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Insulin Resistance and Its Potential Role in Pregnancy-Induced Hypertension

Endocrinology, Diabetes and Hypertension Division (E.W.S.) and Divisions of General Medicine and Women’s Health (C.G.S.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Ellen W. Seely, M.D., Endocrine, Diabetes, and Hypertension Division, Brigham and Women’s Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, Massachusetts 02115.

New-onset hypertension (which includes preeclampsia and gestational hypertension) is a common and morbid complication of pregnancy. Many features of the insulin resistance syndrome have been associated with this condition. These include hypertension, hyperinsulinemia, glucose intolerance, obesity, and lipid abnormalities. Other accompanying abnormalities may include elevated levels of leptin, TNF, tissue plasminogen activator, plasminogen activator inhibitor-1, and testosterone. The documentation of these features before the onset of hypertension in pregnancy suggests that insulin resistance or associated abnormalities may have a role in this disorder. Furthermore, the recognition that features of the insulin resistance syndrome persist many years after pregnancy among women with this condition raises the possibility that these women may have increased risk for future cardiovascular disease. These observations suggest that interventions to reduce insulin resistance may reduce the risk of both hypertension in pregnancy and later life cardiovascular complications, and warrant further study.

E.W.S. is supported by NIH Grants R01HL67332 and SCOR(H) P50HL55000.

Abbreviations: CRP, C-reactive protein; LDL, low density lipoprotein; PAI-1, plasminogen activator inhibitor-1; TPA Ag, tissue plasminogen activator antigen; VCAM, vascular cell adhesion molecule.

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