Anabolic androgenic steroid abuse impairs fibrin clot lysis

Johannes Jakobsen Sidelmann, Jørgen Brodersen Gram, Jon Rasmussen, Caroline Kistorp

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


Abuse of anabolic-androgenic steroids (AAS) is suspected to increase the risk of cardiovascular disease (CVD) and cardiovascular mortality in otherwise healthy individuals. AAS abuse may increase the incidence of CVD by altering the hemostatic balance toward a pro-coagulant state. Studies on the effect of AAS abuse on the fibrinolytic system, however, have either demonstrated a pro-fibrinolytic effect or no effect of AAS abuse, but the overall effect of AAS on fibrinolysis has not been addressed so far. The present cross-sectional study investigated the effect of AAS on fibrin clot lysis, fibrin structure and the hemostatic proteins potentially affecting these measures in current and former AAS abusers and healthy age-matched controls. The study population consisted of 37 current and 33 former AAS abusers, along with 30 healthy age-matched controls. Fibrin clot lysis, fibrin structure properties, fibrinogen, coagulation factor XIII (FXIII) plasminogen, plasmin inhibitor, plasminogen activator inhibitor 1 (PAI-1), and thrombin activatable fibrinolysis inhibitor (TAFI) were determined. Fibrin clot lysis was significantly reduced in participants abusing AAS compared to former abusers and controls, p<0.001. Plasma fibrinogen, plasminogen and plasmin inhibitor were significantly increased in current abusers (P<0.05). No significant differences were observed with respect to measures of fibrin structure properties, PAI-1, and TAFI (P>0.05). In conclusions, AAS abuse depresses fibrin clot lysis. This effect is not associated with alterations in fibrin structure but is rather caused by increased plasma concentrations of fibrinogen, FXIII and plasmin inhibitor. These findings suggest that AAS abuse may be associated with increased thrombotic disease.
TidsskriftSeminars in Thrombosis and Hemostasis
StatusAccepteret/In press - jan. 2020