Review on February 02, 2010
The majority of oral preparations of postmenopausal hormones (PMHs) raise levels of C-reactive protein (C-RP), a precise indicator of inflammation, within around one month of starting therapy. This increase is noticeable in the menopausal woman who is given either estrogen hormones alone or estrogen hormones combined with a progestin, which has now become the most familiar preparation of postmenopausal hormones used. The following data comes from observational studies and randomized trials of the seemingly healthy menopausal woman and indicates that the increase is not due to atherosclerotic burden, other risk factors for cardiovascular disease or other inflammatory disorders.
Raised levels of C-RP foresee increased risks of consequent cardiovascular events in the menopausal woman and in men, though the means by which this occurs are uncertain. In a few investigations, aspirin therapy has decreased levels of C-RP and other inflammatory cytokines in the menopausal woman. It is unknown whether or not aspirin therapy at lower or higher doses inhibits the postmenopausal hormones-induced increase in C-RP levels in the menopausal woman. A new study of 10 menopausal women who were using aspirin therapy showed no change in C-RP levels with postmenopausal hormones therapy.
If the theory that aspirin stops the postmenopausal hormones-induced increase in CR-P levels is correct, then there are several clinical considerations. In terms of postmenopausal hormones, observational studies and randomized trials show increases in HDL cholesterol levels and decreases in LDL cholesterol levels in the menopausal woman. Observational epidemiological studies continue to indicate that a menopausal woman who selects her own postmenopausal hormones therapy has a reduced chance of coronary heart disease. Yet, the HERS study and Women's Health Initiative randomized trial with clinical end points imply rather greater risks within the first two years of therapy
Focusing on aspirin's ability to stop the postmenopausal hormones-induced rise in C-RP levels in the menopausal woman, a daily dosage of around 81mg is currently recommended for primary and secondary prevention. Doses of around 650 mg/d will produce more undesirable effects, but there may also be extra benefits based on other means of action beyond any antiplatelet effect.
If aspirin therapy inhibits the postmenopausal hormones-induced increase in C-RP levels in the menopausal woman, this might imply a possible abolition of the early increase in cardiovascular events laid out in the HERS study and the Women's Health Initiative. So, if the menopausal woman taking postmenopausal hormones holds onto the possible long-term benefit of aspirin therapy, achieves the long-term benefit and has any early increase in events abolished by such therapy then the clinical and public health impact could be significant. Therefore, aspirin therapy has the potential to create a more desirable benefit-risk ratio of postmenopausal hormones therapy in the menopausal woman. The hypothesis that aspirin therapy inhibits the postmenopausal hormones-induced increase in CR-P levels demands thorough testing.