Mesterolone: thrombosis during treatment, and a study of its prothrombotic effects.

Lowe, G.D.O.; Thomson, J. A.; Reavey, M. M.; Forbes, C. D.; Prentice, C. R. M.

doi:10.1111/j.1365-2125.1979.tb00905.x

Cited by 22 publications

(7 citation statements)

References 20 publications

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“…Several studies have suggested an increase in fibrinolysis with androgen administration (6)(7)(8) and plasma testosterone levels are positively correlated with tPA and negatively correlated with PAI activity in hyperlipidaemic men (22). Others have found no changes in fibrino lysis during 3 weeks of treatment with the synthetic androgen mesterolone (2). The fall in PAI found here may be the mechanism for the increase in fibrinolysis previously reported.…”

Section: Discussionsupporting

confidence: 56%

“…investigated as a possible hormonal male contraceptive ( I ) . There is increasing concern that anabolic steroid abuse may eause thrombo embolism, but the evidence so far is largely anecdotal (2)(3)(4). In animal studies, testosterone caused an increase in experimentally-induced thrombosis (5), but synthetic androgens, in particular stanozolol, increase fibrinolysis (6,7).…”

Section: Introductionmentioning

confidence: 99%

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Haemostatic Effects of Supraphysiological Levels of Testosterone in Normal Men

Anderson

Ludlam

1995

Thromb Haemost

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SummaryThe effects of exogenous testosterone on the haemostatic system were studied in a group of 32 healthy men undergoing a clinical trial of hormonal male contraception. The men received 200 mg testosterone oenanthate (TE) weekly i.m., and plasma samples were taken pretreatment, at defined time points up to 52 weeks of treatment, and 4 and 8 weeks after discontinuing TE. This dose of TE caused a 2-fold increase in trough plasma testosterone levels.TE caused a fall in plasma fibrinogen concentration after 16 weeks of treatment. This was sustained for the duration of TE treatment and recovered to pretreatment levels during the recovery phase. There was also a sustained fall in the level of C4b binding protein which showed a rebound to levels above pretreatment during recovery. Levels of antithrombin III and prothrombin fragment F1.2 rose initially during TE treatment, and levels of protein C, protein S (free) and plasminogen activator inhibitor fell, but the concentrations of these factors all returned to pretreatment levels during continued treatment. There was no change in the plasma concentrations of β-thromboglobulin, tissue plasminogen activator, protein S (total), or D-dimer. There was a sustained increase in haemoglobin concentration and haematocrit, without any change in platelet count.The observed changes were consistent with mild activation of the haemostatic system during initial treatment with testosterone. After several months the raised activation markers had returned to pretreatment levels indicating that a new equilibrium had been established which did not appear to be prothrombotic. The increase in prothrombin fragment F1.2 for the first 32 weeks, and at four weeks after discontinuation of treatment, is consistent with prolonged mildly increased prothrombinase activity. The observed substantial fall in fibrinogen is likely to have reduced, whereas the small rise in haemoglobin will have increased, the tendency to arterial thrombosis. We conclude that supraphysiological doses of testosterone do not result in a sustained marked prothrombotic state, but these results do not exclude a small change in thrombotic risk.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Haemostatic Effects of Supraphysiological Levels of Testosterone in Normal Men

Anderson

Ludlam

1995

Thromb Haemost

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“…In adults, associations between anabolic/androgenic steroid abuse and acute arterial or venous thrombosis have been demonstrated 13–17. Underlying mechanisms have been suggested to involve interactions of androgens with platelet aggregation,18 coagulation and fibrinolytic proteins, and the vasculature 19.…”

Section: Discussionmentioning

confidence: 99%

Role of endogenous testosterone concentration in pediatric stroke

Normann

Veber

Fobker

et al. 2009

Annals of Neurology

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Previous studies have indicated a male predominance in pediatric stroke. To elucidate this gender disparity, total testosterone concentration was measured in children with arterial ischemic stroke (AIS; n = 72), children with cerebral sinovenous thrombosis (CSVT; n = 52), and 109 healthy controls. Testosterone levels above the 90th percentile for age and gender were documented in 10 children with AIS (13.9%) and 10 with CSVT (19.2%), totaling 16.7% of patients with cerebral thromboembolism overall, as compared with only 2 of 109 controls (1.8%; p = 0.002). In multivariate analysis with adjustment for total cholesterol level, hematocrit, and pubertal status, elevated testosterone was independently associated with increased disease risk (odds ratio [95% confidence interval]: overall = 3.98 [1.38–11.45]; AIS = 3.88 [1.13–13.35]; CSVT = 5.50 [1.65–18.32]). Further adjusted analyses revealed that, for each 1nmol/l increase in testosterone in boys, the odds of cerebral thromboembolism were increased 1.3‐fold. Ann Neurol 2009;66:754–758

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“…There are reports of thromboembolism following the abuse of anabolic steroids (Lowe et al, 1979;Ferenchick, 1990;Robinson & Wise, 1993). There are reports of thromboembolism following the abuse of anabolic steroids (Lowe et al, 1979;Ferenchick, 1990;Robinson & Wise, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The effect of T on the haemostatic system is largely unknown. There are reports of thromboembolism following the abuse of anabolic steroids (Lowe et al, 1979;Ferenchick, 1990;Robinson & Wise, 1993). However, an increase in fibrinolysis has been described with stanazolol (Kluft et al, 176 H. M. Buckler et al ᭧ 1998 Blackwell Science Ltd, Clinical Endocrinology, 49, 173-178…”

Section: Discussionmentioning

confidence: 99%

The effects of low‐dose testosterone treatment on lipid metabolism, clotting factors and ultrasonographic ovarian morphology in women

Buckler¹,

McElhone²,

Durrington³

et al. 1998

Clinical Endocrinology

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Low-dose testosterome administration to women for over two years did not induce changes in ovarian architecture but had small, potentially atherogenic effects on some parameters of lipid and lipoprotein metabolism. However, no differences were detected in markers of activation of the clotting system to indicate an actual increase in the risk of thrombosis. Overall, this study provides largely reassuring data about the safety of low-dose androgen treatment in women. However, caution should be exercised in women with existing or a familial predisposition to lipid abnormalities, because of the small but significant changes found in HDL-C, apo-A1 and VLDL-C.

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Mesterolone: thrombosis during treatment, and a study of its prothrombotic effects.

Cited by 22 publications

References 20 publications

Haemostatic Effects of Supraphysiological Levels of Testosterone in Normal Men

Haemostatic Effects of Supraphysiological Levels of Testosterone in Normal Men

Role of endogenous testosterone concentration in pediatric stroke

The effects of low‐dose testosterone treatment on lipid metabolism, clotting factors and ultrasonographic ovarian morphology in women

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