The menopause and hormone replacement therapy: lipids, lipoproteins, coagulation and fibrinolytic factors.

OBJECTIVES: To review the recent literature concerning the effects of the menopause and hormone replacement therapy (HRT) on the plasma lipoprotein and hemostatic system, as well as on the interaction between these two coronary heart disease (CHD) risk factor systems. METHODS. Collection of information from relevant scientific journals, and by the use of Medline and Current Contents.
RESULTS: The mainly beneficial effects of unopposed oral estrogen replacement on the plasma lipoprotein pattern are preserved to different degrees after addition of progestin to the regimen. Nortestostorone-derived progestins tend to lower HDL cholesterol levels more than progesterone derivatives. The slight triglyceride-elevating effect on conjugated equine estrogens was in a large study not significantly counteracted by progesterone derivatives but can, according to other studies, be reversed by nortestosterone-derived progestins. A limited number of studies on transdermal administration of estradiol has suggested that the effects on plasma lipoproteins are smaller than during oral administration. There is no convincing evidence that currently used HRT regimens would significantly increase the risk of thrombosis. Nevertheless, the finding in some studies that plasma triglyceride elevations could in theory be associated with impaired fibrinolysis and enhanced coagulation merit further attention as some HRT regimens tend to increase plasma triglyceride levels. From a theoretical point of view, transdermal estrogen delivery would be preferable in women at risk for thrombosis, as they have less pronounced effects on liver functions, including production of hemostatic factors and very-low-density lipoprotein triglycerides.
CONCLUSIONS: While the numerous existing HRT regimens provide many alternative and useful possibilities, further studies are needed concerning (a) novel progestins with minimal HDL cholesterol lowering effects, (b) transdermal and other non-oral routes for HRT, (c) possible antioxidative properties of estrogen and (d) metabolic links between the lipoprotein and hemostatic risk factor systems.