ABSTRACT
OBJECTIVE: The purpose of this study was to assess an early hemoglobin A1c (HgbA1c) value from 5.7-6.4% as an early predictor of progression to gestational diabetes (GDM). STUDY DESIGN: A retrospective cohort study was performed on all women who delivered at a single institution over 2 years who had an early screening HgbA1c test performed at ≤20 weeks of gestation. Women with known preexisting diabetes mellitus or HgbA1c values ≥6.5% were excluded. The primary outcome was GDM development. Secondary outcomes included delivery route, maternal weight gain, birthweight, and neonatal morbidities. Women with an HgbA1c value of 5.7-6.4% were compared with those with an HgbA1c level of <5.7%. RESULTS: Nearly one-third of those patients in the HgbA1c 5.7-6.4% group (27.3%) experience the development of GDM compared with only 8.7% in the HgbA1c <5.7% group (odds ratio, 3.9; 95% confidence level, 2.0-7.7). This 3-fold increase remained significant (adjusted odds ratio, 2.4) after adjustment for age, prepregnancy body mass index, gestational age at HgbA1c collection, gestational age at screening, ethnicity, and method of screening. There were no significant differences in the need for medical treatment, weight gain, delivery route, birthweight, macrosomia, or neonatal morbidities. CONCLUSION: More than 10% of patients in our cohort had an early screening HgbA1c value of 5.7-6.4%. Women in this group have a significantly higher risk of progression to GDM compared with women with normal HgbA1c values and should be considered for closer GDM surveillance and possible intervention.
Subject(s)
Birth Weight , Diabetes, Gestational/blood , Glycated Hemoglobin/analysis , Adult , Biomarkers/blood , Body Mass Index , Cohort Studies , Delivery, Obstetric/methods , Diabetes, Gestational/diagnosis , Female , Gestational Age , Glucose Tolerance Test , Humans , Infant, Newborn , Infant, Newborn, Diseases/epidemiology , Odds Ratio , Pregnancy , Retrospective Studies , Risk Assessment , Weight Gain , Young AdultABSTRACT
Type 2 diabetes frequently results from progressive failure of pancreatic beta-cell function in the presence of chronic insulin resistance. We tested whether chronic amelioration of insulin resistance would preserve pancreatic beta-cell function and delay or prevent the onset of type 2 diabetes in high-risk Hispanic women. Women with previous gestational diabetes were randomized to placebo (n = 133) or the insulin-sensitizing drug troglitazone (400 mg/day; n = 133) administered in double-blind fashion. Fasting plasma glucose was measured every 3 months, and oral glucose tolerance tests (OGTTs) were performed annually to detect diabetes. Intravenous glucose tolerance tests (IVGTTs) were performed at baseline and 3 months later to identify early metabolic changes associated with any protection from diabetes. Women who did not develop diabetes during the trial returned for OGTTs and IVGTTs 8 months after study medications were stopped. During a median follow-up of 30 months on blinded medication, average annual diabetes incidence rates in the 236 women who returned for at least one follow-up visit were 12.1 and 5.4% in women assigned to placebo and troglitazone, respectively (P < 0.01). Protection from diabetes in the troglitazone group 1) was closely related to the degree of reduction in endogenous insulin requirements 3 months after randomization, 2) persisted 8 months after study medications were stopped, and 3) was associated with preservation of beta-cell compensation for insulin resistance. Treatment with troglitazone delayed or prevented the onset of type 2 diabetes in high-risk Hispanic women. The protective effect was associated with the preservation of pancreatic beta-cell function and appeared to be mediated by a reduction in the secretory demands placed on beta-cells by chronic insulin resistance.
