Abstract

The consequences of hyperglycemia appearing during pregnancy were well described in 1917, when Elliot P. Joslin described Case 309, which “showed sugar in 1897 during pregnancy, but following confinement, with resulting dead baby, it disappeared, but returned in 9 years in the form of moderate to severe diabetes… . [W]ith our present knowledge, it is quite possible that such an outcome could be prevented by active treatment of the glycosuria from the very start” (1). Subsequently, O'Sullivan and Mahan's definition of gestational diabetes mellitus (GDM) in 1964 was a formal recognition of the mother's increased risk of future development of diabetes (2). They defined GDM if a pregnant woman undergoing a 3-h 100-g oral glucose tolerance test had glucose values exceeding 2 SDs above the mean on two of the four values. This landmark study described a population of pregnant women with a lifetime risk of diabetes exceeding 70% (3). Multiple studies worldwide have demonstrated a broad ethnic and geographic distribution of GDM, but all studies share the increased risk of subsequent diabetes after delivery (4). Assessment of diabetes risk postpartum is influenced by the criteria used to define GDM, the testing undertaken postpartum, and the length of follow-up. Diagnosis of carbohydrate intolerance in the first trimester of pregnancy may reflect the ascertainment of previously undiagnosed and, presumably, asymptomatic diabetes. Alternatively, pregnancy creates a metabolic stress that may push a woman with compensated type 1 or type 2 diabetes into a decompensated hyperglycemic state. Under these circumstances, one would anticipate a high rate of persistent hyperglycemia in the postpartum state. In fact, the presence of GDM doubles the risk of diabetes within 4 months postpartum, whereas a fasting plasma glucose >121 mg/dl during the pregnancy increased the risk 21-fold (5). Differential criteria for diagnosis of GDM affects the …

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