Karen V. Smirnakis

Postpartum diabetes screening in women with a history of gestational diabetes.

OBJECTIVE: Women with a history of gestational diabetes mellitus (GDM) are at high risk for developing type 2 diabetes (diabetes mellitus, DM). The American Diabetes Association recommends regular postpartum diabetes screening for women with a history of GDM, but the American College of Obstetricians and Gynecologists (ACOG) is not as directive. We sought to examine postpartum glycemic testing in women diagnosed with GDM. METHODS: We conducted an observational cohort study of women diagnosed with GDM at one of two large academic medical centers between 2000 and 2001. Kaplan-Meier estimates of the time from delivery to the first postpartum DM screening tests were determined, and predictors of postpartum DM screening were examined using Cox proportional hazards testing. RESULTS: Only 37% of eligible women underwent the postpartum diabetes screening tests recommended by the American Diabetes Association (fasting glucose or oral glucose tolerance test [OGTT]), with a median time from delivery to the first such testing of 428 days. By comparison, 94% of women underwent postpartum cervical cancer screening using a Papanicolaou (Pap) test, with a median time from delivery to Pap testing of 49 days. Even when random glucose testing was included in a broad definition of postpartum DM screening (random or fasting glucose, glycosylated hemoglobin, or OGTT), only two thirds of women (67%) received a postpartum glycemic assessment. CONCLUSION: In the population studied, only 37% of women with a history of GDM were screened for postpartum DM according to guidelines published by the American Diabetes Association. Efforts to improve postpartum DM screening in this high-risk group are warranted. LEVEL OF EVIDENCE: II-2

Insulin Resistance and Alterations in Angiogenesis. Additive Insults That May Lead to Preeclampsia

Abstract—Altered angiogenesis and insulin resistance, which are intimately related at a molecular level, characterize preeclampsia. To test if an epidemiological interaction exists between these two alterations, we performed a nested case-control study of 28 women who developed preeclampsia and 57 contemporaneous controls. Serum samples at 12 weeks of gestation were measured for sex hormone binding globulin (SHBG; low levels correlate with insulin resistance) and placental growth factor (PlGF; a proangiogenic molecule). Compared with controls, women who developed preeclampsia had lower serum levels of SHBG (208±116 versus 256±101 nmol/L, P =0.05) and PlGF (16±14 versus 67±150 pg/mL, P <0.001), and in multivariable analysis, women with serum levels of PlGF ≤20 pg/mL had an increased risk of developing preeclampsia (odds ratio [OR] 7.6, 95% CI 1.4 to 38.4). Stratified by levels of serum SHBG (≤175 versus >175 mg/dL), women with low levels of SHBG and PlGF had a 25.5-fold increased risk of developing preeclampsia (P =0.10), compared with 1.8 (P =0.38) among women with high levels of SHBG and low levels of PlGF. Formal testing for interaction (PlGF×SHBG) was significant (P =0.02). In a model with 3 (n−1) interaction terms (high PlGF and high SHBG, reference), the risk for developing preeclampsia was as follows: low PlGF and low SHBG, OR 15.1, 95% CI 1.7 to 134.9; high PlGF and low SHBG, OR 4.1, 95% CI 0.45 to 38.2; low PlGF and high SHBG, OR 8.7, 95% CI 1.2 to 60.3. Altered angiogenesis and insulin resistance are additive insults that lead to preeclampsia.