These pages are best viewed with Netscape version 3.0 or higher or Internet Explorer version 3.0 or higher. When viewed with other browsers, some characters or attributes may not be rendered correctly.Summary and Recommendations of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus Boyd E. Metzger, MD INTRODUCTION— The Fourth International Workshop-Conference on Gestational Diabetes Mellitus (GDM) was convened in Chicago, Illinois, on 14 March 1997, under the sponsorship of the American Diabetes Association. The meeting provided a forum for review of new information concerning GDM in the areas of diagnosis and prevalence, perinatal and long-range implications for the mother and her offspring, and management strategies. There is a general consensus that the prevalence of GDM is increasing globally, but there is considerable controversy about the clinical importance of GDM and the magnitude of its impact on mother and offspring. Lack of uniformity in approach to detection and diagnosis of GDM has hampered efforts to resolve these issues. The Summary and Recommendations of the Third International Workshop-Conference on Gestational Diabetes Mellitus emphasized the critical importance of developing new diagnostic criteria that are based on the potential to detect pregnancies at risk for adverse perinatal outcome as a result of maternal hyperglycemia, rather than placing primary emphasis on the identification of mothers at risk for progression to diabetes outside of pregnancy. This objective has not yet been fulfilled; however, efforts are being made to address this via a multicenter study. Conference participants reviewed data indicating that degrees of glucose intolerance less severe than the currently recommended National Diabetes Data Group (NDDG) criteria for GDM (1) may be associated with an increased risk of adverse perinatal outcome. Extrapolation from the whole blood glucose values found by O'Sullivan and Mahan (2) to plasma or serum glucose concentrations to take into account the specific enzymatic methods currently in use, as proposed by Carpenter and Coustan (3), yields lower values for abnormal plasma glucose concentrations and increases the number of pregnancies defined as GDM. Additional studies have been performed, using approaches similar to that of O'Sullivan in his original study, to define abnormal 75-g oral glucose tolerance test (OGTT) values in different populations. This approach has yielded values for plasma glucose concentrations that are similar to the Carpenter/Coustan extrapolations of the 100-g OGTT. The conference participants concluded that the use of either a 100-g or a 75-g diagnostic test is acceptable, pending the development of criteria specifically relating glycemia to adverse pregnancy outcome. Reports indicate that when GDM is diagnosed and treated intensively, the risk of intrauterine fetal death is not greater than that of the general obstetric population, and the overall frequency and severity of perinatal morbidities are less when GDM is managed intensively than when GDM is not managed intensively. Fetal size in excess of that expected for gestational age, primarily resulting from an increase in adipose tissue mass, remains the greatest source of perinatal morbidity in GDM, in particular leading to higher rates of cesarean delivery and birth trauma. There is a need for more accurate estimation of the fetus at risk for birth trauma. Well-standardized neonatal anthropometry can provide a good indication of body composition of the newborn infant. There is ample evidence that intensive treatment of hyperglycemia in women with GDM can markedly reduce the risk of excessive size for gestational age. However, many fetuses of women with GDM are not at high risk for excess growth. Estimation of fetal size by serial ultrasonography may improve our ability to identify the majority of pregnancies that are not at increased risk for macrosomia and birth trauma so the most intensive therapies can be directed to "at-risk" pregnancies. Others have used detailed assessments of maternal glycemia or measurement of amniotic fluid insulin concentration to select a subgroup that is treated more intensively. Utility, cost-effectiveness, safety, and perinatal and long-term outcomes with these different approaches must be evaluated. Long-term follow-up studies indicate the potential for increased risk of obesity and glucose intolerance in offspring of mothers with diabetes, including GDM, present during the index pregnancy. Studies are needed to assess these risks for long-term adverse outcomes in additional populations and in relation to degree of metabolic abnormality of GDM. Data from many different populations in which varying diagnostic
paradigms were used during pregnancy indicate that GDM identifies women at risk for
development of diabetes later in life. The severity of glucose intolerance at the time of
diagnosis of GDM or at initial postpartum evaluation, gestational age at diagnosis,
impaired SUMMARY AND RECOMMENDATIONS— The invited lectures and discussions and the posters submitted by participants stimulated dialog among conferees that culminated in detailed deliberations by four panels. The invited manuscripts that were edited and submitted to peer review are contained in this supplement to Diabetes Care. The edited reports of the four panels have been synthesized into the following report. PANEL I: DIAGNOSIS AND PREVALENCE Members Definition Women who are found to have fasting hyperglycemia or abnormal carbohydrate tolerance in the 1st trimester of pregnancy may have preexisting diabetes and should be treated in the same fashion as women who are known to have diabetes before pregnancy. At 6–12 weeks postpartum, all patients who had carbohydrate intolerance during pregnancy (GDM) should be evaluated and reclassified as indicated in Table 1. Those who do not have diabetes at this time should be evaluated for diabetes at least annually.
Diagnosis In the summary and recommendations of earlier workshop-conferences (4–6), screening for GDM was recommended in all pregnancies. Universal screening or diagnostic testing is still recommended for women in ethnic groups with relatively high rates of carbohydrate intolerance during pregnancy and of diabetes later in life. This would include women of Hispanic, African, Native American, South or East Asian, Pacific Islands, or Indigenous Australian ancestry, particularly when they reside in Westernized countries or in an urban setting. Conversely, certain features place women at low risk for GDM, and it may not be cost-effective to screen these patients. Those at low risk include women who are not members of ethnic groups at increased risk for development of type 2 diabetes, who have no previous history of abnormal glucose tolerance or poor obstetric outcomes usually associated with GDM, and who have all of the following characteristics: age <25 years, normal body weight, and no family history of diabetes. A strategy for detecting GDM that is based on an assessment of risk for GDM is outlined in Table 2. Women with GDM in a previous pregnancy who are found to have abnormal glucose metabolism in a subsequent pregnancy should be considered to have diabetes rather than GDM recurring in the latter pregnancy unless it can be verified that glucose tolerance was normal outside of pregnancy.
Women at high risk for GDM because of marked obesity, a strong family history of type 2 diabetes, personal history of GDM, glucose intolerance, or glucosuria should be evaluated for glucose intolerance as early in pregnancy as possible. A standard 50-g glucose challenge (see below) can be used in these cases. A plasma concentration >200 mg/dl (11.1 mmol/l) under any conditions outside of the context of a formal glucose challenge test suggests a diabetic state and warrants confirmatory evaluation as quickly as possible. A fasting plasma glucose concentration >126 mg/dl (7.0 mmol/l) also meets the threshold for a diagnosis of diabetes and should be confirmed or excluded as soon as feasible by retesting after an overnight fast of 8–14 h.
Evaluation for GDM should be performed between 24 and 28 weeks' gestation in those women not known to have carbohydrate intolerance before the 24th week of gestation. This evaluation may be done in one or two steps. In the two-step procedure, a 50-g oral glucose challenge test (GCT) is followed by a diagnostic OGTT if results of the GCT exceed a predetermined plasma glucose concentration. In the one-step approach, the diagnostic OGTT is administered to all subjects. Various factors determine which method is preferred in a given setting: expected prevalence of GDM, relative cost and patient acceptance of a test that must always be done in the fasted state versus a two-step process for those who test positive at the first step. When the two-step method is used, the GCT is performed without regard to the time of day or time of last meal. Plasma glucose is measured 1 h after ingestion of the glucose load. A value of >140 mg/dl (7.8 mmol/l) identifies a subgroup of women (14–18% of most populations of pregnant women) at risk for GDM. That subgroup includes ~80% of all women with GDM. Using a value of >130 mg/dl (7.2 mmol/l) to define a positive GCT can increase the yield to >90%, but the subgroup with a positive screening test will increase to 20–25% of all pregnant women. Women with a GCT result above the selected threshold require a diagnostic OGTT (Tables 3 and 4). This test should be performed in the morning after an overnight fast of at least 8 h but not more than 14 h and after at least 3 days of unrestricted diet ( >150 g carbohydrate per day) and physical activity. The subject should remain seated and should not smoke throughout the test.
The cutoff values for the 100-g OGTT derived from the original work of O'Sullivan and Mahan (2) designate a population at increased risk for perinatal morbidity as well as the development of type 2 diabetes later in life. The criteria extrapolated from the O'Sullivan and Mahan data by Carpenter and Coustan (3) are lower than the NDDG criteria and therefore result in a higher prevalence of GDM. However, data presented at the workshop-conference indicated that the infants of women who meet these lower criteria are at similar risk for perinatal morbidity, including macrosomia, as those patients identified using the NDDG criteria. Thus, the Carpenter and Coustan criteria (Table 3) were recommended for interpretation of the 100-g OGTT. Cutoff values for the 75-g 2-h OGTT in pregnancy are, of necessity, arbitrary. The lack of definitive data relating such test results to perinatal outcome made it difficult for the panel and the Organizing Committee to arrive at a consensus. Sacks et al. (7) reported results of 75-g 2-h OGTTs in 3,505 pregnant women in Los Angeles, CA. The patient population used in this study had a high prevalence of obesity and of a family history of type 2 diabetes. In an earlier study of the 75-g 2-h OGTT in pregnancy, the Diabetic Pregnancy Study Group of the European Association for the Study of Diabetes found that 10% of a diverse European population had 2-h values >144 mg/dl (8.0 mmol/l) and adopted a cutoff value of 162 mg/dl (9.0 mmol/l). The cutoff values to define GDM on the 75-g test (Table 4) were selected to represent the mean plus 1.5 SDs of the OGTT values in the study of Sacks et al.; however, the 2-h cutoff was raised to 155 mg/dl (8.6 mmol/l) to be more consistent with the 2-h cutoff value that is recommended for the 100-g OGTT (Table 3) and the practices of the European Association for the Study of Diabetes. Recommendations for the future PANEL II: PERINATAL IMPLICATIONS Members Implications The optimal timing of delivery and the need for labor induction and cesarean delivery are controversial. Consequences of excessive fetal growth include birth trauma and maternal morbidity from operative delivery. The cesarean delivery rate is increased in patients with GDM, in part to avoid birth trauma. Knowledge that a mother has GDM or is treated with insulin may also play a role in increasing the rate of cesarean delivery. Other significant neonatal morbidities include hypoglycemia, hyperbilirubinemia, hypocalcemia, and polycythemia. Incidence and severity of morbidities are dependent on gestational age at delivery as well as on metabolic factors. Although a precise definition of neonatal hypoglycemia is not universally accepted, development of neonatal hypoglycemia should be confirmed by accurate laboratory measurement of plasma glucose and not made solely with the use of glucose reagent strips and meter. GDM with onset in late pregnancy is not associated with an increased incidence of congenital malformations. However, data were presented indicating that preexisting diabetes, diagnosed for the first time during pregnancy as GDM with fasting plasma glucose >120 mg/dl (6.7 mmol/l), may be associated with a rate of anomalies that is higher than in the general obstetrics population. Infants of mothers with GDM should not be discharged from the hospital until they are adequately evaluated for the presence of morbidities. Recommendations for the future PANEL III: THERAPEUTIC INTERVENTIONS DURING PREGNANCY Members Metabolic management Nutritional therapy. Medical nutritional therapy is the cornerstone of treatment for GDM. However, relatively little information is available to allow evidence-based recommendations regarding specific dietary approaches to the management of GDM. Consequently, medical nutritional therapy (prescribed by a qualified individual with experience in the management of GDM) should be used as a tool to achieve glycemic goals without inducing excessive ketonemia and ketonuria. Nutritional prescriptions should be individualized to take into account the patient's body habitus, weight gain, and physical activity and should be modified as needed throughout pregnancy to achieve treatment goals. The nutritional prescription should fulfill minimum requirements for pregnancy and should be culturally appropriate. Because there normally is an inverse relationship between pre-pregnancy body weight and optimal weight gain during pregnancy, expected weight gain varies according to the pre-pregnancy weight. A relatively small gain of ~7 kg is recommended for patients who are obese (BMI >29 kg/m2) when they become pregnant, and a proportionally greater weight gain (up to 18 kg) is recommended for patients who are underweight (BMI <19.8 kg/m2) at the onset of pregnancy. Overweight women generally manifest a lowering of glycemia during caloric restriction, supporting the use of moderate caloric restriction to treat those women as long as sufficient calories are provided to prevent excess fat catabolism and ketonuria. No agreement was reached on a minimum caloric requirement for women with GDM, but evidence was cited that diets providing as little as 25 kcal/kg actual body weight have been used with little risk of ketonuria. Limiting carbohydrate intake to 35–45% of total calories (protein 20–25%, fat 35–40%) has been reported to reduce postprandial glycemia compared with diets higher in carbohydrate content. Use of complex carbohydrate was supported, based on the propensity for simple carbohydrates to increase postprandial glycemia, even though the efficacy of complex carbohydrates in reducing perinatal problems has not been tested. Iron was recommended as a nutritional supplement in women at risk for iron deficiency. Other nutritional supplements should be administered according to individual needs. Metabolic surveillance. Self-monitoring of blood glucose appears to be superior to less frequent glucose monitoring in the clinic for detection of glucose concentrations that may warrant intensification of therapy beyond standard dietary management. Urine glucose monitoring is not useful in the management of GDM. Postprandial glucose levels may be more closely related to fetal risks than are fasting levels. Thus, it was recommended that glucose monitoring include postprandial testing and not be confined to fasting and/or premeal testing. No consensus was reached regarding the optimal timing of the postprandial measurements. Post-meal measurements (1-h or 2-h) are used most commonly. When self-monitoring of blood glucose is employed, measures should be in place to assure accuracy of the results, such as the use of meters that store results electronically for review by health care providers. Ongoing validation of the accuracy of patients' monitoring techniques is also important in this regard. Pre-breakfast urine ketone measurements were recommended for patients receiving hypocaloric or carbohydrate-restricted diets to allow the detection and treatment of ketonuria from accelerated fat catabolism. However, the effectiveness of urine ketone monitoring in improving fetal outcome has not been tested. Insufficient data were available to determine whether measurements of glycated hemoglobin or other circulating proteins are of value in the routine management of GDM. However, it was felt that the hypothesis that a relatively low glycated hemoglobin concentration can identify a subgroup of patients with no excess risk of fetal complications on diet therapy alone warrants further investigation. Intensified metabolic therapy. Patients who fail to achieve or maintain glycemic goals or who show signs of excessive fetal growth should receive treatment in addition to standard nutritional management. Treatment with insulin has been used most frequently in such circumstances, and data were presented demonstrating cost-effectiveness in the prevention of fetal complications with maternal insulin therapy. There are no data demonstrating superiority of a particular insulin regimen in GDM. It was recommend that insulin administration be individualized to achieve the glycemic goals stated above. New rapid-acting insulin analogs with peak hypoglycemic action 1–2 h after injection offer the potential for improved control of postprandial glucose excursions, but superiority of these preparations compared with other short-acting insulin preparations in improving perinatal outcome remains to be established. Minimally antigenic insulin preparations were recommended to minimize the transplacental transport of anti-insulin antibodies and the risk of future allergic manifestations in women who develop diabetes requiring insulin therapy after pregnancy. Regular aerobic exercise has been shown to lower fasting and postprandial glucose concentrations in several small studies of previously sedentary individuals. Thus, exercise may be used as an adjunct to nutritional therapy to improve maternal glycemia. The relative impact on fetal outcome of exercise as compared with insulin treatment has not been evaluated. The optimal frequency and intensity of exercise for lowering of maternal glucose concentrations have not been determined, but it appears that a minimum of three episodes of exercise per week, each >15 min, are required to modify maternal glucose levels; 2–4 weeks may be required before a lowering of glycemia occurs. Insufficient evidence exists to recommend any specific type of exercise as being superior to others in the management of GDM. Labor and delivery. Poor metabolic control in late gestation promotes fetal hyperinsulinism and neonatal hypoglycemia, but it is difficult to assess this risk prospectively. Maternal hyperglycemia during labor should be avoided because it may potentiate the risk of neonatal hypoglycemia and accentuate the rise in lactate and decline in pH that normally accompany any fetal hypoxia. In the absence of specific data indicating an optimal range of maternal glycemia during labor, a target range of 80–120 mg/dl (4.4–6.7 mmol/l) for plasma or 70–110 mg/dl (3.9– 6.1 mmol/l) for capillary blood glucose concentrations was recommended. Women with GDM, including those who receive insulin therapy before labor, rarely require exogenous insulin during labor. Thus, it was recommended that capillary or venous plasma glucose levels be monitored at 1- to 4-h intervals from the onset of spontaneous or induced labor and that insulin be administered only if maternal glycemia exceeds the target range. For women with GDM undergoing elective cesarean delivery, insulin can be withheld on the morning of the operation unless the fasting glucose is above the target range. In either setting, sufficient glucose should be administered parenterally to meet basal energy requirements (0.12–0.18 g/kg body weight per h) and to keep capillary or venous plasma glucose concentrations from falling below the target range. Administration of other glucose-containing fluids should be avoided. Women with GDM rarely require exogenous insulin immediately after delivery. Obstetric management Fetal surveillance. Decisions regarding the commencement and frequency of fetal surveillance should be influenced by the severity of maternal hyperglycemia and the presence of other adverse clinical factors, such as past poor obstetric history or coincident hypertensive disorders. At a minimum, mothers with GDM should be taught to monitor fetal movements during the last 8–10 weeks of pregnancy and to report immediately any reduction in the perception of fetal movements. Although no data were available to demonstrate the optimal application of more intensive fetal monitoring, there was agreement that cardiotocography, "non-stress testing," should be considered from 32 weeks' gestation onward in cases where hyperglycemia warrants insulin therapy and at or near term in those requiring only dietary management. No consensus was reached regarding the utility of more complex methods of fetal monitoring, such as the biophysical profile or the assessment by Doppler ultrasound of umbilical blood flow. However, these may be considered in situations where there is excessive or poor fetal growth or there are concomitant medical problems, such as preeclampsia. The use of ultrasound to measure the fetal abdominal circumference at 29–33 weeks' gestation was demonstrated to be useful for identifying a large subset of patients with maternal fasting glucose levels <105 mg/dl (5.8 mmol/l) who were at little risk for fetal macrosomia at term when managed with dietary therapy alone. The optimal application of this approach—including the most appropriate fetal parameters to measure and the optimal timing of the measurements—remains to be determined. Use of fetal ultrasound for detection of congenital anomalies was suggested for women in whom GDM is diagnosed in the 1st trimester or who present with fasting serum or plasma glucose concentrations >120 mg/dl (6.7 mmol/l), because an increased risk of fetal anomalies has been reported in such pregnancies. Amniocentesis for assessment of fetal lung maturity was not felt to be indicated in well-controlled patients after 38 weeks' gestation as long as there is reasonable certainty about the estimation of the gestational age. Use of amniocentesis before 38 weeks' gestation should be guided by the indications for preterm delivery. Maternal surveillance. The risk of hypertensive disorders is increased approximately twofold in women with GDM compared with normal women. Thus, measurement of blood pressure, body weight, and urinary protein was recommended at each prenatal visit to detect the development of pregnancy-induced hypertension (preeclampsia). Standard methods for diagnosis and management of hypertensive disorders are recommended for women with GDM. Route and timing of delivery. There was consensus that the presence of GDM should not of itself constitute an indication for elective cesarean delivery. However, data were presented indicating that rates of cesarean delivery in GDM were higher than could be explained by associated obstetric complications. Although those observations suggest that the diagnosis of GDM does influence delivery decisions in favor of the cesarean route, a consensus was not reached on this issue by the conference attendees. GDM was not felt to be an indication for delivery prior to 38 weeks' gestation in the absence of objective evidence of fetal compromise. However, data were reviewed indicating that delay of delivery past 38 weeks can lead to an increase in the rate of large-for-gestational-age infants without reducing the rate of cesarean deliveries. Thus, consideration may be given to delivery once patients reach 38 completed weeks of gestation. Data are not available to indicate whether or not there is greater risk of perinatal morbidity/mortality in the infants of women with well-controlled GDM if pregnancy is allowed to proceed past 40 weeks' gestation. Nevertheless, it would be reasonable to intensify fetal surveillance when pregnancy is allowed to continue beyond 40 weeks' gestation. Recommendations for the future PANEL IV: LONG-RANGE IMPLICATIONS AND MANAGEMENT AFTER PREGNANCY Members Clinical implications Health care providers should counsel women concerning risks of glucose intolerance and future diabetes by making them aware of the symptoms of diabetes and the need for regular postpartum surveillance, even in the absence of symptoms. The potential for delaying or preventing diabetes in both mothers and offspring represents an opportunity to reduce morbidity and consequent health care costs. Glucose tolerance should be reevaluated in the mother initially at 6–12 weeks postpartum and subsequently as outlined in the Report of the Expert Committee (8), Table 1, and below. Fasting plasma glucose (FPG) >126 mg/dl (7.0 mmol/l) indicates diabetes if confirmed on a separate occasion. If FPG is in the range of 110–125 mg/dl (6.1–6.9 mmol/l), it is designated impaired fasting glucose. FPG <110 mg/dl (6.1 mmol/l) is considered normal; however, an OGTT will provide additional important information. First, the results of the postpartum OGTT are useful in assessing the risk for later development of diabetes. Secondly, the majority of subjects with impaired glucose tolerance have an FPG <110 mg/dl (6.1 mmol/l). It may also be of value to perform an OGTT in those with impaired fasting glucose because some of these subjects will have a 2-h value >200 mg/dl (11.1 mmol/l), thus fulfilling the criteria for a diagnosis of diabetes. If the postpartum evaluation does not indicate diabetes, fasting plasma glucose concentration should be assessed in such women at least annually and in preparation for any future pregnancy. Other cardiovascular risk factors should also be assessed regularly in this high-risk group. Patients should be instructed in lifestyle behaviors aimed at reducing weight and increasing physical activity in the expectation that this will reduce the risk of subsequent diabetes. However, the efficacy of these measures has not yet been shown in prospective clinical trials. Because all subsequent pregnancies carry a risk for GDM or pre-GDM, all women with prior GDM need to participate in a program for planned pregnancies. Evaluation and pre-conception counseling should address appropriate contraception; the need for early evaluation of glucose tolerance in any future pregnancy; the risk of congenital malformations in undiagnosed diabetic pregnancy; and the possibility that further pregnancies may add to the risk of developing diabetes outside of pregnancy. All women who are contemplating pregnancy in the future should be advised to take supplementary folic acid (>400 µg/day) to reduce the risk of neural tube defects in their offspring. The offspring. By the time of puberty, the offspring of women with GDM have increased risk of obesity and abnormal glucose tolerance. These risks are not confined to those who were overweight at birth and may be more directly linked with fetal islet cell function during intrauterine development. Altered metabolic substrates during pregnancy may adversely affect neurobehavioral development at birth and in childhood. Such effects appear to be relatively minor with optimal diabetes and obstetric management and the effective utilization of existing educational and special education programs. The importance of the intrauterine environment is highlighted by studies in the general population that indicate an association between risk of diabetes and cardiovascular disease in adulthood with poor fetal growth and low infant weight gain. Measures aimed at reducing or preventing obesity by modification of lifestyle may also decrease the risk of obesity and diabetes in the offspring. The child's primary care provider should be aware that the child of a mother with GDM has inherent risks of future obesity and diabetes. Breast-feeding should be encouraged, as it is associated with a lower risk of obesity and, in some populations, diabetes in the offspring. However, as in the case of the mother, the efficacy of these measures has not yet been shown in prospective clinical trials. Recommendations for the future More studies are needed during pregnancy, at birth, and during childhood and adolescence to further identify those children most at risk for diabetes and obesity and to understand what contribution is made by maternal metabolic, intrauterine, genetic, lifestyle, and other host risk factors to the lifetime susceptibility to obesity and diabetes. Such studies may foster the development of strategies to prevent obesity, glucose intolerance, and diabetes in the offspring of mothers with GDM and may lead to clinical trials of diabetes prevention in this population. Evidence that transmission of diabetes to subsequent generations may involve intrauterine exposures to hyperglycemia or to other nutrients and agents that may cause stimulation of fetal hyperinsulinism in addition to standard genetic transmission speaks strongly of the need for studies to define the mechanisms that may be involved. Animal models, including transgenic models, may be particularly useful in this regard. Additional prospective studies in humans are needed to identify the children at highest risk and to define maternal, intrauterine, genetic, lifestyle, and other risk factors that may be modified to reduce the risk of diabetes in offspring. References 2. Carpenter MW, Coustan DR: Criteria for screening tests for gestational diabetes. Am J Obstet Gynecol 144:763–773, 1982 3. National Diabetes Data Group: Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 28:1039–1057, 1979 4. Freinkel N, Josimovich J, Conference Planning Committee: American Diabetes Association Workshop-Conference on Gestational Diabetes: summary and recommendations. Diabetes Care 3:499–501, 1980 5. Freinkel N: Summary and recommendations of the Second International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes 34 (Suppl. 2):123–126, 1985 6. Metzger BE, the Organizing Committee: Summary and recommendations of the Third International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes 40 (Suppl. 2):197–201, 1991 7. Sacks DA, Greenspoon JS, Abu-Fadil S, Henry HM, Wolde-Tsadik G, Yao JFF: Toward universal criteria for gestational diabetes: the 75-gram glucose tolerance test in pregnancy. Am J Obstet Gynecol 172:607– 614, 1995 8. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 20:1183–1197, 1997 From the Northwestern University Medical School (B.E.M.), Chicago, Illionois; and the Brown University School of Medicine and the Women and Infants' Hospital of Rhode Island (D.R.C.), Providence, Rhode Island. Address correspondence and reprint requests to Boyd E. Metzger, MD, Northwestern University Medical School, Tarry Building 15-735, 303 East Chicago Ave., Chicago, IL 60611. E-mail: bem@nwu.edu. Received for publication 13 February 1998 and accepted 11 March 1998. B.E.M. has received consulting fees from Abbott Laboratories and has received honoraria from Novo Nordisk and Parke-Davis. Abbreviations: FPG, fasting plasma glucose; GCT, glucose challenge test; GDM, gestational diabetes mellitus; NDDG, National Diabetes Data Group; OGTT, oral glucose tolerance test. Copyright © 1998 American Diabetes Association For Technical Issues contact webmaster@diabetes.org |
-cell
function, and obesity have been identified as predisposing factors for subsequent type 2
diabetes. The value of additional measurements, such as autoantibodies that have been
associated with risk of type 1 diabetes, deserve further assessment in ethnic groups with
the highest incidence of type 1 diabetes.
