Loading…

Anabolic-androgenic steroids: a possible new risk factor of 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 fac...

Full description

Saved in:
Bibliographic Details
Published in:Liver international 2011-03, Vol.31 (3), p.348-353
Main Authors: Schwingel, Paulo Adriano, Cotrim, Helma P., Salles, Bernardo Rios, Almeida, Carlos Eduardo, dos Santos Jr, Crimério Ribeiro, Nachef, Bruno, Andrade, Antonio Ricardo, Zoppi, Cláudio C.
Format: Article
Language:English
Subjects:
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1478-3223
1478-3231
DOI:10.1111/j.1478-3231.2010.02346.x