Original article—alimentary tract
Severe Skin Lesions Cause Patients With Inflammatory Bowel Disease to Discontinue Anti–Tumor Necrosis Factor Therapy

https://doi.org/10.1016/j.cgh.2010.07.022Get rights and content

Background & Aims

Psoriasiform and eczematiform lesions are associated with anti–tumor necrosis factor (TNF)-α therapies. We assessed clinical characteristics, risk factors, and outcomes of skin disease in patients with inflammatory bowel diseases that presented with psoriasiform and eczematiform lesions induced by anti-TNF-α agents.

Methods

We studied 85 patients (69 with Crohn's disease, 15 with ulcerative colitis, and 1 with indeterminate colitis; 62 women) with inflammatory skin lesions (62 psoriasiform and 23 eczematiform lesions).

Results

Twenty-four patients had a history of inflammatory skin lesions and 15 had a familial history of inflammatory skin disease. Locations of eczematiform lesions varied whereas scalp and flexural varieties were mostly psoriasiform. Skin lesions emerged but inflammatory bowel disease was quiescent in 69 patients following treatment with any type of anti-TNF-α agent (60 with infliximab, 20 with adalimumab, and 5 with certolizumab). Topical therapy resulted in partial or total remission in 41 patients. Patients with psoriasiform lesions that were resistant to topical therapy and that changed anti-TNF-α therapies once or twice developed recurring lesions. Overall, uncontrolled skin lesions caused 29 patients to stop taking TNF-α inhibitors.

Conclusions

Inflammatory skin lesions following therapy with TNF-α inhibitors occurred most frequently among women and patients with a personal or familial history of inflammatory skin disease; lesions did not correlate with intestinal disease activity. Recurring and intense skin lesions caused 34% of patients in this study to discontinue use of anti-TNF-α agents.

Section snippets

Study Design

We conducted a retrospective study between January 2004 and September 2009 of patients with new onset or exacerbation of eczematiform or psoriasiform lesions during treatment with anti-TNF agents for IBD observed in the GETAID centers (35 centers in Belgium, France, and Switzerland) and 1 center from Austria. Furthermore, from January 2006 to January 2010, all patients treated with anti-TNF agents in the department of hepatogastroenterology of Lille and presenting with eczematiform or

Description of the Population

A total of 85 patients (23 males and 62 females) with IBD (69 CD, 15 UC, and 1 indeterminate colitis [IC]) were included. Demographic and clinical characteristics of patients are given in Table 1. Skin lesions were overall observed in patients who received infliximab (n = 60), adalimumab (n = 20), and certolizumab pegol (n = 5) therapy. At the time of onset of skin lesions, 79 patients were on maintenance scheduled therapy but 10 patients on infliximab had previous episodic treatment. No

Discussion

Eczematiform and psoriasiform eruptions are, after infections, the most frequent dermatological adverse events in patients receiving anti-TNF-α therapy.12, 13 Their prevalence in patients with IBD is unknown. Recent data from the rheumatologic literature indicates that the incidence rate of new onset psoriasis in patients treated with anti-TNF is around 1.04 (95% confidence interval, 0.97–1.54) per 1000 person-years.14 As psoriasis may be associated with CD,15 psoriasiform lesions may appear

Acknowledgments

In addition to the authors, the following investigators participated in the study: Pierre Desreumaux (CHU Lille), Vered Abitbol (Hôpital Cochin Paris), Arnaud Boureille (CHU Nantes), Hedia Brixi-Benmansour (CHU Reims), Benoît Coffin (Hôpital Louis-Mourier Paris), Mathurin Flamant (CHU Nantes), Eric Lerebours (CHU Rouen), Jacques Moreau (CHU Toulouse), Stéphane Nancey (CHU Lyon), Anne Laure Pelletier (Hôpital Bichat Paris), and Guillaume Savoye (CHU Rouen).

The corresponding author had full

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    Conflicts of interest These authors disclose the following: Jean-François Rahier received lecture fees from speaking at continuing medical education events from Abbott Laboratories and Schering-Plough; Laurent Peyrin Biroulet has received consulting fees from Abbott Laboratories and UCB Pharma; Yoram Bouhnik received lecture fees from Abbott Laboratories and Schering-Plough Corporation; Edouard Louis declared consulting fees or paid advisory board for Abbott, Schering-Plough, and UCB; Pavol Papay received honoraria as consultant for Abbott, Centocor, and UCB Pharma; Matthieu Allez has served or received honoraria for teaching activities from Abbott Pharmaceuticals, Schering-Plough, and UCB Pharma; Jacques Cosnes received consulting fees from Abbott Laboratories and lecture fees from speaking at continuing medical education events from Abbott Laboratories and UCB Pharma; Antoine Cortot has served as consultant for and received honoraria from Ferring and Schering-Plough; David Laharie received honoraria from Abbott Pharmaceuticals and Schering-Plough; Jean-Marie Reimund received lecture fees for speaking at continuing medical education events from Abbott Laboratories and grants for basic research from Ferring Laboratories and UCB Pharma; Marc Lémann declared consulting fees or paid advisory boards for Abbott Laboratories, Cellerix SL, Centocor, Schering-Plough Corporation, UCB Pharma, and received lecture fees from Abbott Laboratories, Schering-Plough Corporation, and UCB Pharma; Emmanuel Delaporte received lecture fees for Abbott, Schering-Plough, and Wyeth; and Jean-Frédéric Colombel has served as a consultant for and received honoraria and research grants from Centocor, Inc, Schering-Plough, UCB Pharma, and Abbott Pharmaceuticals. The remaining authors disclose no conflicts.

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