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P204. Anti-TNFα agents induce psoriasiform eruption in IBD patients: Frequency and outcome

K. Papamichael1, E. Archavlis1, K. Nutsis2, K. Lariou3, A. Tsirogianni4, A. Smyrnidis1, N. Kyriakos1, P. Konstantopoulos1, G.J. Mantzaris1

1A' Gastroenterology Clinic, Evaggelismos Hospital, Athens, Greece; 2Dermatology Clinic, Evaggelismos Hospital, Athens, Greece; 3Department of Pathology, Evaggelismos Hospital, Athens, Greece; 4Department of Immunology, Evaggelismos Hospital, Athens, Greece

Background: Many anti-TNFα agents have shown efficacy in the treatment of autoimmune and idiopathic inflammatory diseases, such as IBD, rheumatoid arthritis, and psoriasis, however they may induce paradoxical inflammation leading to the development of autoimmune diseases similar to those they were designed to treat for. Anti-TNFα-induced skin eruptions including psoriasiform rash are thought to be a class effect resulting from the increased local secretion of pro-inflammatory cytokines, such as IFNα.

Aim: To prospectively evaluate the frequency of psoriasiform eruptions (PSE) in patients with Crohn's disease (CD) and ulcerative colitis (UC) receiving induction and then maintenance scheduled infliximab (IFX) or adalimumab (ADA) therapy

Design: Prospective, single-centre study.

Patients and Method: Consecutive CD and UC patients who received at least two doses of IFX or ADA and were followed in the IBD outpatient clinic every 1–2 months were eligible for the study. In case of a skin rash, patients were examined by a single dermatologist and had skin biopsy if necessary. At baseline and at 6 months interval anti-nuclear antibodies (ANA) and anti-DNA antibodies were measured. Patients with PSE were receiving local therapy; if PSE persisted or expanded despite local treatment anti-TNF therapy was temporarily or permanently stopped and progression or regression of lesions was followed.

Results: 138 IBD [83 males, mean age (SD) 32.4±9.4 years], 104 CD (46 received IFX, 20 ADA and 38 received successively IFX and ADA) and 34 UC (all received IFX) patients were included in the study. PSE appeared in 9 patients (6.5%, 4 males, 7 with CD) and was histologically confirmed. Five patients had received IFX and 4 ADA (3/4 for prior loss of response to IFX). The duration of treatment at presentation of PSE was 10.4 months (8–13) (median, range) for IFX- and 5.4 (3–7) months for ADA-treated patients [the latter group had received successive anti-TNF treatment for 16.5 (12–26) months (median, range)]. One female patient developed PSE on both IFX and ADA. PSE was located in the extremities (1), ears/face (2), external genitalia (1) or in multiple sites (5). ANA (>1:160 titers) were detected in 5/9 patients whereas anti-dsDNA in one patient. Treatment was stopped temporarily in 8/9 patients resulting in full remission of PSE in 3/9 and partial in 5/9 patients. Treatment was stopped permanently in 1 patient. Development of PSE was unrelated to type of disease, gender, age, age at disease onset, type of anti-TNFα, but it appeared after at least 8 months of scheduled maintenance treatment.

Conclusion: A small proportion of IBD patients will develop PSE during anti-TNFα therapy and only very few will have to stop the anti-TNFα treatment. Local treatment and temporal cessation of anti-TNF agents may lead to remission of PSE.