Prevalence and Clinical Significance of Occult Hepatitis B Infection in The Gambia, West Africa.
Africa
advanced liver disease
cirrhosis
hepatocellular carcinoma
occult hepatitis B
prevalence
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
13 09 2022
13 09 2022
Historique:
received:
24
02
2021
accepted:
21
06
2021
pubmed:
24
6
2021
medline:
16
9
2022
entrez:
23
6
2021
Statut:
ppublish
Résumé
Prevalence and clinical outcomes of occult hepatitis B infection (OBI) have been poorly studied in Africa. Using the PROLIFICA cohort, we compared the prevalence of OBI between hepatitis B surface antigen (HBsAg)-negative healthy adults screened from the general population (controls) and HBsAg-negative patients with advanced liver disease (cases), and estimated the population attributable fraction for the effect of OBI on advanced liver disease. OBI prevalence was significantly higher among cases (15/82, 18.3%) than controls (31/330, 9.4%, P = .03). After adjusting for age, sex, and anti-hepatitis C virus (HCV) serology, OBI was significantly associated with advanced liver disease (odds ratio, 2.8; 95% confidence interval [CI], 1.3-6.0; P = .006). In HBsAg-negative people, the proportions of advanced liver disease cases attributable to OBI and HCV were estimated at 12.9% (95% CI, 7.5%-18.1%) and 16.9% (95% CI, 15.2%-18.6%), respectively. OBI is endemic and an independent risk factor for advanced liver disease in The Gambia, West Africa. This implies that HBsAg-negative people with liver disease should be systematically screened for OBI. Moreover, the impact of infant hepatitis B immunization to prevent end-stage liver disease might be higher than previous estimates based solely on HBsAg positivity.
Sections du résumé
BACKGROUND
Prevalence and clinical outcomes of occult hepatitis B infection (OBI) have been poorly studied in Africa.
METHODS
Using the PROLIFICA cohort, we compared the prevalence of OBI between hepatitis B surface antigen (HBsAg)-negative healthy adults screened from the general population (controls) and HBsAg-negative patients with advanced liver disease (cases), and estimated the population attributable fraction for the effect of OBI on advanced liver disease.
RESULTS
OBI prevalence was significantly higher among cases (15/82, 18.3%) than controls (31/330, 9.4%, P = .03). After adjusting for age, sex, and anti-hepatitis C virus (HCV) serology, OBI was significantly associated with advanced liver disease (odds ratio, 2.8; 95% confidence interval [CI], 1.3-6.0; P = .006). In HBsAg-negative people, the proportions of advanced liver disease cases attributable to OBI and HCV were estimated at 12.9% (95% CI, 7.5%-18.1%) and 16.9% (95% CI, 15.2%-18.6%), respectively.
CONCLUSIONS
OBI is endemic and an independent risk factor for advanced liver disease in The Gambia, West Africa. This implies that HBsAg-negative people with liver disease should be systematically screened for OBI. Moreover, the impact of infant hepatitis B immunization to prevent end-stage liver disease might be higher than previous estimates based solely on HBsAg positivity.
Identifiants
pubmed: 34160616
pii: 6308183
doi: 10.1093/infdis/jiab327
pmc: PMC9470103
doi:
Substances chimiques
DNA, Viral
0
Hepatitis B Surface Antigens
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
862-870Subventions
Organisme : Medical Research Council
ID : MC_UU_00026/1
Pays : United Kingdom
Informations de copyright
© The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America.
Déclaration de conflit d'intérêts
Potential conflicts of interest. M. L., M. T., and Y. S. received consultancy fees and research funding support from Gilead US company. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
Références
JAMA Oncol. 2017 Dec 1;3(12):1683-1691
pubmed: 28983565
J Med Virol. 2016 Apr;88(4):674-80
pubmed: 26334654
Int J Infect Dis. 2014 Dec;29:65-70
pubmed: 25449238
Lancet Infect Dis. 2016 Dec;16(12):1399-1408
pubmed: 27638356
AIDS Res Ther. 2017 Mar 8;14(1):11
pubmed: 28270215
J Viral Hepat. 2016 Nov;23(11):897-904
pubmed: 27353593
J Hepatol. 2008 Oct;49(4):652-7
pubmed: 18715666
Hepatology. 2009 Jun;49(6):1868-76
pubmed: 19434719
PLoS One. 2018 Jan 10;13(1):e0190775
pubmed: 29320552
J Hepatol. 2014 Sep;61(3):688-9
pubmed: 24976111
J Hepatol. 2019 Aug;71(2):397-408
pubmed: 31004683
PLoS One. 2015 Jul 06;10(7):e0131912
pubmed: 26148052
Liver Int. 2012 Feb;32(2):231-40
pubmed: 21745272
PLoS One. 2020 Nov 19;15(11):e0242577
pubmed: 33211768
Lancet Glob Health. 2016 Aug;4(8):e559-67
pubmed: 27443781
J Clin Microbiol. 2015 Apr;53(4):1156-63
pubmed: 25631805
J Gastroenterol Hepatol. 2008 Sep;23(9):1426-30
pubmed: 18853999
Liver Int. 2015 Oct;35(10):2318-26
pubmed: 25728498
Vaccine. 2016 Jul 19;34(33):3835-9
pubmed: 27265453
Clin Infect Dis. 2020 Mar 17;70(7):1442-1452
pubmed: 31102406
Gut. 2016 Aug;65(8):1369-76
pubmed: 26109530
Transfus Med Rev. 2015 Jan;29(1):35-44
pubmed: 25447555
JHEP Rep. 2020 Jul 11;2(5):100144
pubmed: 32904132