Abstract Background Observational data has reported anti-TNF related dermatological complications in patients with IBD at 20-22%1,2. Previous histological assessment of some of these lesions have identified skin infiltrates rich in IL-12, IL-17 and IL-233. Underlying aetiology is currently unclear. We aimed to characterise the clinical and inflammatory cytokine profile of patients with IBD who develop dermatological complications of anti-TNF treatment. Methods Patients who were receiving anti-TNF therapy and developed dermatological complications were prospectively recruited from IBD outpatient clinics in a tertiary referral centre. Age and disease matched controls were identified. All patients were reviewed by dermatology to confirm diagnosis. Serum samples and disease phenotype were collected at time of recruitment. Serum cytokine concentrations were quantified using cytometric bead array (IL-8, IL-1, IL-6, IL-10, TNF, IL-12p70)(BD Biosciences) and enzyme linked immunosorbent assays (IL-17 and IL-23) (DuoSet R 72.7%) and small bowel disease (n = 3; 50%) were the most frequent distribution of disease in patients who developed dermatological complications with UC and CD respectively. A trend toward lower mean concentrations of TNF and higher mean concentrations of IL-8, IL-17 9(9):496-503. doi:10.1038/nrgastro.2012.125 2. Freling E, Baumann C, Cuny JF, et al. Cumulative incidence of, risk factors for, and outcome of dermatological complications of anti-TNF therapy in inflammatory bowel disease: a 14-year experience. Am J Gastroenterol. Aug 2015;110(8):1186-96. doi:10.1038/ajg.2015.205 3. Tillack C, Ehmann LM, Friedrich M, et al. Anti-TNF antibody-induced psoriasiform skin lesions in patients with inflammatory bowel disease are characterised by interferon-gamma-expressing Th1 cells and IL-17A/IL-22-expressing Th17 cells and respond to anti-IL-12/IL-23 antibody treatment. Gut. Apr 2014;63(4):567-77. doi:10.1136/gutjnl-2012-302853 4. Toussirot E, Aubin F. Paradoxical reactions under TNF-alpha blocking agents and other biological agents given for chronic immune-mediated diseases: an analytical and comprehensive overview. RMD Open. 2016;2(2):e000239. doi:10.1136/rmdopen-2015-000239 Conflict of interest: Dr. Mchale, Ciarán: No conflict of interest Mc Gettigan, Neasa: No conflict of interest Beatty, Paula: No conflict of interest O’Sullivan, David: No conflict of interest McKenna-Barry, Matthew: No conflict of interest Schilling, Carole: No conflict of interest Dowling, Jennifer: No conflict of interest Roche, Muireann: No conflict of interest Boland, Karen: No conflict of interest
Mchale et al. (Thu,) studied this question.