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阿布昔替尼联合甲泼尼龙治疗难治性皮肤嗜酸性粒细胞增多综合征的快速改善:一例报告

 

Authors Liao B, Li X , Qiu Q, Zhang J, Xu M, Wang X, Liu W , Long R

Received 11 September 2025

Accepted for publication 18 December 2025

Published 20 December 2025 Volume 2025:18 Pages 3565—3569

DOI https://doi.org/10.2147/CCID.S566780

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Anne-Claire Fougerousse

Bei Liao,1– 5,* Xinze Li,1– 5,* Qianjie Qiu,1– 5,* Jing Zhang,1– 5 Meiqin Xu,1– 5 Xiaobing Wang,1– 5 Weijun Liu,1– 5 Ruijie Long1– 5 

1Department of Dermatology, Dermatology Hospital of Jiangxi Province, Nanchang, Jiangxi, People’s Republic of China; 2Department of Dermatology, Jiangxi Provincial Clinical Research Center for Skin Diseases, Nanchang, Jiangxi, People’s Republic of China; 3Department of Dermatology, Candidate Branch of National Clinical Research Center for Skin Diseases, Nanchang, Jiangxi, People’s Republic of China; 4Department of Dermatology, Dermatology Institute of Jiangxi Province, Nanchang, Jiangxi, People’s Republic of China; 5Department of Dermatology, The Affiliated Dermatology Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Ruijie Long, Department of Dermatology, Dermatology Hospital of Jiangxi Province, Nanchang, Jiangxi, 330001, People’s Republic of China, Tel +86 17326067978, Email 2687525845@qq.com Weijun Liu, Department of Dermatology, Dermatology Hospital of Jiangxi Province, Nanchang, Jiangxi, 330001, People’s Republic of China, Tel +86 15180151935, Email liuweijun104@163.com

Abstract: Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent eosinophilia and end-organ damage. Cutaneous manifestations are frequently refractory to conventional therapies, including corticosteroids and immunosuppressants, creating a significant clinical challenge. The Janus kinase (JAK)-STAT pathway has been implicated in eosinophil activation and survival, suggesting a potential role for JAK inhibitors in management. In this context, we present the case of a 58-year-old female with a 10-year history of refractory generalized erythema, papules, and severe pruritus progressing to erythroderma with scaling. Previous treatments including antihistamines, tripterygium glycosides, glycyrrhizin, sodium thiosulfate, and topical glucocorticoids had failed. Laboratory investigations revealed leukocytosis with severe hypereosinophilia (peak 8.65× 109/L, 52.6% of total WBC), hypoalbuminemia, elevated lactate dehydrogenase, and transaminitis. Skin biopsy demonstrated spongiotic edema and eosinophil-rich perivasculitis. Bone marrow examination confirmed eosinophilic hyperplasia (32.5% eosinophils) without evidence of clonality. Comprehensive parasitic and secondary causes were excluded. Following diagnosis of HES, the patient was initiated on methylprednisolone (40 mg/day) combined with abrocitinib (100 mg/day). Within one week, eosinophil count reduced significantly (1.24× 109/L, 7%) with concurrent improvement in liver enzymes. Complete cutaneous remission was achieved at 2-month follow-up, enabling substantial steroid reduction. This case underscores that the combination therapy of abrocitinib and methylprednisolone can offer a promising approach for the HES.

Keywords: hypereosinophilic syndrome, JAK inhibitor, abrocitinib, corticosteroid, refractory, cutaneous manifestations, eosinophilia, targeted therapy