A girl with multiple sclerosis and severe hepatitis

A 15-year-old girl presented with transverse myelitis. The brain and spinal MR imaging was compatible with the diagnosis of multiple sclerosis (MS). Her past medical history was silent and she started intravenous high-dose methylprednisolone 1 g/day for 5 days with clinical improvement. After about 20 days of therapy she had an acute episode of generalized urticaria and angioedema treated with a bolus of methylprednisolone. Blood exams showed marked increase of transaminases (ALT up to 2844 U/L; 54×ULN) with normal GGT, hyperbilirubinemia (total 2.10 mg/dl, direct 0.60 mg/dl) and PT INR value of 1.5. Hepatotropic viruses serologies were not diagnostic, autoimmunity biomarkers were absent and Wilson disease was excluded. Ultrasound imaging reported diffuse parenchymal echogenicity. A liver biopsy showed lesions of acute hepatitis (portal tract inflammation with confluent lobular necrosis). These findings confirm the diagnosis of acute cytotoxic hepatitis induced by drugs (methylprednisolone). In the following days transaminases progressively improved (ALT 365 U/L; 6×ULN), returned to normal value within six-months, and persisted normal. High dose methylprednisolone is the first-line therapy for acute exacerbation of MS. Methylprednisolone-induced liver injury may occur in patients, mostly adults, treated for MS and can be severe and life threatening. It is probably related to a transient immune rebound with spontaneous normalization of liver function test after drug discontinuation. This condition is extremely rare in pediatrics with only one pediatric case reported in literature. The knowledge that high-dose methylprednisolone may induce liver injury is useful in order to close monitoring these patients and prevent acute liver failure.