类风湿关节炎潜伏性结核感染激活的研究进展

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

摘要/Abstract

摘要：

类风湿关节炎是一种慢性全身性自身免疫性疾病,致残率高,随着目标治疗(T2T)理念的推广以及生物制剂和小分子靶向药的出现及应用,疗效及预后显著提高,但患者潜伏性结核感染激活的风险也大大增加。为进一步了解类风湿关节炎患者结核感染及潜伏性结核感染激活风险,对目前临床广泛应用的生物制剂、糖皮质激素以及传统合成改善病情抗风湿药的结核激活风险、潜伏性结核感染的筛查及预防性治疗等方面作一综述。

关键词: 关节炎, 类风湿, 潜伏性结核, 复燃, 生物制剂

中图分类号:

R593.22

刘彤, 王俊祥. 类风湿关节炎潜伏性结核感染激活的研究进展[J]. 临床荟萃, 2024, 39(12): 1135-1140.

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链接本文: https://huicui.hebmu.edu.cn/CN/10.3969/j.issn.1004-583X.2024.12.014

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

参考文献 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.

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