Q: Why has there been a change in the standards of care for gestational diabetes mellitus?
With the obesity epidemic in this country, a greater number of women in their childbearing years are at risk for this continuum of metabolic syndrome, gestational diabetes mellitus (GDM), and type 2 diabetes mellitus (T2DM). GDM has long been defined as glucose intolerance with onset or first recognition during pregnancy.1 Compounding this definition are concerns that undiagnosed type 1 diabetes mellitus (T1DM) or T2DM may have been present at conception or that glucose intolerance may continue after pregnancy, developing into T2DM postpartum or prior to subsequent pregnancies.
In April 2011, the CDC reported that GDM occurs in 2% to 10% of pregnancies and is more likely in women who have a family history of diabetes, are obese, or are African-American, Hispanic/Latino American, or American Indian.2
Furthermore, in 2008, the Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study demonstrated a continuous association of adverse pregnancy outcomes (maternal, fetal, and neonatal) with increasing maternal glucose levels, even at glycemic levels previously considered normal.3 In response, the International Association of Diabetes and Pregnancy Study Groups (IADPSG) developed revised recommendations for diagnosing GDM; these were published in 2010.4 Professional organizations such as the American Diabetes Association (ADA) and the American Association of Clinical Endocrinologists (AACE) are now incorporating these revisions into their guidelines.5,6
Q: What causes GDM?
After 20 weeks’ gestation, there is an approximately 50% increase in insulin resistance in all women, most likely resulting from elevated levels of reproductive/placental hormones and possibly cytokines. As levels rise for the duration of the pregnancy, insulin resistance continually increases.
Women with normal pancreatic function are able to secrete the additional insulin required (as much as 200% to 250% by late pregnancy) to maintain euglycemia. Women predisposed to insulin resistance prior to pregnancy have already begun taxing their pancreatic beta-cells for increased production. As insulin resistance increases during the second and third trimesters, they are less likely to meet the additional demands for insulin, with impaired insulin secretion resulting in a greater risk for hyperglycemia.7
Q: What are the risks of maternal hyperglycemia for the child?
Hyperglycemia during the first trimester, either due to uncontrolled T1DM or undiagnosed T2DM, may cause birth defects, including neural tube and cardiac malformations; it can also contribute to early fetal loss.8,9 Maternal hyperglycemia during the second and third trimesters, as seen with the onset of GDM, is also associated with an increased risk for other complications, and HAPO reported that these complications increased with rising glucose levels previously considered normal.4
According to Pedersen’s hypothesis, maternal hyperglycemia transfers across the placenta, inducing fetal hyperglycemia, compensatory fetal hyperinsulinemia, and consequently increased adipose deposition of nutrients, resulting in macrosomia—the most common complication of GDM.10 Fetal hyperinsulinemia can siphon glucose from the mother, known as steal phenomenon, creating the appearance of maternal euglycemia.11 For this reason, ultrasound surveillance is used to monitor for accelerated fetal growth.
An estimated fetal weight of more than 4,500 g carries a high risk for shoulder dystocia with vaginal delivery, so elective cesarean section is usually recommended.12 Common complications in the infant include neonatal hypoglycemia secondary to fetal hyperinsulinemia, polycythemia, hyperbilirubinemia, and an increased need for neonatal intensive care.4 Furthermore, uncontrolled maternal GDM results in offspring at risk for childhood obesity and impaired glucose tolerance, giving rise to the theory of fetal imprinting and perpetuating a vicious cycle.13-16
In light of worldwide weight trends and with obesity considered the number one risk factor for insulin resistance, which is characterized by elevated triglycerides and free fatty acids, Catalano is revisiting Pedersen’s hypothesis, adding that the availability of maternal lipids for fetal lipogenesis is a possible contributing factor to fetal fat accumulation.17 This could explain why pregnancies complicated by obesity carry many of the same risks, or compound the maternal-fetal risks, that are associated with hyperglycemia in pregnancy.18-20
Q: What are the risks of GDM for the mother?
The immediate risks are an increased incidence of cesarean section, preeclampsia, and preterm delivery.3 Since GDM falls within the continuum for developing T2DM, pregnancy serves as a “stress test” in women who are genetically predisposed. Women who develop GDM have about a 50% risk for developing T2DM within five to 10 years.21
Q: How is GDM diagnosed?
As a result of the obesity and diabetes epidemics in this country, increasing numbers of women have undiagnosed T2DM with pregnancy.22 For this reason, the new guidelines recommend using standard diabetes screening for women with risk factors for T2DM at the first prenatal visit. Women who test positive are given a diagnosis of diabetes and should begin diabetes self-management education and therapeutic intervention, when indicated, without delay. AACE recommends that A1C be used as a screening test, due to potential interfering factors not related to glycemia, and that the diagnosis of diabetes be based on plasma glucose readings.6