Inflammatory Biomarkers, Hormone Replacement Therapy, and Incident Coronary Heart Disease

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Abstract
Several studies indicate that oral postmenopausal hormone replacement therapy (HRT) leads to an increase in plasma C-reactive protein (CRP) levels,1-3 an observation that raises the possibility of an up-regulation of inflammation among women taking these agents. This issue is of clinical concern because CRP represents a potent independent risk marker for the development of cardiovascular events,4-10 and completed and ongoing randomized trials on the prevention of cardiovascular disease have reported an unexpected increase in rates of venous and arterial thrombotic events following initiation of HRT.11,12 It is unclear, however, whether the observed effects of HRT on CRP represent a generalized proinflammatory effect mediated through the upstream cytokine interleukin 6 (IL-6) or whether these effects are due to a secondary mechanism. For example, in the Postmenopausal Estrogen/Progestin Interventions trial, although CRP levels increased with HRT, levels of fibrinogen, E-selectin, and other acute-phase reactants did not.3,13 Furthermore, although it has been hypothesized that elevations in CRP are partly responsible for the hazards associated with HRT use,3 there are no clinical outcomes data addressing this issue.