MxA protein - an interferon beta biomarker in primary progressive multiple sclerosis patients

Background and purpose:  Interferon beta (IFNβ) preparations have some effect on the progressive phase of multiple sclerosis (MS). This limited effect might be partially because of a certain number of IFNβ non‐responders. Myxovirus resistance protein A (MxA) – a marker of IFNβ bioactivity – was corr...

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Published in:European journal of neurology Vol. 15; no. 8; pp. 822 - 826
Main Authors: Millonig, A., Dressel, A., Bahner, D., Bitsch, A., Bogumil, T., Elitok, E., Kitze, B., Tumani, H., Weber, F., Gneiss, C., Deisenhammer, F.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01-08-2008
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Summary:Background and purpose:  Interferon beta (IFNβ) preparations have some effect on the progressive phase of multiple sclerosis (MS). This limited effect might be partially because of a certain number of IFNβ non‐responders. Myxovirus resistance protein A (MxA) – a marker of IFNβ bioactivity – was correlated with the clinical response during an uncontrolled trial, investigating the safety of IFNβ‐1b in primary progressive (PPMS) patients. Methods:  Twenty PPMS were treated with IFNβ‐1b (s.c.) for 1 year. Blood samples were taken before and 1, 2, 3, 6, 9, 12, and 15 months after treatment initiation and MxA protein levels were measured. Patients were clinically evaluated by EDSS and the more sensitive Incapacity Status Scale (ISS) and stratified in a stable and a progressing group. Results:  Using ISS criteria, 11 patients remained stable and nine patients progressed during treatment. The mean area under the curve of log MxA levels during treatment were significantly higher in stable than in progressing patients (10.87 vs. 5.99; P = 0.002). Conclusion:  A good biological response to IFNβ might be associated with a better clinical effect of this drug and could be helpful in future clinical studies for early identification of treatment responders.
Bibliography:ark:/67375/WNG-BHQBZP1V-B
ArticleID:ENE2190
istex:CADC83D96B3823466F51C8DF35C5E8D2556218C7
Addresses: A. Dressel (Department of Neurology, University of Greifswald, Ellernholzstraβe 1/2, 17847 Greifswald, Germany); D. Bahner (Klinik für Neurologie, Klinikum Bad Hersfeld, Seilerweg 29,36251 Bad Hersfeld, Germany); A. Bitsch (Ruppiner Kliniken GmbH, Fehrbelliner Straβe 38, 16816 Neuruppin, Germany); T. Bogumil (Bayer HealthCare Pharmaceuticals Inc., PO Box 1000, Montville, NJ 07045, USA); H. Tumani (University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany); F. Weber (Section of Neurology, Max‐Planck Institute of Psychiatry, Kraepelinstraβe 2‐10, 80804 Munich, Germany); and Dr. Ercan Elitok (Nihon Kohden Europe Gmbh, Raiffeisenstraße 10, 61191 Rosbach v.d.H., Germany).
ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:1351-5101
1468-1331
DOI:10.1111/j.1468-1331.2008.02190.x