title: The role of megestrol acetate as an alternative to conventional hormone replacement therapy.
abstract: OBJECTIVE
  To investigate the effect of megestrol acetate on menopausal symptoms, lipid metabolism, bone metabolism and coagulation.
  
  
  METHODS
  In a prospective observational study, 71 postmenopausal women, for whom conventional hormone replacement therapy (HRT) was unsuitable, were treated with megestrol acetate 40 mg per day. At 0, 3, 6 and 12 months, fasting lipoproteins, bone biochemistry and thrombophilia profiles were measured and symptom score cards (Greene climacteric scale) completed. Bone mineral density measurement was performed at 0 and 12 months.
  
  
  RESULTS
  Forty-one women completed the study. Treatment produced significant decreases in psychological (p < 0.001), vasomotor (p < 0.001) and somatic (p < 0.01) symptoms. There were significant reductions in triglycerides (p < 0.001), total cholesterol (p < 0.001), very-low-density lipoprotein (VLDL) (p < 0.05), low-density lipoprotein (LDL) (p < 0.001), high-density lipoprotein (HDL) cholesterol (p < 0.001) and lipoprotein(a) (p < 0.001). Levels of protein C were reduced (p < 0.05) and fibrinogen increased (p < 0.05). Protein S, plasminogen and antithrombin III levels showed an upward trend, which did not reach statistical significance. Biochemical markers of bone turnover did not change, apart from a significant decrease in alkaline phosphatase. Spinal bone density decreased significantly after 12 months, while femoral neck density remained unchanged.
  
  
  CONCLUSIONS
  Megestrol acetate controls menopausal symptoms, has equivocal effects on cardiovascular risk markers and does not increase bone density. It is useful where estrogen is contraindicated.
authors.affiliation: Department of Biochemistry, Stobhill Hospital, Glasgow G2I 3UW, Scotland.
authors.forename: E
authors.initials: E
authors.lastname: Farish
authors.forename: J F
authors.initials: JF
authors.lastname: Barnes
authors.forename: F
authors.initials: F
authors.lastname: O'Donoghue
authors.forename: C D
authors.initials: CD
authors.lastname: Fletcher
authors.forename: K
authors.initials: K
authors.lastname: Ekevall
authors.forename: D M
authors.initials: DM
authors.lastname: Hart
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D000990:Antithrombin III / Q000032:analysis; D001777:Blood Coagulation; D015519:Bone Density; D001842:Bone and Bones / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D015914:Estrogen Replacement Therapy; D005215:Fasting; D005260:Female; D005269:Femur; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D019290:Megestrol Acetate / Q000627:therapeutic use*; D008593:Menopause; D008875:Middle Aged; D010958:Plasminogen / Q000032:analysis; D011446:Prospective Studies; D011486:Protein C / Q000032:analysis; D017293:Protein S / Q000032:analysis; D013131:Spine; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D017270:Lipoprotein(a); D008074:Lipoproteins; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D011486:Protein C; D017293:Protein S; D014280:Triglycerides; D000990:Antithrombin III; D005340:Fibrinogen; D010958:Plasminogen; D002784:Cholesterol; D000469:Alkaline Phosphatase; D019290:Megestrol Acetate