title: Interferon β-1b and glatiramer acetate effects on permanent black hole evolution.
abstract: OBJECTIVE
  To compare interferon β-1b (IFNβ-1b) and glatiramer acetate (GA) on new lesion (NL) (gadolinium-enhancing, new T2) evolution into permanent black holes (PBH)--a marker of irreversible tissue damage--in patients with relapsing-remitting multiple sclerosis (RRMS).
  
  
  METHODS
  BEYOND was a large, phase III, clinical trial comparing IFNβ-1b 250 μg, IFNβ-1b 500 μg, and GA (2:2:1). Patient scans were reexamined post hoc for PBH in a rater-blinded manner. Two predefined coprimary endpoints compared IFNβ-1b 250 μg with GA: first, number of PBH per patient at year 2 evolving from year 1 NL, then proportion of year 1 NL evolving into PBH at year 2. IFNβ-1b 500 μg and GA were compared in an exploratory fashion.
  
  
  RESULTS
  Approximately 90% (1,957/2,244) of patients had NL at year 1 with follow-up at year 2. Mean numbers of PBH per patient at year 2 evolving from year 1 NL were lower for IFNβ-1b 250 μg than GA (0.30 vs 0.43; p = 0.0451). The proportion of NL evolving into PBH was similar (IFNβ-1b 250 μg vs GA: 21.6% vs 23.5%; p > 0.20). For IFNβ-1b 500 μg, both the mean PBH number per patient at year 2 evolving from year 1 NL (0.26 vs 0.43; p = 0.0037) and proportion of NL evolving into PBH (16.3% vs 23.5%; p = 0.0409) were lower relative to GA.
  
  
  CONCLUSIONS
  IFNβ-1b affected PBH development to a similar or better extent than GA. IFNβ-1b favorably influences an MRI outcome indicative of permanent tissue destruction in the brains of patients with multiple sclerosis.
  
  
  METHODS
  This study provides Class III evidence that IFNβ-1b is associated with a reduction in MRI PBH formation and evolution compared with GA between years 1 and 2 of treatment.
authors.affiliation: University Hospital San Raffaele, Via Olgettina, 20132 Milan, Italy. filippi.massimo@hsr.it
authors.forename: M
authors.initials: M
authors.lastname: Filippi
authors.forename: M A
authors.initials: MA
authors.lastname: Rocca
authors.forename: F
authors.initials: F
authors.lastname: Camesasca
authors.forename: S
authors.initials: S
authors.lastname: Cook
authors.forename: P
authors.initials: P
authors.lastname: O'Connor
authors.forename: B G W
authors.initials: BG
authors.lastname: Arnason
authors.forename: L
authors.initials: L
authors.lastname: Kappos
authors.forename: D
authors.initials: D
authors.lastname: Goodin
authors.forename: D
authors.initials: D
authors.lastname: Jeffery
authors.forename: H-P
authors.initials: HP
authors.lastname: Hartung
authors.forename: G
authors.initials: G
authors.lastname: Comi
authors.forename: J S
authors.initials: JS
authors.lastname: Wolinsky
authors.forename: T
authors.initials: T
authors.lastname: Bogumil
authors.forename: C
authors.initials: C
authors.lastname: Pohl
authors.forename: K
authors.initials: K
authors.lastname: Beckmann
authors.forename: R
authors.initials: R
authors.lastname: Sandbrink
authors.forename: E
authors.initials: E
authors.lastname: Croze
authors.forename: C
authors.initials: C
authors.lastname: Brown
authors.forename: T M
authors.initials: TM
authors.lastname: Desimone
authors.forename: D L
authors.initials: DL
authors.lastname: Arnold
authors.forename: G
authors.initials: G
authors.lastname: Cutter
authors.forename: V
authors.initials: V
authors.lastname: Knappertz
mesh_terms: D000328:Adult; D005260:Female; D005500:Follow-Up Studies; D000068717:Glatiramer Acetate; D006801:Humans; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000627:therapeutic use*; D008279:Magnetic Resonance Imaging; D008297:Male; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000175:diagnosis / Q000188:drug therapy* / Q000473:pathology*; D010455:Peptides / Q000627:therapeutic use*; D011446:Prospective Studies; D016896:Treatment Outcome
chemical_list: D010455:Peptides; D000068576:Interferon beta-1b; D000068717:Glatiramer Acetate; D016899:Interferon-beta