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Gestational Diabetes Mellitus Thomas A Science in medicine Gestational diabetes mellitus Thomas A. Buchanan1 and Anny H. Xiang2 1Departments of Medicine, Obstetrics and Gynecology, and Physiology and Biophysics, and 2Department of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles, California, USA. Gestational diabetes mellitus (GDM) is defined as glucose intolerance of various degrees that is first detected during pregnancy. GDM is detected through the screening of pregnant women for clinical risk factors and, among at-risk women, testing for abnormal glucose tolerance that is usually, but not invariably, mild and asymptomatic. GDM appears to result from the same broad spectrum of physiological and genetic abnormalities that characterize diabetes outside of pregnancy. Indeed, women with GDM are at high risk for having or developing diabetes when they are not pregnant. Thus, GDM provides a unique opportunity to study the early pathogenesis of diabetes and to develop interventions to prevent the disease. Historical perspective currently recommended by the American Diabetes Association For more than a century, it has been known that diabetes antedat- (12) are based on O’Sullivan’s criteria (see above). The detection ing pregnancy can have severe adverse effects on fetal and neona- of GDM, a condition that is generally asymptomatic, involves tal outcomes (1). As early as in the 1940s, it was recognized that screening in 2 sequential steps (Tables 1 and 2), followed by women who developed diabetes years after pregnancy had expe- administration of a 2- or 3-hour OGTT (Table 3) to women deter- rienced abnormally high fetal and neonatal mortality (2). By the mined to be at risk by screening. Women with very high clinical 1950s the term “gestational diabetes” was applied to what was risk characteristics may be diagnosed with probable pregestation- thought to be a transient condition that affected fetal outcomes al (preexisting) diabetes based on the criteria provided in Table adversely, then abated after delivery (3). In the 1960s, O’Sullivan 4. When the diagnostic criteria for a 3-hour OGTT presented in found that the degree of glucose intolerance during pregnancy Table 3 was applied to a group of Caucasian women in Toronto, was related to the risk of developing diabetes after pregnancy. He approximately 7% had GDM (6). The frequency of GDM may vary proposed criteria for the interpretation of oral glucose tolerance among ethnic groups (higher in groups with increased prevalence tests (OGTTs) during pregnancy that were fundamentally statisti- of hyperglycemia) (13–16) and with the use of different diagnostic cal, establishing cut-off values — approximately 2 standard devia- criteria (higher when lower glucose thresholds are applied and vice tions — for diagnosing glucose intolerance during pregnancy (4). versa) (4). Nonetheless, all approaches to GDM detection pinpoint In the 1980s those cut-off points were adapted to modern meth- — and thereby allow diagnosis of — women with glucose tolerance ods for measuring glucose and applied to the modern definition in the upper end of the population distribution during pregnancy. of gestational diabetes — glucose intolerance with onset or first A small minority of those women have glucose levels that would recognition during pregnancy (5). While based on O’Sullivan’s be diagnostic of diabetes outside of pregnancy (Table 4). The great values for predicting diabetes after pregnancy, the diagnosis of majority have lower glucose levels. Both groups impart to their gestational diabetes mellitus (GDM) also identifies pregnancies at offspring an increased risk of perinatal morbidity and long-term increased risk for perinatal morbidity (6–8) and long-term obesity obesity and diabetes that appear to be related at least in part to and glucose intolerance in offspring (9–11). fetal overnutrition in utero. They also incur for themselves a risk of diabetes after pregnancy that is the main focus of this paper. Population perspective Clinical detection of GDM is carried out to identify pregnan- Etiology and pathogenesis cies at increased risk for perinatal morbidity and mortality. Available data do not identify a threshold of maternal glycemia Normal pregnancy at which such risk begins or increases rapidly. A multinational A detailed discussion of glucose regulation in pregnancy is beyond study, the Hyperglycemia and Adverse Pregnancy Outcome study, the scope of this paper. However, 2 points are important for the is underway to explore this issue in a large multiethnic cohort. discussion that follows. First, pregnancy is normally attended by In the absence of a defined glucose threshold for perinatal risk, progressive insulin resistance that begins near mid-pregnancy and many different sets of glycemic criteria have been proposed and progresses through the third trimester to levels that approximate are employed worldwide for the diagnosis of GDM. The criteria the insulin resistance seen in individuals with type 2 diabetes. The insulin resistance appears to result from a combination of Nonstandard abbreviations used: DPP, Diabetes Prevention Program; GAD, increased maternal adiposity and the insulin-desensitizing effects glutamic acid decarboxylase; GDM, gestational diabetes mellitus; MODY, maturity- of hormonal products of the placenta. The fact that insulin resis- onset diabetes of the young; OGTT, oral glucose tolerance test; TRIPOD; Troglitazone tance rapidly abates following delivery suggests that the major in Prevention of Diabetes. contributors to this state of resistance are placental hormones. The Conflict of interest: T.A. Buchanan and A.H. Xiang receive grant support from Take- second point is that pancreatic β cells normally increase their insu- da Pharmaceuticals North America Inc. T.A. Buchanan is also a consultant to Takeda Pharmaceuticals North America Inc. and is on the company’s Actos Speakers’ Bureau. lin secretion to compensate for the insulin resistance of pregnancy Citation for this article: J. Clin. Invest. 115:485–491 (2005). (see Figure 1, for example). As a result, changes in circulating glu- doi:10.1172/JCI200524531. cose levels over the course of pregnancy are quite small compared The Journal of Clinical Investigation http://www.jci.org Volume 115 Number 3 March 2005 485 science in medicine Table 1 Screening for GDM, step 1: clinical risk assessmentA,B Risk category Clinical characteristics Recommended screening High risk (presence of Marked obesity Blood glucose screening at initial antepartum visit or as any is sufficient) Diabetes in first-degree relative(s) soon as possible thereafter; repeat at 24–28 wk if not Personal history of glucose intolerance already diagnosed with GDM by that time Prior delivery of macrosomic infant Current glycosuria Average risk Fits neither low- nor high-risk profile Blood glucose screening between 24 and 28 wk gestation Low risk (all required) Age <25 Blood glucose screening not required Low-risk ethnicityC No diabetes in first-degree relatives Normal prepregnancy weight and pregnancy weight gain No personal history of abnormal glucose levels No prior poor obstetrical outcomes ABased on recommendations of the American Diabetes Association (5). BPerformed at initial antepartum visit. CEthnicities other than Hispanic, African, Native American, South or East Asian, Pacific Islander, or indigenous Australian, all of which have relatively high rates of GDM. Adapted with permission from N. Engl. J. Med. (72). Copyright 1999, Massachussets Medical Society. All rights reserved. with the large changes in insulin sensitivity. Robust plasticity of with GDM have the same markers present in their circulation (17, β cell function in the face of progressive insulin resistance is the 28–31). Although detailed physiological studies of these women are hallmark of normal glucose regulation during pregnancy. lacking, they most likely have inadequate insulin secretion resulting from autoimmune damage to and destruction of pancreatic β cells. Gestational diabetes They appear to have evolving type 1 diabetes, which comes to clini- GDM is a form of hyperglycemia. In general, hyperglycemia results cal attention through routine glucose screening during pregnancy. from an insulin supply that is inadequate to meet tissue demands The frequency of anti–islet cell and anti-GAD antibodies detected in for normal blood glucose regulation. Studies conducted during late GDM tends to parallel ethnic trends in the prevalence of type 1 dia- pregnancy, when, as discussed below, insulin requirements are high betes outside of pregnancy. Patients with anti–islet cell or anti-GAD and differ only slightly between normal and gestational diabetic antibodies often, but not invariably, are lean, and they can rapidly women, consistently reveal reduced insulin responses to nutrients in develop overt diabetes after pregnancy (30). women with GDM (17–23). Studies conducted before or after preg- nancy, when women with prior GDM are usually more insulin resis- Monogenic diabetes and GDM tant than normal women (also discussed below), often reveal insulin Monogenic diabetes mellitus has been identified outside of pregnan- responses that are similar in the 2 groups or reduced only slightly in cy in 2 general forms. Some patients have mutations in autosomes women with prior GDM (18, 22–26). However, when insulin levels (autosomal dominant inheritance pattern, commonly referred to and responses are expressed relative to each individual’s degree of as maturity-onset diabetes of the young [MODY], with
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