Vancomycin-Induced Liver Injury, DRESS, and HLA-A∗32:01.

DRESS syndrome Drug-induced liver injury HLA testing HLA-A∗32:01 Vancomycin

Journal

The journal of allergy and clinical immunology. In practice
ISSN: 2213-2201
Titre abrégé: J Allergy Clin Immunol Pract
Pays: United States
ID NLM: 101597220

Informations de publication

Date de publication:
20 Sep 2023
Historique:
received: 02 02 2023
revised: 02 08 2023
accepted: 11 09 2023
pubmed: 23 9 2023
medline: 23 9 2023
entrez: 22 9 2023
Statut: aheadofprint

Résumé

Intravenous vancomycin therapy can cause liver injury as well as "drug reaction with eosinophilia and systemic symptoms" (DRESS) syndrome. This study aimed to better define the clinical features and HLA associations of vancomycin-induced liver injury. To describe clinical, biochemical, and temporal characteristics of vancomycin-induced liver injury. Cases of liver injury with recent exposure to vancomycin who were enrolled in the US Drug-induced Liver Injury Network between 2004 and 2020 were assessed. Sequencing of HLA alleles was performed on stored blood samples. Among 1697 cases of drug-induced liver injury identified between 2004 and 2021, 9 (0.5%) were attributed to intravenous vancomycin. The 9 cases included 6 men, median age 60 years (range, 23-85 days), and treatment for 26 days (range, 1-34 days). The clinical presentation was DRESS syndrome in 8 patients, of whom 6 received corticosteroids. Liver injury varied from hepatocellular to cholestatic and from mild (n = 5) to fatal (n = 1). In survivors, liver injury and DRESS syndrome ultimately resolved. HLA typing demonstrated the HLA-A∗32:01 allele in 7 vancomycin cases (78%, all with DRESS syndrome), versus 1 of 81 cases (1.2%) exposed but not attributed to vancomycin, and 113 of 1708 cases (6.6%) without vancomycin exposure. The allele frequency in vancomycin cases was 0.44 compared with less than 0.04 in US populations. Vancomycin-induced liver injury is commonly associated with DRESS syndrome and linked to HLA-A∗32:01. HLA-A∗32:01 testing could be considered early to risk-stratify patients using long-term intravenous vancomycin therapy.

Sections du résumé

BACKGROUND BACKGROUND
Intravenous vancomycin therapy can cause liver injury as well as "drug reaction with eosinophilia and systemic symptoms" (DRESS) syndrome. This study aimed to better define the clinical features and HLA associations of vancomycin-induced liver injury.
OBJECTIVE OBJECTIVE
To describe clinical, biochemical, and temporal characteristics of vancomycin-induced liver injury.
METHODS METHODS
Cases of liver injury with recent exposure to vancomycin who were enrolled in the US Drug-induced Liver Injury Network between 2004 and 2020 were assessed. Sequencing of HLA alleles was performed on stored blood samples.
RESULTS RESULTS
Among 1697 cases of drug-induced liver injury identified between 2004 and 2021, 9 (0.5%) were attributed to intravenous vancomycin. The 9 cases included 6 men, median age 60 years (range, 23-85 days), and treatment for 26 days (range, 1-34 days). The clinical presentation was DRESS syndrome in 8 patients, of whom 6 received corticosteroids. Liver injury varied from hepatocellular to cholestatic and from mild (n = 5) to fatal (n = 1). In survivors, liver injury and DRESS syndrome ultimately resolved. HLA typing demonstrated the HLA-A∗32:01 allele in 7 vancomycin cases (78%, all with DRESS syndrome), versus 1 of 81 cases (1.2%) exposed but not attributed to vancomycin, and 113 of 1708 cases (6.6%) without vancomycin exposure. The allele frequency in vancomycin cases was 0.44 compared with less than 0.04 in US populations.
CONCLUSIONS CONCLUSIONS
Vancomycin-induced liver injury is commonly associated with DRESS syndrome and linked to HLA-A∗32:01. HLA-A∗32:01 testing could be considered early to risk-stratify patients using long-term intravenous vancomycin therapy.

Identifiants

pubmed: 37739311
pii: S2213-2198(23)01021-8
doi: 10.1016/j.jaip.2023.09.011
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Published by Elsevier Inc.

Auteurs

Bilal A Asif (BA)

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Md. Electronic address: bilal.a.asif@gmail.com.

Christopher Koh (C)

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Md. Electronic address: christopher.koh@nih.gov.

Elizabeth J Phillips (EJ)

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn.

Jiezhun Gu (J)

Duke Clinical Research Institute, Duke University, Durham, NC.

Yi-Ju Li (YJ)

Duke Clinical Research Institute, Duke University, Durham, NC.

Huiman Barnhart (H)

Duke Clinical Research Institute, Duke University, Durham, NC.

Naga Chalasani (N)

Department of Medicine, Indiana School of Medicine, Indianapolis, Ind.

Robert J Fontana (RJ)

Department of Medicine, University of Michigan School of Medicine, Ann Arbor, Mich.

Paul H Hayashi (PH)

Division of Hepatology and Nutrition, Center for Drug Evaluation and Research, Food and Drug Administration, Silver Spring, Md.

Victor J Navarro (VJ)

Department of Medicine, Einstein Healthcare Network, Philadelphia, Pa.

Jay H Hoofnagle (JH)

Liver Disease Research Branch, Division of Digestive Diseases and Nutrition, NIDDK, NIH, Bethesda, Md.

Classifications MeSH