HLA-A*32:01 is strongly associated with vancomycin-induced drug reaction with eosinophilia and systemic symptoms.
T-cell hypersensitivity
Vancomycin
antibiotic allergy
delayed hypersensitivity
drug reaction with eosinophilia and systemic symptoms
human leukocyte antigen
Journal
The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
16
12
2018
revised:
17
01
2019
accepted:
23
01
2019
pubmed:
19
2
2019
medline:
19
5
2020
entrez:
19
2
2019
Statut:
ppublish
Résumé
Vancomycin is a prevalent cause of the severe hypersensitivity syndrome drug reaction with eosinophilia and systemic symptoms (DRESS), which leads to significant morbidity and mortality and commonly occurs in the setting of combination antibiotic therapy, affecting future treatment choices. Variations in HLA class I in particular have been associated with serious T cell-mediated adverse drug reactions, which has led to preventive screening strategies for some drugs. We sought to determine whether variation in the HLA region is associated with vancomycin-induced DRESS. Probable vancomycin-induced DRESS cases were matched 1:2 with tolerant control subjects based on sex, race, and age by using BioVU, Vanderbilt's deidentified electronic health record database. Associations between DRESS and carriage of HLA class I and II alleles were assessed by means of conditional logistic regression. An extended sample set from BioVU was used to conduct a time-to-event analysis of those exposed to vancomycin with and without the identified HLA risk allele. Twenty-three subjects met the inclusion criteria for vancomycin-associated DRESS. Nineteen (82.6%) of 23 cases carried HLA-A*32:01 compared with 0 (0%) of 46 of the matched vancomycin-tolerant control subjects (P = 1 × 10 HLA-A*32:01 is strongly associated with vancomycin-induced DRESS in a population of predominantly European ancestry. HLA-A*32:01 testing could improve antibiotic safety, help implicate vancomycin as the causal drug, and preserve future treatment options with coadministered antibiotics.
Sections du résumé
BACKGROUND
Vancomycin is a prevalent cause of the severe hypersensitivity syndrome drug reaction with eosinophilia and systemic symptoms (DRESS), which leads to significant morbidity and mortality and commonly occurs in the setting of combination antibiotic therapy, affecting future treatment choices. Variations in HLA class I in particular have been associated with serious T cell-mediated adverse drug reactions, which has led to preventive screening strategies for some drugs.
OBJECTIVE
We sought to determine whether variation in the HLA region is associated with vancomycin-induced DRESS.
METHODS
Probable vancomycin-induced DRESS cases were matched 1:2 with tolerant control subjects based on sex, race, and age by using BioVU, Vanderbilt's deidentified electronic health record database. Associations between DRESS and carriage of HLA class I and II alleles were assessed by means of conditional logistic regression. An extended sample set from BioVU was used to conduct a time-to-event analysis of those exposed to vancomycin with and without the identified HLA risk allele.
RESULTS
Twenty-three subjects met the inclusion criteria for vancomycin-associated DRESS. Nineteen (82.6%) of 23 cases carried HLA-A*32:01 compared with 0 (0%) of 46 of the matched vancomycin-tolerant control subjects (P = 1 × 10
CONCLUSIONS
HLA-A*32:01 is strongly associated with vancomycin-induced DRESS in a population of predominantly European ancestry. HLA-A*32:01 testing could improve antibiotic safety, help implicate vancomycin as the causal drug, and preserve future treatment options with coadministered antibiotics.
Identifiants
pubmed: 30776417
pii: S0091-6749(19)30210-6
doi: 10.1016/j.jaci.2019.01.045
pmc: PMC6612297
mid: NIHMS1521905
pii:
doi:
Substances chimiques
Anti-Bacterial Agents
0
HLA-A Antigens
0
HLA-A*32 antigen
0
Vancomycin
6Q205EH1VU
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
183-192Subventions
Organisme : NIAID NIH HHS
ID : P30 AI110527
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI134648
Pays : United States
Organisme : NHLBI NIH HHS
ID : K12 HL143956
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007347
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024975
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA068485
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD074711
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI139021
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000445
Pays : United States
Organisme : NIAID NIH HHS
ID : R34 AI136815
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI007474
Pays : United States
Organisme : NHLBI NIH HHS
ID : U19 HL065962
Pays : United States
Organisme : NHGRI NIH HHS
ID : U01 HG006378
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002243
Pays : United States
Organisme : NIGMS NIH HHS
ID : RC2 GM092618
Pays : United States
Organisme : NIAID NIH HHS
ID : F30 AI131780
Pays : United States
Organisme : NHGRI NIH HHS
ID : U01 HG004798
Pays : United States
Organisme : NIGMS NIH HHS
ID : P50 GM115305
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR025141
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS032830
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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