VOL. 16 NO. 1  January - February 1998

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Gestational Diabetes: Detection, Management, and Implications

Darcy Barry Carr, MD, and Steven Gabbe, MD

In Brief

Gestational diabetes mellitus (GDM) is the most common medical complication of pregnancy. GDM occurs in women who have insulin resistance and a relative impairment of insulin secretion. These women have a significant risk of developing diabetes later in life. Identifying this group of women is important in not only preventing perinatal morbidity but also improving long-term outcomes for the mothers and their children.

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The definition applies regardless of whether treatment includes diet modification alone or in combination with insulin. It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancy.1

GDM is the most common medical complication and metabolic disorder of pregnancy, occurring in 1–14% of patients depending on the population described and the criteria used for diagnosis.2 Table 1 describes the prevalence of GDM reported by studies3-12 performed at various locations.

Diagnosing and treating pregnancies complicated by GDM is important for preventing adverse perinatal outcomes. Identifying women with GDM who have an increased risk for type 2 diabetes mellitus provides an opportunity to educate, treat, and improve long-term outcome.

The metabolic changes of normal pregnancy are essential to provide adequate nutrients to the growing fetus. Early in pregnancy, maternal estrogen and progesterone increase and promote pancreatic -cell hyperplasia and increased insulin release.13 Increases in peripheral glucose utilization and glycogen storage with a concomitant reduction in hepatic glucose production result in lower maternal fasting glucose levels.14 As pregnancy progresses, increased levels of human chorionic sommatomammotropin (hCS), cortisol, prolactin, progesterone, and estrogen lead to insulin resistance in peripheral tissues.

Table 2 describes the diabetogenic potency and time of peak effect of these hormones.15 Cortisol has the highest diabetogenic potency and has peak effect at 26 weeks gestation. Progesterone also has relatively strong anti-insulin properties that peak at 32 weeks gestation. The timing of these hormonal events is important in regard to scheduling testing for GDM.

The mechanism of insulin resistance is likely a postreceptor defect, since normal insulin binding by insulin-sensitive cells has been demonstrated.16 The pancreas releases 1.5–2.5 times more insulin in order to respond to the resultant increase in insulin resistance.17 Patients with normal pancreatic function are able to meet these demands. Patients with borderline pancreatic function have difficulty increasing insulin secretion and consequently produce inadequate levels of insulin. GDM results when there is delayed or insufficient insulin secretion in the presence of increasing peripheral resistance.

Maternal Morbidity
Maternal morbidity due to GDM may be immediate or long-term. Many studies have documented an increase in pre-eclampsia, polyhydramnios, and operative delivery in pregnancies complicated by GDM.5,18,19 The Toronto Tri-Hospital Gestational Diabetes Project, a prospective cohort study evaluating maternal and fetal outcomes with increasing carbohydrate intolerance, observed a significant association between glucose intolerance and an increased incidence of cesarean delivery, preeclampsia, and length of maternal hospitalization.18

Women with GDM also have a significant risk of developing diabetes later in life. Coustan and associates studied former gestational diabetic women and found diabetes or impaired glucose tolerance (IGT) in 6% of those tested at 0–2 years, 13% at 3–4 years, 15% at 5–6 years, and 30% at 7–10 years postpartum.20 Other studies have documented type 2 diabetes 3–5 years postpartum in 30–50% of women who had a pregnancy complicated by GDM.21,22

Peters and associates found that episodes of insulin resistance due to additional pregnancies increased the rate of developing type 2 diabetes independent of pregnancy-associated weight gain.23 They also found the relative risk for type 2 diabetes was 1.95 for each 10 pounds gained during follow-up after adjusting for the number of pregnancies and other risk factors.23

The implications of GDM are significant, since women with prior GDM are at greater risk for developing hypertension, hyperlipidemia, electrocardiogram abnormalities, and mortality.24 Clark and associates reported that women with GDM have higher triglycerides, free fatty acids, and beta-hydroxybutyrate and lower high-density level (HDL) cholesterol than pregnant control subjects.25 These metabolic differences persisted when body mass index was considered. Meyers-Seifer and associates evaluated women 5–6 years after delivery and documented significantly higher total cholesterol, triglycerides, low-density level (LDL) cholesterol levels, and systolic blood pressure in previous GDM patients.26 These data suggest that women with prior GDM have lipid abnormalities that have been correlated with cardiovascular risk.

Table 1. Prevalence of GDM
Author  Location Prevalence (%)
Abell, Beischer3 Australia 0.7
O’Sullivan4 Boston 2.5
Magee5 Seattle 3.2–5.0
Dooley6 Chicago 3.5–5.5
Sacks7 Los Angeles 3.4
Berkowitz8 Manhattan 4.6
Murphy9 Alaska 5.8
Nahum10 Los Angeles 7.1
Mestman11 Los Angeles 12.3
Benjamin12 Zuni, New Mexico       14.3

Perinatal Morbidity and Mortality
Infants of mothers with GDM (IGDM) are not at increased risk for congenital anomalies unless these women have pre-existing diabetes mellitus. However, IGDM do have an increased risk of perinatal mortality and morbidity, including hyperbilirubinemia, macrosomia and birth trauma, and hypoglycemia.

O’Sullivan observed a fourfold increase in perinatal mortality rates in pregnancies complicated by improperly managed GDM.27 Several other studies have found an increased rate of stillbirths in untreated GDM.3,28 Today, in pregnancies identified and treated appropriately, intrauterine fetal demise is not increased in GDM.2

IGDM have an increased risk of macrosomia, defined as fetal weight >90th percentile for gestational age or >4,000 g.29 Macrosomia complicates ~20% of GDM pregnancies.30 Maternal hyperglycemia leads to fetal hyperglycemia and fetal hyperinsulinemia with subsequent increases in fetal growth. Growth occurs preferentially in adipose and liver tissue, both of which are insulin-sensitive.14

This growth pattern of increased adiposity and organomegaly leads to a disproportionate increase in trunk and shoulder girth compared to head circumference. Consequently, shoulder dystocia is increased two- to sixfold.31 The risk of shoulder dystocia is even further increased in IGDM with fetal weight >4,000 g.31

Brachial plexus injury is one of the most serious complications associated with shoulder dystocia. The incidence increases with fetal weight and occurs in 3–5% of infants weighing <4,500 g and 15–30% of infants weighing >4,500 g.32 Most brachial plexus injuries (80–90%) will completely resolve in the first year, and an additional percentage will have partial recovery. Between 0.2% and 2% will continue to manifest a permanent injury.33

Neonatal hypoglycemia is a common, transient complication in IGDM. It occurs in 50% of macrosomic infants and in 5–15% of infants of mothers with optimally controlled GDM.14 The neonate experiences a drop in blood glucose levels at delivery when the cord is clamped and continues to have exaggerated insulin release secondary to pancreatic -cell hyperplasia. Control of maternal diabetes during the latter half of pregnancy and during labor and delivery influences the occurrence of neonatal hypoglycemia. The frequency of hypoglycemia increases significantly when maternal blood glucose during labor and delivery exceeds 90 mg/dl.34

In addition to the immediate morbidity associated with delivery and the neonatal period, investigators have expressed concern about long-term outcome in children of diabetic mothers. Freinkel postulated that "fuel-mediated teratogenesis" due to abnormal concentrations of maternal glucose, lipids, and amino acids may influence fetal development, leading to changes in metabolism, weight, and behavior.17

Table 2. The Diabetogenic Potency of Hormones in Pregnancy

Hormone  Peak elevation (weeks) Diabetogenic potency
Very weak
Very strong

Adapted from Jovanovic-Peterson L, Peterson C: Review of gestational diabetes mellitus and low-calorie diet and physical exercise as therapy. Diabetes Metab Rev 12:287-308, 1996.

Silverman studied the children of women with both pregestational diabetes and GDM and found IGT in adolescent children was 13 times more frequent than in control adolescents.35 The incidence of IGT in the children was the same for both types of maternal diabetes. Silverman and associates also documented that by 8 years of age, 50% of children of diabetic mothers had weights above the 90th percentile compared to children of women without diabetes.36

Plagemann and associates confirmed that children of mothers with pregestational and GDM have a high incidence of obesity.37 Pettitt and associates studied the children of diabetic Pima Indians from 5 to 19 years of age and found a significantly higher body weight as compared to control subjects.38 They noted that the prevalence of type 2 diabetes was 1.4% in control subjects, 8.6% in children of prediabetic mothers, and 45% in infants of diabetic mothers at 20–24 years of age.38

Intrauterine metabolic experiences may also influence the neurodevelopmental course of children of diabetic mothers. Rizzo and associates studied pregestational and gestational diabetic pregnancies and found that poorer metabolic regulation in the mother was associated with the child’s poorer performance on standard measures of psychomotor development at 6 and 9 years of age.39

Clearly, the detection and appropriate treatment of GDM provides the opportunity to prevent adverse outcomes for both mothers and their children.

Table 3. Diagnostic Criteria for GDM Using the 100 g OGTT
O’Sullivan21* NDDG48** Carpenter and Coustan49**
90 mg/dl
165 mg/dl
145 mg/dl
125 mg/dl
105 mg/dl
190 mg/dl
165 mg/dl
145 mg/dl
95 mg/dl
180 mg/dl
155 mg/dl
140 mg/dl
The diagnosis requires any two values to meet or exceed those listed above.
* Venous whole blood, Somogyi-Nelson analysis.
** Plasma, glucose oxidase.

The NDDG criteria are recommended for the diagnosis of GDM by ACOG and the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus.

In the past, the American College of Obstetricians and Gynecologists (ACOG) recommended that GDM screening be based on risk factor identification. Others have argued that this is inadequate since almost half of all patients with GDM have no identifiable risk factors.2 The latest ACOG Technical Bulletin on Diabetes and Pregnancy suggests that selective screening for GDM is appropriate in some low-risk clinical settings, such as teen clinics. However, universal screening may be more appropriate in other settings.40 Recently, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, working under the sponsorship of the American Diabetes Association (ADA), has stated that universal screening may not be necessary in women who meet all of the following criteria: 1) <25 years of age, 2) normal body weight, 3) no first-degree relatives with diabetes mellitus, 4) not of Hispanic, Native American, Asian, or African-American ethnic groups.41

Proponents of universal screening for GDM emphasize that pregnancy provides a unique opportunity to diagnose a disease that has significant short- and long-term implications for both mothers and children.

Screening for GDM is performed with a 50-g oral glucose load given between 24 and 28 weeks gestation, followed by a 1-hour venous plasma glucose level.40 The screening test is performed at a time when the diabetogenic effects of pregnancy are peaking (Table 2).15 If the test reveals a result >140 mg/dl, the patient is scheduled for a 3-hour, 100-g oral glucose tolerance test (OGTT).40

A threshold of 140 mg/dl identifies 90% of GDM cases with 15% of pregnant patients meeting criteria to take the 3-hour OGTT.40 The sensitivity can be increased further by decreasing the threshold to 130 mg/dl. This cut-off value will increase the number of women who will require a 3-hour OGTT to 25% and, consequently, will increase the cost of identifying each case of GDM.40 Screening after an overnight fast may decrease false negatives and improve the sensitivity of the test.

Patients with high-risk factors, such as a history of a prior macrosomic fetus, chronic steroid use, or a strong family history of diabetes, may benefit from earlier testing, before or at 20 weeks gestation.42 Repeat testing can be done later in pregnancy (around 32–34 weeks) in patients with an initial negative test in the presence other risk factors. In one study, GDM detection increased by ~50% by repeating the test at 33–36 weeks gestation in high-risk individuals (obese, age >33 years, positive 1-hour screen followed by a negative OGTT).43

Assessing blood glucose is also recommended whenever a patient presents with 3+ to 4+ glycosuria on urinanalysis.42 Glycosylated hemoglobin and fructosamine levels do not have adequate sensitivity or specificity to be used as screening tests for GDM.2

A 3-hour OGTT does not need to be conducted in patients with a 1-hour, 50-g plasma glucose screen >185 mg/dl44 or a truly fasting glucose >126 mg/dl.41 Performing a 100-g OGTT when the 1-hour 50-g screening test is >185 mg/dl is likely to produce significant hyperglycemia. In these cases, the diagnosis of GDM can be assumed and therapy initiated.

The 3-hour OGTT should be started in the morning after an overnight fast for at least 8 hours but no more than 14 hours, following at least 3 days of unrestricted diet (>150 g carbohydrate) and physical activity. Venous plasma glucose is measured at fasting and at 1, 2, and 3 hours after a 100-g glucose load. Subjects should remain seated and should not be permitted to smoke tobacco. ACOG and the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus recommend that two or more of the National Diabetes Data Group (NDDG) values be met or exceeded to make the diagnosis of GDM (Table 3).

The diagnostic criteria for GDM are controversial since the currently recommended cutoffs are based on the prediction of subsequent development of diabetes mellitus rather than perinatal outcomes. The initial diagnostic criteria for GDM proposed by O’Sullivan and Mahan were derived from the results of a 3-hour, 100-g OGTT performed on venous whole blood by the Somogyi-Nelson (S-N) technique.21 GDM was diagnosed if two or more blood glucose values were >2 standard deviations above the mean. The diagnostic criteria were chosen by the ability of these results to predict subsequent development of diabetes in these women after pregnancy.

The NDDG revised the criteria in 1979, calculating the equivalent glucose oxidase plasma values from the original data.45 In 1982, Carpenter and Coustan challenged this process.46 Sacks and associates conducted simultaneous determinations using the S-N and glucose oxidase techniques and discovered that the NDDG conversions were above the 95% confidence limits for all but the fasting sample, whereas the Carpenter and Coustan conversions were always within the 95% confidence intervals.47

Many investigators stress the importance of establishing new criteria that are specific to pregnancy and validated by pregnancy outcomes. Several studies have evaluated the current criteria’s ability to predict perinatal outcomes. The Toronto Tri-Hospital Gestational Diabetes Project demonstrated a clear, graded relationship between values on the OGTT and a variety of adverse maternal and fetal outcomes.18 They found an increase in cesarean delivery, macrosomia, preeclampsia, phototherapy, and maternal and neonatal length of hospitalization. Tallarigo and associates and Weiner found that the rate of macrosomia was significantly correlated with the 2-hour value.48,49 Several investigators have found an increased rate of macrosomia is related to a postive glucose challenge followed by a negative OGTT.43,49,50 Even one abnormal GTT value has been related to increased rates of macrosomia.51

Magee and associates compared subjects diagnosed with GDM by the modified Carpenter and Coustan criteria to those diagnosed by the NDDG criteria.5 Using the modified criteria, they found 50% more cases of GDM. The GDM subjects diagnosed by the modified criteria had nearly as many cumulative perinatal morbidities as the NDDG-diagnosed group and significantly more perinatal morbidity than those subjects testing negative. Further studies are needed to confirm this continuous relationship between glucose intolerance and adverse outcomes and to establish appropriate criteria for intervention.

Dietary therapy is the foundation for the treatment of GDM. The ADA has recommended dietary therapy to start with 2,000–2,500 kcal/day (35 kcal/kg present pregnancy weight), with 50–60% carbohydrates (complex, high fiber), 10–20% protein, and 25–30% fat (<10% saturated). New ADA recommendations specify a protein level of 10–20% of calories but now allow greater flexibility in the levels of carbohydrate and fat.52

Jovanovic-Peterson and associates found that the former dietary recommendations lead to significant weight gain and postprandial hyperglycemia requiring insulin therapy in 50% of their patients.53,54 They suggested a diet with less caloric intake calculated by 30 kcal/kg present pregnancy weight for normal-sized individuals, 24 kcal/kg for overweight patients, and 12 kcal/kg for morbidly obese women. The carbohydrate composition was <45% at breakfast, <55% at lunch, and 50% at dinner. Occasionally, the carbohydrate composition was decreased to 33, 45, and 40%, respectively, for further improvement of glycemic control.

Caloric restriction has been studied in obese women with GDM. Restricting caloric intake by 50% (1,200 kcal/day) improves glycemic control but produces ketonemia and ketonuria.55 Therefore, this strategy is not recommended because of potential negative effects on the fetus of increased ketone levels. Moderate (33%) caloric restriction appears to reduce macrosomia rates without adversely affecting neonatal outcomes or causing ketonemia.56

Gunderson recently reviewed intensive nutritional therapy, emphasizing a limit on total carbohydrate and a distribution of carbohydrate throughout the day at several meals and snacks in order to achieve normal blood glucose levels and prevent starvation ketosis.52 Further research evaluating the treatment of GDM with different dietary compositions is needed.

Glucose monitoring should be performed at least weekly with a fasting glucose and postprandial measurement at 1 or 2 hours. However, several studies suggest that more frequent self-monitoring of blood glucose improves glycemic control and decreases adverse pregnancy outcome. de Veciana and associates, in a prospective, randomized trial, found that fasting and 1-hour postprandial glucose monitoring resulted in improved glycemic control and significant decreases in neonatal hypoglycemia, shoulder dystocia, cesarean delivery, birth weight, and percentage of large-for-gestational-age infants when compared with preprandial glucose monitoring.19

Table 4. Initial Insulin Dosing With Three Injections
Type A.M P.M.

4/9 of total insulin
2/9 of total insulin

1/6 of total insulin at bedtime
1/6 of total insulin at dinner

Total daily insulin is calculated by 0.7 U/kg, 0.8 U/kg, 0.9 U/kg, and 1.0 U/kg for 6–18, 18–26, 26–36, and 36–40 weeks, respectively.

Adapted from Jovanovic-Peterson L, Peterson C: Review of gestational diabetes mellitus and low-calorie diet and physical exercise as therapy. Diabetes Metab Rev 12:287-308, 1996

Langer and associates performed a prospective trial comparing a group using conventional management (defined as four home blood glucose tests [fasting and 2-hour postprandial] in addition to weekly fasting blood glucose and 2-hour postprandial levels at the office) versus an intensified management group given memory reflectance meters and instructed to measure seven times daily (fasting, preprandial, 2-hour postprandial, and bedtime).57 Significantly more patients in the intensified group were placed on insulin therapy, and this group had fewer cesarean deliveries and less macrosomia and shoulder dystocia. This study suggests that the conventional method failed to recognize inadequately treated patients, resulting in higher perinatal morbidity.

The ACOG criteria for initiating insulin therapy include a fasting plasma glucose level >105 mg/dl and 2-hour plasma postprandial levels >120 mg/dl.40 It is important to recognize the data suggesting that insulin therapy may achieve lower rates of macrosomia if initiated when fasting blood glucose is >95 mg/dl.58 However, prophylactic insulin treatment in patients whose fasting and postprandial values remain within the recommended range is not advised.

Hospitalization is occasionally necessary to establish optimal control. Total insulin doses can be calculated and given with split dosing by three injections (Table 4). If insulin is required, the target plasma glucose levels are fasting glucose value 60–90 mg/dl, preprandial value 60–105 mg/dl, 2-hour postprandial value <120 mg/dl, 1-hour postprandial value not >130–140 mg/dl, and 2–6 a.m. value 60–90 mg/dl.40

Lispro insulin has a rapid onset, earlier peak, and shorter duration of effect than regular insulin. This pattern of action is similar to healthy pancreatic insulin release in response to a meal.59 Lispro is considered a pregnancy category B drug.60 Animal studies have been performed in pregnancy without any increase in adverse outcomes. Recently, a letter in the New England Journal of Medicine described two cases of congenital anomalies in patients taking lispro.61 Case reports of congenital anomalies in diabetic patients must be viewed with caution, since the baseline risk of malformations is higher in these patients over the general population. Additional study of this insulin in the treatment of diabetes in pregnancy is encouraged.

Exercise has been suggested as a adjuvant therapy in GDM, since glycemic control has been shown to improve with exercise regimens in nonpregnant patients. Jovanovic-Peterson and associates studied 19 women with GDM, assigning 9 to dietary treatment and 10 to diet plus 20 minutes of monitored exercise 3 times a week for 6 weeks.62 They found a significantly lower OGTT and fasting blood glucose in patients assigned to the exercise group beginning 6 weeks after initiating therapy. Avery and associates randomized 33 women to an exercise regimen of 30 minutes 4–3 times a week (under observation by an investigator at the patient’s home only twice per week).63 However, they did not find any difference in the glycemic control between the groups. While more studies are needed, a program of moderate, regular exercise seems appropriate in the management of GDM.

Oral hypoglycemic agents currently are not used in treating GDM. Because these medications cross the placenta and could stimulate the fetal pancreas, tolbutamide, chloropropamide, and other sulfonylureas are not used in pregnancy.58 Glyburide does not cross the placenta in significant amounts and may have a future role in the management of GDM.58

Delivery Timing
Patients with uncomplicated, diet-controlled GDM are allowed to progress to term unless other complications arise. Amniocentesis should be performed to document fetal pulmonary maturity if delivery before 39 weeks gestation is indicated. Fetal surveillance should begin at 40 weeks gestation with twice weekly nonstress testing in pregnancies complicated by diet-controlled GDM. Antenatal testing should be initiated earlier, at 32 weeks gestation, in GDM patients requiring insulin or in pregnancies complicated by hypertension or a prior stillbirth. Fetal movement counting should be performed by all patients after 28 weeks gestation.

Studies have documented an increase in the rate of shoulder dystocia when the birth weight of IGDM exceeds 4,000 g. Consequently, estimated fetal weight plays an important role in the decision-making process for route of delivery. When it is suspected that the fetal weight is >4,250–4,500 g, cesarean delivery should be considered.31 Providers must remember that ultrasonography has a range of error of 10–15% in estimating fetal weight at term.

During labor and delivery, maternal plasma glucose levels are monitored at the bedside every 1–2 hours. Plasma glucose levels should be kept <90 mg/dl in order to decrease the risk or severity of neonatal hypoglycemia.34

The postpartum follow-up of women with GDM is crucial, since some of these women manifest IGT or diabetes mellitus. All should receive contraceptive advice and counseling regarding future pregnancies. Screening for diabetes can be performed at the 6-week postpartum visit, using the criteria established by the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (Table 5).41

Table 5. Diagnostic Criteria for Diabetes Mellitus and IGT
Diagnosis Fasting glucose (mg/dl) Casual glucose (mg/dl) 75-g 2-hour OGTT
>110 and <126mg/dl
>126 mg/dl

200 mg/dl+ symptoms
>140 and <200mg/d >200mg/dl

Adapted from the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 20:1183-97, 1997.


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Kjos and associates evaluated women between the fifth and eighth week postpartum with a 2-hour OGTT and found 81% of patients had normal or unclassifiable OGTT results.64 An additional 10% had IGT, and the remaining 9% had diabetes mellitus. Forty-four percent of women with fasting glucose levels >140 mg/dl had diabetes diagnosed by an OGTT at their initial postpartum visit. These researchers also suggest that routine testing should be performed even in patients with a history of diet-controlled GDM, since they found a 2% prevalence of diabetes mellitus and an 8% prevalence of IGT in these women.

These patients should be informed of their risk of developing type 2 diabetes and educated on the behaviors that may prevent or delay the disease progression. If the postpartum evaluation is normal, patients should be instructed on the symptoms of diabetes and have an annual evaluation of glucose metabolism by a fasting plasma glucose level. Weight loss, exercise, and tobacco cessation should be encouraged, since these lifestyle interventions can reduce overall diabetic morbidity and improve glycemic control. Gregory and associates presented an economic model of the health care dollars and postulated that $32, $140, or $331 million health care dollars could be saved over 10 years, assuming the incidence of diabetes could be reduced by 10, 25, or 50%, respectively, by promoting lifestyle changes in women diagnosed with GDM.65

GDM occurs in women who have insulin resistance and a relative impairment of insulin secretion. These women have a significant risk of developing diabetes later in life. Identifying this group of women is important in not only preventing perinatal morbidity but also improving long-term outcomes for the mother and her children. There continues to be a lack of consensus on the diagnostic criteria and optimal therapy for GDM. Currently, ACOG, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, and the Third International Workshop Conference sponsored by the ADA support the screening indications, diagnostic criteria, and management recommendations mentioned above (Table 3, Figure 1, and dietary intervention from ref. 54). Continued research is imperative to establish diagnostic criteria and management based on maternal and fetal outcomes.


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58Langer O: Management of gestational diabetes. Clin Perinatol 20:1-15, 1993.

59Holleman F, Hoekstra J: Insulin lispro. N Engl J Med 337:176-83, 1997.

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63Avery MD, Leon AS, Kopher RA: Effects of a partially home-based exercise program for women with gestational diabetes. Obstet Gynecol 89:10-15, 1997.

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Darcy Barry Carr, MD, is a maternal-fetal medicine fellow and Steven Gabbe, MD, is chairman of the Department of Obstetrics and Gynecology at the University of Washington School of Medicine in Seattle.

Copyright 1998 American Diabetes Association

Last updated: 1/98
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