Program in Translational NeuroPsychiatric Genomics, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States.
J Neuroimmunol. 2011 Apr;233(1-2):168-74. doi: 10.1016/j.jneuroim.2010.10.038. Epub 2010 Nov 27.
Using retrospectively collected outcome data for treatment naïve subjects treated with either glatiramer acetate (GA) (n=332) or interferon beta (IFN β) (n=424), we replicated the lack of a significant difference in efficacy between these treatments. Further, for both treatments, we observed a decline in the hazard of a relapse over time, which may suggest the existence of subsets of subjects with differential responses to each treatment. The HLA DRB1 1501 allele explained some of this variation in event-free survival while on GA, and we found suggestive evidence that an IRF8 polymorphism influences event-free survival in IFN β treated subjects.
使用回顾性收集的未经治疗的受试者的结果数据，这些受试者接受了格拉替雷（GA）（n=332）或干扰素β（IFNβ）（n=424）治疗，我们复制了这两种治疗方法在疗效方面没有显著差异。此外，对于这两种治疗方法，我们观察到随着时间的推移，复发的风险下降，这可能表明存在对每种治疗方法有不同反应的亚组受试者。在接受 GA 治疗时，HLA DRB1 1501 等位基因解释了 GA 治疗时无事件生存中部分变异，我们发现了有说服力的证据表明，IRF8 多态性影响 IFNβ 治疗受试者的无事件生存。
