New-Onset Psoriasis After Abrocitinib Treatment for Atopic Dermatitis

The coexistence of AD and psoriasis in the same patient has been considered uncommon because of their differing T-cell lineages. AD is a chronic inflammatory skin disease affecting up to 10% of adults and 30% of children globally. It is primarily driven by Th2-mediated cytokines such as IL-4, IL-13, and IL-31.^1,2 In contrast to AD, psoriasis is thought to arise from Th17-mediated cytokines such as IL-17, IL-22, and IL-23.³

Abrocitinib, a selective Janus kinase 1 (JAK1) inhibitor, is one of the newer oral agents approved for moderate to severe AD, working by suppressing key cytokines involved in AD pathogenesis.⁴ Although JAK inhibitors have shown promise in controlling various immune-mediated skin conditions, they may, in rare instances, lead to the emergence of a second immune-mediated disease.

Previous reports have described psoriasis-like eruptions with other JAK inhibitors, including upadacitinib.⁵ However, to date, abrocitinib-induced psoriasis has not been reported in the literature. This case highlights a rare instance of new-onset psoriasis developing in a young patient with AD receiving abrocitinib therapy.⁶

Case Presentation

A 20-year-old male with severe, treatment-resistant AD presented with a new cutaneous eruption. Treatment history included topical corticosteroids, calcineurin inhibitors, prednisone, cyclosporine, methotrexate, and narrowband UVB phototherapy, all with inadequate response. A 6-month trial of dupilumab was discontinued due to limited efficacy and the development of acute pancreatitis.

Abrocitinib 100 mg daily was initiated, later increased to 200 mg following a disease flare, resulting in significant improvement with less than 5% body surface area (BSA) involvement. After 7 months of therapy, a new eruption consisting of salmon-colored, scaly, well-demarcated papules and plaques developed, involving approximately 20% BSA. Lesions were morphologically distinct from prior AD and minimally pruritic.

Biopsy demonstrated psoriasiform epidermal hyperplasia, parakeratosis with neutrophils, and dilated capillaries surrounded by a lymphocytic infiltrate—findings consistent with psoriasis. Based on clinical presentation, histopathology, and temporal association with abrocitinib, a diagnosis of drug-induced new-onset psoriasis was made. Resolution of the eruption occurred after dose reduction to 100 mg daily, with no recurrence observed at follow-up.

Clinical Implications

This case highlights a previously unreported adverse event—new-onset psoriasis associated with abrocitinib therapy for AD—illustrating the complex interplay of immune pathways and paradoxical effects of targeted treatments. Key implications include:

• Phenotypic Switching in Cutaneous IMDs: AD and psoriasis are classically associated with divergent T-helper cell lineages—Th2 for AD and Th17 for psoriasis. Though generally mutually exclusive, there is increasing recognition of phenotypic switching under biologic or targeted immunotherapy.
• JAK1 Inhibitor Paradoxical Effects: While abrocitinib offers broad cytokine inhibition and has demonstrated efficacy in treating both AD and psoriasis, this case underscores that paradoxical reactions such as psoriasis onset may still occur, even with broader immune blockade.
• Monitoring and Management: Clinicians should be vigilant for unexpected skin eruptions in patients on JAK inhibitors. Careful clinical and histologic evaluation is essential, and dose reduction may be an effective strategy for managing mild paradoxical responses without discontinuation of therapy.
• Biologic Overlap: This case contributes to the evolving understanding of immune overlap in dermatology. Subtypes of AD, such as intrinsic or pediatric forms, may have elevated IL-17 expression and histopathologic features resembling psoriasis. Patients with such features may be predisposed to paradoxical switching.

Conclusion

This case illustrates a rare and previously unreported adverse event—new-onset psoriasis associated with abrocitinib therapy for AD. Despite targeting Th2-driven inflammation, abrocitinib may paradoxically trigger Th17-mediated disease. The diagnosis was supported by timing, clinical morphology, and histopathology, with resolution following dose reduction.

As the first documented case of its kind, this report underscores the need for ongoing vigilance and post-marketing surveillance in patients receiving JAK inhibitors. Further research is essential to better understand the immunologic shifts driving such paradoxical responses and to guide safer, more personalized treatment approaches.

Jennifer Fisher, MMSc, PA-C, is a board-certified dermatology physician assistant and medical writer in Connecticut.

References

1. Kolb L, Ferrer-Bruker SJ. Atopic dermatitis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.Updated August 8, 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448071/ 
2. Afshari M, Kolackova M, Rosecka M, Čelakovská J, Krejsek J. Unraveling the skin; a comprehensive review of atopic dermatitis, current understanding, and approaches. Front Immunol. 2024;15:1361005.
3. Guttman-Yassky E, Lowes MA, Fuentes-Duculan J, et al. Low expression of the IL-23/Th17 pathway in atopic dermatitis compared to psoriasis. J Immunol. 2008;181(10):7420-7427.
4. Lé AM, Gooderham M, Torres T. Abrocitinib for the treatment of atopic dermatitis. Immunotherapy. 2023;15(16):1351-1362.
5. Ferrucci, SM, BuffonS, Marzano, AV, Maronese, CA. Phenotypic switch from atopic dermatitis to psoriasis during treatment with upadacitinib. Clinical and Exper Derm. 2022;47(5): 986-987.
6. Becker SL, Haroon A, & Simpson E. New-onset psoriasis with abrocitinib therapy for atopic dermatitis. JAAD Case Reports. https://doi.org/10.1016/j.jdcr.2025.04.002