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IgA 会是大动脉炎疾病活动的生物标志物吗?

Might IgA be a Biomarker of Disease Activity in Takayasu Arteritis?

作者信息

Vantaggio Lorenzo, Pellicano Chiara, Miglionico Marzia, Cusano Giuseppina, Visentini Marcella

机构信息

Department of Translational and Precision Medicine, Sapienza University of Rome, Rome, Italy.

出版信息

Eur J Case Rep Intern Med. 2022 Dec 2;9(12):003664. doi: 10.12890/2022_003664. eCollection 2022.

DOI:10.12890/2022_003664
PMID:36632539
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9829015/
Abstract

UNLABELLED

Takayasu arteritis is a systemic vasculitis of the large vessels and mainly affects Japanese and Southeast Asian women in the second and third decades of life. Inflammatory infiltrate affects the full thickness of the vessel wall, inducing progressive lumen stenosis and occlusion. The main biomarkers of disease activity are the ESR, CRP and serum levels of circulating cytokines. This case report describes the clinical history of a young woman with Takayasu disease with high serum levels of IgA at onset. IgA remained elevated with persistence of disease activity, and normalized only when the patient was treated with an anti-TNF agent (infliximab), which also induced a clinical response in the vasculitis. IgA levels, together with other inflammatory parameters, may be considered a biomarker of disease activity.

LEARNING POINTS

This case report highlights the need to increase the number of humoral markers used to assess disease course in Takayasu arteritis (TA).IgA may be considered a biomarker of TA disease activity.Serum IgA levels may be helpful to identify TA patients not responding to traditional therapy.

摘要

未标注

高安动脉炎是一种大血管的系统性血管炎,主要影响二三十岁的日本和东南亚女性。炎症浸润累及血管壁全层,导致管腔逐渐狭窄和闭塞。疾病活动的主要生物标志物是血沉(ESR)、C反应蛋白(CRP)和循环细胞因子的血清水平。本病例报告描述了一名患有高安病的年轻女性的临床病史,其发病时血清IgA水平较高。随着疾病活动的持续,IgA水平持续升高,仅在患者接受抗TNF药物(英夫利昔单抗)治疗时才恢复正常,该药物也在血管炎中引发了临床反应。IgA水平与其他炎症参数一起,可被视为疾病活动的生物标志物。

学习要点

本病例报告强调需要增加用于评估高安动脉炎(TA)病程的体液标志物数量。IgA可被视为TA疾病活动的生物标志物。血清IgA水平可能有助于识别对传统治疗无反应的TA患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d33/9829015/78be7468c557/3664_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d33/9829015/78be7468c557/3664_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d33/9829015/78be7468c557/3664_Fig1.jpg

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本文引用的文献

1
"Coexistence of IgA nephropathy and renal artery stenosis in Takayasu arteritis: case report and literature review"."巨细胞动脉炎中 IgA 肾病与肾动脉狭窄共存:病例报告及文献复习"。
Rheumatol Int. 2023 Feb;43(2):391-398. doi: 10.1007/s00296-021-05066-0. Epub 2022 Jan 11.
2
Factors associated with event-free survival in Chinese patients with Takayasu's arteritis.与中国 Takayasu 动脉炎患者无事件生存相关的因素。
Clin Rheumatol. 2021 May;40(5):1941-1948. doi: 10.1007/s10067-020-05481-x. Epub 2020 Nov 2.
3
IgA: Structure, Function, and Developability.
免疫球蛋白A:结构、功能及可开发性
Antibodies (Basel). 2019 Dec 5;8(4):57. doi: 10.3390/antib8040057.
4
Management of Takayasu arteritis: a systematic literature review informing the 2018 update of the EULAR recommendation for the management of large vessel vasculitis.大动脉炎的治疗:一项系统文献综述,为 2018 年 EULAR 大血管血管炎治疗建议的更新提供信息。
RMD Open. 2019 Sep 23;5(2):e001020. doi: 10.1136/rmdopen-2019-001020. eCollection 2019.
5
Takayasu Arteritis: Recent Developments.Takayasu 动脉炎:最新进展。
Curr Rheumatol Rep. 2019 Jul 18;21(9):45. doi: 10.1007/s11926-019-0848-3.
6
Takayasu arteritis: an update.高安动脉炎:最新进展
Turk J Med Sci. 2018 Aug 16;48(4):681-697. doi: 10.3906/sag-1804-136.
7
Biological treatments in giant cell arteritis & Takayasu arteritis.巨细胞动脉炎和 Takayasu 动脉炎的生物治疗。
Eur J Intern Med. 2018 Apr;50:12-19. doi: 10.1016/j.ejim.2017.11.003. Epub 2017 Nov 13.
8
Elevated serum levels of immunoglobulin A correlate with the possibility of readmission in patients with microscopic polyangiitis.免疫球蛋白A血清水平升高与显微镜下多血管炎患者再次入院的可能性相关。
J Thorac Dis. 2017 May;9(5):1201-1208. doi: 10.21037/jtd.2017.03.166.
9
Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management.选择性IgA缺乏症:流行病学、发病机制、临床表型、诊断、预后及管理
Scand J Immunol. 2017 Jan;85(1):3-12. doi: 10.1111/sji.12499.
10
The unexplored roles of human serum IgA.人血清IgA的未被探索的作用。
DNA Cell Biol. 2014 Dec;33(12):823-9. doi: 10.1089/dna.2014.2639.