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NEUROLOGY 2005;64:912-913
© 2005 American Academy of Neurology
Brief Communications

MTX-induced white matter changes are associated with polymorphisms of methionine metabolism

M. Linnebank, MD, H. Pels, MD, N. Kleczar, S. Farmand, K. Fliessbach, MD, H. Urbach, MD, K. Orlopp, MD, T. Klockgether, MD, I. G.H. Schmidt-Wolf, MD and U. Schlegel, MD

From the Departments of Neurology (Drs. Linnebank, Pels, Fliessbach, Klockgether, and Schlegel, and N. Kleczar and S. Farmand), Radiology (Dr. Urbach), and Internal Medicine (Drs. Orlopp and Schmidt-Wolf), University Hospital Bonn, Germany.

Address correspondence and reprint requests to Dr. Michael Linnebank, University Hospital Bonn, Department of Neurology, Sigmund-Freud-Str. 25, 53105 Bonn, Germany; e-mail: Michael.Linnebank{at}ukb.uni-bonn.de

Methotrexate (MTX) is a folate antagonist inhibiting nucleic acid and methionine synthesis. Methionine is necessary for CNS myelination. In 42 patients with primary CNS lymphoma (PCNSL) treated with a systemic and intraventricular high-dose MTX-based polychemotherapy, the presence of a risk haplotype defined by polymorphisms influencing methionine metabolism referred a relative risk for CNS white matter changes of 4.7 (p = 0.001). The authors conclude that methionine metabolism influences MTX neurotoxicity.


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