Abstract
Anabolic androgenic steroids (AAS), simply called “androgens”, represent the most widespread drugs used to enhance performance and appearance in a sporting environment. High-dosage and/or long-term AAS administration has been associated frequently with significant alterations in the cardiovascular system, some of these with severe endpoints. The induction of a prothrombotic state is probably the most life-threatening consequence, suggested by numerous case reports in AAS-abusing athletes, and by a considerable number of human and animal studies assessing the influence of exogenous androgens on hemostasis. Despite over fifty years of research, data regarding the thrombogenic potential of exogenous androgens are still scarce. The main reason is the limited possibility of conducting human prospective studies. However, human observational studies conducted in athletes or patients, in vitro human studies, and animal experiments have pointed out that androgens in supraphysiological doses induce enhanced platelet activity and thrombopoiesis, leading to increased platelet aggregation. If this tendency overlaps previously existing coagulation and/or fibrinolysis dysfunctions, it may lead to a thrombotic diathesis, which could explain the multitude of thromboembolic events reported in the AAS-abusing population. The influence of androgen excess on the platelet activity and fluid–coagulant balance remains a subject of debate, urging for supplementary studies in order to clarify the effects on hemostasis, and to provide new compelling evidence for their claimed thrombogenic potential.
Highlights
Anabolic androgenic steroids (AAS) are synthetic derivatives of testosterone, primarily designed to have both an enhanced anabolic and a reduced androgenic activity compared to the parent molecule [1,2]
We focused on reviewing a segment of the global field of existing data—the effects of exogenous androgens on platelet hemostatic activity and thrombopoiesis
Supporting the putative pro-aggregant action of suprapharmacological AAS, we have shown in a previous published study that high doses of nandrolone decanoate (DECA), chronically administered (10 mg/kg body weight, for 12 weeks), induced a significant increase in platelet aggregation triggered by adenosine diphosphate (ADP) (2.5 μM) in the platelet-rich plasma (PRP) from male Wistar rats [152]
Summary
Anabolic androgenic steroids (AAS) are synthetic derivatives of testosterone, primarily designed to have both an enhanced anabolic and a reduced androgenic activity compared to the parent molecule [1,2]. Over 100 synthetic substances have been introduced in clinical practice as treatments for various conditions, such as hypogonadism, anemia secondary to bone marrow insufficiency or renal failure, hereditary angioedema, osteoporosis, catabolic states associated with HIV infection, cancer, burns, chronic obstructive pulmonary disease, alcoholic hepatitis, or neuromuscular diseases [3,4,5] Their powerful anabolic properties have led to an illicit use, with them being currently abused in high doses by athletes for enhanced performance, or in the bodybuilding community for cosmetic reasons [5,6,7]. AAS-induced cardiovascular events are mostly present in a young and healthy population, with no associated risk factors or proven atherosclerotic lesions [19,20,21,22,23,24] This suggests that the pathophysiological mechanism might be atherothrombotic rather than atherogenic, or vasospastic. This review covers the available literature data regarding the influence of androgens usage on platelet function and thrombopoiesis, focusing on their thrombogenic potential in supraphysiological administration, probably the most important cardiovascular side effect emerging from AAS abuse
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