Interferon beta treatment does not induce organ-specific autoantibodies in multiple sclerosis

T. Menge, N. C. Schloot, M. Schott, B. Hemmer, H. Wiendl, M. Roden, H. P. Hartung, B. C. Kieseier

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Indications:83 patients with multiple sclerosis.

Patients:209 patients. IFNβ group negative for neutralizing antibodies (NABs): n=106, 75 females and 31 males, mean age 40.7 years, 47 received Extavia. IFNβ group with positive NABs: n=103, 69 females and 34 males, mean age 41.7 years, 36 received Extavia. Control group (no treatment): n=57, 41 females and 16 males, mean age 39.5 years.

TypeofStudy:A study evaluating whether interferon (IFN) beta (including Extavia) treatment induce organ-specific autoantibodies (AAbs) in patients with multiple sclerosis (MS).

DosageDuration:Dosage not stated. Mean duration: 46.1 months for patients with negative NABs and 41.4 months for those with positive NABs.

Results:When stratified for the presence of NABs, prevalences for neither anti-GAD65, anti-TPO, nor anti-Tg were remarkably elevated in any of the subgroups. Titers of positive AAbs were not remarkably different between subgroups for anti-GAD65, anti-TPO, or anti-Tg, even though positive AAbs were highly elevated in the majority of cases (median anti-GAD65: 28.1 U/mL; anti-TPO: 288.7 U/mL). Gender was a confounding factor for anti-TPO and anti-Tg, being more prevalent in females (anti-TPO: 89% versus 67%; anti-Tg: 90% versus 68%). Age was also a confounder: anti-TPO positive patients were older (44.7 versus 40.3 years) and anti-GAD65 seropositive patients younger (32.0 versus 41.0 years). Expanded Disability Status Scale, disease duration, or IFNβ product were not associated with either AAbs status.

AdverseEffects:No adverse events were mentioned.

AuthorsConclusions:Our results underscore the longstanding safety profile of IFNβ therapy in MS, especially in light of upcoming immunotherapies that may convey the potential to induce autoimmunity, e.g., autoimmune thyroiditis.

FreeText:AAbs were determined by commercial radioligand assays against glutamic acid decarboxylase (GAD65) and against thyroperoxidase (TPO) and thyroglobulin (Tg) with predefined cutoff levels. Presence of NABs was assessed by capture enzyme linked immunosorbent assay and ex vivo myxovirus resistance protein A real time polymerase chain reaction.

Original languageEnglish
Pages (from-to)900-902
Number of pages3
JournalNeurology
Volume73
Issue number11
DOIs
StatePublished - Sep 2009

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