title: Cardiovascular risk markers during treatment with estradiol and trimegestone or dydrogesterone.
abstract: OBJECTIVE
  To study cardiovascular risk markers in women taking estradiol/trimegestone or estradiol/dydrogesterone.
  
  
  METHODS
  Multicenter, randomized, prospective, double-blind study of 184 healthy post-menopausal women randomized to 6 cycles of either estradiol (2mg)+trimegestone (0.5mg) (T-group) or estradiol (2mg)+dydrogesterone (10mg) (DYDR group). Cardiovascular risk markers were measured before, after cycle 1, 3 and 6 and at 4 weeks post-treatment.
  
  
  RESULTS
  Fibrinogen was reduced in both groups but more markedly in the DYDR group. Factor VIIc activity levels decreased in both groups with a greater change in the T-group. Factor VII antigen was increased in both groups with a greater increase in the DYDR group. Factor VIIa was increased in the DYDR group only. Plasminogen levels were also increased in both groups with a greater increase in the T-group. There were no statistically significant changes in lipid variables between the different regimens. Changes in total cholesterol and LDL cholesterol were correlated positively with changes in factor VIIc in the DYDR group and negatively with changes in factor VIIc in the T-group. Trigemestone was associated with a better bleeding pattern.
  
  
  CONCLUSIONS
  Trimegestone was associated with less procoagulant changes in factor VIIa and factor VIIc activity and larger decrease in PAI-1 activity compared with the dydrogesterone preparation. These results reflect less androgenic properties of the trimegestone preparation. The fibrinogen level and Lp(a) were more decreased during dydrogesterone treatment. Further investigation is required to clarify the relative importance of beneficial effects with respect to cardiovascular risk.
authors.affiliation: Department of Obstetrics and Gynecology, Sahlgrenska University Hospital, Göteborg, Sweden. margareta.hellgren@vgregion.se
authors.forename: M
authors.initials: M
authors.lastname: Hellgren
authors.forename: J
authors.initials: J
authors.lastname: Conard
authors.forename: L
authors.initials: L
authors.lastname: Norris
authors.forename: C
authors.initials: C
authors.lastname: Kluft
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001779:Blood Coagulation Factors / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D004394:Dydrogesterone / Q000627:therapeutic use*; D004958:Estradiol / Q000627:therapeutic use*; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000627:therapeutic use*; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D006801:Humans; D008055:Lipids / Q000097:blood*; D008875:Middle Aged; D017698:Postmenopause; D011372:Progestins / Q000627:therapeutic use*; D011397:Promegestone / Q000031:analogs & derivatives* / Q000627:therapeutic use; D012307:Risk Factors; D013923:Thromboembolism / Q000209:etiology; D014592:Uterine Hemorrhage / Q000139:chemically induced
chemical_list: D015415:Biomarkers; D001779:Blood Coagulation Factors; D004967:Estrogens; D008055:Lipids; D011372:Progestins; C050319:trimegestone; D004958:Estradiol; D004394:Dydrogesterone; D011397:Promegestone