Fingolimod limits the formation of black holes



Oommen VV, Tauhid S, Healy BC, Chua AS, Malik MT, Diaz-Cruz C, Dupuy SL, Weiner HL, Chitnis T, Bakshi R.The Effect of Fingolimod on Conversion of Acute Gadolinium-Enhancing Lesions to Chronic T1 Hypointensities in Multiple Sclerosis. J Neuroimaging. 2015 Oct 8. doi: 10.1111/jon.12307. [Epub ahead of print]

BACKGROUND:Brain lesions converting to chronic T1 hypointensities ("chronic black holes" [CBH]), indicate severe tissue destruction (axonal loss and irreversible demyelination) in multiple sclerosis (MS). Two mechanisms by which fingolimod could limit MS lesion evolution include sequestration of lymphocytes in the periphery or direct neuroprotective effects. We investigated the effect of fingolimod on the evolution of acute gadolinium-enhancing (Gd+) brain lesions to CBH in patients with MS.
METHODS:This was a retrospective non-randomized comparison of patients with Gd+ brain lesions at the time of starting oral fingolimod [.5 mg/day, n = 26, age (mean ± SD) 39.2 ± 10.6 years, Expanded Disability Status Scale (EDSS) score - median (range): 1.75 (0, 6.5)] to those on no therapy [n = 30, age 41.7 ± 9.3 years; EDSS 1.0 (0, 6)]. Each lesion was classified by whether it converted to a CBH in the year following treatment.
RESULTS: In the fingolimod group, 99 Gd+ baseline lesions (mean ± SD, range: 3.8 ± 5.1; 1, 21 per patient) were identified of which 25 (25%) evolved to CBH (1.0 ± 2.0; 0, 10 per patient). The untreated group had 62 baseline Gd+ lesions (2.1 ± 2.3; 1, 13), 26 (42%) of which evolved to CBH (.9 ± 1.4; 0, 7) (P = .063). Thirteen patients (50%) receiving fingolimod and 17 untreated patients (57%) developed CBH (P = .79).
CONCLUSION: This pilot study shows a trend of fingolimod on reducing the conversion rate from acute to chronic destructive MS lesions. Such an effect awaits verification in larger randomized prospective studies.
This study suggests that fingolimod slows the conversion of lesions into T1 black holes. These are thought to be areas of damage. The authors suggests and influence on lesion development or neuroprotection. If fingolimod was such a good neuroprotective maybe we would have found that fingo would inhibit progressive MS. It didn't and so the the effect may have been to limit the damage caused by the inflammatory lesions once they had formed, such as regulating how much they evolve. This may relate to the influence on brain atrophy which fingo has an effect on.

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