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Anabolic‐androgenic steroids: a possible new risk factor of toxicant‐associated fatty liver disease
Author(s) -
Schwingel Paulo Adriano,
Cotrim Helma P.,
Salles Bernardo Rios,
Almeida Carlos Eduardo,
dos Santos Crimério Ribeiro,
Nachef Bruno,
Andrade Antonio Ricardo,
Zoppi Cláudio C.
Publication year - 2011
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2010.02346.x
Subject(s) - fatty liver , medicine , steatohepatitis , insulin resistance , toxicant , steatosis , endocrinology , risk factor , gastroenterology , nonalcoholic fatty liver disease , insulin , disease , toxicity
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.