Abstract
In “Serum Neurofilament Light Association With Progression in Natalizumab-Treated Patients With Relapsing-Remitting Multiple Sclerosis,” Bridel et al. evaluated serum neurofilament light chain (sNfL) levels serially after initiation of natalizumab in patients with relapsing-remitting multiple sclerosis (RRMS) and found that they do not capture or predict clinical/radiologic trajectory. Kropshofer et al. commented that their conclusion that sNfL is not a valid biomarker for disease progression is in opposition to the results from other large studies, noting that the editorial about this article, written by Goldschmidt and Fox, suggested that this may be because prior studies demonstrate natural history, without natalizumab treatment. Nonetheless, Kropshofer et al. noted that they found an association between baseline sNfL and 3-month disability progression in patients treated with siponimod, irrespective of prior disease activity, indicating that baseline sNfL can be used for neuroprognostication, regardless of treatment with anti-inflammatory therapy. Bridel et al. clarified that their conclusion was that sNfL may not be well suited to monitor or predict progression in patients with RRMS on natalizumab. They noted that their results may differ from those from other studies because their patients (1) all had RRMS and (2) were all treated with natalizumab. They also commented that almost half of patients on siponimod in the EXPAND study developed new or enlarging brain lesions on 2-year follow-up imaging, so that is not the ideal population to study the relationship between sNfL and progression. They recommend performance of additional larger studies on the relationship between sNfL and progression in patients on natalizumab and/or ocrelizumab. In “Serum Neurofilament Light Association With Progression in Natalizumab-Treated Patients With Relapsing-Remitting Multiple Sclerosis,” Bridel et al. evaluated serum neurofilament light chain (sNfL) levels serially after initiation of natalizumab in patients with relapsing-remitting multiple sclerosis (RRMS) and found that they do not capture or predict clinical/radiologic trajectory. Kropshofer et al. commented that their conclusion that sNfL is not a valid biomarker for disease progression is in opposition to the results from other large studies, noting that the editorial about this article, written by Goldschmidt and Fox, suggested that this may be because prior studies demonstrate natural history, without natalizumab treatment. Nonetheless, Kropshofer et al. noted that they found an association between baseline sNfL and 3-month disability progression in patients treated with siponimod, irrespective of prior disease activity, indicating that baseline sNfL can be used for neuroprognostication, regardless of treatment with anti-inflammatory therapy. Bridel et al. clarified that their conclusion was that sNfL may not be well suited to monitor or predict progression in patients with RRMS on natalizumab. They noted that their results may differ from those from other studies because their patients (1) all had RRMS and (2) were all treated with natalizumab. They also commented that almost half of patients on siponimod in the EXPAND study developed new or enlarging brain lesions on 2-year follow-up imaging, so that is not the ideal population to study the relationship between sNfL and progression. They recommend performance of additional larger studies on the relationship between sNfL and progression in patients on natalizumab and/or ocrelizumab.
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