Naïve hepatitis B e antigen-negative chronic hepatitis B patients are at risk of carotid atherosclerosis: A prospective study.
Cardiovascular risk
Carotid plaques
Endothelial dysfunction
Hepatitis B virus
Intima-media thickness
Subclinical atherosclerosis
Journal
World journal of gastroenterology
ISSN: 2219-2840
Titre abrégé: World J Gastroenterol
Pays: United States
ID NLM: 100883448
Informations de publication
Date de publication:
14 Aug 2021
14 Aug 2021
Historique:
received:
16
02
2021
revised:
13
05
2021
accepted:
09
07
2021
entrez:
9
9
2021
pubmed:
10
9
2021
medline:
11
9
2021
Statut:
ppublish
Résumé
There is an increased risk of atherosclerosis in patients with chronic hepatitis C or human immunodeficiency virus, but there is scarce data on hepatitis B virus infection. The hypothesis of this study is that hepatitis B virus infection increases the risk of carotid plaques and subclinical atherosclerosis in naïve hepatitis B e antigen (HBeAg) negative subjects. To assess the rate of carotid plaques and subclinical atherosclerosis in naïve HBeAg negative subjects in comparison with a cohort of healthy controls. Prospective case-control collaborative study conducted in two tertiary hospitals. Four hundred and two subjects prospectively recruited at the outpatient clinic were included from May 2016 to April 2017: 201 naïve HBeAg-negative hepatitis B virus-infected [49 chronic hepatitis B (CHB) and 152 inactive carriers(ICs)] and 201 healthy controls. Anthropomorphic and metabolic measures, liver stiffness and carotid Doppler ultrasound were performed. Subclinical atherosclerosis was established on an intima-media thickness increase of ≥1.2 mm and/or the presence of carotid plaques. Normally distributed quantitative variables were compared with the Student Carotid plaques were found more often in CHB (32.7%) than ICs (17.1%) or controls (18.4%) ( Untreated HBeAg-negative CHB is an independent risk factor for carotid plaques and subclinical atherosclerosis, while ICs present a similar risk to controls.
Sections du résumé
BACKGROUND
BACKGROUND
There is an increased risk of atherosclerosis in patients with chronic hepatitis C or human immunodeficiency virus, but there is scarce data on hepatitis B virus infection. The hypothesis of this study is that hepatitis B virus infection increases the risk of carotid plaques and subclinical atherosclerosis in naïve hepatitis B e antigen (HBeAg) negative subjects.
AIM
OBJECTIVE
To assess the rate of carotid plaques and subclinical atherosclerosis in naïve HBeAg negative subjects in comparison with a cohort of healthy controls.
METHODS
METHODS
Prospective case-control collaborative study conducted in two tertiary hospitals. Four hundred and two subjects prospectively recruited at the outpatient clinic were included from May 2016 to April 2017: 201 naïve HBeAg-negative hepatitis B virus-infected [49 chronic hepatitis B (CHB) and 152 inactive carriers(ICs)] and 201 healthy controls. Anthropomorphic and metabolic measures, liver stiffness and carotid Doppler ultrasound were performed. Subclinical atherosclerosis was established on an intima-media thickness increase of ≥1.2 mm and/or the presence of carotid plaques. Normally distributed quantitative variables were compared with the Student
RESULTS
RESULTS
Carotid plaques were found more often in CHB (32.7%) than ICs (17.1%) or controls (18.4%) (
CONCLUSION
CONCLUSIONS
Untreated HBeAg-negative CHB is an independent risk factor for carotid plaques and subclinical atherosclerosis, while ICs present a similar risk to controls.
Identifiants
pubmed: 34497439
doi: 10.3748/wjg.v27.i30.5112
pmc: PMC8384736
doi:
Substances chimiques
Hepatitis B e Antigens
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5112-5125Informations de copyright
©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict-of-interest statement:Riveiro-Barciela M has received research grants from Gilead and served as speaker for Gilead and Grifols. Esteban R has received research grants from Gilead and has served as advisors for Gilead, Bristol-Myers Squibb and Novartis. Buti M has received research grants from Gilead and has served as advisors for Gilead, Bristol-Myers Squibb and Novartis. The rest of authors have no personal or financial conflicts of interest.
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