Effect of hormone replacement therapy on lipids and coagulation factors in postmenopausal women smokers

Abstract

Postmenopause and smoking impair lipid profile, induce hypercoagulability and reduce fibrinolytic capacity [1, 2]. Postmenopause induced lipid changes can be reversed by oestrogen replacement [3]. Oestrogens also reduce fibrino-gen level [4] and have beneficial effects on endothelium [5]. Although several studies showed that hormone replacement therapy may increase the risk of thromboembolic diseases, procoagulant oestrogen activity has not clearly been demonstrated. It is well known that smoking accelerates oestrogen metabolism [6, 7], which may attenuate its beneficial effects. The present study was undertaken to determine if there is difference in beneficial effects of oestrogens between smokers and non-smokers in terms of coagulation process and lipids. The examination was a longitudinal one-year, before/after therapeutic study, which included healthy postmenopausal women (FSH levels at least 40 U/l), 30 smokers and 32 non-smokers who were under 55 years of age and postmenopausal period shorter than 5 years. Women with surgically induced menopause received unopposed oral oestrogens, while those with spontaneous menopause were treated with combined oral oestrogen/progestogen therapy. Before entering the study and in three-months intervals total LDL, HDL cholesterol, triglyc?rides and VLDL were determined, as well School of Medicine, Belgrade as plasma fibrinogen prothrombin time, and activated partial thromboplastin time. Neither beneficial nor adverse effects of oestrogens on lipids and coagulation were observed during one-year follow-up in smokers, although subjects with longer smoking history had higher triglyc?rides levels after 12 months of therapy. On the contrary, oestrogen replacement reduced total and LDL cholesterol and increased HDL cholesterol in non-smokers, with no change in triglyc?rides and VLDL level. A decrease in fibrinogen levels and coagulation activity, expressed by protrombin time and partial thromboplastin time, were also observed in hormone replacement therapy in postmenopausal women who did not smoke. Peroral hormone replacement therapy does not induce favorable lipid changes in smokers. Higher triglyc?rides levels observed after one-year therapy in women with a longer smoking history indicate that transdermal replacement maybe more suitable in this group. Peroral oestrogen replacement has no anticoagulant or procoagulant activity in smokers during the early postmenopausal period.