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1
Rheumatoid factor IgM autoantibodies control IgG homeostasis.类风湿因子 IgM 自身抗体控制 IgG 稳态。
Front Immunol. 2022 Oct 21;13:1016263. doi: 10.3389/fimmu.2022.1016263. eCollection 2022.
2
Management of Rheumatoid Arthritis: An Overview.类风湿关节炎的治疗:概述。
Cells. 2021 Oct 23;10(11):2857. doi: 10.3390/cells10112857.
3
Role of Vitamin C in Prophylaxis and Treatment of Gout-A Literature Review.维生素 C 在痛风预防和治疗中的作用——文献综述。
Nutrients. 2021 Feb 22;13(2):701. doi: 10.3390/nu13020701.
4
From Rheumatoid Factor to Anti-Citrullinated Protein Antibodies and Anti-Carbamylated Protein Antibodies for Diagnosis and Prognosis Prediction in Patients with Rheumatoid Arthritis.从类风湿因子到抗瓜氨酸化蛋白抗体和抗氨甲酰化蛋白抗体:类风湿关节炎患者的诊断和预后预测。
Int J Mol Sci. 2021 Jan 12;22(2):686. doi: 10.3390/ijms22020686.
5
C-reactive protein and implications in rheumatoid arthritis and associated comorbidities.C反应蛋白及其在类风湿关节炎和相关合并症中的意义。
Semin Arthritis Rheum. 2021 Feb;51(1):219-229. doi: 10.1016/j.semarthrit.2020.11.005. Epub 2020 Dec 17.
6
Current Understanding of an Emerging Role of HLA-DRB1 Gene in Rheumatoid Arthritis-From Research to Clinical Practice.HLA-DRB1 基因在类风湿关节炎中新兴作用的研究现状——从研究到临床实践。
Cells. 2020 May 2;9(5):1127. doi: 10.3390/cells9051127.
7
Immunoglobulin G structure and rheumatoid factor epitopes.免疫球蛋白 G 的结构和类风湿因子表位。
PLoS One. 2019 Jun 14;14(6):e0217624. doi: 10.1371/journal.pone.0217624. eCollection 2019.
8
Deficiency of Adenosine Deaminase 2 (DADA2): Updates on the Phenotype, Genetics, Pathogenesis, and Treatment.腺苷脱氨酶 2 缺乏症(DADA2):表型、遗传学、发病机制和治疗的最新进展。
J Clin Immunol. 2018 Jul;38(5):569-578. doi: 10.1007/s10875-018-0525-8. Epub 2018 Jun 27.
9
Physiological functions and pathogenic potential of uric acid: A review.尿酸的生理功能及致病潜力:综述
J Adv Res. 2017 Sep;8(5):487-493. doi: 10.1016/j.jare.2017.03.003. Epub 2017 Mar 14.
10
Adenosine Deaminase Deficiency - More Than Just an Immunodeficiency.腺苷脱氨酶缺乏症——不仅仅是一种免疫缺陷病。
Front Immunol. 2016 Aug 16;7:314. doi: 10.3389/fimmu.2016.00314. eCollection 2016.

类风湿关节炎患者与非关节炎患者的腺苷脱氨酶、C反应蛋白、尿酸及类风湿关节炎水平比较:一项综述

Comparison of Adenosine Deaminase, C-reactive Protein, Uric Acid, and Rheumatoid Arthritis Levels in Patients With Rheumatoid Arthritis and Those Without Arthritis: A Review.

作者信息

Makhe Priyanka A, Vagga Anjali A

机构信息

Biochemistry, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Wardha, IND.

出版信息

Cureus. 2024 Apr 1;16(4):e57433. doi: 10.7759/cureus.57433. eCollection 2024 Apr.

DOI:10.7759/cureus.57433
PMID:38699124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11063568/
Abstract

One of the hallmarks of rheumatoid arthritis (RA) is inflammation of the synovial membrane, and oxidative stress is a mediator of tissue damage. RA is characterized by persistent joint inflammation, which leads to pain, edema, and finally joint destruction. Numerous biochemical markers can cause RA because of their impact on systemic and local inflammation. Numerous biomarkers have been investigated for their potential application in the diagnosis and prognosis of RA. In this review article, we evaluate the role of RA factor or rheumatoid factor (RF), uric acid, C-reactive protein (CRP), and adenosine deaminases (ADAs) as biomarkers in patients with and without arthritis. Studies that analyze and compare the levels of uric acid, ADAs, CRP, and RF in patients with and without arthritis. Although recent research has shown higher levels of uric acid, ADA, CRP, and RA in patients with RF compared to healthy controls, these findings may indicate a role for these markers in reflecting inflammation and disease activity. In the metabolism of purines, the enzyme ADA is involved. The liver produces CRP, which is then released into the bloodstream. In inflammatory situations, there is a rise in CRP levels. This biomarker is frequently used for systemic inflammatory assessment in RA. The pathophysiology and severity of RA have both been connected to uric acid, which has historically been linked to gout. One particular biomarker for RA is RF. When compared to a healthy control group of individuals with arthritis, this review provides valuable insights into the diagnostic and prognostic use of uric acid, CRP, ADAs, and RF.

摘要

类风湿关节炎(RA)的一个标志是滑膜炎症,氧化应激是组织损伤的介质。RA的特征是持续性关节炎症,可导致疼痛、水肿,最终导致关节破坏。许多生化标志物因其对全身和局部炎症的影响而可引发RA。人们已经对众多生物标志物在RA诊断和预后方面的潜在应用进行了研究。在这篇综述文章中,我们评估了类风湿因子(RF)、尿酸、C反应蛋白(CRP)和腺苷脱氨酶(ADA)作为关节炎患者和非关节炎患者生物标志物的作用。分析和比较关节炎患者和非关节炎患者尿酸、ADA、CRP和RF水平的研究。尽管最近的研究表明,与健康对照组相比,RF阳性患者的尿酸、ADA、CRP和RF水平更高,但这些发现可能表明这些标志物在反映炎症和疾病活动方面的作用。在嘌呤代谢中,涉及ADA酶。肝脏产生CRP,然后释放到血液中。在炎症情况下,CRP水平会升高。这种生物标志物常用于RA的全身炎症评估。RA的病理生理学和严重程度都与尿酸有关,尿酸在历史上一直与痛风有关。RF是RA的一种特定生物标志物。与健康对照组的关节炎患者相比,本综述为尿酸、CRP、ADA和RF的诊断和预后应用提供了有价值的见解。