From the Department of Neurology (S.N., J.K., T.D.), University Hospital Basel, University of Basel; Division of Developmental- and Neuropaediatrics (S.N.), University Children's Hospital of Basel (UKBB), University of Basel; and Department of Biomedicine (J.K., T.D.), University Hospital Basel, Switzerland.
Neurol Neuroimmunol Neuroinflamm. 2020 Aug 14;7(6). doi: 10.1212/NXI.0000000000000874. Print 2020 Nov.
To investigate the dynamics of immune cells recovery after treatment discontinuation of fingolimod in real-life clinical practice, we analyzed the course of lymphocyte reconstitution and its potential influencing factors in patients with multiple sclerosis (MS).
We analyzed leukocyte, lymphocyte, and granulocyte counts of 58 patients at 3, 6, and 12 months after fingolimod cessation and the following parameters as potential risk factors for a prolonged lymphopenia up to 12 months: age; sex; Expanded Disability Status Scale, and disease duration at the time of fingolimod start; type and number of previous immunomodulatory treatments; fingolimod treatment duration; lymphocyte count at baseline before fingolimod, at fingolimod stop, and at the time of therapy switch; time interval between fingolimod cessation and new treatment initiation; type of the follow-up immunomodulatory treatment; and corticosteroid administration after fingolimod cessation.
All patients showed a drop of the lymphocyte count under fingolimod with no relevant leukopenia or neutropenia. One year after discontinuation, still 22% of the patients were lymphopenic and 54% of them did not reach 80% of the baseline lymphocyte value. Low lymphocyte counts before fingolimod start, under fingolimod, and at therapy switch, successive treatment with rituximab, and pretreatment with mitoxantrone were significantly associated with a prolonged immune cell recovery.
Prolonged lymphopenia after fingolimod cessation exists in a subgroup of patients with MS and should be considered in clinical practice, particularly when changing treatment regimens.
在真实临床实践中，研究停用芬戈莫德后免疫细胞恢复的动态，我们分析了多发性硬化症（MS）患者淋巴细胞重建的过程及其潜在的影响因素。
我们分析了 58 例患者在停用芬戈莫德后 3、6 和 12 个月的白细胞、淋巴细胞和粒细胞计数，以及以下参数作为淋巴细胞减少持续至 12 个月的潜在危险因素：年龄；性别；扩展残疾状况量表，以及开始使用芬戈莫德时的疾病持续时间；以前免疫调节治疗的类型和数量；芬戈莫德治疗持续时间；在开始芬戈莫德之前、停止芬戈莫德时和开始治疗转换时的淋巴细胞计数；停止芬戈莫德和开始新治疗之间的时间间隔；随访免疫调节治疗的类型；以及停止芬戈莫德后皮质类固醇的应用。
所有患者在芬戈莫德下均表现出淋巴细胞计数下降，无相关白细胞减少或中性粒细胞减少。停药 1 年后，仍有 22%的患者出现淋巴细胞减少，54%的患者未达到基线淋巴细胞值的 80%。在开始芬戈莫德之前、在芬戈莫德下和在治疗转换时的低淋巴细胞计数、连续使用利妥昔单抗治疗以及米托蒽醌预处理与免疫细胞恢复延长显著相关。
停用芬戈莫德后淋巴细胞减少持续存在于 MS 患者的亚组中，在临床实践中应予以考虑，特别是在改变治疗方案时。
