Population genetic testing and SERPINA1 sequencing identifies unidentified alpha-1 antitrypsin deficiency alleles and gene-environment interaction with hepatitis C infection.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2023
Historique:
received: 19 01 2023
accepted: 16 05 2023
medline: 4 9 2023
pubmed: 31 8 2023
entrez: 31 8 2023
Statut: epublish

Résumé

Alpha-1 antitrypsin deficiency (AATD), a relatively common autosomal recessive genetic disorder, is underdiagnosed in symptomatic individuals. We sought to compare the risk of liver transplantation associated with hepatitis C infection with AATD heterozygotes and homozygotes and determine if SERPINA1 sequencing would identify undiagnosed AATD. We performed a retrospective cohort study in a deidentified Electronic Health Record (EHR)-linked DNA biobank with 72,027 individuals genotyped for the M, Z, and S alleles in SERPINA1. We investigated liver transplantation frequency by genotype group and compared with hepatitis C infection. We performed SERPINA1 sequencing in carriers of pathogenic AATD alleles who underwent liver transplantation. Liver transplantation was associated with the Z allele (ZZ: odds ratio [OR] = 1.31, p<2e-16; MZ: OR = 1.02, p = 1.2e-13) and with hepatitis C (OR = 1.20, p<2e-16). For liver transplantation, there was a significant interaction between genotype and hepatitis C (ZZ: interaction OR = 1.23, p = 4.7e-4; MZ: interaction OR = 1.11, p = 6.9e-13). Sequencing uncovered a second, rare, pathogenic SERPINA1 variant in six of 133 individuals with liver transplants and without hepatitis C. Liver transplantation was more common in individuals with AATD risk alleles (including heterozygotes), and AATD and hepatitis C demonstrated evidence of a gene-environment interaction in relation to liver transplantation. The current AATD screening strategy may miss diagnoses whereas SERPINA1 sequencing may increase diagnostic yield for AATD, stratify risk for liver disease, and inform clinical management for individuals with AATD risk alleles and liver disease risk factors.

Identifiants

pubmed: 37651384
doi: 10.1371/journal.pone.0286469
pii: PONE-D-23-01752
pmc: PMC10470904
doi:

Substances chimiques

SERPINA1 protein, human 0
alpha 1-Antitrypsin 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0286469

Subventions

Organisme : NLM NIH HHS
ID : R01 LM010685
Pays : United States
Organisme : NHLBI NIH HHS
ID : R38 HL143619
Pays : United States

Informations de copyright

Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Bryce A Schuler (BA)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Lisa Bastarache (L)

Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Janey Wang (J)

Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Jing He (J)

Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Sara L Van Driest (SL)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Joshua C Denny (JC)

All of Us Research Program, National Institutes of Health, Bethesda, Maryland, United States of America.
National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.

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Classifications MeSH