Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2025
Cladribine Is Associated With Stable Cortical Gray Matter Lesion Burden in Multiple Sclerosis: A 7T MRI Study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zurawski Jonathan, Tauhid Shahamat, Healy Brian C, Chu Renxin, Houtchens Maria K, Jalkh Youmna, Khalil Samar, Quattrucci Molly, Mateen Farrah J, Napoli Salvatore, Rizvi Syed, Singhal Tarun, Bakshi Rohit
Аннотация
BACKGROUND AND PURPOSE: Cladribine, an FDA-approved disease-modifying immunotherapy for multiple sclerosis (MS), penetrates the CSF and mitigates T cells and B cells, and thus may impact the development of cortical gray matter lesions (CLs) and leptomeningeal enhancement (LME). 7T MRI is a highly sensitive tool for monitoring these outcomes in relapsing-remitting (RR) MS.
METHODS: MS subjects (n = 19, age [mean ± standard deviation]: 48.8 ± 10.0 years, 63.1% RRMS, 36.9% secondary progressive MS, Expanded Disability Status Scale [EDSS] score 4.1 ± 2.0) underwent 7T MRI with 0.7-mm3 voxels within a mean 1.9 months of oral cladribine initiation and ∼1 year later in this real-world study. CLs and LME were quantified by an expert. Wilcoxon signed rank tests and paired t-tests compared baseline to follow-up data.
RESULTS: A total of 88.2% of subjects had CLs at baseline (mean 14.1 CLs/patient, range 1-77). No subjects accrued new CLs, and CL volume remained stable (0.33 ± 0.48 mL baseline vs. 0.31 ± 0.46 mL follow-up, p = 0.22). LME was found in 88.9% of subjects at baseline. LME foci number was stable in seven (41.2%), increased in five (29.4%), and decreased in five (29.4%) subjects at follow-up, but overall LME burden was stable (3.1 ± 1.8 vs. 3.2 ± 1.6 foci per subject, p = 1.0). No EDSS or timed 25-foot walk change was noted (both p > 0.35). No subjects had clinical relapses or new T2 or gadolinium-enhancing white matter lesions during the study.
CONCLUSION: These observational data suggest that cladribine therapy stabilizes cortical demyelination in MS over the first year of treatment. Overall, LME burden remained stable over 1 year; however, within-subject resolution and accrual were noted.
METHODS: MS subjects (n = 19, age [mean ± standard deviation]: 48.8 ± 10.0 years, 63.1% RRMS, 36.9% secondary progressive MS, Expanded Disability Status Scale [EDSS] score 4.1 ± 2.0) underwent 7T MRI with 0.7-mm3 voxels within a mean 1.9 months of oral cladribine initiation and ∼1 year later in this real-world study. CLs and LME were quantified by an expert. Wilcoxon signed rank tests and paired t-tests compared baseline to follow-up data.
RESULTS: A total of 88.2% of subjects had CLs at baseline (mean 14.1 CLs/patient, range 1-77). No subjects accrued new CLs, and CL volume remained stable (0.33 ± 0.48 mL baseline vs. 0.31 ± 0.46 mL follow-up, p = 0.22). LME was found in 88.9% of subjects at baseline. LME foci number was stable in seven (41.2%), increased in five (29.4%), and decreased in five (29.4%) subjects at follow-up, but overall LME burden was stable (3.1 ± 1.8 vs. 3.2 ± 1.6 foci per subject, p = 1.0). No EDSS or timed 25-foot walk change was noted (both p > 0.35). No subjects had clinical relapses or new T2 or gadolinium-enhancing white matter lesions during the study.
CONCLUSION: These observational data suggest that cladribine therapy stabilizes cortical demyelination in MS over the first year of treatment. Overall, LME burden remained stable over 1 year; however, within-subject resolution and accrual were noted.