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Darcy Barry Carr, MD, and Steven Gabbe, MD
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 114% 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.
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 1.52.5 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.
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 02 years, 13% at 34 years, 15% at 56 years, and 30% at 710 years postpartum.20 Other studies have documented type 2 diabetes 35 years postpartum in 3050% 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 56 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.
Perinatal Morbidity and Mortality
OSullivan 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 35% of infants weighing <4,500 g and 1530% of infants weighing >4,500 g.32 Most brachial plexus injuries (8090%) 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 515% 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 ß-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
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 2024 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 childs 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.
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 3234 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 3336 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 OSullivan 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 criterias 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.
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
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 6090 mg/dl, preprandial value 60105 mg/dl, 2-hour postprandial value <120 mg/dl, 1-hour postprandial value not >130140 mg/dl, and 26 a.m. value 6090 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 43 times a week (under observation by an investigator at the patients 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
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 >4,2504,500 g, cesarean delivery should be considered.31 Providers must remember that ultrasonography has a range of error of ±1015% in estimating fetal weight at term.
During labor and delivery, maternal plasma glucose levels are monitored at the bedside every 12 hours. Plasma glucose levels should be kept <90 mg/dl in order to decrease the risk or severity of neonatal hypoglycemia.34
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
1Metzger BE, Organizing Committee: Summary and recommendations of the Third International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes 40:197-201, 1991.
2Coustan DR: Gestational diabetes. In Diabetes in America, 2nd Edition. Harris MI, Cowie CC, Stern MP, Boyko EJ, Reiber GE, Bennett PH, Eds. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 1995, p. 703-17.
3Abell DA, Beischer NA: Evaluation of the three-hour oral glucose tolerance test in detection of significant hyperglycemia and hypoglycemia in pregnancy. Diabetes 24:874-80, 1973.
4OSullivan JB, Mahan CM, Charles D, Dandrow R: Screening criteria for high-risk gestational diabetic patients. Am J Obstet Gynecol 116:895-900, 1973.
5Magee MS, Walden CE, Benedetti TJ, Knopp RH: Influence of diagnostic criteria on the incidence of gestational diabetes and perinatal morbidity. JAMA 269:609-15, 1993.
6Dooley SL, Metzger BE, Cho NH: Gestational diabetes mellitus: influence of race on disease prevalence and perinatal outcomes in a U.S. population. Diabetes Care 40 (Suppl. 2):25-29, 1991.
7Sacks DA, Abu-Fadil S, Karten GJ, Forsythe AB, Hackett JR: Screening for gestational diabetes with the one-hour 50 g glucose test. Obstet Gynecol 70:89-93, 1987.
8Berkowitz GS, Roman SH, Lapinski RH, Alvarez M: Maternal characteristics, neonatal outcome, and the time of diagnosis of gestational diabetes. Am J Obstet Gynecol 167:976-82,1992.
9Murphy NJ, Bulkow LR, Schraer CD, Lanier AP: Prevalence of diabetes mellitus in pregnancy among Yupik Eskimos, 1987-1988. Diabetes Care 16 (Suppl. 1):315-17, 1993.
10Nahum GG, Huffaker BJ: Correlation between first- and early third-trimester glucose screening test results. Obstet Gynecol 76:709-13,1990.
11Mestman JH: Outcome of diabetes screening in pregnancy and perinatal morbidity in infants of mothers with mild impairment in glucose tolerance. Diabetes Care 3:447-52, 1980.
12Benjamin E, Winters D, Mayfield J, Gohdes D: Diabetes in pregnancy in Zuni Indian women. Diabetes Care 16:1231-35, 1993.
13Kuhl C, Holst JJ: Plasma glucagon and insulin: glucagon ratio in gestational diabetes. Diabetes 25:16, 1976.
14Landon MB: Diabetes mellitus and other endocrine diseases. In Obstetrics Normal and Problem Pregnancies, 3rd Edition. Gabbe SG, Niebyl JR, Simpson JL, Eds. New York, Churchill Livingstone, 1996, p. 1037-81.
15Jovanovic-Peterson L, Peterson CM: Review of gestational diabetes mellitus and low-calorie diet and physical exercise as therapy. Diabetes Metab Rev 12:287-308, 1996.
16Puavalai G, Drobry EC, Domont LA, Baumann G: Insulin receptors and insulin
resistance in human pregnancy: evidence for a post receptor defect in insulin action.
17Freinkel N: Banting Lecture 1980: Of pregnancy and progeny. Diabetes 29:1023-35, 1980.
18Sermer M, Naylor D, Gare DJ, Kenshole AB, Ritchie JWK, Farine D, Cohen HR, McArthur K, Holzapfel S, Biringer A, Chen E, for the Toronto Tri-Hopital Gestational Diabetes Investigators: Impact of increasing carbohydrate intolerance on maternal-fetal outcomes in 3,637 women without gestational diabetes. Am J Obstet Gynecol 173:146-56, 1995.
19de Veciana M, Major CA, Morgan MA, Asrat T, Toohey JS, Lien JM, Evans AT: Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy. N Engl J Med 333:1237-41, 1995.
20Coustan DR, Carpenter MW, OSullivan PS, Carr SR: Gestational diabetes mellitus: predictors of subsequent disordered glucose metabolism. Am J Obstet Gynecol 168:1139-45, 1993.
21OSullivan JB, Mahan CM: Criteria for the oral glucose tolerance test in pregnancy. Diabetes 13:278-85, 1964.
22Mestman JH, Anderson GV, Guadalupe V: Follow-up study of 369 subjects with abnormal carbohydrate metabolism during pregnancy. Obstet Gynecol 39:421-25, 1972.
23Peters RK, Kjos SL, Xiang A, Buchanan TA: Long-term diabetogenic effect of single pregnancy in women with previous gestational diabetes mellitus. Lancet 347:227-30, 1996.
24OSullivan JB: Subsequent morbidity among GDM women. In Carbohydrate Metabolism in Pregnancy and the Newborn. Sutherland HW, Stowers JM, Eds. New York, Churchill Livingstone, 1984, p. 174-80.
25Clark CM Jr, Qiu Chunfu, Amerman B, Porter B, Fineberg N, Aldasouqi S, Golichowski A: Gestational diabetes: should it be added to the syndrome of insulin resistance? Diabetes Care 20:867-71, 1997.
26Meyers-Seifer CH, Vohr BR: Lipid levels in former gestational diabetic mothers. Diabetes Care 19:1351-56, 1996.
27OSullivan JB, Charles D, Mahan CM, Dandrow RV: Gestational diabetes and perinatal mortality rate. Am J Obstet Gynecol 116:901-904, 1973.
28Pettitt DJ, Knowler WC, Baird HR, Bennett PH: Gestational diabetes: infant and maternal complications of pregnancy in relation to third-trimester glucose tolerance in Pima Indians. Diabetes Care 3:458-64, 1980.
29Hod M, Rabinerson D, Peled Y: Gestational diabetes mellitus: is it a clinical entity? Diabetes Reviews 3:602-13, 1995.
30Gabbe SG, Mestman JH, Freeman RK: Management and outcome of Class A diabetes mellitus. Am J Obstet Gynecol 127:465-69, 1977.
31American College of Obstetricians and Gynecologists: Shoulder Dystocia. ACOG Practice Patterns #7. Washington, DC, ACOG, 1997.
32Benedetti TJ: Dystocia: causes, consequences, correct response. Contemp OB/GYN 36:37-48, 1991.
33Blank A, Grave GD: Effects of gestational diabetes on perinatal morbidity reassesed. Report of the International Workshop on Adverse Perinatal Outcomes of Gestational Diabetes Mellitus, December 3-4, 1992. Diabetes Care 18:127-29, 1995.
34Kuhl C, Andersen GE, Hertel J, Molsted-Pedersen L: Metabolic events in infants of diabetic mothers during first 24 hours after birth. Acta Paediatr Scand 71:19-25, 1982.
35Silverman BL, Metzger BE, Cho NH, Loeb CA: Impaired glucose tolerance in adolescent offspring of diabetic mothers. Diabetes Care 18:611-17, 1995.
36Silverman BL, Rizzo T, Green OC, Cho NH, Winter RJ, Ogata ES: Long-term prospective evaluation of offspring of diabetic mothers. Diabetes 40:121-25, 1991.
37Plagemann A, Harder T, Kohlhoff R, Rohde W, Dorner G: Overweight and obesity in infants of mothers with long-term insulin-dependent diabetes or gestational diabetes. Int J Obesity 21:451-56, 1997.
38Pettitt DJ, Knowler WC, Bennett PH, Aleck KA, Baird HR: Obesity in offspring of diabetic Pima Indian women despite normal birth weight. Diabetes Care 10:76-80, 1987.
39Rizzo T, Dooley SL, Metzger BE, Cho NH, Ogata ES, Silverman BL: Prenatal and perinatal influences on long-term psychomotor development in offspring of diabetic mothers. Am J Obstet Gynecol 173:1753-58, 1995.
40American College of Obstetricians and Gynecologists: Diabetes and Pregnancy. ACOG Technical Bulletin # 200. Washington, DC, ACOG, 1994.
41Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 20:1183-97, 1997.
42Gabbe SG: Identifying patients with GDM. OB/Gyn Clin Alert, May 1993.
43Jovanovic L, Peterson CM: Screening for gestational diabetes: optimum timing and criteria for retesting. Diabetes 4 (Suppl. 2):21-23, 1985.
44Landy HJ, Gomez-Marin O, OSullivan MJ: Diagnosing gestational diabetes mellitus: use of a glucose screen without administering the glucose tolerance test. Obstet Gynecol 87:395-400, 1996.
45National Diabetes Data Group: Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 28:1039-57, 1979.
46Carpenter MW, Coustan DR: Criteria for screening tests for gestational diabetes. Am J Obstet Gynecol 144:768-73, 1982.
47Sacks DA, Abu-Fadil S, Greenspoon JS, Fotheringham N: Do the current standards for glucose tolerance testing represent a valid conversion of OSullivans original criteria? Am J Obstet Gynecol 161:638-41, 1989.
48Tallarigo L, Giampietro O, Penno G, Miccoli R, Gregori G, Navalesi R: Relation of glucose tolerance to complications of pregnancy in nondiabetic women. N Engl J Med 315:989-92, 1986.
49Weiner CP: Effect of varying degrees of normal glucose metabolism on maternal and perinatal outcome. Am J Obstet Gynecol 159:862-70, 1988.
50Leikin EL, Jenkins JH, Pomerantz GA, Klein L: Abnormal glucose screening tests in pregnancy: a risk factor for fetal macrosomia. Obstet Gynecol 569:570-73, 1987.
51Langer O, Brustman L, Anyaegbunam A, Mazze R: The significance of one abnormal glucose tolerance test value on adverse outcome in pregnancy. Am J Obstet Gynecol 157:758-63, 1987.
52Gunderson EP: Intensive nutrition therapy for gestational diabetes. Diabetes Care 20:221-26, 1997.
53Jovanovic-Peterson L, Peterson CM: Dietary manipulation as a primary treatment strategy for pregnancies complicated by diabetes. J Am Coll Nutr 9:320-25, 1990.
54Mulford MI, Jovanovic-Peterson L, Peterson CM: Alternative therapies for the management of gestational diabetes. Clin Perinatol 20:619-34, 1993.
55Magee MS, Knopp RH, Benedetti TJ: Metabolic effects of 1200 kcal diet in obese pregnant women with gestational diabetes. Diabetes 39:234-40, 1990.
56Knopp RH, Magee MS, Raisys V: Hypocaloric diets and ketogenesis in the management of obese gestational diabetic women. J Am Coll Nutr 10:649-67, 1991.
57Langer O, Rodriguez DA, Xenakis EMJ, McFarland MB, Berkus MD, Arredondo F: Intensified versus conventional management of gestational diabetes. Am J Obstet Gynecol 170:1036-47, 1994.
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.
60Humalog package insert, Indianapolis, Indiana, Eli Lilly and Company.
61Diamond T, Kormas N: Possible adverse fetal effect of insulin lispro. N Engl J Med 337:1009, 1997.
62Jovanovic-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 161:415-19, 1989.
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.
64Kjos SL, Buchanan TA, Greenspoon JS, Montoro M, Bernstein GS, Mestman JH: Gestational diabetes mellitus: the prevalence of glucose intolerance and diabetes mellitus in the first two months postpartum. Obstet Gynecol 163:93-98, 1990.
65Gregory KD, Kjos SL, Peters RK: Cost of non-insulin-dependent diabetes in women with a history of gestational diabetes: implications for prevention. Obstet Gynecol 81:782-86, 1993.
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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