AI Article Synopsis

  • Tumor necrosis factor (TNF) α inhibitors, commonly used for treating inflammatory bowel disease (IBD), can sometimes provoke unexpected inflammatory responses in patients.
  • A case study of a 62-year-old male with ulcerative colitis showed he developed Sweet syndrome after two months on adalimumab, leading to skin lesions characteristic of neutrophilic dermatosis.
  • The researchers recommend stopping adalimumab and increasing prednisolone dosage while exploring the cause of the symptoms, noting that the risk of drug hypersensitivity syndrome in this case was considered low.

Article Abstract

Tumor necrosis factor (TNF) α inhibitors are widely used to treat inflammatory bowel disease (IBD); however, some patients have unexpected inflammatory episodes during anti-TNF therapy. The objective of our research was to highlight a paradoxical case of anti-TNF-agent-induced Sweet syndrome compared with Sweet syndrome treated by anti-TNF agents. We describe a 62-year-old male with a history of ulcerative colitis presenting with multiple polymorphic indurated skin macules and plaques after 2 months of adalimumab therapy. Neutrophilic dermatosis was diagnosed based on the clinical presentation and skin biopsy and may have resulted from extraintestinal manifestations of a flare-up of IBD or been induced by adalimumab therapy. We conclude that when facing this dilemma, adalimumab should be discontinued, and the dose of prednisolone should be increased before determining the definitive cause. Based on drug hypersensitivity syndrome (DHS) risk assessment in the 10-D assessment system, this case was classified as grade 1 (no risk). Finally, we review the molecular and cellular mechanisms connecting cytokine dysregulation to Sweet syndrome.

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Source
http://dx.doi.org/10.5414/CP204088DOI Listing

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