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Case Reports
. 2006 Oct;40(10):1868-71.
doi: 10.1345/aph.1H171. Epub 2006 Aug 22.

Methylprednisolone-induced toxic hepatitis

Affiliations
Case Reports

Methylprednisolone-induced toxic hepatitis

Firdevs Topal et al. Ann Pharmacother. 2006 Oct.

Abstract

Objective: To report the third published case, as of April 8, 2006, of methylprednisolone-induced toxic hepatitis.

Case summary: A 47-year-old woman was admitted to our clinic with weakness, fatigue, pruritus, and scleral icterus that had developed 10 days prior to presentation. She had been taking topiramate for one year for treatment of chronic isolated central nervous system vasculitis. One week before her symptoms developed, she had completed a self-prescribed 7 day course of oral methylprednisolone for treatment of left arm weakness. She believed that methylprednisolone was appropriate since it had been used previously for acute episodes of vasculitis. Results of liver function tests performed on admission were alanine aminotransferase 2478 U/L, aspartate aminotransferase 1600 U/L, total bilirubin 10 mg/dL, direct bilirubin 8 mg/dL, alkaline phosphatase 138 U/L, and gamma-glutamyl transferase 242 U/L. Topiramate and methylprednisolone were the only drugs she had been taking before admission, and no other causes of liver dysfunction (eg, infection, ischemia, systemic disease) were identified. Topiramate was stopped, and enzyme levels decreased to normal values within 45 days without treatment. There had been no increase in enzyme levels during hospitalization upon the accidental use of topiramate. Based on the history and laboratory findings, the final diagnosis was mixed hepatocellular and cholestatic liver injury caused by methylprednisolone.

Discussion: Steroids have rarely been associated with hepatotoxicity; moreover, they are the treatment of choice for severe hepatitis. To date, only 2 cases of methylprednisolone-induced hepatotoxicity have previously been reported. Our case is similar to those with regard to mixed hepatocellular and cholestatic liver injury. Resolution of the hepatotoxicity occurred after discontinuation of the drug, with conservative treatment measures. An objective causality assessment based on the Naranjo scale suggests that hepatotoxicity was probably related to methylprednisolone.

Conclusions: Although rare, hepatotoxicity related to methylprednisolone should be considered in patients who develop elevated enzyme levels while receiving this steroid.

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