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(Hypertension. 2002;40:886.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Insulin Resistance But Not Inflammation Is Associated With Gestational Hypertension

Myles Wolf; Laura Sandler; Ricardo Jimenez-Kimble; Anand Shah; Jeffrey L. Ecker; Ravi Thadhani

From the Renal Unit, Department of Medicine (M.W., L.S., R.J.-K., A.S., R.T.) and the Department of Obstetrics and Gynecology (J.L.E., R.T.), Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Myles Wolf, MD, MMSc, Bulfinch 127, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114. E-mail mswolf{at}partners.org

Hypertensive disorders of pregnancy, including gestational hypertension and preeclampsia, are leading causes of pregnancy-associated morbidity. Although insulin resistance and inflammation contribute to preeclampsia, prospective data regarding mechanisms of gestational hypertension are sparse. We conducted a prospective, nested case-control study to test the hypotheses that insulin resistance, marked by reduced sex hormone–binding globulin (SHBG) levels, and inflammation, marked by increased C-reactive protein levels, are similarly associated with gestational hypertension. We measured first-trimester C-reactive protein and SHBG levels in 51 women who subsequently developed gestational hypertension and 102 randomly selected normotensive pregnant controls. Compared with controls, first-trimester SHBG levels were significantly reduced among women who later developed gestational hypertension (176±73 versus 203±79 nmol/L; P=0.03), but there was no difference in C-reactive protein levels. There was statistically significant interaction among nulliparity, first-trimester SHBG levels, and risk of gestational hypertension, such that increasing SHBG levels were associated with significantly reduced risk of gestational hypertension among nulliparous women (odds ratio, 0.64 per 50-nmol/L increase; 95% confidence interval, 0.46, 0.90; P<0.01) but not among multiparous women. This association remained significant after adjusting for potential confounders (odds ratio, 0.55; 95% confidence interval, 0.31, 0.98; P=0.04). We conclude that insulin resistance, but not inflammation, is an independent risk factor for gestational hypertension among nulliparous women. Furthermore, important mechanistic differences exist in the pathogenesis of gestational hypertension comparing nulliparous and multiparous women.

Key Words: hypertension, gestational • insulin resistance • prospective studies

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