Psoriasiform Dermatitis Following JAK Inhibitor Therapy for Hidradenitis Suppurativa and Crohn's Disease

Upadacitinib, a selective JAK1 inhibitor approved for hidradenitis suppurativa (HS) and Crohn's disease (CD), has been implicated in paradoxical inflammatory reactions; however, upadacitinib-induced psoriasiform dermatitis in patients treated for HS has not been previously described to the best of our knowledge. We report a 55-year-old woman with HS, CD, rheumatoid arthritis, and systemic lupus erythematosus, receiving upadacitinib 30 mg daily, who developed a pruritic erythematous scaly plaque on the lower back without personal or family history of psoriasis. Punch biopsy demonstrated psoriasiform dermatitis with acanthosis, focal hypogranulosis, uniform elongation of rete ridges, spongiosis, parakeratosis, and a superficial perivascular lymphocytic infiltrate. Given upadacitinib's established efficacy for both HS and CD, the drug was continued, and topical augmented betamethasone dipropionate was initiated, achieving adequate control at two-week follow-up. This case inverts the established paradigm in which JAK inhibitors serve as rescue agents for paradoxical reactions triggered by anti-TNF-α biologics. Comparable psoriasiform eruptions have been reported with baricitinib and tofacitinib, primarily in rheumatoid arthritis, a comorbidity present in our patient and an important interpretive caveat. We hypothesize that interferon-gamma (IFN-γ)-mediated STAT1 dysregulation intrinsic to HS pathogenesis may lower the threshold for JAK inhibitor-induced immune imbalance, although this mechanism remains speculative and warrants further investigation. Paradoxically, upadacitinib has also resolved psoriasiform eruptions in HS, underscoring the bidirectional and unpredictable nature of JAK1 inhibitor-mediated immune modulation. Psoriasiform dermatitis may represent a paradoxical cutaneous reaction to upadacitinib in patients with HS, warranting vigilant dermatologic monitoring and further investigation into individual susceptibility factors.