Intramuscular Interferon Beta-1A Therapy Initiated during a First Demyelinating Event in Multiple Sclerosis

Jacobs, Lawrence; Beck, Roy W.; Simon, Jack H.; Kinkel, Revere P.; Brownscheidle, Carol M.; Murray, Thomas J.; Simonian, Nancy A.; Slasor, Peter; Sandrock, AW

doi:10.1056/nejm200009283431301

Cited by 1,394 publications

(859 citation statements)

References 17 publications

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“…In April 1996, the Controlled High-Risk Subjects Avonex MS Prevention Study (CHAMPS) group began enrolling across North America [24]. Participants experienced a unifocal attack of demyelinating disease no more than 27 days before randomization and had characteristic MRI brain findings.…”

Section: Clinically Isolated Syndromementioning

confidence: 99%

Interferon Beta and Glatiramer Acetate Therapy

McGraw

Lublin

2013

Neurotherapeutics

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Section: Clinically Isolated Syndromementioning

confidence: 99%

Interferon Beta and Glatiramer Acetate Therapy

McGraw

Lublin

2013

Neurotherapeutics

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“…The Controlled High-Risk Subjects Avonex MS Prevention Study (CHAMPS) enrolled 383 patients with a CIS and abnormal MRI consistent with demyelination. 30 Patients received standard treatment with intravenously administered methylprednisolone for their CIS, and were randomized to receive 30 g IFN␤1a-IM or placebo once weekly within 27 days of onset of the CIS. After a planned interim analysis at 22 months demonstrated a decreased rate of clinically definite MS (CDMS), the trial was terminated.…”

Section: Clinically Isolated Syndromesmentioning

confidence: 99%

Interferon-β Treatment for Multiple Sclerosis

Bermel

Rudick

2007

Neurotherapeutics

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Summary:Multiple sclerosis (MS) is the leading nontraumatic cause of neurologic disability in young adults. Interferon-␤, approved for use in 1993, was the first treatment to modify the course and prognosis of the disease and remains a mainstay of MS treatment. Numerous large-scale clinical trials in early, active patient populations have established the clinical efficacy of interferon-␤ in reducing relapses and delaying disability progression. Although its mechanism of action remains incompletely understood, a reduction in active lesions seen on magnetic resonance imaging implies primary anti-inflammatory properties, a mechanism supported by basic immunologic research. Variation in individual patient responsiveness to interferon-␤ may be due to disease variability or differential induction of interferon-stimulated genes. The magnitude of the therapeutic effect appears to be similar among products, but the optimal dose, route, and frequency of administration of the drug remain uncertain.

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“…Early treatment is important to avoid permanent damage and might slow or delay progression (Jacobs et al, 2000;Kappos et al, 2007). However, due to the variety of clinical presentations and its large differential diagnosis, early identification of the disease is especially problematic (Rolak and Fleming, 2007;Swanton et al, 2007).…”

mentioning

confidence: 99%