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Association between Mycobacterium tuberculosis infection and the risk of inflammatory arthritides

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dc.contributor.author김치영-
dc.contributor.author안성수-
dc.contributor.author정인경-
dc.contributor.author하장우-
dc.contributor.author한민경-
dc.date.accessioned2024-12-06T02:11:17Z-
dc.date.available2024-12-06T02:11:17Z-
dc.date.issued2024-09-
dc.identifier.issn0392-856X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/200708-
dc.description.abstractObjective 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.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherClinical And Experimental Rheumatology S.A.S-
dc.relation.isPartOfCLINICAL AND EXPERIMENTAL RHEUMATOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHArthritis, Psoriatic* / epidemiology-
dc.subject.MESHArthritis, Psoriatic* / immunology-
dc.subject.MESHArthritis, Rheumatoid* / epidemiology-
dc.subject.MESHArthritis, Rheumatoid* / immunology-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHDatabases, Factual-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHIncidence-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHMycobacterium tuberculosis / immunology-
dc.subject.MESHProportional Hazards Models-
dc.subject.MESHRepublic of Korea / epidemiology-
dc.subject.MESHRetrospective Studies-
dc.subject.MESHRisk Assessment-
dc.subject.MESHRisk Factors-
dc.subject.MESHSpondylitis, Ankylosing* / epidemiology-
dc.subject.MESHSpondylitis, Ankylosing* / immunology-
dc.subject.MESHTime Factors-
dc.subject.MESHTuberculosis* / diagnosis-
dc.subject.MESHTuberculosis* / epidemiology-
dc.subject.MESHTuberculosis* / immunology-
dc.titleAssociation between Mycobacterium tuberculosis infection and the risk of inflammatory arthritides-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorMinkyung Han-
dc.contributor.googleauthorJang Woo Ha-
dc.contributor.googleauthorInkyung Jung-
dc.contributor.googleauthorChi Young Kim-
dc.contributor.googleauthorSung Soo Ahn-
dc.identifier.doi10.55563/clinexprheumatol/cccp8o-
dc.contributor.localIdA04916-
dc.contributor.localIdA02233-
dc.contributor.localIdA03693-
dc.contributor.localIdA06125-
dc.contributor.localIdA05436-
dc.relation.journalcodeJ00555-
dc.identifier.eissn1593-098X-
dc.identifier.pmid38757281-
dc.identifier.urlhttps://www.clinexprheumatol.org/abstract.asp?a=20667-
dc.contributor.alternativeNameKim, Chi Young-
dc.contributor.affiliatedAuthor김치영-
dc.contributor.affiliatedAuthor안성수-
dc.contributor.affiliatedAuthor정인경-
dc.contributor.affiliatedAuthor하장우-
dc.contributor.affiliatedAuthor한민경-
dc.citation.volume42-
dc.citation.number9-
dc.citation.startPage1812-
dc.citation.endPage1819-
dc.identifier.bibliographicCitationCLINICAL AND EXPERIMENTAL RHEUMATOLOGY, Vol.42(9) : 1812-1819, 2024-09-
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

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