Interleukin-6 and flow-mediated dilatation as markers of increased vascular inflammation in women receiving hormone therapy

Menopause. 2005 Sep-Oct;12(5):552-8. doi: 10.1097/01.gme.0000172267.24949.70. Epub 2005 Sep 1.

Abstract

Objective: The lack of a beneficial long-term cardiovascular effect of hormone therapy and the early incidence of cardiovascular adverse events observed in recent randomized studies have been related to a heightened inflammatory effect of hormone therapy.

Design: We evaluated the effect of different postmenopause therapies on inflammatory markers and endothelial function in 205 postmenopausal women before and after therapy.

Results: all postmenopausal women, estrogens alone increased plasma levels of C-reactive protein (CRP) but decreased all other markers of inflammation including interleukin-6 (IL-6) (CRP: +75% +/- 11%, intracellular adhesion molecule: -21% +/- 4%, vascular cell adhesion molecule: -15% +/- 6%, E-selectin: -18% +/- 4%, s-thrombomodulin -10.5% +/- 3.7%, IL-6 -14% +/- 6%; percent changes, P < 0.01 compared with baseline). Raloxifene and tibolone did not significantly affect the overall inflammatory milieu. In a minority of patients, estrogen-progestogen associations and tibolone increased IL-6 levels and induced unfavorable changes on inflammation markers (CRP: +93% +/- 8%, intracellular adhesion molecule: -3% +/- 2%, vascular cell adhesion molecule: -5% +/- 2%, E-selectin: +6% +/- 2%, s-thrombomodulin: +5% +/- 2%, IL-6: +12% +/- 4%; percent changes compared with baseline). Patients with increased IL-6 levels were older and had a longer time since menopause. In all patients except those with increased IL-6 levels, hormone therapy improved endothelial function, whereas tibolone and raloxifene did not significantly change endothelial function compared with baseline. A worsening of endothelial function was detected in patients with increased IL-6 levels during therapy.

Conclusions: Postmenopausal hormone therapy is associated with decreased vascular inflammation; however, in patients with a longer time since menopause, postmenopause hormone therapy may increase inflammation and worsen endothelial function. These unfavorable vascular effects may be detected by an elevation in IL-6 levels and by a lack of improvement in endothelial function.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Androgen Antagonists / therapeutic use
  • Biomarkers / blood
  • Brachial Artery / diagnostic imaging
  • C-Reactive Protein / analysis*
  • Cell Adhesion Molecules / blood*
  • Contraceptive Agents, Female / therapeutic use
  • Cyproterone Acetate / therapeutic use
  • Dydrogesterone / therapeutic use
  • Estradiol / therapeutic use
  • Estrogen Receptor Modulators / therapeutic use
  • Estrogens / therapeutic use
  • Estrogens, Conjugated (USP) / therapeutic use
  • Female
  • Hormone Replacement Therapy*
  • Humans
  • Interleukin-6 / blood*
  • Medroxyprogesterone Acetate / therapeutic use
  • Middle Aged
  • Multivariate Analysis
  • Norethindrone / analogs & derivatives
  • Norethindrone / therapeutic use
  • Norethindrone Acetate
  • Norpregnenes / therapeutic use
  • Postmenopause
  • Prospective Studies
  • Raloxifene Hydrochloride / therapeutic use
  • Thrombomodulin / blood*
  • Ultrasonography

Substances

  • Androgen Antagonists
  • Biomarkers
  • Cell Adhesion Molecules
  • Contraceptive Agents, Female
  • Estrogen Receptor Modulators
  • Estrogens
  • Estrogens, Conjugated (USP)
  • Interleukin-6
  • Norpregnenes
  • Thrombomodulin
  • Raloxifene Hydrochloride
  • Cyproterone Acetate
  • Estradiol
  • C-Reactive Protein
  • Dydrogesterone
  • Norethindrone Acetate
  • Medroxyprogesterone Acetate
  • tibolone
  • Norethindrone