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  • Presentation

Paradoxical Rashes and JAK Inhibitor-Associated Acne in Hidradenitis and IBD Patients

Description

Dr. Alexandra Charo discussed paradoxical rashes and JAK inhibitor-associated acne in patients with hidradenitis suppurativa and inflammatory bowel disease. She emphasized using broader terms like “biologic-induced” or “paradoxical” rash because these eruptions occur with multiple biologics, not just TNF inhibitors. Paradoxical rashes often show mixed morphologies, such as psoriasiform and eczematous features, and pathology may reveal both psoriasiform and spongiotic dermatitis. She reviewed incidence, dose dependence, and proposed pathophysiology, noting that TNF blockade may unleash interferon-driven inflammation, while other biologics may involve different mechanisms. Clinical presentations can vary widely, including inverse psoriasis-like eruptions, psoriasiform eczema, palmoplantar disease, impetiginized plaques, and psoriatic alopecia. Management can be difficult; switching within the same TNF class often fails, so additional therapy aimed at the interferon pathway may be needed, including methotrexate, apremilast, light therapy, or JAK inhibitors. She then shifted to JAK inhibitor-associated acne, particularly with JAK1 agents, describing it as potentially recalcitrant and recommending evaluation for Demodex because many cases may need ivermectin rather than standard acne therapy.

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Conclusions

  • Paradoxical rashes are a biologic-associated phenomenon seen across multiple drug classes, not just TNF inhibitors.
  • These rashes often have mixed and varied morphologies, including psoriasiform, eczematous, inverse, palmoplantar, impetiginized, and alopecia-like presentations.
  • The underlying mechanism is thought to involve immune pathway shifts, especially interferon dysregulation, rather than classic psoriasis pathways alone.
  • Paradoxical rashes can be dose-dependent and may be more common with higher-dose or higher-frequency biologic regimens.
  • Switching from one TNF inhibitor to another often does not reliably resolve the rash, so these eruptions can be refractory.
  • Management is often more successful when the rash itself is treated, including with agents that target the interferon pathway such as JAK inhibitors, methotrexate, apremilast, or light therapy.
  • For some patients, continuing the needed biologic while adding rash-directed therapy can be effective.
  • JAK inhibitor–associated acne is a recognized adverse effect, especially with JAK1-selective agents.
  • When JAK-associated acne occurs, clinicians should consider demodex infestation as a frequent contributor and treat accordingly when present.
  • Overall, the presentation concludes that recognizing the specific rash phenotype is essential for choosing whether to treat through, add adjunctive therapy, or change the underlying medication.
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