High C-reactive protein levels are associated with oral hormonal menopausal therapy but not with intrauterine levonorgestrel and transdermal estradiol.

OBJECTIVE

Oral hormone replacement therapy (HRT) has been linked to increased cardiovascular (CVD) morbidity. HRT causes a sustained increase in C-reactive protein (CRP), an excellent marker of subclinical inflammation and CVD. The aim of the study was to support our hypothesis that CRP, which is synthesized in the liver, is not increased in association with transdermal/intrauterine HRT.

MATERIAL AND METHODS

A case-control study was performed in which CRP measurements in women receiving levonorgestrel intrauterine system combined with transdermal estradiol (LNG/TDE, n=27) were followed for 9 months or longer. CRP concentrations in these women were compared with those of either oral HRT users (n=20) or controls (n=19).

RESULTS

No significant differences were found in CRP concentrations between the LGN/TDE and control groups (1.8+/-1.2 and 1.8+/-1.8 mg/L, respectively). However, CRP was significantly increased in the oral HRT group (5.5+/-2.9 mg/L, p<0.001).

CONCLUSIONS

CRP is significantly increased by oral HRT but not by the LNG/TDE combination after 9 months of treatment. This trend may explain the preponderance of some menopausal women on HRT being at increased risk for the development of CVD. Therefore, the use of LNG/TDE is acceptable for relief of severe climacteric symptoms possibly not imposing an increased CVD risk documented upon oral HRT.