Contributing factors to death due to tuberculosis and COVID-19 co-infection in a cohort in northeastern Brazil
DOI:
https://doi.org/10.23925/1984-4840.2025v27a8Keywords:
COVID-19, Tuberculosis, Coinfection, DeathAbstract
Objective: To identify the factors that increase the risk of death in people with tuberculosis and COVID-19 co-infection. Methods: This was a retrospective cohort study conducted in the state of Pernambuco, Brazil. A total of 10,572 patients diagnosed with tuberculosis, regardless of whether they contracted COVID-19, were evaluated. Risk factors for death from COVID-19 were identified using bivariate analysis and multivariate logistic regression with a stepwise forward approach. Results: Among the 10,572 patients with tuberculosis, pulmonary tuberculosis was the most prevalent in 8,833 patients (83.5%), followed by 488 patients with peripheral lymph node tuberculosis (28%). Of these, 2,643 patients (25%) contracted COVID-19. Of the 814 tuberculosis patients who died, COVID-19 was responsible for 98 deaths (12%). Bivariate analysis demonstrated that being male increased the likelihood of dying from COVID-19 by 60%. Logistic regression analysis identified the following factors associated with an increased risk of death from COVID-19: male sex (RR = 1.71, 95% CI 1.0 to 2.92), age (RR = 1.04, 95% CI % 1.02 to 1.05), diabetes (RR = 1.95, 95% CI 1.17 to 3.23), abandonment of tuberculosis treatment (RR = 3.41, 95% CI 1.19 to 9.76) and admission to a ward or intensive care unit due to COVID-19 (RR = 4.79, 95% CI 2.17 to 10.57). Conclusions: People with tuberculosis who did not adhere to tuberculosis treatment or who required hospitalization or intensive care due to COVID-19 had a higher risk of dying from COVID-19.
References
Starshinova A, Guglielmetti L, Rzhepishevska O, Ekaterincheva O, Zinchenko Y, Kudlay D. Diagnostics and management of tuberculosis and COVID-19 in a patient with pneumothorax (clinical case). J Clin Tuberc Other Mycobact Dis. 2021;24:100259. doi: 10.1016/j.jctube.2021.100259.
Migliori G, Thong P, Akkerman O, Alffenaar J, Álvarez-Navascués F, Assao-Neino M, et al. Worldwide effects of coronavirus disease pandemic on tuberculosis services, January–April 2020. Emerg Infect Dis. 2020;26:2709. doi: 10.3201/eid2611.203163.
Visca D, Ong C, Tiberi S, Centis R, D´ambrosio L, Chen B, et al. Tuberculosis and COVID-19 interaction: a review of biological, clinical and public health effects. Pulmonology. 2021;27:151-65. doi: 10.1016/j.pulmoe.2020.12.012.
Daneshmandi Z, Pourdowlat G, Rekabi M, Honarpisheh P, Mirzendedel M, Sadati E, et al. Coronavirus disease 2019 and Mycobacterium tuberculosis reactivation and coinfections: A review of the literature. J Prev Diagn Treat Strategies Med. 2022;1:76. doi: 10.4103/jpdtsm.jpdtsm_6_22.
Luke E, Swafford K, Shirazi G, Venketaraman V. TB and COVID-19: an exploration of the characteristics and resulting complications of co-infection. Front Biosc (Schol Ed). 2022;14:6. doi: 10.31083/j.fbs1401006.
Kumar R, Bhattacharya B, Meena V, Soneja M, Wig N. COVID-19 and TB co-infection - Finishing touch in perfect recipe to severity or death. J Infect. 2020;81:39-40. doi: 10.1016/j.jinf.2020.06.062.
TB/COVID-19 global study group. Tuberculosis and COVID-19 co-infection: description of the global cohort. Eur Respir J. 2022;59:2102538. doi: 10.1183/13993003.02538-2021.
Diebold S, Kaisho T, Hemmi H, Akira S, Sousa C. Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA. Science. 2004;303(5663):1529-31. doi: 10.1126/science.1093616.
Boehme K, Compton T. Innate sensing of viruses by toll-like receptors. J Virol. 2004;78(15): 7867-73. doi: 10.1128/jvi.78.15.7867-7873.2004.
Berghöfer B, Frommer T, Haley G, Fink L, Bein G, Hackstein H. TLR7 ligands induce higher IFN-α production in females. J Immunol. 2006;177(4):2088-96. doi: 10.4049/jimmunol.177.4.2088.
Marriott I, Huet-Hudson Y. Sexual dimorphism in innate immune responses to infectious organisms. Immunol Res. 2006;34:177-92. doi: 10.1385/IR:34:3:177.
Schurz H, Salie M, Tromp G, Hoal E, Kinnear C, Möller M. The X chromosome and sex-specific effects in infectious disease susceptibility. Hum Genomics. 2019;13(1):1-12. doi: 10.1186/s40246-018-0185-z.
Chanana N, Palmo T, Sharma K, Kumar R, Graham B, Pasha Q. Sex-derived attributes contributing to SARS-CoV-2 mortality. Am J Physiol Endocrinol Metab. 2020;319(3):562-7. doi: 10.1152/ajpendo.00295.2020.
Hewagama A, Patel D, Yarlagadda S, Strickland F, Richardson B. Stronger inflammatory/cytotoxic T-cell response in women identified by microarray analysis. Genes Immun. 2009;10(5):509-16. doi: 10.1038/gene.2009.12.
Shepherd R, Cheung A, Pang K, Saffery R, Novakovic B. Sexual dimorphism in innate immunity: the role of sex hormones and epigenetics. Front Immunol. 2021;11:604000. doi: 10.3389/fimmu.2020.604000.
Takahashi T, Ellingson M, Wong P, Israelow B, Lucas C, Klein J, et al. Sex differences in immune responses that underlie COVID-19 disease outcomes. Nature. 2020;588(7837):315-20. doi: 10.1038/s41586-020-2700-3.
Bwire G. Coronavirus: why men are more vulnerable to COVID-19 than women? SN Compr Clin Med. 2020;2(7):874-6. doi: 10.1007/s42399-020-00341-w.
Salah H, Mehta J. Hypothesis: sex-related differences in ACE2 activity may contribute to higher mortality in men versus women with COVID-19. J Cardiovasc Pharmacol Ther. 2021;26(2):114-8. doi: 10.1177/1074248420967792.
Faurholt‐Jepsen D, Range N, PrayGod G, Jeremiah K, Faurholt-Jepsen M, Aabye M, et al. Diabetes is a strong predictor of mortality during tuberculosis treatment: a prospective cohort study among tuberculosis patients from Mwanza, Tanzania. Trop Med Int Health. 2013;18(7):822-9. doi: 10.1111/tmi.12120.
Ayelign B, Negash M, Genetu M, Wondmagegn T, Shibabaw T. Immunological impacts of diabetes on the susceptibility of Mycobacterium tuberculosis. J Immunol Res. 2019;2019:1-8. doi: 10.1155/2019/6196532.
Kumar N, Babu S. Influence of diabetes mellitus on immunity to human tuberculosis. Immunology. 2017;152(1):13-24. doi: 10.1111/imm.12762.
Aggarwal A, Agarwal R, Dhooria S, Prasad K, Sehgal I, Muthu V. Active pulmonary tuberculosis and coronavirus disease 2019: A systematic review and meta-analysis. PloS One. 2021; 16(10):1-21. doi: 10.1371/journal.pone.0259006.
Sy K, Haw N, Uy J. Previous and active tuberculosis increases risk of death and prolongs recovery in patients with COVID-19. Infect Dis. 2020; 52(12):902-7. doi: 10.1080/23744235.2020.1806353.
Lin C, Chen T, Lu P, Lai C, Yang Y, Lin W, et al. Effects of gender and age on development of concurrent extrapulmonary tuberculosis in patients with pulmonary tuberculosis: a population based study. PLoS One. 2013;8:63936. doi: 10.1371/journal.pone.0063936.
Banta J, Ani C, Bvute K, Lloren J, Darnell T. Pulmonary vs. extra-pulmonary tuberculosis hospitalizations in the US [1998–2014]. J Infect Public Health. 2020;13:131-9. doi: 10.1016/j.jiph.2019.07.001.
Pang Y, An J, Shu W, Huo F, Chu N, Gao M, et al. Epidemiology of extrapulmonary tuberculosis among inpatients, China, 2008–2017. Emerg Infect Dis. 2019;25:457. doi: 10.3201/eid2503.180572.
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