Department of Neurology, Brigham and Women's Hospital, Partners MS Center, Harvard Medical School, Boston, MA.
Department of Radiology, Brigham and Women's Hospital, Partners MS Center, Harvard Medical School, Boston, MA.
J Neuroimaging. 2016 Mar-Apr;26(2):184-7. doi: 10.1111/jon.12307. Epub 2015 Oct 8.
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.
This was a retrospective nonrandomized 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.
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).
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.
脑损伤转化为慢性 T1 低信号（“慢性黑洞”[CBH]），表明多发性硬化症（MS）中存在严重的组织破坏（轴突丢失和不可逆的脱髓鞘）。芬戈莫德限制 MS 病变进展的两种机制包括将淋巴细胞隔离在周围或直接神经保护作用。我们研究了芬戈莫德对 MS 患者急性钆增强（Gd+）脑病变向 CBH 演变的影响。
这是一项回顾性非随机比较研究，比较了开始口服芬戈莫德时（[.5 mg/天，n = 26，年龄（平均值 ± 标准差）39.2 ± 10.6 岁，扩展残疾状况量表[EDSS]评分中位数（范围）：1.75（0，6.5）]和未接受治疗的患者（n = 30，年龄 41.7 ± 9.3 岁；EDSS 1.0（0，6））的 Gd+脑病变。根据治疗后一年是否转化为 CBH 对每个病变进行分类。
在芬戈莫德组中，发现 99 个 Gd+基线病变（平均值 ± 标准差，范围：3.8 ± 5.1；1 个患者中有 21 个），其中 25 个（25%）转化为 CBH（1.0 ± 2.0；0，10 个患者中有 10 个）。未接受治疗的患者中有 62 个基线 Gd+病变（2.1 ± 2.3；1 个患者中有 13 个），其中 26 个（42%）转化为 CBH（0.9 ± 1.4；0，10 个患者中有 7 个）（P =.063）。接受芬戈莫德治疗的 13 名患者（50%）和未接受治疗的 17 名患者（57%）发生 CBH（P =.79）。
这项初步研究表明，芬戈莫德具有降低急性向慢性破坏性 MS 病变转化的趋势。这种效果有待更大规模的随机前瞻性研究证实。
