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Anabolic-androgenic steroids: a possible new risk factor of toxicant-associated fatty liver disease.
Liver International : Official Journal of the International Association for the Study of the Liver 2011 March
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.
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.
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