P762 Onset of inflammatory bowel disease during treatment with secukinumab: Can anti-IL-17A be a trigger for inflammatory bowel disease?
R. Rodríguez Moncada*1, J. M. Vázquez Morón1, M. Rojas Feria2, J. M. Herrera Justiniano3, B. Maldonado Pérez4, M. Castro Fernández2, A. Núñez Ortiz3, V. Cabello Rubio3, H. Pallarés Manrique1, E. Gómez Delgado1, A. Bejarano García1
1Hospital Juan Ramón Jiménez, Gastroenterology Unit, Huelva, Spain, 2Universitary Hospital Virgen de Valme, Gastroenterology Unit, Seville, Spain, 3Universitary Hospital Virgen del Rocío, Gastroenterology Unit, Seville, Spain, 4Universitary Hospital Virgen de la Macarena, Gastroenterology Unit, Seville, Spain
Secukinumab is a monoclonal antibody that acts specifically on interleukin 17A (IL-17A), and is approved for the treatment of plaque psoriasis (PP), psoriatic arthritis (PA) and ankylosing spondylitis (AS). Although it is a pro-inflammatory cytokine raised to the level of intestinal mucosa in patients with inflammatory bowel disease (IBD), it is paradoxical that blocking the IL-17 pathway using secukinumab is not associated to a reduction in bowel inflammation, it even seems to make it worse. This is also due to the fact that IL-17 seems to act as protector against inflammation, contributing to the inhibition of the Th1 response and maintaining the integrity of the enterocyte’s epithelial barrier and intestinal homeostasis. Although so far it has not been identified as a trigger of IBD. We describe several of the first cases (Table 1). In addition to this series of cases, only two other cases of onset of IBD during treatment with secukinumab have been reported, both during 2018.
Descriptive study of a series of cases with emergence of IBD during treatment with secukinumab due to PP, PA or AS in five hospitals in South of Spain.
353 patients started treatment with secukinumab by indication of rheumatology or dermatology. During treatment, five patients (1.4%) developed an IBD. A sixth case was detected in a hospital where we don′t know number of patients treated with secukinumab. Four of those six patients (66%) were women, with an average age of 41 years (IQR 26.5–47.2). Indications for treatment were 3 PA, 2 PP and 1 SA. Three patients (50%) had previously received anti-TNFα. Four patients were diagnosed with Crohn′s disease (66%) and two patients with ulcerative colitis (33%). The average time to develop IBD was 8.5 weeks from the start of the treatment (IQR 3.7–21.5). After the diagnosis of IBD, secukinumab was withdrawn in five patients and treatment was started with ustekinumab (two patients), infliximab (two patients) or golimumab (one patient). All patients reached a clinical improvement to IBD and rheumatological/dermatological pathology.
Secukinumab and onset of IBD. Cases in hospitals from Seville and Huelva.
This study documents the negative relationship between secukinumab and IBD. Thus, it could be that this drug, as well as possibly triggering an outbreak of activity, sets off cases of subclinical or latent disease, especially in genetically predisposed patients; therefore, in these cases, we should consider using other safer therapeutic options for the treatment of these rheumatological and dermatological entities (e.g. anti-TNFα or anti-IL12/23 drugs).