Elevated liver enzymes under therapy with methylphenidate in a boy with T-cell leukemia

Abstract

The established standard of pharmacotherapy of the attention deficit hyperactivity disorder is methylphenidate, a drug with very few side effects. A 4-year-old boy with T cell acute lymphoblastic leukemia, and severe damage to the white matter induced by chemo- and radiotherapy was treated with methylphenidate in increasing doses due to marked attention deficit hyperactivity disorder. Liver enzymes, i.e. aspartate aminotransferase, alanine aminotransferase and gamma glutamyltranspeptidase, were slightly elevated prior to therapy. Three weeks into methylphenidate therapy, the patient suffered from recurrent vomiting. Liver enzymes were elevated with alanine aminotransferase at 1260 U/L, aspartate aminotransferase at 499 U/L and gamma glutamyltranspeptidase 284 U/L. Creatine kinase was elevated at 405 U/L, while bilirubin and renal function parameters were within normal levels. Following discontinuation of therapy, liver enzymes returned almost to normal levels within a week. Hepatotoxic reactions to methylphenidate are extremely rare. As methylphenidate inhibits the liver cytochrome P450 system, synergistic toxic effects are possible in theory. An elevated creatine kinase level would be possible within the framework of autoimmune reactions. Patients with increased risk (i.e. age below 6 years, hepatic stress due to prior pharmacotherapy) should be treated with methylphenidate, only under close clinical and laboratory monitoring.

Keywords

Methylphenidate - creatine kinase - liver enzymes - hepatotoxicity