL, Schaefer-Graf U, Sardesi S, et al. A randomized
controlled trial using glycemic plus fetal ultrasound
parameters versus glycemic parameters to determine insulin
therapy in gestational diabetes with fasting hyperglycemia.
Diabetes Care. 2001;24:19041910.
115. American Diabetes Association. Summary and recommendations of the First International Conference-Workshop
on Gestational Diabetes Mellitus. Diabetes Care. 1980
3:499501.
116. Frenkel N. Summary and recommendations of the

Second International Workshop-Conference on Gestational
Diabetes. Diabetes. 1985;34(Suppl 2):S123S126.
32
117. Metzger BE, Coustan DR. Summary and recommendations

of the Fourth International Workshop-Conference on
Gestational Diabetes. The Organizing Committee. Diabetes
Care. 1998;21(Suppl 2):B161B167.
118. Langer O. Maternal glycemic criteria for insulin therapy
in gestational diabetes mellitus. Diabetes Care. 1998;21
(Suppl 2):B91B98.
119. Gunderson EP. Gestational diabetes and nutritional
recommendations. Curr Diab Rep. 2004;4:377386.
120. Franz MJ, Monk A, Barry B, et al. Effectiveness of medical
nutrition therapy provided by dietitians in the management
of non-insulin-dependent diabetes mellitus: a randomized,
controlled clinical trial. J Am Diet Assoc. 1995;95:1009
1017.
124. Gunderson EP, Murtaugh MA, Lewis CE, Quesenberry

CP, West DS, Sidney S. Excess gains in weight and waist
circumference associated with childbearing: The Coronary
Artery Risk Development in Young Adults Study (CARDIA).
Int J Obes Relat Metab Disord. 2004;28:525535.
125. Callaway LK, Prins JB, Chang AM, McIntyre HD. The
prevalence and impact of overweight and obesity in an
Australian obstetric population. Med J Aust. 2006;184:
5659.
126. Crane JM, White J, Murphy P, Burrage L, Hutchens D.
The effect of gestational weight gain by body mass index on
maternal and neonatal outcomes. J Obstet Gynaecol Can.
2009;31:2835.
127. Tennant PW, Rankin J, Bell R. Maternal body mass index
and the risk of fetal and infant death: a cohort study from the
North of England. Hum Reprod. 2011;26:15011511.
128. Bhattacharya S, Campbell DM, Liston WA, Bhattacharya
S. Effect of body mass index on pregnancy outcomes in
nulliparous women delivering singleton babies. BMC Public
Health. 2007;7:168.
129. Magee MS, Knopp RH, Benedetti TJ. Metabolic effects of
1200-kcal diet in obese pregnant women with gestational
diabetes. Diabetes. 1990;39:234240.
130. IOM (Institute of Medicine) and NRC (National Research
Council). Weight Gain During Pregnancy: Reexamining the
Guidelines. Washington, DC: The National Academies
Press; 2009.
131. Snyder J. Gray-Donald K, Koski KG. Predictors of infant
birth weight in gestational diabetes. Am J Clin Nutr.
1994;59:14091414.
132. Knopp RH, Magee MS, Raisys V, Benedetti T, Bonet B.
Hypocaloric diets and ketogenesis in the management of
obese gestational diabetic women. J Am Coll Nutr.
1991;10:649667.
133. Algert S, Shragg P, Hollingsworth DR. Moderate caloric
restriction in obese women with gestational diabetes. Obstet
Gynecol. 1985;65:487491.
134. Rizzo T, Metzger BE, Burns WJ, Burns K. Correlations
between antepartum maternal metabolism and child
intelligence. N Engl J Med. 1991;325:911916.
135. Jovanovic L, Metzger B, Knopp RH, et al. The Diabetes in

Early Pregnancy Study: -hydroxybutyrate levels in type 1
diabetic pregnancy compared with normal pregnancy.
NICHD-Diabetes in Early Pregnancy Study Group (DIEP).
National Institute of Child Health and Development.
Diabetes Care November. 1998;21:19781984.
136. American Diabetes Association. American Diabetes
Association: gestational diabetes (position statement).
Diabetes Care. 2000;23(Suppl 1):S77S79.
137. American Diabetes Association. Gestational diabetes.
Diabetes Care. 2004;27(Suppl 1):S88S90.
148. Smith JG, Manuck TA, White J, Merrill DC. Insulin

glargine versus neutral protamine Hagedorn insulin for
treatment of diabetes in pregnancy. Am J Perinatol. 2009;
26:5762.
149. Egerman RS, Ramsey RD, Kao LW, et al. Perinatal
outcomes in pregnancies managed with antenatal insulin
glargine. Am J Perinatol. 2009;26:591595.
150. Imbergamo MP, Amato MC, Sciortino G, et al. Use of
glargine in pregnant women with type 1 diabetes mellitus: a
case-control study. Clin Ther. 2008;30:14761484.
138. Tieu J, Crowther CA, Middleton P. Dietary advice in

pregnancy for preventing gestational diabetes. Cochrane
Database Syst Rev. 2008;2:CD006674.
151. Kurtzhals P, Schffer L, Srensen A, et al. Correlations

of receptor binding and metabolic and mitogenic potencies
of insulin analogs designed for clinical use. Diabetes.
2000;49:9991005.
139. Fraser RB, Ford FA, Milner RD. A controlled trial of a high
dietary fibre intake in pregnancyeffects on plasma glucose
and insulin levels. Diabetologia. 1983;25:238241.
152. Lauszus FF. The clinical significance of IGF-I in maternal

serum during pregnancy in type 1 diabetes. Curr Diabetes
Rev. 2007;3:194197.
140. Jovanovic-Peterson L, Peterson CM, Reed GF, et al.

Maternal postprandial glucose levels and infant birth weight:
the Diabetes in Early Pregnancy Study. The National
Institute of Child Health and Human Development-Diabetes
in Early Pregnancy Study. Am J Obstet Gynecol. 1991;
164:103111.
153. Thrailkill KM, Quattrin T, Baker L, Kuntze JE, Compton

PG, Martha PM Jr. Cotherapy with recombinant human
insulin-like growth factor I and insulin improves glycemic
control in type 1 diabetes. RhIGF-I in IDDM Study Group.
RhIGF-I in IDDM Study Group. Diabetes Care. 1999;22:
585592.
141. Brand-Miller J, Hayne S, Petocz P, Colagiuri S.

Low-glycemic index diets in the management of diabetes: a
meta-analysis of randomized controlled trials. Diabetes Care.
2003;26:22612267.
154. Hofmann T, Horstmann G, Stammberger I. Evaluation of

the reproductive toxicity and embryotoxicity of insulin
glargine (LANTUS) in rats and rabbits. Int J Toxicol.
2002;21:181189.
142. Bartley PC, Bogoev M, Larsen J, Philotheou A. Long-term

efficacy and safety of insulin detemir compared to neutral
protamine Hagedorn insulin in patients with type 1 diabetes
using a treat-to-target basal-bolus regimen with insulin aspart
at meals: a 2-year, randomized, controlled trial. Diabet Med.
2008;25:442449.
155. Lepercq J, Jacqueminet S, Hieronimus S, Timsit J,

Grimaldi A. Use of insulin glargine throughout pregnancy in
102 women with type 1 diabetes. Diabetes Metab. 2010;
36:209212.
143. Hermansen K, Fontaine P, Kukolja KK, Peterkova V, Leth

G, Gall MA. Insulin analogues (insulin detemir and insulin
aspart) versus traditional human insulins (NPH insulin and
regular human insulin) in basal-bolus therapy for patients
with type 1 diabetes. Diabetologia. 2004;47:622629.
144. Russell-Jones D, Simpson R, Hylleberg B, Draeger E,
Bolinder J. Effects of QD insulin detemir or neutral
protamine Hagedorn on blood glucose control in patients
with type I diabetes mellitus using a basal-bolus regimen. Clin
Ther. 2004;26:724736.
146. Price N, Bartlett C, Gillmer M. Use of insulin glargine

during pregnancy: a case-control pilot study. BJOG.
2007;114:453457.
147. Fang YM, MacKeen D, Egan JF, Zelop CM. Insulin glargine
compared with neutral protamine Hagedorn insulin in the
treatment of pregnant diabetics. J Matern Fetal Neonatal
Med. 2009;22:249253.
157. Pratoomsoot C, Smith HT, Kalsekar A, Boye KS, Arellano

J, Valentine WJ. An estimation of the long-term clinical and
economic benefits of insulin lispro in type 1 diabetes in the
UK. Diabet Med. 2009;26:803814.
158. Loukovaara S, Immonen I, Teramo KA, Kaaja R.
Progression of retinopathy during pregnancy in type 1
diabetic women treated with insulin lispro. Diabetes Care.
2003;26:11931198.
159. Durnwald CP, Landon MB. A comparison of lispro and
regular insulin for the management of type 1 and type 2
diabetes in pregnancy. J Matern Fetal Neonatal Med.
2008;21:309313.
160. Bhattacharyya A, Brown S, Hughes S, Vice PA. Insulin
lispro and regular insulin in pregnancy. QJM. 2001;94:
255260.
161. Aydin Y, Berker D, Direktr N, et al. Is insulin lispro
safe in pregnant women: does it cause any adverse outcomes
on infants or mothers? Diabetes Res Clin Pract. 2008;80:
444448.
145. Mathiesen ER, Damm P, Jovanovic L, et al. Basal insulin

analogues in diabetic pregnancy: a literature review and
baseline results of a randomised, controlled trial in type 1
diabetes. Diabetes Metab Res Rev. 2011;27:543551.
156. Negrato CA, Rafacho A, Negrato G, et al. Glargine vs.

NPH insulin therapy in pregnancies complicated by diabetes:
an observational cohort study. Diabetes Res Clin Pract.
2010;89:4651.
33
162. Persson B, Swahn ML, Hjertberg R, Hanson U, Nord E,

Nordlander E, Hansson LO. Insulin lispro therapy in
pregnancies complicated by type 1 diabetes mellitus. Diabetes
Res Clin Pract. 2002;58:115121.
163. Cypryk K, Sobczak M, Pertyska-Marczewska M, et al.
Pregnancy complications and perinatal outcome in diabetic
women treated with Humalog (insulin lispro) or regular
human insulin during pregnancy. Med Sci Monit.
2004;10:PI29P132.
164. Wyatt JW, Frias JL, Hoyme HE, et al. Congenital anomaly
rate in offspring of mothers with diabetes treated with insulin
lispro during pregnancy. Diabet Med. 2005;22:803807.
165. Bhattacharyya A, Vice PA. Insulin lispro, pregnancy, and
retinopathy. Diabetes Care. 1999;22:21012104.
166. Buchbinder A, Miodovnik M, McElvy S, et al. Is insulin
lispro associated with the development or progression of
diabetic retinopathy during pregnancy? Am J Obstet Gynecol.
2000;183:11621165.
167. Hironimus S, Cupelli C, Bongain A, Durand-Rville M,
Berthier F, Fnichel P. Pregnancy in type 1 diabetes: insulin
pump versus intensified conventional therapy [in French].
Gynecol Obstet Fertil. 2005;33:389394.
168. Lapolla A, Dalfr MG, Masin M, et al. Analysis of outcome
of pregnancy in type 1 diabetics treated with insulin pump
or conventional insulin therapy. Acta Diabetol. 2003;40:
143149.
169. Misso ML, Egberts KJ, Page M, OConnor D, Shaw J.
Continuous subcutaneous insulin infusion (CSII) versus
multiple insulin injections for type 1 diabetes. Cochrane
Database Syst Rev. 2010;1:CD005103.
170. Mukhopadhyay A, Farrell T, Fraser RB, Ola B. Continuous

subcutaneous insulin infusion vs intensive conventional
insulin therapy in pregnant diabetic women: a systematic
review and meta-analysis of randomized, controlled trials.
Am J Obstet Gynecol. 2007;197:447456.
34
171. Gabbe SG. New concepts and applications in the use of the
insulin pump during pregnancy. J Matern Fetal Med. 2000;
9:4245.
172. Simmons D, Thompson CF, Conroy C, Scott DJ. Use of
insulin pumps in pregnancies complicated by type 2 diabetes
and gestational diabetes in a multiethnic community.
Diabetes Care. 2001;24:20782082.
173. Chen R, Ben-Haroush A, Weissmann-Brenner A,
Melamed N, Hod M, Yogev Y. Level of glycemic control and
pregnancy outcome in type 1 diabetes: a comparison between
multiple daily insulin injections and continuous subcutaneous
insulin infusions. Am J Obstet Gynecol. 2007;197:404.e1e5.
174. Kremer CJ, Duff P. Glyburide for the treatment of
gestational diabetes. Am J Obstet Gynecol. 2004;190:1438
1439.
175. Jacobson GF, Ramos GA, Ching JY, Kirby RS, Ferrara A,
Field DR. Comparison of glyburide and insulin for the
management of gestational diabetes in a large managed care
organization. Am J Obstet Gynecol. 2005;193:118124.
176. Ramos GA, Jacobson GF, Kirby RS, Ching JY, Field DR.
Comparison of glyburide and insulin for the management of
gestational diabetics with markedly elevated oral glucose
challenge test and fasting hyperglycemia. J Perinatol.
2007;27:262267.
177. Lain KY, Garabedian MJ, Daftary A, Jeyabalan A.
Neonatal adiposity following maternal treatment of
gestational diabetes with glyburide compared with insulin.
Am J Obstet Gynecol. 2009;200:501506.
178. Hebert MF, Ma X, Naraharisetti SB, et al. Are we
optimizing gestational diabetes treatment with glyburide?
The pharmacologic basis for better clinical practice. Clin
Pharmacol Ther. 2009;85:607614.
179. Dhulkotia JS, Ola B, Fraser R, Farrell T. Oral hypoglycemia
agents vs. insulin in management of gestational diabetes:
a systemic review and metaanalysis. Am J Obstet Gynecol.
2009;203:457.e1e9.
180. Conway DL, Gonzales O, Skiver D. Use of glyburide for
the treatment of gestational diabetes: the San Antonio
experience. J Matern Fetal Neonatal Med. 2004;15:5155.
181. Rochon M, Rand L, Roth L, Gaddipati S. Glyburide for the
management of gestational diabetes: risk factors predictive of
failure and associated pregnancy outcomes. Am J Obstet
Gynecol. 2006;195:10901094.
182. Yogev Y, Melamed N, Chen R, Nassie D, Pardo J, Hod M.
Glyburide in gestational diabetes--prediction of treatment
failure. J Matern Fetal Neonatal Med. 2011;24:842842.
183. Kahn BF, Davies JK, Lynch AM, Reynolds RM, Barbour
LA. Predictors of glyburide failure in the treatment of
gestational diabetes. Obstet Gynecol. 2006;107:13031309.
184. Chmait R, Dinise T, Moore T. Prospective observational
study to establish predictors of glyburide success in women
with gestational diabetes mellitus. J Perinatol. 2004;24:617
622.
185. Goetzl L, Wilkins I. Glyburide compared to insulin for the
treatment of gestational diabetes mellitus: a cost analysis.
J Perinatol. 2002;22:403406.
186. Gutzin SJ, Kozer E, Magee LA, Feig DS, Koren G. The
safety of oral hypoglycemic agents in the first trimester of
pregnancy: a meta-analysis. Can J Clin Pharmacol.
2003;10:179183.
187. Baillargeon JP, Jakubowicz DJ, Iuorno MJ, Jakubowicz S,
Nestler JE. Effects of metformin and rosiglitazone, alone and
in combination, in nonobese women with polycystic ovary
syndrome and normal indices of insulin sensitivity. Fertil
Steril. 2004;82:893902.
188. Gagnon C, Baillargeon JP. Suitability of recommended
limits for fasting glucose tests in women with polycystic ovary
syndrome. CMAJ. 2007;176:933938.
189. Genazzani AD, Ricchieri F, Lanzoni C. Use of metformin
in the treatment of polycystic ovary syndrome. Womens
Health (Lond Engl). 2010;6:577593.
190. Glueck CJ, Bornovali S, Pranikoff J, Goldenberg N,

Dharashivkar S, Wang P. Metformin, pre-eclampsia, and
pregnancy outcomes in women with polycystic ovary
syndrome. Diabet Med. 2004;21:829836.
203. Mayer-Davis EJ, Rifas-Shiman SL, Hu F, Colditz G,

Gilman M. Breast feeding and risk for childhood obesity:
does diabetes or obesity status matter? Diabetes Care October.
2006;22312237.
191. Gilbert C, Valois M, Koren G. Pregnancy outcome after

first-trimester exposure to metformin: a meta-analysis. Fertil
Steril. 2006;86:658663.
204. Schaefer-Graf UM, Hartmann R, Pawliczak J, et al.

Association of breast-feeding and early childhood overweight
in children from mothers with gestational diabetes mellitus.
Diabetes Care. 2006;29:11051107.
192. Salvesen KA, Vanky E, Carlsen SM. Metformin treatment

in pregnant women with polycystic ovary syndromeis
reduced complication rate mediated by changes in the
uteroplacental circulation? Ultrasound Obstet Gynecol.
2007;29:433437.
193. Bolton S, Cleary B, Walsh J, Dempsey E, Turner MJ.
Continuation of metformin in the first trimester of women
with polycystic ovarian syndrome is not associated with
increased perinatal morbidity. Eur J Pediatr. 2009;168:
203206.
194. Charles B, Norris R, Xiao X, Hague W. Population
pharmacokinetics of metformin in late pregnancy. Ther
Drug Monit. 2006;28:6772.
195. Eyal S, Easterling TR, Carr D, et al. Pharmacokinetics of
metformin during pregnancy. Drug Metab Dispos.
2010;38:833840.
196. Balsells M, Corcoy R, Adelantado JM, Garca-Patterson
A, Altirriba O, de Leiva A. Gestational diabetes mellitus:
metabolic control during labour. Diabetes Nutr Metab.
2000;13:257262.
197. Andersen O, Hertel J, Schmlker L, Khl C. Influence of
the maternal plasma glucose concentration at delivery on
the risk of hypoglycaemia in infants of insulin-dependent
diabetic mothers. Acta Paediatr Scand. 1985;74:268273.
198. Miodovnik M, Mimouni F, Tsang RC. Management of
the insulin-dependent diabetic during labor and delivery.
Influences on neonatal outcome. Am J Perinatol. 1987;4:106
114.
199. Curet LB, Izquierdo LA, Gilson GJ, Schneider JM,
Perelman R, Converse J. Relative effects of antepartum and
intrapartum maternal blood glucose levels on incidence of
neonatal hypoglycemia. J Perinatol. 1997;17:113115.
200.
Lean ME, Pearson DW, Sutherland HW. Insulin
management during labour and delivery in mothers with
202. Mimouni F. Perinatal asphyxia in infants of diabetic mothers

is associated with maternal vasculopathy and hyperglycaemia
in labour. Neonat Epidemiol Follow-up. 1987:400A.
206. Plagemann A, Harder T, Franke K, Kohlhoff R. Long-term

impact of neonatal breast-feeding on body weight and glucose
tolerance in children of diabetic mothers. Diabetes Care.
2002;25:1622.
207. Rodekamp E, Harder T, Kohlhoff R, Franke K,
Dudenhausen JW, Plagemann A. Long-term impact of
breast-feeding on body weight and glucose tolerance in
children of diabetic mothers: role of the late neonatal period
and early infancy. Diabetes Care. 2005;28:14571462.
208. Mayer-Davis EJ, Rifas-Shiman SL, Zhou L, Hu FB,
Colditz GA, Gillman MW. Breast-feeding and risk for
childhood obesity: does maternal diabetes or obesity status
matter? Diabetes Care. 2006;29:22312237.
209. Pettitt DJ, Forman MR, Hanson RL, Knowler WC,
Bennett PH. Breastfeeding and incidence of non-insulindependent diabetes mellitus in Pima Indians. Lancet.
1997;350:166168.
210. Pettitt DJ, Knowler WC. Long-term effects of the
intrauterine environment, birth weight, and breast-feeding in
Pima Indians. Diabetes Care. 1998;21(Suppl 2):B138B141.
211. Young TK, Martens PJ, Taback SP, Sellers EA, Dean HJ,
Cheang M, Flett B. Type 2 diabetes mellitus in children:
prenatal and early infancy risk factors among native
Canadians. Arch Pediatr Adolesc Med. 2002;156:651655.
212. Virtanen SM, Rsnen L, Ylnen K, et al. Early
introduction of dairy products associated with increased risk
of IDDM in Finnish children. The Childhood in Diabetes in
Finland Study Group. Diabetes. 1993;42:17861790.
213. OReilly M, Avalos G, Dennedy MC, OSullivan EP,
Dunne FP. Breast-feeding is associated with reduced
postpartum maternal glucose intolerance after gestational
diabetes. Ir Med J. 2012;105(5 Suppl):3136.
214. Owen CG, Martin RM, Whincup PH, Smith GD, Cook
DG. Does breastfeeding influence risk of type 2 diabetes in
later life? A quantitative analysis of published evidence. Am
J Clin Nutr. 2006;84:10431054.
215. Glueck CJ, Wang P. Metformin before and during pregnancy
and lactation in polycystic ovary syndrome. Expert Opin Drug
Saf. 2007;6:191198.
201. Feldberg D, Dicker D, Samuel N, Peleg D, Karp M,

Goldman JA. Intrapartum management of insulin-dependent
diabetes mellitus (IDDM) gestants. A comparative study of
constant intravenous insulin infusion and continuous
subcutaneous insulin infusion pump (CSIIP). Acta Obstet
Gynecol Scand. 1988;67:333338.
205. Gunderson EP. Breastfeeding after gestational diabetes

pregnancy: subsequent obesity and type 2 diabetes in women
and their offspring. Diabetes Care. 2007;30(Suppl 2):S161
S168.
35
216. Glueck CJ, Salehi M, Sieve L, Wang P. Growth, motor, and

social development in breast- and formula-fed infants of
metformin-treated women with polycystic ovary syndrome.
J Pediatr. 2006;148:628632.
217. Feig DS, Briggs GG, Kraemer JM, et al. Transfer of
glyburide and glipizide into breast milk. Diabetes Care.
2005;28:18511855.
218. Glatstein MM, Djokanovic N, Garcia-Bournissen F,
Finkelstein Y, Koren G. Use of hypoglycemic drugs during
lactation. Can Fam Physician. 2009;55:371373.
219. Petersen KR, Skouby SO, Sidelmann J, Mlsted-Pedersen
L, Jespersen J. Effects of contraceptive steroids on
cardiovascular risk factors in women with insulin-dependent
diabetes mellitus. Am J Obstet Gynecol. 1994;171:400405.
220. Garg SK, Chase HP, Marshall G, Hoops SL, Holmes DL,
Jackson WE. Oral contraceptives and renal and retinal
complications in young women with insulin-dependent
diabetes mellitus. JAMA. 1994;271:10991102.
229. Kimmerle R, Heinemann L, Berger M. Intrauterine devices

are safe and effective contraceptives for type I diabetic
women. Diabetes Care. 1995;18:15061507.
230. Kjos SL, Ballagh SA, La Cour M, Xiang A, Mishekk DR
Jr. The copper T380A intrauterine device in women with
type II diabetes mellitus. Obstet Gynecol. 1994;84:1006
1009.
231. Sturridge F, Guillebaud J. A risk-benefit assessment of
the levonorgestrel-releasing intrauterine system. Drug Saf.
1996;15:430440.
221. Klein BE, Moss SE, Klein R. Oral contraceptives in women

with diabetes. Diabetes Care. 1990;13:895898.
222. Skouby SO, Khl C, Mlsted-Pedersen L, Petersen K,
Christensen MS. Triphasic oral contraception: Metabolic
effects in normal women and those with previous gestational
diabetes. Am J Obstet Gynecol. 1985;153:495500.
233. Petersen KR. Pharmacodynamic effects of oral contraceptive

steroids on biochemical markers for arterial thrombosis.
Studies in non-diabetic women and in women with insulindependent diabetes mellitus. Dan Med Bull. 2002;49:4360.
223. Kjos SL, Shoupe D, Douyan S, et al. Effect of low dose

oral contraceptives on carbohydrate metabolism in women
with recent gestational diabetes: results of a controlled,
randomized, prospective study. Am J Obstet Gynecol.
1990;163:18821827.
234. Godsland IF, Crook D, Simpson R, et al. The effects of

different formulations of oral contraceptive agents on
lipid and carbohydrate metabolism. N Engl J Med.
1990;323:13751381.
225. Skouby SO, Andersen O, Saurbrey N, Khl C. Oral

contraception and insulin sensitivity: in vivo assessment in
normal women and women with previous gestational
diabetes. J Clin Endocrinol Metab. 1987;64:519523.
228. Skouby SO, Mlsted-Pedersen L, Kosonen A. Consequences

of intrauterine contraception in diabetic women. Fertil Steril.
1984;42:568572.
232. Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a

levonorgestrel intrauterine system on women with type 1
diabetes: a randomized trial. Obstet Gynecol. 2005;105:
811815.
224. Kjos SL, Peters RK, Xiang A, Thomas D, Schaefer U,

Buchanan TA. Contraception and the risk of type 2 diabetes
mellitus in Latina women with prior gestational diabetes
mellitus. JAMA. 1998;280:533538.
36
227. Weisberg E, Fraser IS, Lacarra M, et al. Efficacy, bleeding

patterns, and side effects of a 1-year contraceptive vaginal
ring. Contraception. 1999;59:311318.
226. Creasy GW, Fisher AC, Hall N, Shangold GA. Transdermal

contraceptive patch delivering norelgestromin and ethinyl
estradiol. Effects on the lipid profile. J Reprod Med.
2003;48:179186.
235. Kim CH, Ahn JW, Kang SP, Kim SH, Chae HD, Kang
BM. Effect of levothyroxine treatment on in vitro
fertilization and pregnancy outcome in infertile women
with subclinical hypothyroidism undergoing in vitro
fertilization/intracytoplasmic sperm injection. Fertil Steril.
2011;95:16501654.
236. Bech K, Hier-Madsen M, Geldt-Rasmussen U, Jensen
BM, Mlsted-Pedersen L, Khl C. Thyroid dysfunction and
autoimmune manifestations in insulin-dependent diabetes
during and after pregnancy. Acta Endocrinol (Copenh).
1991;124:534539.
Acknowledgments
The members of the Task Force thank the Endocrine Society Clinical Guidelines Subcommittee and Clinical
Affairs Core Committee for their careful critical review of earlier versions of this manuscript and their helpful
comments and suggestions. We also thank the members of the Endocrine Society who kindly reviewed the draft
version of this manuscript when it was posted on the Societys website and who sent additional comments and
suggestions. We express our great appreciation to Stephanie Kutler and Lisa Marlow for their administrative support
and to Deborah Hoffman for her writing assistance in the process of developing this guideline. Lastly, as chair, Ian
personally expresses his gratitude to his fellow committee members for their perseverance, dedication, and
camaraderie during this guidelines lengthy and challenging gestation.
Financial Disclosure of Task Force

Ian Blumer, MD (chair) is a speaker for Astra-Zeneca, Bristol Myers Squibb, Eli Lilly, Medtronic, Novo Nordisk,
Roche and Sanofi-Aventis. He is also a member of advisory board for Bayer, Eli Lilly, GlaxoSmithKline, Novo
Nordisk, Janssen Pharmaceuticals, and Takeda. David R. Hadden, MD is a member of the data monitoring
committee for Novo Nordisk and a technical editor for Wiley-Blackwell Publishing. M. Hassan Murad, MD, Lois
Jovanovic, MD, Jorge H. Mestman, MD, Eran Hadar, MD and Yariv Yogev, MD have no relevant financial
relationships to declare.
* Evidence-based reviews for this guideline were prepared under contract with the Endocrine Society.
37
CME Learning Objectives and Post-Test Questions

LEARNING OBJECTIVES
Upon completion of this educational activity, learners will be able to:
Recognize the appropriate target level of glycemic control (as reflected by the HbA1C) for a woman
with established diabetes before attempting to conceive.
Evaluate self-monitored blood glucose target levels for a woman with gestational diabetes and the
appropriate therapeutic intervention if these targets are being exceeded.
Determine the appropriate frequency for ocular assessment for a pregnant woman with diabetes and
known retinopathy.
Select appropriate antihyperglycemic medication for a breastfeeding woman with type 2 diabetes.
CME Question #1
A 25-year-old woman with a 5-year history of type 1 diabetes advises you she would like to try to conceive as soon
as possible. Her current haemoglobin A1C (HbA1C) is 8.5 percent.
What advice should you give her?
38
A) She can safely proceed with trying to conceive.

B) She should defer trying to conceive until her HbA1C is <6 percent.
C) She should defer trying to conceive until her HbA1C is as close to normal as possible when this can be
safely achieved.
D) She should begin using continuous glucose monitoring.
CME Question #2
A 30-year-old woman is 24 weeks pregnant and is diagnosed with gestational diabetes. After 1 week of medical
nutrition therapy and exercise her self-monitored blood glucose (SMBG) levels are averaging 100 mg/dl (5.6
mmol/L) before meals and 130 mg/dl (7.2 mmol/L) 2 hours after meals.
What is the preferred next step in managing this patient?
A) Make no change to her current therapy as her SMBG values are within target.
B) Recommend she start glyburide.
C) Recommend she start metformin.
D) Recommend she start insulin therapy.
CME Question #3
A 29-year-old woman with type 1 diabetes and hypertension is newly pregnant. She has known, stable
retinopathy. Her HbA1C is 6.5 percent. Her blood pressure is 125/85.
What advice should you give her regarding her retinopathy?
A) Tell her that her retinopathy can worsen during pregnancy and arrange for regular eye exams during the
pregnancy.
B) Tell her that as her retinopathy is stable it is unlikely to progress during the pregnancy.
C) Advise her of the great dangers to her vision if she continues the pregnancy and recommend she terminate
the pregnancy.
D) Recommend she see an eye care professional in the near future then again after she has delivered.
CME Question #4
A 32-year-old woman with type 2 diabetes being treated with glyburide has just delivered a healthy infant at term.
She will be breastfeeding the baby.
What should you recommend for this woman?
A) She should discontinue the glyburide and take insulin instead.
B) She should continue the glyburide.
C) She should not breastfeed the infant.
To claim your CME credit, please go to https://www.endocrine.org/education-and-practice-management/

continuing-medical-education/publication-cme.
D) She should discontinue the glyburide and take metformin instead.
39
CME Answers and Explanations

CME Question #1
Correct answer: C, A woman with overt diabetes should defer trying to conceive until her HbA1C is as close to
normal as possible when this can be safely achieved.
Discussion: Maternal hyperglycemia in the first few weeks of pregnancy increases the risk of fetal mal-formations,
spontaneous abortions, and perinatal mortality. Although the exact degree of risk of a congenital anomaly for a
given HbA1C is not precisely known, it has been reported that the risk progressively rises in concert with the
degree of periconceptional HbA1C elevation. A limiting factor, however, in striving to achieve an optimal HbA1C
is the occurrence of hypoglycemia.
CME Question #2
Correct answer: D, Recommend she start insulin therapy.
40
Discussion: Target SMBG values for a woman with gestational (or overt) diabetes are equal to or less than 95 mg/
dl (5.3 mmol/L) before meals (equal to or less than 90 mg/dl (5.0 mmol/L) fasting if this can be safely achieved); equal
to or less than 140 mg/dl (7.8 mmol/L) one hour after the start of a meal; equal to or less than 120 mg/dl (6.7
mmol/L) two hours after the start of a meal. Elevated blood glucose in a pregnant woman is associated with an
increased risk of harm to the fetus. Insulin therapy is the preferred blood glucose-lowering medication in women
diagnosed with gestational diabetes prior to 25 weeks gestation.
CME Question #3
Correct answer: A, Tell her that her retinopathy can worsen during the pregnancy and arrange for regular eye
exams during the pregnancy.
Discussion: Established retinopathy can rapidly progress duringand up to one year afterpregnancy and can
lead to sight-threatening deterioration. The greater the degree of preconceptional retinopathy, the greater is the
risk of retinopathy progressing during pregnancy. Additional risk factors for progression of retinopathy during pregnancy include pre-existing hypertension, poorly controlled hypertension during pregnancy, preeclampsia, and poor
glycemic control at the onset of and during pregnancy. Pregnant women with established retinopathy should be
seen by their eye specialist every trimester, then within three months of delivering, then as needed.
CME Question #4
Correct answer: B, She should continue the glyburide.
Discussion: Glyburide is not found in significant quantities in breast milk and is not associated with hypoglycemia
in nursing infants. Metformin can also be safely taken by breast feeding women.
41
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Diabetes and Pregnancy:

Diabetes and Pregnancy:

An Endocrine Society Clinical Practice Guideline

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Activity Expiration Date: November 2016

Conclusions: Using an evidence-based approach, this

An Endocrine Society Clinical Practice Guideline

Consensus Process: One group meeting, several

be provided to all women with diabetes who are

with diabetes seeking to conceive be treated with

1.3c. We suggest that insulin-treated women with

fully using the long-acting insulin analogs insulin

withdrawing contraceptive measures or otherwise

who are seeking pregnancy have a detailed ocular

retinopathy be seen by their eye specialist every

considering pregnancy have their renal function

Diabetes and Pregnancy

1.3b. We suggest that a change to a womans insulin

1.3d. We suggest that women with diabetes success-

conceive. (Ungraded recommendation) We suggest

(particularly the duration of the womans diabetes and

preconceptional renal dysfunction have their renal

is seeking pregnancy and has CAD, its severity should

1.7a. We recommend that satisfactory blood pressure

1.9a. We recommend against the use of statins in

1.6b. We suggest that all women with diabetes and

1.7b. We recommend that a woman with diabetes

women with diabetes who are attempting to conceive.

An Endocrine Society Clinical Practice Guideline

1.7c. We suggest that in the exceptional case where

the degree of renal dysfunction is severe and there is

tensin-receptor blockers have been continued up to

has sufficient numbers of vascular risk factors

tion, we recommend measurement of serum TSH and,

nancy for overweight and obese women with diabetes.

2.0. Gestational diabetes

(see Table 1) with a fasting plasma glucose, HbA1C,

Testing for gestational diabetes at 24 to 28

Overt diabetes (type 1, type 2, or other)

Overt diabetes (type 1, type 2, or other)

Diabetes and Pregnancy

patient should not smoke during the test. One or more

diabetes target blood glucose levels as close to normal

pharmacological therapy if lifestyle therapy is insufficient to maintain normoglycemia in women with

An Endocrine Society Clinical Practice Guideline

2.4a. We recommend that postpartum care for

should be undertaken 6 to 12 weeks after delivery in

or not the child was born to a mother with gestational

2.4d. We recommend that all women who have had

should be discontinued immediately after delivery for

in all pregnant women with gestational or overt

Table 3. Glycemic Targets Preconceptionally for

1 h after the start of a meal