Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

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

Research output: Contribution to journalJournal articleResearchpeer-review

DOI

  1. Isolated Distal Deep Vein Thrombosis: Perspectives from the GARFIELD-VTE Registry

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Upper Extremity DVT versus Lower Extremity DVT: Perspectives from the GARFIELD-VTE Registry

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Characteristics and Management of Patients with Venous Thromboembolism: The GARFIELD-VTE Registry

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Smoking is Associated with Increased Risk of Major Bleeding: A Prospective Cohort Study

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

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, R2 = 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.

Original languageEnglish
JournalThrombosis and Haemostasis
ISSN0340-6245
DOIs
Publication statusPublished - 5 Jan 2021

    Research areas

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

ID: 65861543