Menopause and High Attributable Risk of ElevatedC-Reactive Protein Level to Conventional Coronary Heart Disease Risk Factors

By Samantha S. | Updated: Aug 02, 2016


Review on February 04, 2010

menopause experiment

The initiation and development of cardiovascular disease is believed to be partly linked to inflammation and much attention has been given to C-reactive protein (CRP), an acute-phase reactant released mainly by hepatocytes. While low-grade inflammation can forecast coronary heart disease (CHD), the point to which elevated CRP level is attributable to firmly-set CHD risk factors in post-menopause women needs further exploration. If increased CRP level is closely related to standard CHD risk factors, then normal screening of this biomarker would apparently be less valuable to clinicians. Thus, the study below was carried out to assess the extent to which high CRP levels may simply reflect expression of the pathobiologic changes caused by normal CHD risk factors. This study determined the use of estrogen hormone therapy in females who had surgical or natural menopause.

Results from this study show that the occurrence of high CRP level was greater among post-menopause women using estrogen hormone therapy than among estrogen hormone therapy nonusers or past users. Such findings are in line with earlier studies showing higher CRP levels in post-menopause women than in men and higher levels in post-menopause women receiving estrogen hormone therapy than in post-menopause women not using hormone therapy. However, because of the small number of post-menopause women receiving estrogen hormone therapy, this variable was not considered in the multiple logistic regression model.

Menopause inflamation

 This study supports/emphasizes the role that conventional CHD risk factors play in atherothrombosis by showing that a key biomarker of systemic inflammation, increased CRP level, is usually related to borderline or abnormal CHD risk factors and hardly ever/seldom occurs without them. A lot of evidence shows a strong relationship between inflammatory biomarkers and CHD risk factors in post-menopause women who may be using estrogen hormone therapy.

The findings detailed above suggest that high CRP level is mainly attributable to traditional CHD risk factors in post-menopause women. Therefore, measurement of CRP levels in post-menopause women who may be using or have used hormone therapy may have little clinical benefit as a screening tool for CHD risk assessment unless randomized clinical trials can prove that lowering CRP levels counteracts CHD events further than well-established lifestyle and pharmacologic modalities. Until then, greater effort should be made to encourage smoking cessation, more physical activity, and lowering of elevated blood pressure, lipid levels, and visceral adiposity in post-menopause women because all of these factors help to reduce CHD.

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