European journal of neurology · 2026
Association of Serum hs-CRP and TNF-α With Therapeutic Response to Erenumab for Migraine Prevention: A Registry for Migraine (REFORM) Study.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Karlsson William K, Christensen Rune H, Al-Khazali Haidar M, Olsen Dorte A, Madsen Jonna S, Ashina Messoud, Ashina Håkan
Аннотация
BACKGROUND: Experimental studies show inflammatory cytokines can modulate calcitonin gene-related peptide (CGRP) signaling, suggesting systemic inflammatory markers might reflect biological processes relevant to anti-CGRP therapies. We aimed to determine whether serum high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-alpha (TNF-α) are associated with erenumab response in adults with migraine and assess longitudinal biomarker changes during and after treatment.
METHODS: In this prospective, observational single-center study, adults with episodic or chronic migraine self-administered 140 mg erenumab subcutaneously every 4 weeks for 24 weeks. Serum was collected at baseline, Week 24 (end of treatment), and Week 48 (24 weeks post-treatment). Treatment response was defined as a ≥ 50% reduction in monthly migraine days from baseline to Weeks 13-24. Logistic and linear regression models evaluated associations between baseline biomarkers and response, while longitudinal changes were analyzed using linear mixed-effects models.
RESULTS: Of 679 enrolled participants, serum was analyzed in 623. Among 541 with sufficient data to determine response, 281 (51.9%) were responders. Neither baseline hs-CRP (OR 1.04; 95% CI 0.96-1.12; p = 0.30) nor TNF-α (OR 0.75; 95% CI 0.49-1.16; p = 0.20) predicted treatment response. TNF-α increased from baseline to Week 24 (mean rise 3.0%; 95% CI 0.5%-5.4%; p = 0.030), but no responder-non-responder differences were found.
CONCLUSIONS: Peripheral inflammatory biomarkers such as hs-CRP and TNF-α neither predict response nor change meaningfully during CGRP-receptor blockade. These results suggest broadly applied inflammatory markers do not capture treatment-relevant biology and highlight the need for mechanism-specific biomarkers to advance personalized migraine therapy.
METHODS: In this prospective, observational single-center study, adults with episodic or chronic migraine self-administered 140 mg erenumab subcutaneously every 4 weeks for 24 weeks. Serum was collected at baseline, Week 24 (end of treatment), and Week 48 (24 weeks post-treatment). Treatment response was defined as a ≥ 50% reduction in monthly migraine days from baseline to Weeks 13-24. Logistic and linear regression models evaluated associations between baseline biomarkers and response, while longitudinal changes were analyzed using linear mixed-effects models.
RESULTS: Of 679 enrolled participants, serum was analyzed in 623. Among 541 with sufficient data to determine response, 281 (51.9%) were responders. Neither baseline hs-CRP (OR 1.04; 95% CI 0.96-1.12; p = 0.30) nor TNF-α (OR 0.75; 95% CI 0.49-1.16; p = 0.20) predicted treatment response. TNF-α increased from baseline to Week 24 (mean rise 3.0%; 95% CI 0.5%-5.4%; p = 0.030), but no responder-non-responder differences were found.
CONCLUSIONS: Peripheral inflammatory biomarkers such as hs-CRP and TNF-α neither predict response nor change meaningfully during CGRP-receptor blockade. These results suggest broadly applied inflammatory markers do not capture treatment-relevant biology and highlight the need for mechanism-specific biomarkers to advance personalized migraine therapy.