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New acute and chronic black holes in patients with multiple sclerosis randomised to interferon beta-1b or glatiramer acetate
  1. D Cadavid1,
  2. J Cheriyan1,2,
  3. J Skurnick3,
  4. J A Lincoln1,
  5. L J Wolansky2,
  6. S D Cook1
  1. 1
    Department of Neurology and Neuroscience, University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School, Newark, New Jersey, USA
  2. 2
    Department of Radiology, University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School, Newark, New Jersey, USA
  3. 3
    Department of Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School, Newark, New Jersey, USA
  1. Correspondence to Dr D Cadavid, Experimental Neurology Group, Biogen Idec, 14 Cambridge Center, Bldg 6A, 6th Floor, Cambridge, MA 02142, USA; cadavidi{at}umdnj.edu

Abstract

Background: Hypointense lesions on T1 weighted MRI, referred to as black holes (BH), are a marker of demyelination/axonal loss in multiple sclerosis (MS). There is some evidence that glatiramer acetate (GA) may decrease the conversion of new brain lesions to BH.

Methods: Monthly 3-Tesla brain MRI scans were used for up to 2 years to study the development and evolution of new BH in 75 patients with MS randomised to GA or Interferon β-1b (IFNβ1b) in the BECOME study.

Findings: Of 1224 newly enhancing lesions (NEL) appearing at baseline through 24 months in 61 patients, 767 (62.7%) showed an acute BH (ABH). The majority of ABH were transient and of similar duration by treatment group. Of 571 ABH in which MRI follow-up scans were available for ⩾1 year, 103 (18.8%) were still visible ⩾12 months after onset and were considered chronic BH (CBH). Only 12.1% of the 849 NEL with MRI follow-up ⩾1 year converted to CBH, 9.8% with IFNβ1b and 15.2% with GA (p = 0.02). The conversion from ABH to CBH was also lower with IFNβ1b (15.2%) than with GA (21.4%), of borderline significance (p = 0.06). The majority of patients who developed NEL did not develop CBH; however, about a quarter had conversion rates from ABH to CBH greater than 20%.

Interpretation: Only a minority of new brain lesions in patients with MS treated with GA or IFNβ1b convert to CBH.

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Footnotes

  • Funding The BECOME study was supported by Bayer Schering Pharma AG, distributors of IFNβ1b, but was investigator-initiated and remains the intellectual property of New Jersey Medical School/University of Medicine & Dentistry of New Jersey.

  • Competing interests Since May 2008, DC has been a full-time employee of Biogen Idec, a competitor of the manufacturers of IFNβ1b and GA. Since July 2008, LJW has been a full-time employee of RadPharm, Princeton, New Jersey. The work in the BECOME study was not related to their employment at Biogen Idec or RadPharm. The sponsor was not allowed to participate in any of the following phases of the study: conduct of the study, data collection, data management, data analysis and preparation of the manuscript. DC, LJW and JS had some of their academic salary supported by the clinical trial contract. DC and SDC received honoraria from the sponsor during the course of the study (<$10 000).

  • Ethics approval Ethics approval was provided by IRB from UMDNJ-New Jersey Medical School, number M167-2002.

  • Patient consent Obtained.

  • Provenance and Peer review Not commissioned; externally peer reviewed.

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