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Published on: May 15, 2019
Case Report: Abrocitinib treatment for refractory palmoplantar pustulosis
Xiaoyan Luo1, Yaxin Huang2, Mengdie Yang1
1Department of Dermatology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Abstract:
Palmoplantar pustulosis (PPP) is a chronic relapsing inflammatory dermatosis characterized by recurrent sterile pustules on the palms and soles and often shows inadequate or unsustained responses to conventional systemic therapies and biologics. We report a 58-year-old woman with a 3-year history of refractory PPP. Before referral, oral prednisone and acitretin provided only transient disease control, with rapid relapse during dose tapering. Apremilast combined with topical halometasone cream and 308-nm excimer laser therapy failed to adequately control the plantar lesions. After referral, the patient declined cyclosporine and methotrexate because of concerns regarding potential systemic adverse effects. Baseline PPPASI and DLQI scores were 46.0 and 23, respectively. Secukinumab 300 mg with topical halometasone reduced the scores to 22.0 and 18 by week 8, indicating a partial but clinically inadequate response. Clinically active plantar lesions persisted, and new intensely pruritic erythematous papules developed on the lower extremities, accompanied by peripheral eosinophilia (0.62 × 10⁹/L) and elevated serum IgE (256 kIU/L). Secukinumab and topical halometasone were discontinued at week 8, and abrocitinib was initiated at 100 mg once daily. PPPASI decreased to 1.5 and 1.2 and DLQI to 8 and 3 at weeks 4 and 8, respectively. By week 8, the lower-extremity papules had markedly improved, and the eosinophil count and serum IgE had returned to their reference ranges. At week 16, disease control remained stable without treatment-related adverse events or laboratory abnormalities. This case suggests that abrocitinib may represent a potential treatment option for selected patients with refractory PPP who exhibit a partial but clinically inadequate response to secukinumab and concurrent clinical and laboratory changes suggestive of Th2-associated inflammation.
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