4.0 Article

Aphthous mouth ulcers as an initial manifestation of secukinumab-induced inflammatory bowel disease

Journal

ANNALES DE DERMATOLOGIE ET DE VENEREOLOGIE
Volume 145, Issue 11, Pages 676-682

Publisher

MASSON EDITEUR
DOI: 10.1016/j.annder.2018.07.009

Keywords

Secukinumab; Oral aphthous ulcers; Tocilizumab; Inflammatory bowel disease

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Background. - Secukinumab, a humanized monoclonal antibody targeting interleukin 17A, has been associated with the development of inflammatory bowel diseases. We report a case of a female patient developing recurrent oral ulcers prior to inflammatory bowel disease induced by secukinumab. The patient had developed similar oral ulcers 6 years earlier while on tocilizumab (targeting IL6R), suggesting an immunological link between the two episodes. Patients and methods. - A 36-year-old female patient had refractory spondylarthrosis. In 2010, she had presented oral aphthous ulcers during treatment with tocilizumab. In 2011, tocilizumab was stopped and the ulcers resolved. In 2016, secukinumab was introduced and led to recurrence of oral aphthous ulcers followed by ileitis-pancolitis. Corticosteroids and ustekinumab resulted in partial remission. Discussion. - The patient developed inflammatory bowel disease during treatment with secukinumab, preceded by recurrent oral aphthous ulcers. She had presented similar oral ulcers 6 years earlier while on a treatment targeting IL6R. IL6 is a pleiotropic cytokine that may activate the Th17 pathway. Thus, tocilizumab could have induced an anti-11.17-like effect, accounting for the occurrence of oral aphthous ulcers, possibly related to mild inflammatory bowel disease. Conclusion. - The occurrence of oral ulcers during treatment with secukinumab may herald inflammatory bowel disease. In patients with a previous history of recurrent aphthous stomatitis, especially where induced by previous biologics, consideration must be given to the risk-benefit ratio of prescribing an anti-IL17 antibody. (C) 2018 Elsevier Masson SAS. Alt rights reserved.

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