Perturbation of the Hematopoietic Profile by Anabolic Androgenic Steroids

Objective. The aim of this study was to investigate the hematopoietic profile in AAS abusers, during or short after their last abuse and approximately six months later. Moreover, we studied if supraphysiological doses of testosterone influence the concentration of hemoglobin and erythropoietin in healthy volunteers. Design and Methods. Subjects ( ) were recruited through an antidoping hotline. The hematological profile was measured when the subjects entered the study and approximately 6 months later. Testosterone enanthate (500？mg) was administered to healthy volunteers ( ). Gene expression was studied in human hek293 cells exposed to 1？μM testosterone. Results. Decreased levels of hemoglobin, erythrocyte volume fraction, and erythrocyte counts were observed after 6 months without the use of AAS. Results in volunteers show that hemoglobin increased 3% four and 15 days after testosterone administration, whereas EPO was significantly increased by 38% four days after dose. Agreeingly, in vitro study shows that testosterone induces the mRNA level of EPO with 65% after 24-hour exposure. Conclusion. These results indicate that supraphysiological doses of testosterone may cause a perturbation in the hematopoietic profile. This is of interest in relation to the adverse cardiovascular effects observed in AAS abusers. 1. Introduction The group of anabolic-androgenic steroids (AAS) includes testosterone and its analogue synthetic derivatives and chemical congeners. They are commonly abused by athletes and sportsmen to improve muscle mass and enhance exercise performance. AAS are the most frequently detected doping agents, testosterone being the predominant steroid (http://www.wada-ama.org). Notably, the abuse of these agents among nonprofessional athletes, as well as among people who want to enhance their physical appearance, is a growing public health problem and has become a major society concern [1–3]. The adverse effects of AAS on the cardiovascular system include adverse changes in cholesterol levels [4], endothelial dysfunction [5], and alterations of the structure of the heart, such as enlargement and thickening of the left ventricle which impairs its contraction and relaxation [6, 7]. Several case reports suggest that AAS may induce thrombotic events such as myocardial infarction [8–13]. A possible mechanism contributing to thrombogenesis is an increase in hemoglobin (Hb) associated with AAS use [14]. Such increases in hematocrit values have been associated with cardiovascular risks including atherosclerosis, coronary artery disease, and myocardial