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New acute and chronic black holes in multiple sclerosis patients randomized to interferon beta-1b or glatiramer acetate
  1. Diego Cadavid (cadavidi{at}umdnj.edu)
  1. UMDNJ-New Jersey Medical School, United States
    1. Jojy Cheriyan (jojy_cheriyan{at}yahoo.com)
    1. UMDNJ-New Jersey Medical School, United States
      1. Joan Skurnick (skurnick{at}umdnj.edu)
      1. UMDNJ-New Jersey Medical School, United States
        1. John A Lincoln (lincolja{at}umdnj.edu)
        1. UMDNJ-New Jersey Medical School, United States
          1. Leo J Wolansky (wolansky{at}radpharm.com)
          1. UMDNJ-New Jersey Medical School, United States
            1. Stuart D Cook (cooksd{at}umdnj.edu)
            1. UMDNJ-New Jersey Medical School, United States

              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: We used monthly 3 Tesla brain MRI scans for up to 2 years to study the development and evolution of new BH in 75 MS patients randomized to GA or Interferon β-1b (IFNb1b) in the BECOME study.

              Findings: Of 1,224 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 MS patients treated with GA or IFNβ1b convert to CBH.

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