Risks of Blood Volume Changes in Hypogonadal Men Treated with Testosterone Enanthate for Erectile Impotence

Abstract

Administration of anabolic steroids carries many risks. We present a series of 15 patients with primary hypogonadism who as a group had statistically significant increases in whole body hematocrit and red blood cell volume while on testosterone therapy of 300 mg. intramuscularly every 3 weeks. A small decrease in plasma volume over-all was not significant. Subsequent analyses compared subgroups whose whole body hematocrit during testosterone therapy was either 48% or greater (9) or less than 48% (6). Interaction effects indicated that the subgroups were similar when off testosterone but when on testosterone the former group exhibited an increase in red blood cell volume and a decrease in plasma volume, while the latter group had little change in either measurement. Subsequent to stopping testosterone therapy 2 patients in the whole body hematocrit 48% or greater group suffered strokes and 1 had transient ischemic attacks while on therapy. No one in the whole body hematocrit less than 48% group has had any cerebrovascular symptoms. Clinical implications, as well as cost-effective and practical suggestions for detecting possible dangerous hemoconcentration are discussed.

Pharmacokinetics, Efficacy, and Safety of a Permeation-Enhanced Testosterone Transdermal System in Comparison with Bi-Weekly Injections of Testosterone Enanthate for the Treatment of Hypogonadal Men*

“…By increasing blood viscosity, polycythemia reduces cerebral blood flow and poses an additional risk factor for stroke in patients with underlying cardiovascular disease (25). In the present study, the percentage of patients who had at least one supraphysiological hematocrit elevation was nearly 3-fold higher in the IM injection group compared with the TTD group.…”

“…The statistical association between hematocrit and E 2 levels in both treatment groups, which was stronger than the correlation to the patients' age, has not been reported previously and deserves further investigation. Although none of the patients in the present study with elevated hematocrits experienced any thromboembolic events, such concerns regarding have been raised in other studies (1,25,27,28). Periodic monitoring of hematocrit is, therefore, recommended for patients receiving T replacement therapy (29).…”

“…Whereas the erythropoietic-stimulating effect of androgens (22,23) has been used to treat a variety of anemias (24), administration of T has also been reported to cause polycythemia in some patients, particularly those Ͼ50 years of age (25)(26)(27). By increasing blood viscosity, polycythemia reduces cerebral blood flow and poses an additional risk factor for stroke in patients with underlying cardiovascular disease (25).…”

Diagnostic, traitement et surveillance de l’hypogonadisme de survenue tardive chez l’homme: Recommandations officielles de l’International Society for the Study of the Aging Male (ISSAM) et commentaires

“…A l'inverse, une 616vation supraphysiologique de l'hrmatocrite peut ~tre observre occasionnellement lors d'une androg6noth6rapie, obligeant ~ interrompre le traitement [11,16,22,26,29,42], 6tant donn6 le risque d'augmenter la viscosit6 sanguine et de favoriser les thromboses.…”

Influence of exogenous oestrogen or (anti-) androgen administration on soluble transferrin receptor in human plasma

“…Interestingly, there is no difference in serum erythropoietin levels between men and women, even though there is a significant difference in their testosterone and Hb levels (Miller et al 1985). So, it seems that the androgenmediated increases in Hb levels and Hct are not exclusively mediated by erythropoietin, and testosterone may have a direct effect on bone marrow stem cells (Shahidi 1973, Krabbe et al 1978, Mooradian et al 1987, Krauss et al 1991. Our study monitored the effects of sex steroids on Hb and the Hct in transsexuals undergoing cross-sex hormone administration, making use of a quantitative assay of bone marrow erythropoietic activity, the soluble transferrin receptor (sTfR).…”