Association between Mycobacterium tuberculosis infection and the risk of inflammatory arthritides

被引:1
|
作者
Han, M. [1 ]
Ha, J. W. [2 ]
Jung, I. [3 ]
Kim, C. Y. [4 ]
Ahn, S. S. [2 ]
机构
[1] Yonsei Univ, Coll Med, Dept Biomed Syst Informat, Biostat Collaborat Unit, Seoul, South Korea
[2] Yonsei Univ, Yongin Severance Hosp, Coll Med, Dept Internal Med,Div Rheumatol, Yongin, Gyeonggi Do, South Korea
[3] Yonsei Univ, Coll Med, Dept Biomed Syst Informat, Div Biostat, Seoul, South Korea
[4] Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea
关键词
tuberculosis; inflammatory arthritis; risk; rheumatoid arthritis; ankylosing spondylitis; psoriatic arthritis; PATHOGENESIS;
D O I
10.55563/clinexprheumatol/cccp8o
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective Tuberculosis is a highly contagious disease that has a significant impact on global health. Emerging evidence suggests that tuberculosis can lead to an altered immune response. We investigated the association between tuberculosis and the onset of inflammatory arthritides (IA). Methods Patients with incident tuberculosis in the South Korean National Claims database from 2010 to 2021 were included, and those who had undergone appendectomy during 2010-2011 served as controls. The onset of IA (including seropositive rheumatoid arthritis [SPRA], ankylosing spondylitis [AS], and psoriatic arthritis [PsA]) after tuberculosis was compared between patients with tuberculosis and the control group. Sensitivity analysis was performed using stabilised inverse probability of treatment weighting (sIPTW). Results A total of 408,685 patients with tuberculosis and 159,675 controls were included. During the mean follow-up of 7.5 years, a total of 1,957 (0.3%) were diagnosed with IA (SPRA, 1,397; AS, 481; and PsA, 79). Multivariable Cox hazard analysis indicated that the overall risk of IA was elevated in the tuberculosis group (hazard ratio [HR], 1.71; 95% confidence interval [CI], 1.51-1.93) compared with controls. This increased incidence in patients with tuberculosis was identical among IA subgroups even after adjustment (SPRA [HR, 1.72; 95% CI, 1.49-2.00], AS [HR, 1.64; 95% CI, 1.30-2.06], and PsA [HR, 2.59; 95% CI, 1.32-5.07]) and was replicated in the sIPTW. Conclusion The increased overall risk of developing IA after tuberculosis corroborates the hypothesis that tuberculosis can trigger dysregulated immunity. This necessitates an increased awareness of autoimmunity in this patient group.
引用
收藏
页码:1812 / 1819
页数:8
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