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BRIEF COMMUNICATIONS: Dana Ekstein, Eduard Linetsky, Oded Abramsky, and Dimitrios Karussis Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis Neurology 2005; 65: 456-458 [Abstract] [Full text] [PDF]

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Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis

Bernd C. Kieseier, Hans-Peter Hartung   (19 October 2005)

Reply to Kieseier et al

Dana Ekstein, Oded Abramsky   (19 October 2005)

Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis 19 October 2005
Bernd C. Kieseier, Dept Neurology, Heinrich-Heine University Duesseldorf Moorenstrasse 5, 40225 Duesseldorf, Germany, Hans-Peter Hartung Send Correspondence to journal: Re: Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis bernd.kieseier{at}uni-duesseldorf.de Bernd C. Kieseier, et al.	Ekstein et al report that interferon beta could promote immune-mediated diseases of the nervous system. [1] This is unclear considering interferon beta is known to exhibit multiple immunomodulatory effects within the peripheral immune compartment which would probably inhibit rather than induce inflammation.[2] Of the six cases reported, one patient did not have neuropathy or leukemia. It is possible that a pre-existing neuropathy prior to the initiation of therapy with interferon beta was missed. Coexistence of chronic immune-mediated demyelination of the central and peripheral nervous system has been reported. It is known that patients with inflammatory disorders of the peripheral nervous system sometimes exhibit demyelinating lesions of the CNS on MRI as well as delayed visual evoked responses.[3] Even the association of an acute axonal form of Guillain-Barré Syndrome and multiple sclerosis (MS) has been described.[4] It is possible that in few patients the immune response is mounted against target antigens shared between the central and peripheral nervous systems. Interferon beta is proven to be clinically effective in MS and apparently also in some patients with chronic inflammatory demyelinating polyradiculoneuropathy.[5] Given the predominant mode of action of this drug within the peripheral immune compartment and the similarities in the immunopathogenesis between immune-mediated demyelination of the central and peripheral nervous systems, it seems unlikely that interferon beta promotes inflammation within the peripheral nerve. In the case reported by Ekstein et al, the patient did not exhibit any or only a weak clinical response to interferon beta. The authors may have just observed the natural course of the disease. References 1. Ekstein D, Linetsky E, Abramsky O, Karussis D. Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis. Neurology 2005;65:456-458. 2. Yong VW. Differential mechanisms of action of interferon-beta and glatiramer acetate in MS. Neurology 2002;59:802-808. 3. Köller H, Kieseier BC, Jander S, Hartung HP. Chronic inflammatory demyelinating polyneuropathy. N Engl J Med 2005;352:1343-1356. 4. Capello E, Roccatagliata L, Schenone A et al. Acute axonal form of Guillain- Barré syndrome in a multiple sclerosis patient: chance association or linked disorders? Eur J Neurol 2000;7:223-225. 5. Vallat JM, Hahn AF, Leger JM et al. Interferon beta-1a as an investigational treatment for CIDP. Neurology 2003;60:S23-28. Disclosure: The authors report no conflicts of interest
Reply to Kieseier et al 19 October 2005
Dana Ekstein, Department of Neurology and the Agnes Ginges Center for Neurogenetics, Hadassah-Hebrew Universit Hadassah Ein-Karem Medical Center, Jerusalem, Israel, Oded Abramsky Send Correspondence to journal: Re: Reply to Kieseier et al dekstein{at}md.huji.ac.il Dana Ekstein, et al.	We appreciate Drs. Kieseier and Hartung's thoughtful comments and agree that more studies are needed to document a clear association between interferon beta treatment and neuropathy in MS. Meanwhile, we believe that the temporal relationship between the initiation of treatment and appearance of neuropathy, and improvement of neuropathy when drug is discontinued, strongly suggest that interferons may cause peripheral neuropathy in some MS patients. Although previously reported [6], the mechanism of this paradoxical and probably rare effect is unknown. Reference 6. Pirko I, Kuntz NL, Patterson M, Keegan BM, Weinshenker BG, Rodriguez M. Contrasting effects of IFNbeta and IVIG in children with central and peripheral demyelination. Neurology 2003;60:1697-1699. Dana Disclosure: The authors report no conflicts of interest.