ArticleJournal of asthma and allergy2021
Development of Rheumatoid Arthritis During Anti-Interleukin-5 Therapy in a Patient with Refractory Chronic Eosinophilic Pneumonia.
Article in Journal of asthma and allergy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Sequential autoimmune and neoplastic manifestations during long-term benralizumab therapy for severe eosinophilic asthma: A descriptive case report.Respiratory medicine case reports · 2026Article
- Articular manifestations related to anti-interleukin-5 therapies in severe asthma: a case series.ERJ open research · 2024Article
- Anti-IL-5 biologics and rheumatoid arthritis: a single-centre 500 patient year exposure analysis.RMD open · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo 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.
conclusionThe 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.
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