Major adverse cardiovascular events and hyperuricemia during tuberculosis treatment.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2023
2023
Historique:
received:
26
08
2023
accepted:
31
10
2023
medline:
20
11
2023
pubmed:
17
11
2023
entrez:
16
11
2023
Statut:
epublish
Résumé
Hyperuricemia is common during tuberculosis (TB) treatment, especially in association with pyrazinamide (PZA). This study investigated the relationship between major adverse cardiovascular events (MACEs) and hyperuricemia during TB treatment. We conducted a single-center retrospective cohort study. From January 2010 through June 2017, we assessed all consecutive TB patients at Chonnam National University Hospital in South Korea. Hyperuricemia was defined as serum uric acid levels exceeding 7.0 mg/dL (men) and 6.0 mg/dL (women). Of the 1,143 patients included, PZA was administered to 1,081 (94.6%), and hyperuricemia was detected in 941 (82.3%). Eight patients experienced MACEs. Multivariate analysis using logistic regression indicated that prior ischemic heart disease was associated with MACE development (OR,14.087; 95% CI,3.304-60.061; P < 0.000), while hyperuricemia was not (OR, 1.505; 95% CI, 0.184-12.299; P = 0.703). For patients without drug-resistant TB, the absence of hyperuricemia was associated with higher mortality (OR, 2.609; 95% CI, 1.066-6.389; P = 0.036), whereas hyperuricemia was associated with less worse outcomes (OR,0.316; 95% CI,0.173-0.576; P < 0.000). Although most patients treated with PZA developed hyperuricemia, it was not associated with MACE development. Hyperuricemia during TB treatment was associated with better outcomes, possibly due to consistent adherence to TB treatment.
Sections du résumé
BACKGROUND
BACKGROUND
Hyperuricemia is common during tuberculosis (TB) treatment, especially in association with pyrazinamide (PZA). This study investigated the relationship between major adverse cardiovascular events (MACEs) and hyperuricemia during TB treatment.
METHODS
METHODS
We conducted a single-center retrospective cohort study. From January 2010 through June 2017, we assessed all consecutive TB patients at Chonnam National University Hospital in South Korea. Hyperuricemia was defined as serum uric acid levels exceeding 7.0 mg/dL (men) and 6.0 mg/dL (women).
RESULTS
RESULTS
Of the 1,143 patients included, PZA was administered to 1,081 (94.6%), and hyperuricemia was detected in 941 (82.3%). Eight patients experienced MACEs. Multivariate analysis using logistic regression indicated that prior ischemic heart disease was associated with MACE development (OR,14.087; 95% CI,3.304-60.061; P < 0.000), while hyperuricemia was not (OR, 1.505; 95% CI, 0.184-12.299; P = 0.703). For patients without drug-resistant TB, the absence of hyperuricemia was associated with higher mortality (OR, 2.609; 95% CI, 1.066-6.389; P = 0.036), whereas hyperuricemia was associated with less worse outcomes (OR,0.316; 95% CI,0.173-0.576; P < 0.000).
CONCLUSIONS
CONCLUSIONS
Although most patients treated with PZA developed hyperuricemia, it was not associated with MACE development. Hyperuricemia during TB treatment was associated with better outcomes, possibly due to consistent adherence to TB treatment.
Identifiants
pubmed: 37972037
doi: 10.1371/journal.pone.0294490
pii: PONE-D-23-24904
pmc: PMC10653473
doi:
Substances chimiques
Antitubercular Agents
0
Uric Acid
268B43MJ25
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0294490Informations de copyright
Copyright: © 2023 Shin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Tubercle. 1980 Mar;61(1):41-9
pubmed: 6989067
N Engl J Med. 2008 Oct 23;359(17):1811-21
pubmed: 18946066
J Cardiol. 2016 Feb;67(2):170-6
pubmed: 26228000
Lipids Health Dis. 2018 Apr 11;17(1):80
pubmed: 29642917
Am J Hypertens. 2006 Oct;19(10):1055-62
pubmed: 17027827
N Engl J Med. 1966 Sep 1;275(9):457-64
pubmed: 5917940
Ann Intern Med. 1999 Jul 6;131(1):7-13
pubmed: 10391820
Cardiol J. 2008;15(1):21-5
pubmed: 18651381
Int J Cardiol. 2013 Jul 15;167(1):262-9
pubmed: 22261690
J Clin Rheumatol. 2015 Oct;21(7):346-8
pubmed: 26398460
Am J Cardiol. 2001 Jun 15;87(12):1411-4
pubmed: 11397367
Lancet. 2019 Apr 20;393(10181):1642-1656
pubmed: 30904262
N Engl J Med. 1994 Apr 28;330(17):1179-84
pubmed: 8139628
J Coll Physicians Surg Pak. 2004 Mar;14(3):136-8
pubmed: 15228843
Am J Med. 1969 Oct;47(4):575-92
pubmed: 4898522
Atherosclerosis. 2015 Jul;241(1):211-8
pubmed: 25670232
Circulation. 2007 May 15;115(19):2526-32
pubmed: 17470699
PLoS Med. 2007 Jul 24;4(7):e238
pubmed: 17676945
Ann Rheum Dis. 2013 May;72(5):694-700
pubmed: 22736095
Eur J Heart Fail. 2015 Nov;17(11):1144-51
pubmed: 26424212
Curr Opin Rheumatol. 2014 Mar;26(2):186-91
pubmed: 24419750
Nihon Kokyuki Gakkai Zasshi. 1999 Feb;37(2):115-8
pubmed: 10214039
Curr Pharm Des. 2013;19(13):2432-8
pubmed: 23173592
Cochrane Database Syst Rev. 2015 May 29;(5):CD003343
pubmed: 26022367
Angiology. 2016 Mar;67(3):272-80
pubmed: 26032849
Kidney Int. 2004 Mar;65(3):1041-9
pubmed: 14871425
J Am Heart Assoc. 2017 Jun 29;6(7):
pubmed: 28663251
Eur Rev Med Pharmacol Sci. 2014;18(9):1295-306
pubmed: 24867507
J Intern Med. 2009 Dec;266(6):558-70
pubmed: 19563390
JAMA. 2000 May 10;283(18):2404-10
pubmed: 10815083