Anabolic-androgenic steroids: a possible new risk factor of toxicant-associated fatty liver disease
Article first published online: 11 OCT 2010
© 2010 John Wiley & Sons A/S
Volume 31, Issue 3, pages 348–353, March 2011
How to Cite
Schwingel, P. A., Cotrim, H. P., Salles, B. R., Almeida, C. E., dos Santos, C. R., Nachef, B., Andrade, A. R. and Zoppi, C. C. (2011), Anabolic-androgenic steroids: a possible new risk factor of toxicant-associated fatty liver disease. Liver International, 31: 348–353. doi: 10.1111/j.1478-3231.2010.02346.x
- Issue published online: 1 FEB 2011
- Article first published online: 11 OCT 2010
- Received 16 June 2010, Accepted 22 August 2010
- anabolic agents;
- drug use;
- non-alcoholic fatty liver disease;
- toxicant-associated fatty liver disease
Background: Industrial toxin and drugs have been associated with non-alcoholic fatty liver disease (NAFLD); in these cases, the disease has been termed toxicant-associated steatohepatitis (TASH).
Aim: This study hypothesizes that the use of anabolic-androgenic steroids (AAS) could also be a risk factor to TASH or better toxicant-associated fatty liver disease (TAFLD) development.
Methodology: Case–control study including 180 non-competitive recreational male bodybuilders from August/2007 to March/2009. Ninety-five had a history of intramuscular AAS use (cases; G1) and 85 were non-users (controls; G2). They underwent a clinical evaluation and abdominal ultrasound, and their blood levels of aminotransferases, creatine phosphokinase (CPK), lipids, glucose and insulin were measured. TAFLD criteria: history of AAS use >2 years; presence of hepatic steatosis on ultrasound and/or aminotransferase alterations with normal CPK levels; exclusion of ethanol intake ≥20 g/day or use of other drugs; and exclusion of obesity, dyslipidaemia, diabetes and other liver diseases. Homeostasis model assessment for insulin resistance ≥3 was considered insulin resistant. Independent t-test, odds ratio (OR) and 95% confidence intervals (95% CI) were calculated.
Results: All cases were asymptomatic. Clinical and laboratorial data were similar in G1 and G2 (P>0.05). TAFLD criteria were observed in 12.6% of the G1 cases and 2.4% of controls had criteria compliant with non-alcoholic fatty liver related to metabolic conditions. OR was 6.0 (95% CI: 1.3–27.6).
Conclusions: These results suggest that AAS could be a possible new risk factor for TAFLD. In this type of fatty liver disease, the individuals had a low body fat mass and they did not present insulin resistance.