Effects of estrogen and selective estrogen receptor modulators on hemostasis and inflammation: potential differences among drugs.
Postmenopausal hormone replacement therapy (HRT), tamoxifen, and raloxifene all share an increase of about three-fold in the risk of venous thromboembolism (VTE). Currently, it is thought that HRT transiently increases the risk of myocardial infarction (MI), followed by subsequent reduction in risk, at least among women with established coronary heart disease. Raloxifene and tamoxifen are not known to share this apparent clinical effect. Study of hemostasis and inflammation factors, as surrogate end points, can be useful to form hypotheses concerning the pathophysiology related to clinical effects of these agents. Data presented here suggest differences among these agents that might relate to differences in clinical outcomes. From the vascular perspective, future studies need to focus on interactions of treatment with these biochemical parameters and their genetic correlates in order to define low- or high-risk subgroups for intervention with these therapies.
Cushman
M
M
Department of Medicine, University of Vermont, Colchester 05446, USA. mcushman@zoo.uvm.edu
D020847:Estrogen Receptor Modulators / Q000627:therapeutic use*; D015914:Estrogen Replacement Therapy; D005260:Female; D006487:Hemostasis / Q000187:drug effects*; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000188:drug therapy*; D009203:Myocardial Infarction / Q000453:epidemiology / Q000517:prevention & control; D017698:Postmenopause; D012307:Risk Factors; D020845:Selective Estrogen Receptor Modulators / Q000627:therapeutic use*
D020847:Estrogen Receptor Modulators; D020845:Selective Estrogen Receptor Modulators