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生物类似药阿达木单抗(CinnoRA)诱导的银屑病和银屑病关节炎患者嗜酸性粒细胞增多症:一例报告

Eosinophilia Induced by Biosimilar Adalimumab (CinnoRA) in a Patient with Psoriasis and Psoriatic Arthritis: A Case Report.

作者信息

Saedpanah Roya, Rashidi Atiye, Firooz Alireza

机构信息

Center for Research and Training in Skin Diseases and Leprosy (CRTSDL), Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Clin Cosmet Investig Dermatol. 2025 Sep 4;18:2183-2188. doi: 10.2147/CCID.S546208. eCollection 2025.

Abstract

BACKGROUND

Psoriasis is a chronic inflammatory skin disorder that can significantly impact quality of life. Biologic therapies, such as TNF-alpha inhibitors, have improved clinical outcomes but may rarely cause hematologic abnormalities, including eosinophilia. Eosinophilia is uncommon but can be associated with allergic reactions or organ involvement.

CASE PRESENTATION

We report a 33-year-old male with psoriasis and psoriatic arthritis who developed asymptomatic marked eosinophilia after eight doses of biosimilar adalimumab (CinnoRA). Baseline peripheral blood eosinophil percentage was 3.2%, which increased to 19.9% during therapy. Alternative causes, including parasitic infection, allergy, and hematologic disease, were excluded. CinnoRA was discontinued, and eosinophil counts normalized during follow-up.

CONCLUSION

This case illustrates that unexplained eosinophilia can occur during TNF-alpha inhibitor therapy. While routine monitoring is not universally recommended based on a single case, clinicians should consider eosinophilia as a possible adverse reaction, especially in symptomatic patients or those with persistently elevated counts.

摘要

背景

银屑病是一种慢性炎症性皮肤病,会对生活质量产生重大影响。生物疗法,如肿瘤坏死因子-α抑制剂,改善了临床疗效,但可能很少引起血液学异常,包括嗜酸性粒细胞增多。嗜酸性粒细胞增多并不常见,但可能与过敏反应或器官受累有关。

病例介绍

我们报告一名33岁患有银屑病和银屑病关节炎的男性,在使用八剂生物类似药阿达木单抗(CinnoRA)后出现无症状的明显嗜酸性粒细胞增多。基线外周血嗜酸性粒细胞百分比为3.2%,在治疗期间增至19.9%。排除了包括寄生虫感染、过敏和血液系统疾病在内的其他病因。停用CinnoRA后,嗜酸性粒细胞计数在随访期间恢复正常。

结论

该病例表明,在肿瘤坏死因子-α抑制剂治疗期间可能出现不明原因的嗜酸性粒细胞增多。虽然基于单个病例并不普遍推荐常规监测,但临床医生应将嗜酸性粒细胞增多视为可能的不良反应,尤其是在有症状的患者或计数持续升高的患者中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a8/12418804/0b389ab1cf44/CCID-18-2183-g0001.jpg

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