The factors predicting development of serious infections in ANCA-associated vasculitis.
Journal
Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG
ISSN: 2532-179X
Titre abrégé: Sarcoidosis Vasc Diffuse Lung Dis
Pays: Italy
ID NLM: 9610928
Informations de publication
Date de publication:
29 Jun 2023
29 Jun 2023
Historique:
received:
22
05
2022
accepted:
25
03
2023
medline:
29
6
2023
pubmed:
29
6
2023
entrez:
29
6
2023
Statut:
epublish
Résumé
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a rare autoimmune disease usually involving small vessels and progressing with necrotizing inflammation. Treatment requires long-term use of immunosuppressive agents to inhibit disease activity. Serious infections (SIs) are a common complication in AAV. The aim of this study was to identify the risk factors for serious infections which required hospitalization in patients with AAV. In this retrospective cohort study., we included 84 patients admitted to the Ankara University Faculty of Medicine in the last 10 years with a diagnosis of AAV. In 42 (50%) of 84 patients followed up with the diagnosis of AAV, an infection requiring hospitalization was identified. The patients' total corticosteroid dose, use of pulse steroids, induction regimen, levels of C-reactive protein (CRP) and the presence of pulmonary and renopulmonary involvement were found to be associated with the frequency of infection (p=0.015, p=0.016, p=0.010, p=0.03, p= 0.026 and p=0.029, respectively). In multivariable analysis, it was found that renopulmonary involvement (p=0.002, HR=4.95, 95% CI= 1.804-13.605), age of over 65 (p=0.049, HR=3.37, 95% CI=1.004-11.369) and high CRP levels (p=0.043, HR=1.006, 95% CI=1.000-1.011) constituted independent predictors of serious infection risk. The frequency of infection is known to be increased in ANCA-associated vasculitis. Our study showed that renopulmonary involvement, age and elevated CRP levels on admission are independent risk factors of infection.
Sections du résumé
BACKGROUND
BACKGROUND
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a rare autoimmune disease usually involving small vessels and progressing with necrotizing inflammation. Treatment requires long-term use of immunosuppressive agents to inhibit disease activity. Serious infections (SIs) are a common complication in AAV.
OBJECTIVE
OBJECTIVE
The aim of this study was to identify the risk factors for serious infections which required hospitalization in patients with AAV.
METHODS
METHODS
In this retrospective cohort study., we included 84 patients admitted to the Ankara University Faculty of Medicine in the last 10 years with a diagnosis of AAV.
RESULTS
RESULTS
In 42 (50%) of 84 patients followed up with the diagnosis of AAV, an infection requiring hospitalization was identified. The patients' total corticosteroid dose, use of pulse steroids, induction regimen, levels of C-reactive protein (CRP) and the presence of pulmonary and renopulmonary involvement were found to be associated with the frequency of infection (p=0.015, p=0.016, p=0.010, p=0.03, p= 0.026 and p=0.029, respectively). In multivariable analysis, it was found that renopulmonary involvement (p=0.002, HR=4.95, 95% CI= 1.804-13.605), age of over 65 (p=0.049, HR=3.37, 95% CI=1.004-11.369) and high CRP levels (p=0.043, HR=1.006, 95% CI=1.000-1.011) constituted independent predictors of serious infection risk.
CONCLUSION
CONCLUSIONS
The frequency of infection is known to be increased in ANCA-associated vasculitis. Our study showed that renopulmonary involvement, age and elevated CRP levels on admission are independent risk factors of infection.
Identifiants
pubmed: 37382076
doi: 10.36141/svdld.v40i2.13243
pmc: PMC10494754
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e2023015Références
N Engl J Med. 1996 Jul 4;335(1):16-20
pubmed: 8637536
J Rheumatol. 2017 Oct;44(10):1468-1475
pubmed: 28765251
Ann Rheum Dis. 2010 Jun;69(6):1036-43
pubmed: 19574233
Arthritis Rheum. 2001 Apr;44(4):912-20
pubmed: 11318006
Rheumatology (Oxford). 2021 Jun 18;60(6):2745-2754
pubmed: 33253372
Ann Rheum Dis. 2009 Dec;68(12):1827-32
pubmed: 19054820
Mucosal Immunol. 2017 Mar;10(2):299-306
pubmed: 27966551
Ann Rheum Dis. 2009 May;68(5):658-63
pubmed: 18504289
Ann Rheum Dis. 2011 Mar;70(3):488-94
pubmed: 21109517
Rheumatology (Oxford). 2021 Aug 2;60(8):3553-3564
pubmed: 33752235
Clin Rheumatol. 2018 Aug;37(8):2133-2141
pubmed: 29557539
J Rheumatol. 2020 Mar;47(3):407-414
pubmed: 31203229
PLoS One. 2019 Jul 10;14(7):e0218705
pubmed: 31291263
QJM. 1994 Nov;87(11):671-8
pubmed: 7820541
Arthritis Rheum. 2001 Mar;44(3):666-75
pubmed: 11263782
Clin J Am Soc Nephrol. 2012 Feb;7(2):240-7
pubmed: 22134625
J Chronic Dis. 1987;40(5):373-83
pubmed: 3558716
Arthritis Rheum. 1990 Aug;33(8):1065-7
pubmed: 2390119
BMC Infect Dis. 2019 Jul 26;19(1):664
pubmed: 31349802
Arthritis Rheum. 2004 Feb 15;51(1):83-91
pubmed: 14872460
Perit Dial Int. 2008 Jun;28 Suppl 3:S183-7
pubmed: 18552253
Rheumatology (Oxford). 2005 Apr;44(4):495-501
pubmed: 15613403
J Rheumatol. 2014 Sep;41(9):1849-55
pubmed: 25086076
Arthritis Rheum. 2013 Jan;65(1):1-11
pubmed: 23045170
Eur J Immunol. 2016 Oct;46(10):2286-2301
pubmed: 27595500
Rheumatology (Oxford). 2014 Dec;53(12):2306-9
pubmed: 24729399
BMC Nephrol. 2018 Jun 14;19(1):138
pubmed: 29902982
Arthritis Rheum. 2000 May;43(5):1021-32
pubmed: 10817555