摘要
Objective: This study shows the effect of hormone replacement therapy(HRT), using oral estrogen exclusively or in combination with progestin, on platelet activation in healthy menopaused women. Background: Recent evidence from studies of postmenopausal HRT in healthy women demonstrated a short-time increased risk of coronary heart disease. Platelet activation, which generates vasoconstrictory thromboxane A2(TxA2), has been related to the risk of cardiovascular diseases. Methods: Bymeans of a placebo-controlled study twenty-seven postmenopausal patients were continuously orally administered estrogen in combination with progestin or estrogen exclusively for an 8-week period. Platelet activation was evaluated by flow cytometric P-selectin expression and by enzyme immunoassay plasmatic TxA2(TxB2) concentrations. Results: P-selectin binding index changed from 6.3±3.6 to 7.0±3 in the placebo group(n=10); from 5.9+2.2 to 7.9±3.3 in the E+P group(n=8) and from 6.4+2.7 to 7.1±1.9 in the E group(n=9). Plasma concentrations of TxB2 before and after intervention, changed from 1.2±1.2 to 1.5±1.4(pg/well) in the placebo group; significantly(p=0.005) in the E+P group(n=8), from 0.9±0.3 to 6.1±6.5(pg/well), and from 1.3±1.5 to 0.8±0.4(pg/well) in the E group(n=8; mean±standard deviation, basal x therapy, p< 0.05). Conclusions: Healthy menopaused women who were administered estradiol in association with norethisterone continuously had an increase of plasmatic thromboxane, possibly determined by platelet activation, which indicates a higher short-term thrombotic risk. P-selectin expression analyses failed to demonstrate the impact of HRT on platelets.
Objective: This study shows the effect of hormone replacement therapy(HRT), using oral estrogen exclusively or in combination with progestin, on platelet activation in healthy menopaused women. Background: Recent evidence from studies of postmenopausal HRT in healthy women demonstrated a short-time increased risk of coronary heart disease. Platelet activation, which generates vasoconstrictory thromboxane A2(TxA2), has been related to the risk of cardiovascular diseases. Methods: Bymeans of a placebo-controlled study twenty-seven postmenopausal patients were continuously orally administered estrogen in combination with progestin or estrogen exclusively for an 8-week period. Platelet activation was evaluated by flow cytometric P-selectin expression and by enzyme immunoassay plasmatic TxA2(TxB2) concentrations. Results: P-selectin binding index changed from 6.3±3.6 to 7.0±3 in the placebo group(n=10); from 5.9+2.2 to 7.9±3.3 in the E+P group(n=8) and from 6.4+2.7 to 7.1±1.9 in the E group(n=9). Plasma concentrations of TxB2 before and after intervention, changed from 1.2±1.2 to 1.5±1.4(pg/well) in the placebo group; significantly(p=0.005) in the E+P group(n=8), from 0.9±0.3 to 6.1±6.5(pg/well), and from 1.3±1.5 to 0.8±0.4(pg/well) in the E group(n=8; mean±standard deviation, basal x therapy, p< 0.05). Conclusions: Healthy menopaused women who were administered estradiol in association with norethisterone continuously had an increase of plasmatic thromboxane, possibly determined by platelet activation, which indicates a higher short-term thrombotic risk. P-selectin expression analyses failed to demonstrate the impact of HRT on platelets.
