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Androgenic‐anabolic steroid drug‐induced liver injury

Bodybuilders and athletes frequently abuse androgenicanabolic steroids (AAS), which have both physiological and metabolic consequences. The prevalence of AAS abuse is increasing, with reported rates of 15–30% in weight trainers in health clubs and gyms. AAS are increasingly being used for their cosmetic benefit, with the number of reported steroid users increasing in the high school population group; approximately 6.6% of year 12 students in America were reported to have taken AAS in 1988. More recent reports estimate rates of 3–12% of male and 0.5–2% of female adolescents. Similar figures have been reported in several countries in Europe, and in Australia and Brazil, with a lifetime prevalence of AAS use between 1% and 6% for high school students, and between 9% and 38% among bodybuilders. This trend has not only resulted in an increase in anabolic-steroid-associated reproductive and endocrine disorders, myocardial hypertrophy, stroke, aggression, and depression, but has also been associated with hepatocellular injury. Due to the illicit nature of AAS and the relative paucity of reported cases, there is little consensus on diagnosis, monitoring or therapy for AAS-induced hepatocellular injury. We report the case of a 46-year-old man who presented to the emergency department with a 3-month history of painless jaundice and weight loss of 9 kg over 3 weeks. He had ceased his AAS use 5 months prior to presentation. He reported nausea, pruritus and anorexia. He had ingested stanozolol (40 mg) and methandrostenolone (40 mg) daily for 2 months, and reported stopping usage 5 months prior to his initial symptoms. There was no other exposure to drugs associated with cholestatic liver injury. There was no history of significant alcohol intake, intravenous drug use or herbal medication intake, and his body mass index was 28.5. Examination revealed jaundice, icterus and a mildly tender right-upper quadrant. There was no encephalopathy, and he was haemodynamically stable. Liver function tests showed a mixed cholestatic and hepatitic pattern, with alkaline phosphatase 295 U/L, gamma glutamyl transpeptidase 114 UL, alanine transaminase 125 U/L and bilirubin of 302 mmol/L (conjugated bilirubin of 127 mmol/L). There was no synthetic dysfunction. Viral and autoimmune serologies were unremarkable. Ultrasound of the liver and computed tomography of the abdomen were normal. A liver biopsy showed intrahepatic cholestasis and occasional necroinflammatory foci, consistent with a drug reaction and proliferation (indicative of stanozolol usage) (Fig. 1). He was commenced on ursodeoxycholic acid treatment, and at week 7 post-discharge, he had complete resolution of his jaundice, and liver function tests and ursodeoxycholic acid was ceased. In the setting of controlled medical use, AAS are rarely associated with jaundice. Abuse of AAS is becoming an increasingly common problem; four out of every five users of AAS have been found to be non-athletes, taking these drugs for cosmetic reasons, with most taking larger doses than previously recorded. 17a-AAS include the compounds methyltestosterone, methandrostenolone, oxymetholone, oxandrolone and stanozolol. Long-term AAS use has been linked to a spectrum of liver injury, such as peliosis, adenoma and hepatocellular carcinoma. Stanozolol is a 17a-AAS that is often misused by athletes and bodybuilders. Druginduced liver injury secondary to AAS usually presents with painless jaundice. The level of jaundice appears to be dose-dependent. The pattern of liver function derangement most often described in association with AAS is a mixed cholestatic and hepatitic picture, which corresponds with the intrahepatic cholestasis and hepatocellular necrosis found in liver biopsy. AAS have been shown in adult male rats to result in moderate inflammatory or degenerative lesions in Figure 1 Necroinflammatory appearance with cholestasis. bs_bs_banner