Serum S100B in primary progressive multiple sclerosis patients treated with interferon-beta-1a

S100B belongs to a family of calcium-binding proteins implicated in intracellular and extracellular regulatory activities. This study of serum S100B in primary progressive multiple sclerosis (PPMS) is based on data obtained from a randomized, controlled trial of Interferon β-1a in subjects with PPMS. The key questions were whether S100B levels were associated with either disability or MRI findings in primary progressive MS and whether Interferon β-1a has an effect on their S100B levels. Serial serum S100B levels were measured using an ELISA method. The results demonstrated that serum S100B is not related to either disease progression or MRI findings in subjects with primary progressive MS given Interferon β-1a. Furthermore there is no correlation between S100B levels and the primary and secondary outcome measures

Interferon beta-1b treatment does not induce autoantibodies

Background: There is little information regarding the potential of interferon beta ( IFN beta) 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 IFN beta on hepatic, thyroid, and other markers of autoimmunity using data from the European placebo-controlled double-blind, multicenter study of IFN beta-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 IFN beta-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 IFN beta-1b treatment. Adverse events possibly indicative of other diseases with autoimmune links were not associated with respective AAb status. Conclusion: Interferon beta- 1b treatment did not induce autoantibody formation in this population of patients with secondary progressive multiple sclerosis