Affiliations: Hospital for Children and Adolescents, University of
Leipzig, Leipzig, Germany
Note: [] Correspondence: Dr. Matthias K. Bernhard, Hospital for Children
and Adolescents, University of Leipzig, Liebigstr. 20a, D-04103 Leipzig,
Germany. Tel.: +49 341 97 26250; E-mail: Matthias.
Bernhard@medizin.uni-leipzig.de
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.
