Approach to the patient with gestational diabetes after delivery

Abstract

The diagnosis of gestational diabetes mellitus (GDM) identifies patients with a pancreatic β-cell defect. In some patients, the defect is transient or stable, but in most it is progressive, imparting a high risk of diabetes for at least a decade after the index pregnancy. The β-cell defects in GDM can result from many causes, including genetic variants typical of monogenic forms of diabetes and autoimmunity typical of evolving type 1 diabetes. No specific disease-modifying therapies are available for those patients. The majority of women with GDM have clinical characteristics indicating a risk for type 2 diabetes (T2D). Available evidence indicates that T2D can be prevented or delayed by intensive lifestyle modification and by medications, particularly those that ameliorate insulin resistance. Clinical management should include assessment of glucose tolerance in the postpartum period to detect diabetes or assess diabetes risk. Women who don't have diabetes should be advised about their risk and participate in family planning to prevent subsequent pregnancies with undiagnosed hyperglycemia. All patients should be monitored for rising glycemia indicative of progressive β-cell deterioration. We suggest a combination of fasting glucose and glycosylated hemoglobin measurements for this purpose. Monitoring should be initiated at least annually and should be intensified if glycemia is rising and/or impaired. Lifestyle modification is advised to reduce the risk for T2D. Like monitoring, lifestyle modification should be intensified for rising glycemia and/or development of impaired glucose levels. At present, there is insufficient evidence to recommend medications to prevent T2D. Close follow-up and monitoring will allow initiation of pharmacological treatment as soon as diabetes develops. Children of women with GDM are at increased risk for obesity and diabetes. They should receive education, monitoring, and lifestyle advice to minimize obesity and diabetes risk. Copyright © 2011 by The Endocrine Society.