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 1-14% of patients depending on the population described and the criteria used for diagnosis.[2] Table 1 describes the prevalence of GDM reported by studiesp[3-12] performed at various locations.

Table 1. Prevalence of GDM Author Location Prevalence Abell, Beischer[3] Australia 0.7 O'Sullivan[4] Boston 2.5 Magee[5] Seattle 3.2-5.0 Dooley[6] Chicago 3.5-5.5 SackS[7] Los Angeles 3.4 Berkowitz[8] Manhattan 4.6 Murphy[9] Alaska 5.8 Nahum[10] Los Angeles 7.1 Mestman[11] Los Angeles 12.3 Benjamin[12] Zuni, New Mexico 14.3

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.

Pathophysiology

The metabolic changes of normal pregnancy are essential to provide adequate nutrients to the growing fetus. Early in pregnancy, maternal estrogen and progesterone increase and promote pancreatic Β-cell hyperplasia and increased, insulin release.[13] Increases in peripheral glucose utilization and glycogen storage with a concomitant reduction in hepatic glucose production result in lower maternal fasting glucose levels.[14] As pregnancy progresses, increased levels of human chronic sommatornammotropin (hCS), cortisol, prolactin, progesterone, and estrogen lead to insulin resistance in peripheral tissues.

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 antiinsulin properties that peak at 32 weeks gestation. The timing of these hormonal events is important in regard to scheduling testing for GDM.

Table 2. The Diabetogenic Potency of Hormones in Pregnancy Hormone Peak elevation (weeks) Diabetogenic potency Prolactin 10 Weak Estradiol 26 Very weak hCS 26 Moderate Cortisol 26 Very strong Progesterone 32 Strong

Adapted from Jovanovic-Peterson L, Peterson C: Review of gestational diabetes mellitus and low-calorie diet and physical exercise as therapy. Diabetes Metab Rev 12:287-308, 1996.

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 1.5-2.5 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.

Maternal Morbidity

Maternal morbidity due to GDM may be immediate or long-term. Many studies have documented an increase in preeclampsia, polyhydramnios, and operative delivery in pregnancies complicated by GDM.[5,18,19] The Toronto Tri-Hospital Gestational Diabetes Project, a prospective cohort study evaluating maternal and fetal outcomes with increasing carbohydrate intolerance,...