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Development of Rheumatoid Arthritis During Anti-Interleukin-5 Therapy in a Patient with Refractory Chronic Eosinophilic Pneumonia

PURPOSE: To report the case of a patient with refractory chronic eosinophilic pneumonia who developed rheumatoid arthritis during anti-interleukin (IL)-5 therapy. CASE REPORT: The case of a 66-year-old male ex-smoker with allergic rhinitis who had dyspnea and chronic cough for 6 months and who was u...

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Detalles Bibliográficos
Autores principales: Kawabata, Hiroki, Satoh, Minoru, Yatera, Kazuhiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8631983/
https://www.ncbi.nlm.nih.gov/pubmed/34858033
http://dx.doi.org/10.2147/JAA.S342993
Descripción
Sumario:PURPOSE: To report the case of a patient with refractory chronic eosinophilic pneumonia who developed rheumatoid arthritis during anti-interleukin (IL)-5 therapy. CASE REPORT: The case of a 66-year-old male ex-smoker with allergic rhinitis who had dyspnea and chronic cough for 6 months and who was ultimately diagnosed with chronic eosinophilic pneumonia is reported. Long-term corticosteroid therapy was necessary due to recurrence of the chronic eosinophilic pneumonia during tapering of the corticosteroid. As a steroid sparing strategy, mepolizumab was initiated, and the steroid was tapered gradually. When the dose of prednisolone was 2 mg/day, he developed polyarthralgia. Mepolizumab was changed to benralizumab considering the possibility that arthralgia was a side effect of mepolizumab; however, the arthralgia continued and he was ultimately diagnosed with rheumatoid arthritis. Methotrexate was initiated and his arthritis improved. Thereafter, benralizumab was discontinued after 5 injections, and he subsequently required neither systemic corticosteroids nor biologics. CONCLUSION: The present case may suggest that suppression of IL-5 induces rheumatoid arthritis in certain patients; however, it is also possible that initial steroid therapy improved subclinical RA and made it remain undiagnosed, and the parallel OCS tapering during IL-5 therapy could have contributed to unveil the underlying RA. Further studies are required to establish guidelines on the optimum use of anti-IL-5 therapy and to understand the interactions between chronic eosinophilic pneumonia, anti-IL-5 therapy, tapering of corticosteroid and development of rheumatoid arthritis.