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Association between Mycobacterium tuberculosis infection and the risk of inflammatory arthritides

Authors
 Minkyung Han  ;  Jang Woo Ha  ;  Inkyung Jung  ;  Chi Young Kim  ;  Sung Soo Ahn 
Citation
 CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, Vol.42(9) : 1812-1819, 2024-09 
Journal Title
CLINICAL AND EXPERIMENTAL RHEUMATOLOGY
ISSN
 0392-856X 
Issue Date
2024-09
MeSH
Adult ; Aged ; Arthritis, Psoriatic* / epidemiology ; Arthritis, Psoriatic* / immunology ; Arthritis, Rheumatoid* / epidemiology ; Arthritis, Rheumatoid* / immunology ; Case-Control Studies ; Databases, Factual ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Mycobacterium tuberculosis / immunology ; Proportional Hazards Models ; Republic of Korea / epidemiology ; Retrospective Studies ; Risk Assessment ; Risk Factors ; Spondylitis, Ankylosing* / epidemiology ; Spondylitis, Ankylosing* / immunology ; Time Factors ; Tuberculosis* / diagnosis ; Tuberculosis* / epidemiology ; Tuberculosis* / immunology
Abstract
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.
Full Text
https://www.clinexprheumatol.org/abstract.asp?a=20667
DOI
10.55563/clinexprheumatol/cccp8o
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biomedical Systems Informatics (의생명시스템정보학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Chi Young(김치영)
Ahn, Sung Soo(안성수) ORCID logo https://orcid.org/0000-0002-9002-9880
Jung, Inkyung(정인경) ORCID logo https://orcid.org/0000-0003-3780-3213
Ha, Jang Woo(하장우)
Han, Minkyung(한민경) ORCID logo https://orcid.org/0000-0002-5011-5557
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/200708
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