Impact of interferon beta-1a on neurologic disability in relapsing multiple sclerosis

Rudick, RA; Goodkin, Donald E.; Jacobs, L. D.; Cookfair, Diane L.; Herndon, Robert M.; Richert, John R.; Salazar, Andrés M.; Fischer, Jill S.; Granger, Carl V.; Simon, Jack H.; Alam, John; Simonian, Nancy A.; Campion, Marilyn; Bartoszak, David M.; Bourdette, Dennis; Braiman, Jonathan; Brownscheidle, Carol M.; Coats, Michael E.; Cohan, Stanley; Dougherty, D. S.; Kinkel, R. Philip; Mass, Michele; Munschauer, Frederick E.; Priore, Roger L.; Pullicino, Patrick; Scherokman, Barbara; Weistock-Guttman, B.; Whitham, Ruth H.

doi:10.1212/wnl.49.2.358

Cited by 213 publications

(88 citation statements)

References 8 publications

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“…This trial also reported a reduction in the unconfirmed 1-point EDSS worsening over the first 2 years of the study (Ϫ28%; p ϭ 0.037). Also, in a secondary analysis of data from the extension phase of this trial, 23 after excluding determinations made during acute attacks, these authors reported a significant reduction in the unconfirmed 1.5 point EDSS progression rate over 3 years in the treated patients compared with control subjects (Ϫ48%; p ϭ 0.004) using survival analysis methods. This last analysis, however, is of uncertain reliability.…”

Section: Analysis Of the Evidence Immunomodulatory Treatments Intermentioning

confidence: 93%

“…[18][19][20][21][22][23][24][25][26][27] Thus, in general, when comparing the different findings of these trials, both the magnitude of the reported effects on clinical and MRI outcomes, as well as their statistical significance, seem to be greater with increasing dosages of IFN␤. Nevertheless, because of differences in trial design, differences in the MS populations studied, and the fact that the results were obtained in independent clinical trials, this observation can only be considered as weak (Class III) evidence of a dose response.…”

Section: Analysis Of the Evidence Immunomodulatory Treatments Intermentioning

confidence: 99%

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Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

et al. 2002

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Overview. Clinical types of MS.MS is a chronic recurrent inflammatory disorder of the CNS. The disease results in injury to the myelin sheaths, the oligodendrocytes, and, to a lesser extent, the axons and nerve cells themselves. [1][2][3][4][5] The symptoms of MS vary, depending in part on the location of plaques within the CNS. Common symptoms include sensory disturbances in the limbs, optic nerve dysfunction, pyramidal tract dysfunction, bladder or bowel dysfunction, sexual dysfunction, ataxia, and diplopia. 5Four different clinical courses of MS have been defined. 6 The first, relapsing-remitting MS (RRMS), is characterized by self-limited attacks of neurologic dysfunction. These attacks develop acutely, evolving over days to weeks. Over the next several weeks to months, most patients experience a recovery of function that is often (but not always) complete. Between attacks the patient is neurologically and symptomatically stable. The second clinical course, secondary progressive MS (SPMS), begins as RRMS, but at some point the attack rate is reduced and the course becomes characterized by a steady deterioration in function unrelated to acute attacks. The third clinical type, primary progressive MS (PPMS), is characterized by a steady decline in function from the beginning without acute attacks. The fourth type, progressive-relapsing MS (PRMS), also begins with a progressive course although these patients also experience occasional attacks. Outcome measures in MS clinical trials.Evaluation of the relative effectiveness of different therapies requires consideration of which outcome measure or measures are relevant to the goals of therapy. Clearly, the most important therapeutic aim of any disease-modifying treatment of MS is to prevent or postpone long-term disability. However, long-term disability in MS often evolves slowly over many years.1-3 Clinical trials, by contrast, study patients for only short periods of time (2 or 3 years) and, therefore, use only short-term outcome measures to assess efficacy. As a result, it is important to validate any short-term measure by its correlation with the actual patient outcome many years later. For a discussion of these issues, interested readers should consult the full-length assessment on the Neurology Web site at www.neurology.org.Scope of this guideline. The purpose of this assessment is to consider the clinical utility of these disease-modifying agents including the anti-inflammatory, immunomodulatory, and immunosuppressive treatments that are currently available.

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Section: Analysis Of the Evidence Immunomodulatory Treatments Intermentioning

confidence: 93%

Section: Analysis Of the Evidence Immunomodulatory Treatments Intermentioning

confidence: 99%

Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

et al. 2002

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“…Tolerance of the drug was acceptable, considering the inherent discomfort of the IM injection route. Subsequent re-analysis of the data by the investigators 38 included a change of EDSS greater than two points, or sustained progression by one point for one year, with the conclusion that the previous results underestimated the effect of IFNβ-1a. Further post-hoc analysis revealed benefit in some areas of neuropsychological testing and degree of brain atrophy in patients treated with IFNβ-1a.…”

Section: Dovepressmentioning

confidence: 99%

Early stage and long term treatment of multiple sclerosis with interferon-β

Applebee

Panitch²

2009

BTT

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“…The effect of interfering with the signaling pathways of these cytokines have been tested by the development of a variety of anticytokine agents some of which are currently in the market or are being assessed in clinical trials of autoimmune diseases. Some of these anti-cytokine compounds include etanercept/enbrel, adalimumab/humira, infliximab/remicade, certolizumab pegol/cimzia, alefacept /amevive, avonex, and betaseron, which are used as therapeutic agents in autoimmune diseases such as RA, psoriasis, MS and Crohn's disease [160][161][162][163][164]. These drugs have shown beneficial in subsiding inflammation associated with some of the autoimmune diseases; however, they were effective only in a subset of patients.…”

Section: N O T F O R D I S T R I B U T I O Nmentioning

confidence: 99%

Autoimmunity and Apoptosis - Therapeutic Implications

Rashedi

Panigrahi²,

Ezzati³

et al. 2007

CMC

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Acquisition of a complex immune system during evolution provided organisms with the most effective defense mechanism against "foreign" or "non-self" invaders. This efficient protection against pathogens, however, has been achieved at the expense of a higher risk for "self"-directed reaction or autoimmunity. Establishment of self-tolerance and homeostasis in the immune system is regulated at different physiological stages of immune cells development. The breakdown in discrimination between "self" and "non-self" causes an aberrant immune response against autoantigens that promote damage to the "self" cells and tissue(s), resulting in various autoimmune phenotypes. Whereas activation and clonal proliferation of autoreactive T-and B-lymphocytes underlies the pathogenesis of autoimmune diseases, the mechanism by which self-tolerance is lost and autoimmune responses are induced is not clear yet. Autoimmunity is a multi-step process that occurs as a consequence of complex interaction between genetic susceptibility and non-genetic factors. Programmed cell death, as a key mechanism to regulate immune system function, has a crucial influence on both the selection process of immune cells and the maintenance of this immune tolerance in peripheral repertoire. Thus, defects in apoptotic death pathways may contribute to the development of autoimmune response in susceptible individuals in certain conditions.

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Impact of interferon beta-1a on neurologic disability in relapsing multiple sclerosis

Cited by 213 publications

References 8 publications

Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

Early stage and long term treatment of multiple sclerosis with interferon-β

Autoimmunity and Apoptosis - Therapeutic Implications

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Impact of interferon beta-1a on neurologic disability in relapsing multiple sclerosis

Cited by 213 publications

References 8 publications

Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

Disease modifying therapies in multiple sclerosis: Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines [RETIRED]

Early stage and long term treatment of multiple sclerosis with interferon-&beta;

Autoimmunity and Apoptosis - Therapeutic Implications

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Early stage and long term treatment of multiple sclerosis with interferon-β