Recipient and donor PTX3 rs2305619 polymorphisms increase the susceptibility to invasive fungal disease following haploidentical stem cell transplantation: a prospective study.
Haploidentical stem cell transplantation
Invasive fungal disease
PTX3 rs2305619 polymorphism
Journal
BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551
Informations de publication
Date de publication:
26 Mar 2022
26 Mar 2022
Historique:
received:
01
08
2021
accepted:
22
03
2022
entrez:
29
3
2022
pubmed:
30
3
2022
medline:
31
3
2022
Statut:
epublish
Résumé
Invasive fungal disease (IFD) is a severe complication after haploidentical stem cell transplantation (haplo-HSCT) and has a poor prognosis. It has been shown that genetic polymorphism may be one possible reason for the increased risk of IFD. This study aimed to assess the role of genetic polymorphism in the level of susceptibility to IFD after haplo-HSCT. In this study, we prospectively enrolled 251 patients who received haplo-HSCT at the Peking University Institute of Hematology from 2016 to 2018. Forty-three single nucleotide polymorphisms (SNPs) of the genomic DNA were genotyped in blood samples from both recipient and donor. Twenty-two patients (8.8%) were diagnosed with proven or probable IFD. The independent risk factors for IFD were grades 3-4 acute graft-versus-host disease, cytomegalovirus reactivation, and recipient and donor rs2305619 (PTX3) (P < 0.05) in multivariate analysis. Meanwhile, we combined the variables to develop the IFD risk scoring system and stratified patients into low- (0-2) and high-risk (3-4) groups. The 30-day and 100-day cumulative incidence of IFD in the low- and high-risk groups were 2.1% and 10.2%, 4.2% and 20.3%, respectively (P = 0.015). PTX3 rs2305619 polymorphism increase the susceptibility of IFD after haplo-HSCT in the Chinese Han population, and the IFD scoring system could be useful in risk stratification for IFD after HSCT.
Sections du résumé
BACKGROUND
BACKGROUND
Invasive fungal disease (IFD) is a severe complication after haploidentical stem cell transplantation (haplo-HSCT) and has a poor prognosis. It has been shown that genetic polymorphism may be one possible reason for the increased risk of IFD. This study aimed to assess the role of genetic polymorphism in the level of susceptibility to IFD after haplo-HSCT.
METHODS
METHODS
In this study, we prospectively enrolled 251 patients who received haplo-HSCT at the Peking University Institute of Hematology from 2016 to 2018. Forty-three single nucleotide polymorphisms (SNPs) of the genomic DNA were genotyped in blood samples from both recipient and donor.
RESULTS
RESULTS
Twenty-two patients (8.8%) were diagnosed with proven or probable IFD. The independent risk factors for IFD were grades 3-4 acute graft-versus-host disease, cytomegalovirus reactivation, and recipient and donor rs2305619 (PTX3) (P < 0.05) in multivariate analysis. Meanwhile, we combined the variables to develop the IFD risk scoring system and stratified patients into low- (0-2) and high-risk (3-4) groups. The 30-day and 100-day cumulative incidence of IFD in the low- and high-risk groups were 2.1% and 10.2%, 4.2% and 20.3%, respectively (P = 0.015).
CONCLUSIONS
CONCLUSIONS
PTX3 rs2305619 polymorphism increase the susceptibility of IFD after haplo-HSCT in the Chinese Han population, and the IFD scoring system could be useful in risk stratification for IFD after HSCT.
Identifiants
pubmed: 35346077
doi: 10.1186/s12879-022-07298-2
pii: 10.1186/s12879-022-07298-2
pmc: PMC8962575
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
292Informations de copyright
© 2022. The Author(s).
Références
J Pediatric Infect Dis Soc. 2018 Aug 17;7(3):191-198
pubmed: 28549148
Biol Blood Marrow Transplant. 2014 Aug;20(8):1080-8
pubmed: 24582783
Curr Top Microbiol Immunol. 2010;341:83-96
pubmed: 20397074
Clin Infect Dis. 2009 Feb 1;48(3):265-73
pubmed: 19115967
Clin Microbiol Infect. 2012 Oct;18(10):997-1003
pubmed: 22085092
Clin Infect Dis. 2020 Sep 12;71(6):1367-1376
pubmed: 31802125
PLoS One. 2012;7(2):e32273
pubmed: 22384201
Semin Immunopathol. 2015 Mar;37(2):97-106
pubmed: 25420452
N Engl J Med. 2008 Oct 23;359(17):1766-77
pubmed: 18946062
Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):39-41
pubmed: 19147076
Exp Hematol. 2016 Oct;44(10):917-23
pubmed: 27403536
Curr Med Sci. 2019 Dec;39(6):906-912
pubmed: 31845221
Blood. 2012 May 31;119(22):5311-9
pubmed: 22282500
J Clin Oncol. 2007 Dec 1;25(34):5471-89
pubmed: 17909198
Curr Clin Microbiol Rep. 2016 Jun;3(2):81-91
pubmed: 27547700
Genet Mol Res. 2015 Feb 02;14(1):925-30
pubmed: 25730030
Nature. 2002 Nov 14;420(6912):182-6
pubmed: 12432394
PLoS One. 2016 Mar 10;11(3):e0150632
pubmed: 26963509
Biol Blood Marrow Transplant. 2005 Dec;11(12):945-56
pubmed: 16338616
Infect Dis Clin North Am. 2019 Jun;33(2):545-566
pubmed: 31005138
N Engl J Med. 2014 Jan 30;370(5):421-32
pubmed: 24476432
Biol Blood Marrow Transplant. 2015 Jun;21(6):1117-26
pubmed: 25840339
Ann Transl Med. 2020 Sep;8(18):1142
pubmed: 33240991
J Infect. 2016 Sep;73(3):280-8
pubmed: 27343564
J Exp Med. 2007 Apr 16;204(4):793-804
pubmed: 17389238
Blood. 2017 May 11;129(19):2693-2701
pubmed: 28270451
Clin Infect Dis. 2014 Aug 15;59(4):569-77
pubmed: 24803380
Genes Immun. 2015 Jan-Feb;16(1):83-8
pubmed: 25427560
Clin Microbiol Infect. 2013 Nov;19(11):1029-34
pubmed: 23565830
Blood. 2015 Jun 18;125(25):3956-62
pubmed: 25940714