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肿瘤坏死因子-α抑制剂诱发色素性紫癜性皮病:一例报告

TNF-α inhibitor induced pigmented purpuric dermatoses: a case report.

作者信息

Jhaveri Divita, Zhao Frances

机构信息

Rheumatology Advanced Trainee, Princess Alexandra Hospital, Brisbane, Australia.

Internal Medicine Registrar, Princess Alexandra Hospital, Brisbane, Australia.

出版信息

BMC Rheumatol. 2022 Apr 29;6(1):34. doi: 10.1186/s41927-022-00255-1.

DOI:10.1186/s41927-022-00255-1
PMID:35484596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9052443/
Abstract

BACKGROUND

We present a rare case of TNF-α inhibitor induced pigmented purpuric dermatoses (PPD) and explore its mechanisms and management.

CASE PRESENTATION

A 44-year-old woman presented with non-pruritic non-tender petechial rash on bilateral lower limbs after being started on Adalimumab, with the rash progressing to worsen on Golimumab, both used for managing her seronegative peripheral arthritis. Laboratory panel revealed a negative vasculitis screen and skin biopsy confirmed the condition. After ceasing the TNF-α inhibitors and changing to Secukinumab, an Interleukin-17 inhibitor, the lesions stopped erupting and slowly resolved.

CONCLUSION

PPD is a benign skin condition and has been associated with various medications and exposure to chemicals in the literature. Different mechanisms have been proposed in the literature however its exact aetiology is unknown. To date, there is no standardized treatment however patients should be reassured that PPD is benign and will often regress by itself once the causative agent has been removed.

摘要

背景

我们报告一例罕见的肿瘤坏死因子-α(TNF-α)抑制剂诱发的色素性紫癜性皮病(PPD)病例,并探讨其发病机制及治疗方法。

病例介绍

一名44岁女性在开始使用阿达木单抗后双侧下肢出现非瘙痒性、非压痛性瘀点皮疹,在换用戈利木单抗后皮疹进展恶化,这两种药物均用于治疗她的血清阴性外周关节炎。实验室检查显示血管炎筛查阴性,皮肤活检确诊病情。停用TNF-α抑制剂并换用白细胞介素-17抑制剂司库奇尤单抗后,皮疹停止新发并逐渐消退。

结论

PPD是一种良性皮肤疾病,文献报道其与多种药物及接触化学物质有关。文献中提出了不同的发病机制,但其确切病因尚不清楚。迄今为止,尚无标准化治疗方法,但应向患者保证PPD是良性的,一旦去除致病因素,通常会自行消退。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/49506f7f142a/41927_2022_255_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/708e8a905e58/41927_2022_255_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/ae29011313cc/41927_2022_255_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/49506f7f142a/41927_2022_255_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/708e8a905e58/41927_2022_255_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/ae29011313cc/41927_2022_255_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbaf/9052443/49506f7f142a/41927_2022_255_Fig3_HTML.jpg

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Paradoxical immune-mediated inflammation in inflammatory bowel disease patients receiving anti-TNF-α agents.
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Indian Dermatol Online J. 2012 Jan;3(1):17-20. doi: 10.4103/2229-5178.93486.
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