P45 Interstitial pneumonitis induced by secukinumab therapy in a patient with psoriatic arthritis

Background Inhibition of pro-inflammatory interleukin-17A (IL-17A) with secukinumab (an anti-IL-17A antibody) has been utilised in patients with chronic autoimmune disease such as psoriasis seronegative spondyloarthopathies. In mouse models, IL-17A was involved in the development of pulmonary inflammation and progression of fibrosis, with blockade of IL-17A implicated as a potential therapeutic target in such conditions. Here we report a case of, seemingly paradoxical, interstitial lung disease (ILD) secondary to secukinumab therapy in a 61-year-old patient with psoriatic arthritis. Methods Please refer to the results section. Results Initial therapy was with adalimumab achieving good disease control for 9 years, at which point his arthritis began to progress. Secukinumab was commenced with good clinical response from his arthritis, however he developed a persistent cough with blood-stained secretions, and shortness of breath on exertion. A CT thorax was arranged at 21 weeks after initiation of secukinumab, and showed florid bibasal, lingula and middle lobe ground glass density air space opacification. He went on to have bronchoscopy with bronchoalveolar lavage (BAL) and differential cell count. BAL was negative for atypical infection including P. jirovecii, growing upper respiratory tract flora only. Microscopy of BAL showed lymphocytosis in keeping with the diagnosis of drug induced ILD, with no atypical cells. The patient made a significant improvement on withdrawal of secukinumab therapy within 7-8 weeks of cessation - both clinically and radiologically. Conclusion A review of the current literature at this time indicates this is now a third case of secukinumab induced ILD. Given this potentially idiosyncratic reaction we suggest further work may be necessary to understand the underlying immunogenic potential of secukinumab, and an increased awareness as well as vigilance in reporting, to determine those at-risk populations of this phenomenon. Disclosures C. Saleh None. S. Bilgrami None. T. Gatheral None. L. Ottewell None.