Effectiveness of CGRP (-Receptor) monoclonal antibodies after treatment re-initiation

Background
Monoclonal Antibodies targeting the calcitonin gene-related peptide (CGRP) or its receptor have proven to be effective and well-tolerated therapy options in the prophylactic treatment of migraine. After successful treatment with CGRP (receptor) antibodies, European and German guidelines recommend a treatment cessation to re-evaluate further need for prophylactic treatment. Patients frequently express concerns regarding a break-induced reduction in effectiveness after re-initiation of treatment. Data on this topic is rare.
Methods
This retrospective longitudinal cohort study analyzes clinical routine real-world data from migraine patients being treated with CGRP antibodies. The observation period includes the last three months before, the time during, and the first three months after the break. Primary scientific goals are changes in monthly headache days (MHD), monthly migraine days (MMD), and intake days of acute medication (AMD) during the observation period. We analyzed for significant differences in those using the Friedmann test and post hoc test. We also tried to isolate possible predictors of variances in MHD, MMD, and AMD differences between the three months prior to and following the treatment pause by creating multiple linear regression models for MHD, MMD, and AMD differences between those periods.
Results
65 patients (22 EM, 43 CM) fulfilled our inclusion criteria. During the pause, MHD increased by 66.11% (9.06±7.49 to 15.05±7.87, p < .001) and decreased by 40,73% after re-initiation (to 8.92±7.03, p < .001). MMD increased by 99.24% (5.28±2.85 to 10.52±6.07, p < .001) and after re-initiation decreased by 45.82% (to 5.70±3.28, p < .001). AMD increased by 61.52% (5.64±4.99 to 9.11±5.31, p < .001), and decreased by 37.98% after re-initiation (to 5.65±3.77, p < .001). Comparing MHD, MMD, and AMD before and following the break, revealed no significant differences (p = 1.000). There was no significant predictive value in our multiple linear regression model of MHD (p = .296, corrected R squared = .031), MMD (p = .444, corrected R squared = .001), and AMD (p = .919, corrected R squared = -.089).
Conclusion
CGRP antibodies maintain their effectiveness even after the break. Our data does not support patients’ concerns about a break-induced reduction in the effectiveness of further prophylaxis.