BACKGROUND AND AIM: To measure inflammatory markers in postmenopausal women on different forms of hormone replacement therapy (HRT). METHOD: C-reactive protein (CRP), fibrinogen, plasma viscosity (PV), albumin and white blood cell (WBC) count were determined in 749 postmenopausal women. RESULTS: CRP concentration was significantly higher in women on estrogen monotherapy (difference of the median (d) 0.96 mg/l, P = 0.013), compared to those without HRT, but there was no difference in women on combined HRT. Fibrinogen concentration was significantly lower in women on estrogen monotherapy (d 0.25g/l, P = 0.004) and combined HRT (d 0.4 g/l, P < 0.001), compared to women without HRT. Similarly, PV was significantly lower in women on estrogen monotherapy (d 0.017 mPa x s, P = 0.007) and women on combined HRT (d 0.039mPa x s, P < 0.001), compared to those without HRT. No differences were found for WBC count and the negative acute phase marker albumin in the various treatment groups. In contrast to oral estrogen administration, levels of CRP, fibrinogen and PV in women on transdermal estrogen therapy did not differ from the no-HRT group. There was no association between these markers of inflammation and plasma estrogen levels. CONCLUSION: Oral estrogen monotherapy was associated with highest concentrations of CRP. In contrast, other markers of inflammation were either similar or lower in the oral HRT group, compared to the group of women without HRT, suggesting that higher CRP concentrations reflect estrogen effects on CRP expression rather than a systemic pro-inflammatory effect.
BACKGROUND AND AIM: To measure inflammatory markers in postmenopausal women on different forms of hormone replacement therapy (HRT). METHOD:C-reactive protein (CRP), fibrinogen, plasma viscosity (PV), albumin and white blood cell (WBC) count were determined in 749 postmenopausal women. RESULTS:CRP concentration was significantly higher in women on estrogen monotherapy (difference of the median (d) 0.96 mg/l, P = 0.013), compared to those without HRT, but there was no difference in women on combined HRT. Fibrinogen concentration was significantly lower in women on estrogen monotherapy (d 0.25g/l, P = 0.004) and combined HRT (d 0.4 g/l, P < 0.001), compared to women without HRT. Similarly, PV was significantly lower in women on estrogen monotherapy (d 0.017 mPa x s, P = 0.007) and women on combined HRT (d 0.039mPa x s, P < 0.001), compared to those without HRT. No differences were found for WBC count and the negative acute phase marker albumin in the various treatment groups. In contrast to oral estrogen administration, levels of CRP, fibrinogen and PV in women on transdermal estrogen therapy did not differ from the no-HRT group. There was no association between these markers of inflammation and plasma estrogen levels. CONCLUSION: Oral estrogen monotherapy was associated with highest concentrations of CRP. In contrast, other markers of inflammation were either similar or lower in the oral HRT group, compared to the group of women without HRT, suggesting that higher CRP concentrations reflect estrogen effects on CRP expression rather than a systemic pro-inflammatory effect.
Authors: Brian C Cooper; Natalie Z Burger; Michael J Toth; Mary Cushman; Cynthia K Sites Journal: Am J Obstet Gynecol Date: 2007-02 Impact factor: 8.661
Authors: Elizabeth A Lawson; Karen K Miller; Vani A Mathur; Madhusmita Misra; Erinne Meenaghan; David B Herzog; Anne Klibanski Journal: J Clin Endocrinol Metab Date: 2007-05-22 Impact factor: 5.958
Authors: Sridevi Devaraj; Anthony T Cheung; Ishwarlal Jialal; Steven C Griffen; Danh Nguyen; Nicole Glaser; Thomas Aoki Journal: Diabetes Date: 2007-08-08 Impact factor: 9.461