Biochemical markers surrogating on vascular effects of sex steroid hormones.
The main mechanism of possible cardioprotection by estrogens appears to be a direct effect on the vasculature, resulting in an improvement of endothelial function and inhibition of atherogenesis. Numerous observational and experimental studies have demonstrated a positive correlation between estrogens and various biochemical markers surrogating direct vascular effects. In general, most markers are influenced in a similar way by oral and transdermal hormone therapy, although oral therapy may have a faster and more pronounced effect. The main difference between oral and transdermal administration may be confined to markers that are mainly or exclusively produced in the liver. Clinical studies demonstrate that progestogen addition can have an impact on the beneficial estrogen-induced changes of biochemical markers. Concerning the effects of tibolone, inconsistent data have been found. Overall, tibolone-induced beneficial changes on the various biochemical markers appear to be less marked compared with those of hormone therapy. The few data available on the direct effects of androgens on the vascular wall indicate a less favorable action of androgens on biochemical markers than of estrogens. The practical relevance of marker measurements is currently under discussion. Although evidence strongly supports some of these markers as predictors of acute events, it remains to be established whether modifying circulating levels of these markers will influence outcomes.
Mueck
Alfred O
AO
Section of Endocrinology and Menopause, University Women's Hospital, Tuebingen, Germany. endo.meno@med.uni-tuebingen.de
Seeger
Harald
H
D000728:Androgens / Q000494:pharmacology; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D001808:Blood Vessels / Q000187:drug effects*; D018932:Chemokine CCL2 / Q000097:blood; D004333:Drug Administration Routes; D004958:Estradiol / Q000008:administration & dosage / Q000627:therapeutic use; D015914:Estrogen Replacement Therapy / Q000706:statistics & numerical data; D005260:Female; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood; D008954:Models, Biological; D009569:Nitric Oxide / Q000097:blood; D009652:Norpregnenes / Q000494:pharmacology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D017698:Postmenopause; D011372:Progestins / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
D000728:Androgens; D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D012739:Gonadal Steroid Hormones; D018836:Inflammation Mediators; D017270:Lipoprotein(a); D009652:Norpregnenes; D017395:Plasminogen Activator Inhibitor 1; D011372:Progestins; C051321:SERPINE1 protein, human; D006710:Homocysteine; D009569:Nitric Oxide; D004958:Estradiol; C027385:tibolone