Effect of Anabolic–Androgenic Steroid Abuse on the Contact Activation System

Johannes Jakobsen Sidelmann; Jørgen Brodersen Gram; Yaseelan Palarasah; Jon Jarløv Rasmussen; Caroline Kistorp

doi:10.1055/a-1346-3384

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2021; 121(10): 1268-1273
DOI: 10.1055/a-1346-3384

Coagulation and Fibrinolysis

Effect of Anabolic–Androgenic Steroid Abuse on the Contact Activation System

Johannes Jakobsen Sidelmann

¹Unit for Thrombosis Research, Department of Regional Health Research, University of Southern, Esbjerg, Denmark

²Department of Clinical Biochemistry, University Hospital of Southern Denmark, Esbjerg, Denmark

,

Jørgen Brodersen Gram

¹Unit for Thrombosis Research, Department of Regional Health Research, University of Southern, Esbjerg, Denmark

²Department of Clinical Biochemistry, University Hospital of Southern Denmark, Esbjerg, Denmark

,

Yaseelan Palarasah

¹Unit for Thrombosis Research, Department of Regional Health Research, University of Southern, Esbjerg, Denmark

²Department of Clinical Biochemistry, University Hospital of Southern Denmark, Esbjerg, Denmark

³Department of Cancer and Inflammation Research, University of Southern Denmark, Odense, Denmark

,

Jon Jarløv Rasmussen

⁴Department of Endocrinology, Copenhagen University Hospital – Rigshospitalet, Copenhagen, Denmark

,

Caroline Kistorp

⁴Department of Endocrinology, Copenhagen University Hospital – Rigshospitalet, Copenhagen, Denmark

› Institutsangaben

Abstract

The effect of anabolic–androgenic steroid (AAS) abuse on the contact activation system (CAS) is not known in detail. We hypothesized that current AAS abuse reduces the kallikrein-generating capacity of CAS significantly and investigated the impact of AAS on the proteins and capacity of CAS in current and former AAS abusers and healthy age-matched controls. Men 18 to 50 years of age were included as current AAS abusers, former AAS abusers, or controls. Blood samples were collected after overnight fasting. Kallikrein generation (lag time, peak height, and endogenous kallikrein potential [EKP]), coagulation factor XII (FXII), prekallikrein, high-molecular-weight kininogen (HK), and Complement C1 esterase inhibitor (C1inh) were assessed. Groups were compared by analysis of variance or Kruskal–Wallis test and probabilities were corrected for multiple comparisons. Associations were evaluated by linear regression models. The EKP was significantly reduced in current (n = 37) AAS abusers (984 ± 328 nmol/L × min) compared with former (n = 33) abusers (1,543 ± 481 nmol/L × min) and controls (n = 30) (1,521 ± 339 nmol/L × min), p < 0.001. Current abusers had higher levels of FXII and C1inh and lower levels of prekallikrein and HK than controls, p ≤ 0.025. Stepwise regression analysis showed that EKP was associated with C1inh and prekallikrein in current AAS abusers, R ² = 0.70, p < 0.001. We conclude that current AAS abuse reduces the kallikrein-generating capacity of CAS by increasing the concentration of C1inh and reducing the concentration of prekallikrein. These changes may contribute to the anti-inflammatory effect of testosterone.

Keywords

factor XII - prekallikrein - C1 esterase inhibitor - high-molecular-weight kininogen - anabolic–androgenic steroids

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Referenzen

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