title: The influence of physiological and surgical menopause on coronary heart disease risk markers.
abstract: OBJECTIVE
  To investigate the influence of physiological and surgical menopause on serum concentrations of coronary heart disease (CHD) risk markers and sex hormones.
  
  
  METHODS
  Physiological menopausal transition was investigated in two studies. In a longitudinal study, 16 women were followed from 2 years before until 2 years after physiological menopause. In a case-control study, 27 early postmenopausal women were compared with 27 age-matched late premenopausal women. Surgical menopause was investigated in 11 women undergoing a prophylactic bilateral salpingo-oophorectomy. The following parameters were measured: serum concentrations of estradiol, follicle-stimulating hormone, inhibin A, inhibin B, asymmetric dimethylarginine, lipids, leptin, homocysteine, C-reactive protein, and coenzyme Q10, as well as weight and body mass index.
  
  
  RESULTS
  After physiological and surgical menopause, serum estradiol and inhibin A and B decreased, whereas follicle-stimulating hormone increased (all P values < 0.01). Serum asymmetric dimethylarginine, total and low-density lipoprotein cholesterol, and leptin concentrations were significantly higher in postmenopausal women compared with premenopausal women (all P values < 0.05). Serum homocysteine concentrations increased significantly during the physiological menopausal transition. Total and low-density lipoprotein cholesterol increased after surgical menopause (both P values = 0.01). None of the other parameters studied were influenced significantly by the menopausal transition. No difference in change in the various CHD risk markers investigated was observed between physiological and surgical menopause.
  
  
  CONCLUSIONS
  The CHD risk profile was affected unfavorably by both physiological and surgical menopause. Changes in most CHD risk markers were small, despite the substantial changes in hormonal parameters.
authors.affiliation: Project Aging Women and the Institute for Cardiovascular Research-Vrije Universiteit and the Department of Obstetrics and Gynecology, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Marieke O
authors.initials: MO
authors.lastname: Verhoeven
authors.forename: Marius J
authors.initials: MJ
authors.lastname: van der Mooren
authors.forename: Tom
authors.initials: T
authors.lastname: Teerlink
authors.forename: René H M
authors.initials: RH
authors.lastname: Verheijen
authors.forename: Peter G
authors.initials: PG
authors.lastname: Scheffer
authors.forename: Peter
authors.initials: P
authors.lastname: Kenemans
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D015415:Biomarkers / Q000097:blood*; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D003327:Coronary Disease / Q000097:blood*; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007265:Inhibins / Q000097:blood; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008137:Longitudinal Studies; D008593:Menopause / Q000502:physiology*; D008875:Middle Aged; D010052:Ovariectomy; D012307:Risk Factors; D014451:Ubiquinone / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D015415:Biomarkers; D020738:Leptin; D008055:Lipids; C487735:dimethylarginine; C422362:inhibin A; C422364:inhibin B; D006710:Homocysteine; D014451:Ubiquinone; D004958:Estradiol; D007265:Inhibins; D005640:Follicle Stimulating Hormone; D002097:C-Reactive Protein; D001120:Arginine; C024989:coenzyme Q10