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Thrombotic thrombocytopenic purpura associated with adalimumab (Humira) treatment in Crohn disease

xenobiotics. It is postulated that that high doses of stanozolol may cause proliferation of hepatocytes, which was demonstrated in our patient’s liver biopsy. The druginduced liver injury caused by AAS is thought to be due to direct hepatotoxicity of the AAS, which appears to be dependent on individual susceptibility. The drug-induced cholestasis appears to be reversible upon withdrawal of AAS. Supportive care with reversal of coagulopathy and empirical usage of ursodeoxycholic acid has shown improvement of hepatic dysfunction. The case presented here differs from those previously reported in that the obstructive jaundice developed only 5 months after commencing AAS, whereas most cases have been described at the time of commencement or within weeks of usage. Recovery was prolonged, requiring 5 months of abstinence from stanozolol use. Common drugs causing cholestasis or cholestatic hepatitis, such as clavulanic acid, flucloxacillin and terbinafine, need to be considered initially. However, it is important to consider abuse of AAS in cases where the diagnosis is proving difficult, particularly in certain demographics such as young age. Our case also demonstrates that the utility of a liver biopsy as findings suggestive of hepatotoxicity secondary to cholestasis may aid in the diagnosis of patients. AAS-induced hepatocellular damage can be a challenging diagnosis for clinicians, largely due to its covert usage. A high index of suspicion is required to make the diagnosis, and counselling regarding abstinence from ongoing use is required to prevent progressive drug-induced liver disease.