ESTROGEN REPLACEMENT THERAPY AND COAGULATION - RELATIONSHIP TO LIPID AND LIPOPROTEIN CHANGES

Objective: To examine the relationship of estrogen-induced changes in lipids and lipoproteins with alterations in the coagulation system. Me thods: Coagulation and lipid indices were measured in 31 postmenopausa l women, ages 40-60 years, after a 3-month course of 0.625-mg conjugat ed equine estrogen. We analyzed changes in variables from baseline to 3 months using t tests for paired samples or the Wilcoxon matched-pair s signed-rank test. Results: Unopposed estrogen replacement therapy pr oduced statistically significant decreases in antithrombin-III antigen (P = .006) and activity (P = .001) and total protein S (P = .003) and a significant increase in protein C antigen (P = .017). C4b-binding p rotein also decreased significantly from baseline to 3 months (P < .00 1). Mean fibrinogen level decreased by 18.2 mg/dL, not a statistically significant change (P = .213). Estrogen produced the expected statist ically significant changes in lipids and lipoproteins. Several correla tions between changes in lipids and lipoproteins and coagulation indic es were statistically significant. Protein C antigen and activity chan ges correlated directly with high-density lipoprotein cholesterol chan ges (r = .52, P less than or equal to .005; r = .38, P less than or eq ual to .05; respectively), and protein C antigen also correlated direc tly with increases in apoprotein A-I (r = .54, P less than or equal to .005). Triglyceride changes correlated directly with changes in prote in C antigen (r = .36, P less than or equal to .05) and activity (I = .49, P less than or equal to .005) and inversely with C4b-binding prot ein (r = -.58, P less than or equal to .01). Apoprotein B was correlat ed with free protein S (r = .48, P less than or equal to .01). Conclus ions: Although several estrogen-induced changes may decrease atheroscl erotic potential and hypercoagulability, others may promote coagulabil ity. These divergent effects may be manipulated pharmacologically by o ther estrogen compounds or by the addition of various progestins. Copy right (C) 1997 by The American College of Obstetricians and Gynecologi sts.