Treatment approaches to patients with multiple sclerosis and coexisting psoriasis : a longitudinal multicenter observational cohort study

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Abstract

Neurologists frequently encounter multiple sclerosis (MS) patients with coexisting autoimmune disorders such as psoriasis (PsO). The evolving landscape of immunotherapies has made treatment decisions more complex, yet also opened opportunities for therapies targeting shared immunopathogenic mechanisms. However, evidence for this patient group remains limited to case reports and small series. In this multicenter observational study, 420 MS patients were screened, identifying 38 with PsO. These were compared with MS-only patients regarding demographics, disease course, Expanded Disability Status Scale (EDSS), and disease-modifying therapy (DMT) use. DMT histories, reasons for discontinuation, and adverse events were analyzed. Logistic regression assessed PsO and MS worsening, using dimethyl fumarate (DMF) as reference. MS/PsO patients were older at diagnosis (37.6 vs. 33.0 years). EDSS and disease course showed no statistically significant differences. DMF was most frequently used (68%), with low rates of PsO (8%) and MS worsening (15%). PsO worsening was common under teriflunomide (75%), interferons (38%), and sphingosine-1-phosphate (S1P) modulators (40%). Logistic regression suggested higher odds under teriflunomide (OR = 16.5, p = 0.028), interferons (OR = 16.5, p = 0.004), and S1P-modulators (OR = 8.25, p = 0.047). Anti-CD20 therapies (OR = 2.75, p = 0.257) and natalizumab (OR = 1.83, p = 0.635) showed non-significant trends. Interleukin-17 (IL-17) inhibitors were well tolerated, with >50% stable in both conditions and no significant MS worsening (OR = 1.67, p = 0.546). IL-17 inhibitors and DMF showed a favorable tolerability in MS/PsO. Teriflunomide, interferons, and S1P-modulators frequently exacerbate PsO. CD20 therapies and natalizumab remain effective for MS but may worsen PsO; IL-17–based combinations appear promising in highly active disease.

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Neurotherapeutics, 23, 3, Elsevier B.V., [Amsterdam], 2026, https://doi.org/10.1016/j.neurot.2026.e00914

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