GESTATIONAL DIABETES. . . . . . . . . . . . . . . . . . . . . . .. 1 107
SCREENING AND DIAGNOSIS .................... 1108
MATERNAL AND FETAL EFFECTS .....i............. 1110 . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 1 111
Diabetes may exist bore the inception ofpregnancy, or may not appear until labour. The prognosis is generaly believed to be ominous or mother and chil, but a review of the literature shows that less than 25 percent of the mothers died from diabetic coma, while premature labour occurred in ony one third of the cases.
-J. Whitridge Williams (1903)
In the early 1900s, overt diabetes complicating pregnancy was associated with horriic morbidity and mortality for a mother and her fetus. Although tremendously mitigated by the discovery of insulin, overt and gestational diabetes still are formidable complications of pregnancy.
According to the Centers for Disease Control and Prevention (2017), the number of adults diagnosed with diabetes in the United States is 23.r1 million. And, almost a quarter of people with diabetes in the United States remain undiagnosed.
tion more likely to develop type 2 diabetes, population growth within minority group at particular risk for type 2 diabetes, and a dramatic rise in obesity rates-also referred to as diabesiy.
he term reflects the strong relationship of diabetes and the current obesity epidemic in the United States and underlines the critical need for diet and lifestyle interventions to change the trajectory of both.
here is keen interest in events that precede diabetes, and this includes the intrauterine environment. Here, early imprinting is believed to have efects later in life (Saudek, 2002). For example, in utero exposure to maternal hyperglycemia leads to fetal hyperinsulinemia, causing an increase in fetal fat cells. his leads to obesity and insulin resistance in childhood (Feig, 2002). These factors in turn lead to impaired glucose tolerance and diabetes in adulthood. This cycle of fetal exposure to diabetes leading to childhood obesity and glucose intolerance is discussed further in Chapter 48 (p. 941).
In nonpregnant individuals, the type of diabetes is based on its presumed etiopathogenesis and its pathophysiological manifestations. Absolute insulin deficiency, generally autoimmune in etiology, characterizes ype 1 diabetes. In contrast, insulin resistance, relative insulin deiciency, or elevated glucose production characterizes ype 2 diabetes (Table 57-1). Both types are generally preceded by a period of abnormal glucose homeostasis oten referred to as prediabetes. The terms insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) are now obsolete. Pancreatic �-cell destruction can begin at any age, but type 1 diabetes is clinically apparent most often before age 30. Type 2 diabetes usually develops with advancing age but is increasingly identified in younger obese adolescents.
TABLE 57-1. Etiological Classification of Diabetes Mellitus
Type 1: �-Cell destruction, usually absolute insulin deficiency Immune-mediated
Type 2: Ranges from predominantly insulin resistance to predominantly an insulin secretory defect with insulin resistance
Genetic mutations of �-cell function-MODY 1-6, others Genetic defects in insulin action
Genetic syndromes-Down, Klinefelter, Tuner