title: Interferon beta-1b treatment does not induce autoantibodies.
abstract: BACKGROUND
  There is little information regarding the potential of interferon beta (IFNbeta) to induce or exacerbate autoimmune disease. Existing data from uncontrolled studies are contradictory and do not differentiate between autoimmune dysfunction, which is frequent in patients with multiple sclerosis (MS), and untoward drug effects.
  
  
  OBJECTIVE
  To evaluate the impact of IFNbeta on hepatic, thyroid, and other markers of autoimmunity using data from the European placebo-controlled double-blind, multicenter study of IFNbeta-1b in patients with secondary progressive MS (SPMS).
  
  
  METHODS
  Serum samples obtained at baseline and at 6-month intervals for 24 months were analyzed for the following autoantibodies (AAbs): antinuclear (ANA), antimitochondrial (AMA), smooth muscle (SMA), liver kidney microsome (LKM), thyroid microsome (TPO), and human thyroglobulin (TG). AAb status at baseline and during treatment was related to respective laboratory and clinical deviations.
  
  
  RESULTS
  The analysis of AAb data included 355 patients receiving IFNbeta-1b and 353 receiving placebo. There was no difference between treatment groups in de novo AAb positivity. A greater proportion of women were AAb positive at baseline and during treatment. No association was found between liver enzyme elevations and ANA, AMA, or SMA antibody formation in either treatment group. Laboratory-based thyroid alterations during the study were significantly related to TG/TPO status at baseline but were not associated with IFNbeta-1b treatment. Adverse events possibly indicative of other diseases with autoimmune links were not associated with respective AAb status.
  
  
  CONCLUSIONS
  Interferon beta-1b treatment did not induce autoantibody formation in this population of patients with secondary progressive multiple sclerosis.
authors.affiliation: Department of Neurology, Free University Hospital, Amsterdam, The Netherlands. ch.polman@vumc.nl
authors.forename: C H
authors.initials: CH
authors.lastname: Polman
authors.forename: L
authors.initials: L
authors.lastname: Kappos
authors.forename: F
authors.initials: F
authors.lastname: Dahlke
authors.forename: R
authors.initials: R
authors.lastname: Graf
authors.forename: K
authors.initials: K
authors.lastname: Beckmann
authors.forename: T
authors.initials: T
authors.lastname: Bogumil
authors.forename: C
authors.initials: C
authors.lastname: Pozzilli
authors.forename: A J
authors.initials: AJ
authors.lastname: Thompson
mesh_terms: D001323:Autoantibodies / Q000097:blood / Q000187:drug effects* / Q000276:immunology; D015415:Biomarkers; D056486:Chemical and Drug Induced Liver Injury; D015331:Cohort Studies; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000009:adverse effects* / Q000276:immunology; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000503:physiopathology; D008107:Liver Diseases / Q000097:blood / Q000276:immunology; D008297:Male; D008928:Mitochondria / Q000276:immunology; D009103:Multiple Sclerosis / Q000139:chemically induced* / Q000188:drug therapy* / Q000276:immunology; D015990:Placebo Effect; D017678:Sex Distribution; D013954:Thyroglobulin / Q000276:immunology; D013959:Thyroid Diseases / Q000097:blood / Q000139:chemically induced / Q000276:immunology; D013961:Thyroid Gland / Q000187:drug effects / Q000276:immunology / Q000503:physiopathology; D016896:Treatment Outcome
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D000068576:Interferon beta-1b; D016899:Interferon-beta; D013954:Thyroglobulin