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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

¹ Hormone & Vascular Biology Group, Academic Unit of Endocrinology, Division of Genomic Medicine, The University of Sheffield, Sheffield, S10 2RX, UK, ² Department of Cardiology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, S10 2JF, UK, ³ Center for Diabetes & Endocrinology, Barnsley District General Hospital, Barnsley District Hospital NHS Trust, Barnsley, S57 5RT, UK and ⁴ Faculty of Health & Well-being, Sheffield Hallam University, Collegiate Crescent, Sheffield, S10 2BD, UK

(Correspondence should be addressed to K S Channer, Department of Cardiology, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK; Email: Kevin.Channer{at}sth.nhs.uk)

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).

Conclusion: Physiological testosterone replacement does not adversely affect blood coagulation status.