Antibiotic use and development of nonalcoholic fatty liver disease: A population-based case-control study.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
10 2023
Historique:
revised: 08 06 2023
received: 11 04 2023
accepted: 20 06 2023
medline: 19 9 2023
pubmed: 30 6 2023
entrez: 30 6 2023
Statut: ppublish

Résumé

Antibiotics affect the gut microbiome. Preclinical studies suggest a role of gut dysbiosis in the development of nonalcoholic fatty liver disease (NAFLD), but data from large cohorts with liver histology are lacking. In this nationwide case-control study, Swedish adults with histologically confirmed early-stage NAFLD (total n = 2584; simple steatosis n = 1435; steatohepatitis (NASH) n = 383; non-cirrhotic fibrosis n = 766) diagnosed January 2007-April 2017 were included and matched to ≤5 population controls (n = 12 646) for age, sex, calendar year and county of residence. Data for cumulative antibiotic dispensations and defined daily doses were accrued until 1 year before the matching date. Using conditional logistic regression, multivariable-adjusted odds ratios (aORs) were calculated. In a secondary analysis, NAFLD patients were compared with their full siblings (n = 2837). Previous antibiotic use was seen in 1748 (68%) NAFLD patients versus 7001 (55%) controls, corresponding to 1.35-fold increased odds of NAFLD (95% CI = 1.21-1.51) in a dose-dependent manner (p Antibiotic use may be a risk factor for incident NAFLD, especially in individuals without the metabolic syndrome. The risk was highest for fluoroquinolones and remained robust in sibling comparisons with whom individuals share genetic and early environmental susceptibilities.

Sections du résumé

BACKGROUND AND AIMS
Antibiotics affect the gut microbiome. Preclinical studies suggest a role of gut dysbiosis in the development of nonalcoholic fatty liver disease (NAFLD), but data from large cohorts with liver histology are lacking.
METHODS
In this nationwide case-control study, Swedish adults with histologically confirmed early-stage NAFLD (total n = 2584; simple steatosis n = 1435; steatohepatitis (NASH) n = 383; non-cirrhotic fibrosis n = 766) diagnosed January 2007-April 2017 were included and matched to ≤5 population controls (n = 12 646) for age, sex, calendar year and county of residence. Data for cumulative antibiotic dispensations and defined daily doses were accrued until 1 year before the matching date. Using conditional logistic regression, multivariable-adjusted odds ratios (aORs) were calculated. In a secondary analysis, NAFLD patients were compared with their full siblings (n = 2837).
RESULTS
Previous antibiotic use was seen in 1748 (68%) NAFLD patients versus 7001 (55%) controls, corresponding to 1.35-fold increased odds of NAFLD (95% CI = 1.21-1.51) in a dose-dependent manner (p
CONCLUSIONS
Antibiotic use may be a risk factor for incident NAFLD, especially in individuals without the metabolic syndrome. The risk was highest for fluoroquinolones and remained robust in sibling comparisons with whom individuals share genetic and early environmental susceptibilities.

Identifiants

pubmed: 37387502
doi: 10.1111/liv.15663
doi:

Substances chimiques

Anti-Bacterial Agents 0
Fluoroquinolones 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2186-2197

Subventions

Organisme : Swiss National Science Foundation
Pays : Switzerland

Informations de copyright

© 2023 The Authors. Liver International published by John Wiley & Sons Ltd.

Références

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Auteurs

Fahim Ebrahimi (F)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Department of Gastroenterology and Hepatology, Clarunis University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland.

Tracey G Simon (TG)

Division of Gastroenterology and Hepatology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Harvard Medical School, Boston, Massachusetts, USA.
Clinical and Translational Epidemiology Unit (CTEU), Massachusetts General Hospital, Boston, Massachusetts, USA.

Hannes Hagström (H)

Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden.
Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.

Jiangwei Sun (J)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

David Bergman (D)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Anders Forss (A)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Gastroenterology Unit, Department of Gastroenterology, Dermatovenereology and Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Bjorn Roelstraete (B)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Lars Engstrand (L)

Centre for Translational Microbiome Research, Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Science for Life Laboratory (SciLifeLab), Stockholm, Sweden.

Jonas F Ludvigsson (JF)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
Department of Medicine, Columbia University College of Physicians and Surgeons, New York City, New York, USA.

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