title: Hemostatic factors and estrogen during the menopausal transition.
abstract: BACKGROUND
  It has been speculated that gender differences in cardiovascular disease (CVD) mortality can be attributed to the effects of estrogens on inflammation and hemostatic marker profiles. Therefore, we evaluated endogenous hormone concentrations, menopause transition stages, and adoption of exogenous hormone use in relation to hemostatic and inflammation marker concentrations in women.
  
  
  METHODS
  Longitudinally, we studied 3302 participants from the Study of Women's Health Across the Nation, aged 42-52 yr at baseline and self-identified as African-American (28%), Caucasian (47%), Chinese (8%), Hispanic (8%), or Japanese (9%). Serum samples from baseline and years 2001, 2003, and 2005 were assayed for estradiol and FSH. Hormone concentrations were related to CVD markers, including fibrinogen, factor VII-c, plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator, and human serum C-reactive protein (hsCRP).
  
  
  RESULTS
  Lower estradiol levels were associated with higher levels of PAI-1 and tissue plasminogen activator, but there were no significant relationships with fibrinogen, factor VII-c, or hsCRP. Higher FSH concentrations were associated with higher PAI-1 and factor VII levels, but lower fibrinogen and hsCRP levels. Transitions from premenopause and early perimenopause to postmenopause were not associated with significant differences in levels of hemostatic factors. The hsCRP concentrations were approximately 25% higher, and the PAI-1 concentrations approximately 20% lower among women who initiated hormone therapy, compared with nonusers.
  
  
  CONCLUSIONS
  Endogenous estrogens may reduce CVD risk via modulation of fibrinolytic factors, but not coagulation or inflammatory markers. Notably, conclusions derived from studies of exogenous hormones and CVD risk may not parallel or explain the effects of endogenous hormones or perimenopausal hormone changes on CVD risk.
authors.affiliation: Department of Epidemiology, University of Michigan School of Public Health, 339 East Liberty Street, Suite 310, Ann Arbor, Michigan 48104, USA. mfsowers@umich.edu
authors.forename: MaryFran R
authors.initials: MR
authors.lastname: Sowers
authors.forename: Karen A
authors.initials: KA
authors.lastname: Matthews
authors.forename: Mary
authors.initials: M
authors.lastname: Jannausch
authors.forename: John F
authors.initials: JF
authors.lastname: Randolph
authors.forename: Daniel
authors.initials: D
authors.lastname: McConnell
authors.forename: Kim
authors.initials: K
authors.lastname: Sutton-Tyrrell
authors.forename: Roderick
authors.initials: R
authors.lastname: Little
authors.forename: Bill
authors.initials: B
authors.lastname: Lasley
authors.forename: Richard
authors.initials: R
authors.lastname: Pasternak
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000032:analysis; D004958:Estradiol / Q000097:blood*; D015914:Estrogen Replacement Therapy; D005260:Female; D005342:Fibrinolysis; D005640:Follicle Stimulating Hormone / Q000097:blood; D006487:Hemostasis; D006801:Humans; D008137:Longitudinal Studies; D008593:Menopause / Q000097:blood*; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D004958:Estradiol; D005640:Follicle Stimulating Hormone; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator