Paradoxical psoriasiform inflammatory reaction during the use of tumor necrosis factor-alpha inhibitors in patients with Crohn’s disease (a review of the literature and presentation of two clinical cases)

Abstract

Psoriasiform rash (paradoxical inflammation) induced by tumor necrosis factor-alpha (TNFα) inhibitors is observed in about 5–10% of patients with inflammatory bowel diseases treated by these genetically engineered agents. Its predictors include gender (mostly female), smoking, higher body mass index, and formation of anti-neutrophil antibodies. There is no correlation between the paradoxical inflammation and specific agent; the rash can develop with the use of any TNFα inhibitor, such as infliximab, adalimumab, or certolizumab pegol. The first line of treatment for pharmacologically induced psoriasis includes topical corticosteroids (mostly, high potency agents clobetasol and betamethasone) and combination steroid-containing agents (betamethasone + calcipotriol). If this treatment is ineffective or the rash recurs during the use of TNFα inhibitors, the rash is qualified as a class-specific effect, with consideration of switching the patient to a genetically engineered product with another mechanism of action. In such a case, there is a strong indication for ustekinumab. Despite a relatively high incidence of the paradoxical inflammation with TNFα inhibitors and a bulk of published data, some questions remain unanswered. In particular, further studies are required into the time intervals between the achievement of a clinically significant effect of TNFα inhibitors on the symptoms of inflammatory bowel diseases and the skin rash formation, which means the possibility of treatment withdrawal and change of the treatment strategy, as well as studies on the long-term prognosis of the skin lesions. In this context, clinical case presentation and the accumulated experience would subsequently help to formulate actual clinical recommendations on the management of this patient category.