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Excerpt
Departments of Surgery, Physiology, and Biophysics and Biochemistry/Molecular Biology, and Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, Minnesota
J Clin Endocrinol Metab 2001;86:3629–3634
In observational studies, hormone replacement therapy correlates with a lower rate of coronary artery disease in postmenopausal women than in age-matched control women. Paradoxically, the risk of venous thrombosis is increased both in women given hormone replacement therapy for primary or secondary prevention of coronary artery disease and men treated for prostate cancer or sex transformation. This prospective, randomized trial was designed to demonstrate effects of unopposed estrogen on regulators of activated coagulation and the acute-phase response in healthy postmenopausal women. The study enrolled 26 women aged 55 to 80 years during an 18-month period. One group received a daily tablet containing 0.625 mg of conjugated equine estrogen (Premarin), and the other, a placebo tablet, for 3 months.
Plasma levels of total tissue factor pathway inhibitor (TFPI) and TFPI activity fell significantly after 3 months of estrogen therapy. The decrease in TFPI correlated with a concurrent decline in plasma low-density lipoprotein. Neither group exhibited significant changes in prothrombin or plasminogen activator inhibitor-1, but plasminogen increased significantly with estrogen treatment. There were no changes in plasma fibrinogen or P-selectin levels. Among inflammatory markers, mean plasma levels of C-reactive protein increased significantly in women given estrogen, and interindividual variation in C-reactive protein also increased. There were no significant changes in circulating α1-protease inhibitor in the estrogen group, but fluctuations between baseline and final levels were reduced.
Unopposed estrogen therapy seems to simultaneously influence elements of the extrinsic coagulation pathway and of the acute-phase inflammatory response in postmenopausal women. Conceivably, concomitant changes in these substances may lower the risk of arterial disease while at the same time changing the threshold for thrombotic events.
