title: Testosterone does not adversely affect fibrinogen or tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) levels in 46 men with chronic stable angina.
abstract: OBJECTIVE
  In women, sex hormones cause increased morbidity and mortality in patients with coronary heart disease (CHD) and adversely affect the coagulation profile. We have studied the effect of physiological testosterone replacement therapy in men on coagulation factor expression, to determine if there is an increased risk of thrombosis.
  
  
  METHODS
  Double-blind, randomized, placebo-controlled trial of testosterone in 46 men with chronic stable angina. Measurements of free, total and bioavailable testosterone, luteinising hormone (LH) and follicle-stimulating hormone (FSH), estradiol, plasminogen activator inhibitor-1 (PAI-1), fibrinogen, tissue plasminogen activator (tPA) and full blood count were made at 0, 6 and 14 weeks.
  
  
  RESULTS
  Bioavailable testosterone levels were: 2.58 +/- 0.58 nmol/l at baseline, compared with 3.35 +/- 0.31 nmol/l at week 14 (P < 0.001) after treatment compared with 2.6 +/- 0.18 nmol/l and 2.44 +/- 0.18 nmol/l in the placebo group (P was not significant). There was no change in fibrinogen (3.03 +/- 0.18 g/l at baseline and 3.02 +/- 0.18 g/l at week 14, P = 0.24), tPA activity (26.77 +/- 4.9 Iu/ml and 25.67 +/- 4.4 Iu/ml, P = 0.88) or PAI-1 activity (0.49 +/- 0.85 Iu/ml and 0.36 +/- 0.06 Iu/ml, P = 0.16) with active treatment and no differences between the groups (at week 14, P value 0.98, 0.59 and 0.8 for fibrinogen, PAI-1 and tPA respectively). Haemoglobin concentration did not change over time, in the testosterone group (1.44 +/- 0.02 g/l and 1.45 +/- 0.02 g/l, P = 0.22).
  
  
  CONCLUSIONS
  Physiological testosterone replacement does not adversely affect blood coagulation status.
authors.affiliation: Hormone & Vascular Biology Group, Academic Unit of Endocrinology, Division of Genomic Medicine, The University of Sheffield, Sheffield S10 2RX, UK.
authors.forename: A M
authors.initials: AM
authors.lastname: Smith
authors.forename: K M
authors.initials: KM
authors.lastname: English
authors.forename: C J
authors.initials: CJ
authors.lastname: Malkin
authors.forename: R D
authors.initials: RD
authors.lastname: Jones
authors.forename: T H
authors.initials: TH
authors.lastname: Jones
authors.forename: K S
authors.initials: KS
authors.lastname: Channer
mesh_terms: D000279:Administration, Cutaneous; D000728:Androgens / Q000008:administration & dosage* / Q000097:blood; D000787:Angina Pectoris / Q000453:epidemiology / Q000378:metabolism*; D001777:Blood Coagulation / Q000187:drug effects*; D002908:Chronic Disease; D005340:Fibrinogen / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012307:Risk Factors; D013739:Testosterone / Q000008:administration & dosage* / Q000097:blood; D013927:Thrombosis / Q000453:epidemiology; D010959:Tissue Plasminogen Activator / Q000097:blood*
chemical_list: D000728:Androgens; D017395:Plasminogen Activator Inhibitor 1; D013739:Testosterone; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator