Tumor necrosis factor alpha inhibitors (anti‐TNF‐α) completely revolutionized the treatment of inflammatory bowel disease (IBD). However, anti‐TNF‐α‐induced cutaneous side effects have been increasingly reported in the literature. Particularly, psoriasis and… Click to show full abstract
Tumor necrosis factor alpha inhibitors (anti‐TNF‐α) completely revolutionized the treatment of inflammatory bowel disease (IBD). However, anti‐TNF‐α‐induced cutaneous side effects have been increasingly reported in the literature. Particularly, psoriasis and the recently recognized psoriasiform lesions are of particular concern, as anti‐TNF‐α agents are also used in the treatment of psoriasis, seemingly reflecting an immunological paradox. The clinical management of these cutaneous lesions is particularly challenging, owing to the potential need of anti‐TNF‐α discontinuation and scarcity of other therapeutic options. Therefore, optimization of current topical and systemic therapies and incorporation of new therapeutic agents is of great interest. Our aim is to review data in the literature regarding the clinical management of these cutaneous lesions and provide a therapeutic algorithm, supported by our experience as a tertiary referral center for IBD. Although in older reports no distinction was made, anti‐TNF‐α‐induced psoriasiform lesions are not only more prevalent but also bear notable differences from classical psoriasis, possibly reflecting a different nosological entity. Onset of lesions has been related to periods of IBD remission, as supported by low levels of fecal calprotectin. Psoriasiform lesions can be adequately managed either by topical (glucocorticoids, calcineurin inhibitors, and antibiotics) or systemic (phototherapy, acitretin, glucocorticoids, and antibiotics) therapies and/or switch to other anti‐TNF‐α agents. Data referring to patients who were able to continue on the same IBD therapy ranged from 30.7 to 100%, reinforcing the importance of an adequate control of these lesions. The recently approved ustekinumab offers another step in the management of anti‐TNF‐α‐intolerant patients.
               
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