IBD Treatment-Associated Rashes: Paradoxical Reactions and JAK-Inhibitor Skin Eruptions

Conclusions

• IBD patients can develop skin eruptions from multiple causes, so a broad differential and biopsy are often needed to distinguish paradoxical drug reactions from infection, contact dermatitis, or other dermatoses.
• Paradoxical rashes associated with IBD therapies are not always classic psoriasis and can present as psoriasiform eczema, impetiginized intertriginous disease, palmoplantar eruptions, or psoriatic alopecia.
• These paradoxical reactions are seen most commonly with anti-TNF agents but can also occur with other biologics and are thought to involve interferon-driven pathways rather than true psoriasis alone.
• Switching from one anti-TNF to another often does not resolve the rash, whereas moving to another mechanism or treating through with adjunctive therapy may be more effective.
• Therapies that target the interferon/JAK pathway, along with methotrexate, apremilast, or phototherapy, can improve paradoxical rashes when the underlying IBD treatment must be maintained.
• JAK inhibitor–associated acneiform eruptions frequently warrant evaluation for alternative diagnoses, because some are actually fungal folliculitis or Demodex-associated disease rather than ordinary acne.
• Upadacitinib and other JAK1-selective agents appear more strongly linked to acne than less JAK1-predominant inhibitors.
• When JAK-associated acne is atypical or treatment-resistant, scraping or biopsy can reveal treatable organisms such as Demodex or Malassezia, and targeted therapy such as ivermectin or antifungals can lead to resolution.