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From the Department of Neurology (M.L., A.S., U.S., S.S., T.K., U.W.), University Hospital Bonn, Bonn, Germany; Department of Pediatrics and Clinical Chemistry (S.K., R.J.A.W.), University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Department of Clinical Genetics (W.J.K., M.L.T.V.), Erasmus Medical Center, Rotterdam, The Netherlands; Department Pediatrics (J.G.), University Hospital Göttingen, Göttingen, Germany; Department of Epileptology (K.F.), University Hospital Bonn, Bonn, Germany; Department of Neurology (P.S., W.K.), Sächsisches Krankenhaus Hubertusburg, Wermsdorf, Germany; Department of Neurology (U.S.), University Hospital Bochum, Knappschaftskrankenhaus, Bochum, Germany.
Address correspondence and reprint requests to Dr. Michael Linnebank, University Hospital Bonn, D-53105 Bonn, Germany; e-mail: michael.linnebank{at}ukb.uni-bonn.de
A combined genotype of polymorphisms of methionine metabolism has been associated with CNS demyelination in methotrexate-treated patients. Within a sample of 86 patients with X-linked adrenoleukodystrophy, this genotype was overrepresented in a subgroup of 15 patients with adrenomyeloneuropathy (AMN) with CNS demyelination (adrenoleukomyeloneuropathy) in comparison to 49 AMN patients without CNS demyelination ("pure" AMN; p = 0.002), suggesting that methionine metabolism might contribute to the phenotypic variability in adrenoleukodystrophy.
Disclosure: The authors report no conflicts of interest.
Received August 22, 2005. Accepted in final form October 20, 2005.
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