11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Assessing ‘No Evidence of Disease Activity’ Status in Patients with Relapsing-Remitting Multiple Sclerosis Receiving Fingolimod in Routine Clinical Practice: A Retrospective Analysis of the Multiple Sclerosis Clinical and Magnetic Resonance Imaging Outcomes in the USA (MS-MRIUS) Study

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          ‘No evidence of disease activity’ (NEDA), a composite measure of clinical and magnetic resonance imaging outcomes, provides a comprehensive assessment of disease activity, but is not extensively reported in clinical practice. NEDA-3 is defined as patients with no new/enlarged T2 or gadolinium-enhancing lesions, no relapses, and no disability progression (according to Expanded Disability Status Scale scores). NEDA-4 comprises the components of NEDA-3 and a fourth criterion of ≤ 0.4% annualized brain volume loss.

          Objective

          The objective of this study was to assess NEDA status among patients with relapsing-remitting multiple sclerosis receiving fingolimod in clinical practice.

          Methods

          Clinical and magnetic resonance imaging data were retrospectively collected from 590 patients who initiated fingolimod at 33 multiple sclerosis centers in the USA. Patients were required to have a magnetic resonance imaging scan in the 6 months before or 1 month after fingolimod initiation (index period) and in the 9–24 months after fingolimod initiation (post-index period). Magnetic resonance imaging data were systematically quantified at a centralized reading facility. The proportions of patients with NEDA-3 or NEDA-4 status during fingolimod treatment were assessed.

          Results

          During the follow-up period (median: 16 months), data to assess NEDA-3 and NEDA-4 were available for 586 and 325 patients, respectively. In the post-index period, 58.7% of patients achieved NEDA-3 status (no relapses, 85.2%; no new/enlarged T2/gadolinium-enhancing lesions, 76.3%; no disability progression, 87.9%) and 37.2% achieved NEDA-4 status (no relapses, 86.5%; no new/enlarged T2/gadolinium-enhancing lesions, 78.8%; no disability progression, 91.1%; brain volume loss ≤ 0.4, 58.2%).

          Conclusion

          Among patients receiving fingolimod, over half achieved NEDA-3 status and over one-third achieved NEDA-4 status.

          Electronic supplementary material

          The online version of this article (10.1007/s40263-017-0482-4) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references20

          • Record: found
          • Abstract: found
          • Article: not found

          Evaluation of no evidence of disease activity in a 7-year longitudinal multiple sclerosis cohort.

          With multiple and increasingly effective therapies for relapsing forms of multiple sclerosis (MS), disease-free status or no evidence of disease activity (NEDA) has become a treatment goal and a new outcome measure. However, the persistence of NEDA over time and its predictive power for long-term prognosis are unknown.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The measurement and clinical relevance of brain atrophy in multiple sclerosis.

            Brain atrophy has emerged as a clinically relevant component of disease progression in multiple sclerosis. Progressive loss of brain tissue bulk can be detected in vivo in a sensitive and reproducible manner by MRI. Clinical studies have shown that brain atrophy begins early in the disease course. The increasing amount of data linking brain atrophy to clinical impairments suggest that irreversible tissue destruction is an important determinant of disease progression to a greater extent than can be explained by conventional lesion assessments. In this review, we will summarise the proposed mechanisms contributing to brain atrophy in patients with multiple sclerosis. We will critically discuss the wide range of MRI-based methods used to quantify regional and whole-brain-volume loss. Based on a review of current information, we will summarise the rate of atrophy among phenotypes for multiple sclerosis, the clinical relevance of brain atrophy, and the effect of disease-modifying treatments on its progression.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Effect of relapses on development of residual deficit in multiple sclerosis.

              To determine the percentage of patients with residual deficits following multiple sclerosis (MS) exacerbations and the magnitude of those deficits using a database of pooled placebo patients from clinical trials. A database of patients assigned to the placebo group in several randomized clinical trials was queried to determine those patients with Expanded Disability Status Scale (EDSS) and Scripps Neurologic Rating Scale assessments prior to, at the time of, and after an acute exacerbation of MS. The extent of deficit present at these time points was compared to determine the acute effect of exacerbations and the degree of persistent disability. Forty-two percent of patients had residual deficit of at least 0.5 and 28% had residual of >or=1.0 EDSS units, at an average of 64 days after an exacerbation. The results were reproduced across subsequent exacerbations and were sustained over time. The subgroup of patients with measurable change in EDSS during the exacerbation had more extensive residual impairment on the follow-up visits. Similar results were seen when the Scripps score was examined. MS exacerbations produce a measurable and sustained effect on disability.
                Bookmark

                Author and article information

                Contributors
                716-8597540 , bw8@buffalo.edu
                Journal
                CNS Drugs
                CNS Drugs
                CNS Drugs
                Springer International Publishing (Cham )
                1172-7047
                1179-1934
                21 December 2017
                21 December 2017
                2018
                : 32
                : 1
                : 75-84
                Affiliations
                [1 ]State University of New York at Buffalo, Jacobs Multiple Sclerosis Center for Treatment and Research, Jacobs Pediatric Multiple Sclerosis Center of Excellence, New York State Multiple Sclerosis Consortium, Buffalo, NY USA
                [2 ]ISNI 0000 0001 1515 9979, GRID grid.419481.1, Novartis Pharma AG, ; Basel, Switzerland
                [3 ]IQVIA, Basel, Switzerland
                [4 ]IQVIA, Burlington, MA USA
                [5 ]The Elliot Lewis Center for Multiple Sclerosis Care, Boston, MA USA
                [6 ]Christiana Care Multiple Sclerosis Center, Newark, DE USA
                [7 ]Minneapolis Clinic of Neurology, Golden Valley, MN USA
                [8 ]ISNI 0000 0004 1936 9887, GRID grid.273335.3, Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, , State University of New York at Buffalo, ; Buffalo, NY USA
                [9 ]ISNI 0000 0004 1936 9887, GRID grid.273335.3, Translational Imaging Center at Clinical Translational Science Institute, University at Buffalo, , State University of New York at Buffalo, ; Buffalo, NY USA
                Article
                482
                10.1007/s40263-017-0482-4
                5843701
                29270772
                83af8ba6-6733-4950-8205-d05d95f67e39
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: Novartis Pharma AG
                Categories
                Original Research Article
                Custom metadata
                © Springer International Publishing AG, part of Springer Nature 2018

                Comments

                Comment on this article