期刊
MULTIPLE SCLEROSIS JOURNAL
卷 22, 期 10, 页码 1297-1305出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/1352458515616701
关键词
Atrophy; brain; fingolimod; multiple sclerosis; NEDA
资金
- Novartis Pharma AG, Basel, Switzerland
Background: No evidence of disease activity' (NEDA), defined as absence of magnetic resonance imaging activity (T2 and/or gadolinium-enhanced T1 lesions), relapses and disability progression (NEDA-3'), is used as a comprehensive measure of treatment response in relapsing multiple sclerosis (RMS), but is weighted towards inflammatory activity. Accelerated brain volume loss (BVL) occurs in RMS and is an objective measure of disease worsening and progression. Objective: To assess the contribution of individual components of NEDA-3 and the impact of adding BVL to NEDA-3 (NEDA-4') Methods: We analysed data pooled from two placebo-controlled phase 3 fingolimod trials in RMS and assessed NEDA-4 using different annual BVL mean rate thresholds (0.2%-1.2%). Results: At 2years, 31.0% (217/700) of patients receiving fingolimod 0.5mg achieved NEDA-3 versus 9.9% (71/715) on placebo (odds ratio (OR) 4.07; p<0.0001). Adding BVL (threshold of 0.4%), the respective proportions of patients achieving NEDA-4 were 19.7% (139/706) and 5.3% (38/721; OR 4.41; p<0.0001). NEDA-4 status favoured fingolimod across all BVL thresholds tested (OR 4.01-4.41; p<0.0001). Conclusion: NEDA-4 has the potential to capture the impact of therapies on both inflammation and neurodegeneration, and deserves further evaluation across different compounds and in long-term studies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据