doi:10.3969/j.issn.1004-583X.2024.12.014

Abstract

CLC Number:

R593.22

Add to citation manager EndNote|Ris|BibTeX

URL: https://huicui.hebmu.edu.cn/EN/10.3969/j.issn.1004-583X.2024.12.014

https://huicui.hebmu.edu.cn/EN/Y2024/V39/I12/1135

References 43

[1]	Bagcchi S. WHO's global tuberculosis report 2022[J]. Lancet Microbe, 2023, 4(1): e20.
[2]	Yamada T, Nakajima A, Inoue E, et al. Increased risk of tuberculosis in patients with rheumatoid arthritis in Japan[J]. Ann Rheum Dis, 2006, 65(12): 1661-1663. doi: 10.1136/ard.2005.047274 pmid: 16837491
[3]	邓日辉, 刘丽燕, 刘明岭, 等. 类风湿关节炎患者发生潜伏性结核感染的多因素分析[J]. 实用医学杂志, 2022, 38(17): 2165-2169.
[4]	Ji X, Hu L, Wang Y, et al. Risk of tuberculosis in patients with rheumatoid arthritis treated with biological and targeted drugs: Meta-analysis of randomized clinical trials[J]. Chin Med J (Engl), 2022, 135(4): 409-415.
[5]	Weyand CM, Goronzy JJ. The immunology of rheumatoid arthritis[J]. Nat Immunol, 2021, 22(1): 10-18. doi: 10.1038/s41590-020-00816-x pmid: 33257900
[6]	Martineau AR, Wilkinson RJ, Wilkinson KA, et al. A single dose of vitamin D enhances immunity to mycobacteria[J]. Am J Respir Crit Care Med, 2007, 176(2): 208-213.
[7]	Winthrop KL, Park SH, Gul A, et al. Tuberculosis and other opportunistic infections in tofacitinib-treated patients with rheumatoid arthritis[J]. Ann Rheum Dis, 2016, 75(6): 1133-1138. doi: 10.1136/annrheumdis-2015-207319 pmid: 26318385
[8]	Kanagawa H, Niki Y, Kobayashi T, et al. Mycobacterium tuberculosis promotes arthritis development through toll-like receptor 2[J]. J Bone Miner Metab, 2015, 33(2): 135-141. doi: 10.1007/s00774-014-0575-9 pmid: 24633489
[9]	Mcgarry T, Veale DJ, Gao W, et al. Toll-like receptor 2 (TLR2) induces migration and invasive mechanisms in rheumatoid arthritis[J]. Arthritis Res Ther, 2015, 17(1): 153.
[10]	Zafari P, Golpour M, Hafezi N, et al. Tuberculosis comorbidity with rheumatoid arthritis: Gene signatures, associated biomarkers, and screening[J]. IUBMB Life, 2021, 73(1): 26-39. doi: 10.1002/iub.2413 pmid: 33217772
[11]	Greenwald M, Ball J, Deodar A. A mode of error: Immunoglobulin binding protein (a subset of anti-citrullinated proteins) can cause false positive tuberculosis test results in rheumatoid arthritis[J]. J Clin Tuberc Other Mycobact Dis, 2017, 9: 5-9. doi: 10.1016/j.jctube.2017.08.004 pmid: 31723711
[12]	Tubach F, Salmon D, Ravaud P, et al. Risk of tuberculosis is higher with anti-tumor necrosis factor monoclonal antibody therapy than with soluble tumor necrosis factor receptor therapy: The three-year prospective French research axed on tolerance of biotherapies registry[J]. Arthritis Rheum, 2009, 60(7): 1884-1894.
[13]	中华医学会风湿病学分会. 类风湿关节炎诊断及治疗指南[J]. 中华风湿病学杂志, 2010, 14(4): 265-270.
[14]	Roach DR, Bean AG, Demangel C, et al. TNF regulates chemokine induction essential for cell recruitment, granuloma formation, and clearance of mycobacterial infection[J]. J Immunol, 2002, 168(9): 4620-4627. doi: 10.4049/jimmunol.168.9.4620 pmid: 11971010
[15]	Cantini F, Niccoli L, Goletti D. Adalimumab, etanercept, infliximab, and the risk of tuberculosis: Data from clinical trials, national registries, and postmarketing surveillance[J]. J Rheumatol Suppl, 2014, 91: 47-55. doi: 10.3899/jrheum.140102 pmid: 24789000
[16]	Ogura H, Murakami M, Okuyama Y, et al. Interleukin-17 promotes autoimmunity by triggering a positive-feedback loop via interleukin-6 induction[J]. Immunity, 2008, 29(4): 628-636. doi: 10.1016/j.immuni.2008.07.018 pmid: 18848474
[17]	Komatsu N, Okamoto K, Sawa S, et al. Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis[J]. Nat Med, 2014, 20(1): 62-68. doi: 10.1038/nm.3432 pmid: 24362934
[18]	Nakahara H, Song J, Sugimoto M, et al. Anti-interleukin-6 receptor antibody therapy reduces vascular endothelial growth factor production in rheumatoid arthritis[J]. Arthritis Rheum, 2003, 48(6): 1521-1529.
[19]	Ogata A, Mori M, Hashimoto S, et al. Minimal influence of tocilizumab on IFN-gamma synthesis by tuberculosis antigens[J]. Mod Rheumatol, 2010, 20(2): 130-133. doi: 10.1007/s10165-009-0243-4 pmid: 19898919
[20]	Okada M, Kita Y, Kanamaru N, et al. Anti-IL-6 receptor antibody causes less promotion of tuberculosis infection than anti-TNF-alpha antibody in mice[J]. Clin Dev Immunol, 2011, 2011: 404929.
[21]	Sims NA. The JAK1/STAT3/SOCS3 axis in bone development, physiology, and pathology[J]. Exp Mol Med, 2020, 52(8): 1185-1197. doi: 10.1038/s12276-020-0445-6 pmid: 32788655
[22]	Morris R, Kershaw NJ, Babon JJ. The molecular details of cytokine signaling via the JAK/STAT pathway[J]. Protein Sci, 2018, 27(12): 1984-2009. doi: 10.1002/pro.3519 pmid: 30267440
[23]	Ono T, Hayashi M, Sasaki F, et al. RANKL biology: Bone metabolism, the immune system, and beyond[J]. Inflamm Regen, 2020, 40: 2. doi: 10.1186/s41232-019-0111-3 pmid: 32047573
[24]	Labranche TP, Jesson MI, Radi ZA, et al. JAK inhibition with tofacitinib suppresses arthritic joint structural damage through decreased RANKL production[J]. Arthritis Rheum, 2012, 64(11): 3531-3542.
[25]	Kondo N, Kuroda T, Kobayashi D. Cytokine networks in the pathogenesis of rheumatoid arthritis[J]. Int J Mol Sci, 2021, 22(20).
[26]	Ghoreschi K, Jesson MI, Li X, et al. Modulation of innate and adaptive immune responses by tofacitinib (CP-690, 550)[J]. J Immunol, 2011, 186(7): 4234-4243. doi: 10.4049/jimmunol.1003668 pmid: 21383241
[27]	Maiga M, Lun S, Guo H, et al. Risk of tuberculosis reactivation with tofacitinib (CP-690550)[J]. J Infect Dis, 2012, 205(11): 1705-1708. doi: 10.1093/infdis/jis269 pmid: 22474037
[28]	Valor-Mendez L, Manger B, Wacker J, et al. Lymph node and pulmonary tuberculosis during upadacitinib treatment in a psoriatic arthritis patient[J]. Rheumatol Adv Pract, 2022, 6(2): rkac32.
[29]	Cantini F, Niccoli L, Goletti D. Tuberculosis risk in patients treated with non-anti-tumor necrosis factor-alpha (TNF-alpha) targeted biologics and recently licensed TNF-alpha inhibitors: Data from clinical trials and national registries[J]. J Rheumatol Suppl, 2014, 91: 56-64.
[30]	Youssef J, Novosad SA, Winthrop KL. Infection risk and safety of corticosteroid use[J]. Rheum Dis Clin North Am, 2016, 42(1): 157-176.
[31]	Dixon WG, Suissa S, Hudson M. The association between systemic glucocorticoid therapy and the risk of infection in patients with rheumatoid arthritis: Systematic review and meta-analyses[J]. Arthritis Res Ther, 2011, 13(4): R139.
[32]	Breedveld FC, Dayer JM. Leflunomide: Mode of action in the treatment of rheumatoid arthritis[J]. Ann Rheum Dis, 2000, 59(11): 841-849. pmid: 11053058
[33]	Leitner J, Drobits K, Pickl WF, et al. The effects of cyclosporine A and azathioprine on human T cells activated by different costimulatory signals[J]. Immunol Lett, 2011, 140(1-2): 74-80. doi: 10.1016/j.imlet.2011.06.010 pmid: 21756939
[34]	Pyo J, Cho SK, Kim D, et al. Systemic review: Agreement between the latent tuberculosis screening tests among patients with rheumatic diseases[J]. Korean J Intern Med, 2018, 33(6): 1241-1251. doi: 10.3904/kjim.2016.222 pmid: 29277097
[35]	邓国防, 王庆文, 陈秋奇, 等. 风湿性疾病患者合并结核分枝杆菌潜伏感染诊治的专家共识[J]. 中国防痨杂志, 2022, 44(9): 869-879.
[36]	Liu X, Zhang L, Zhang F, et al. Prevalence and risk factors of active tuberculosis in patients with rheumatic diseases: A multi-center, cross-sectional study in China[J]. Emerg Microbes Infect, 2021, 10(1): 2303-2312.
[37]	Latent tuberculosis infection: Updated and consolidated guidelines for programmatic management[M]. Geneva: World Health Organization, 2018.
[38]	Sterling TR, Njie G, Zenner D, et al. Guidelines for the treatment of latent tuberculosis infection: Recommendations from the national tuberculosis controllers association and CDC, 2020[J]. MMWR Recomm Rep, 2020, 69(1): 1-11. doi: 10.15585/mmwr.rr6901a1 pmid: 32053584
[39]	Iannone F, Cantini F, Lapadula G. Diagnosis of latent tuberculosis and prevention of reactivation in rheumatic patients receiving biologic therapy: International recommendations[J]. J Rheumatol Suppl, 2014, 91: 41-46. doi: 10.3899/jrheum.140101 pmid: 24788999
[40]	Gomez-Reino JJ, Carmona L, Angel DM. Risk of tuberculosis in patients treated with tumor necrosis factor antagonists due to incomplete prevention of reactivation of latent infection[J]. Arthritis Rheum, 2007, 57(5): 756-761.
[41]	Cantini F, Nannini C, Niccoli L, et al. Guidance for the management of patients with latent tuberculosis infection requiring biologic therapy in rheumatology and dermatology clinical practice[J]. Autoimmun Rev, 2015, 14(6): 503-509. doi: 10.1016/j.autrev.2015.01.011 pmid: 25617816
[42]	Ledingham J, Wilkinson C, Deighton C. British thoracic society (BTS) recommendations for assessing risk and managing tuberculosis in patients due to start anti-TNF-alpha treatments[J]. Rheumatology (Oxford), 2005, 44(10): 1205-1206.
[43]	Denis B, Lefort A, Flipo RM, et al. Long-term follow-up of patients with tuberculosis as a complication of tumour necrosis factor (TNF)-alpha antagonist therapy: Safe re-initiation of TNF-alpha blockers after appropriate anti-tuberculous treatment[J]. Clin Microbiol Infect, 2008, 14(2): 183-186.

RichHTML

PDF (PC)

Knowledge

Abstract

Cite this article

share this article

References 43

Related Articles 15

Recommended Articles

Metrics

Comments

[1]	Dong Hong, Li Zhenbin, Ma Xu, Luo Yaping, Jiao Aijun, Zhang Xufei, Sun Caixia. Rheumatoid arthritis combined with insomnia: A multicenter cross-sectional survey [J]. Clinical Focus, 2024, 39(10): 882-888.
[2]	Song Yijing, Li Jian, Song Qin, Shao Li. Predictive value of C-reactive protein combined with triglyceride glucose index for coronary heart disease risk in patients with rheumatoid arthritis [J]. Clinical Focus, 2024, 39(6): 506-511.
[3]	. [J]. Clinical Focus, 2023, 38(8): 753-756.
[4]	. [J]. Clinical Focus, 2023, 38(7): 663-667.
[5]	. [J]. Clinical Focus, 2023, 38(3): 279-284.
[6]	Zhang Yueyue, Xie Meifang, Sun Gen. Rheumatoid arthritis complicated with T-cell large granular lymphocytic leukemia: A case report and literature review [J]. Clinical Focus, 2022, 37(8): 728-732.
[7]	Hu Fangfang, Zhong Shiling, Di Yazhen, Wu Ling. Vascular endothelial function of juvenile idiopathic arthritis in pediatric patients: A systematic review and meta-analysis [J]. Clinical Focus, 2022, 37(3): 204-210.
[8]	Lin Changyi, Song Minghui, Wu Peicheng. Difference between remitting seronegative symmetrical synovitis with pitting edema syndrome and seronegative rheumatoid arthritis [J]. Clinical Focus, 2022, 37(3): 262-265.
[9]	. [J]. Clinical Focus, 2022, 37(2): 188-192.
[10]	. [J]. Clinical Focus, 2022, 37(1): 92-96.
[11]	Liu Ziyi, Wang Jibo. Analysis of clinical characteristics and related factors of rheumatoid arthritis complicated with malignant tumors in patients [J]. Clinical Focus, 2021, 36(3): 246-250.
[12]	. [J]. Clinical Focus, 2021, 36(1): 75-79.
[13]	Chen Wenyu, Wang Juanjuan, Wang Zhiming. Clinical feature of pleural effusion in 78 patients with rheumatoid arthritis [J]. Clinical Focus, 2016, 31(2): 214-217.
[14]	Xie Qingyun, Wei Meng, Fu Peiliang, Sun Jiuyi, Qian Qirong. Association study between single nucleotide polymorphisms of interleukin 23 receptor and rheumatoid arthritis [J]. Clinical Focus, 2016, 31(1): 40-44.
[15]	Wang Lei;Zhang Guimin;Li Li;Yu Zhibo;Yan Yonglong;Zhang Fengxiao;Sun Lijun. Application of high frequency energy Doppler ultrasound in monitoring of rheumatoid arthritis treatment [J]. Clinical Focus, 2015, 30(12): 1405-1409.