Hepatitis B e antigen loss in adults and children with chronic hepatitis B living in North America: A prospective cohort study.
e antigen
hepatitis B
prospective cohort
Journal
Journal of viral hepatitis
ISSN: 1365-2893
Titre abrégé: J Viral Hepat
Pays: England
ID NLM: 9435672
Informations de publication
Date de publication:
11 2021
11 2021
Historique:
received:
31
03
2021
accepted:
23
07
2021
pubmed:
7
8
2021
medline:
3
2
2022
entrez:
6
8
2021
Statut:
ppublish
Résumé
Hepatitis B e antigen (HBeAg) is a soluble viral protein in plasma of patients with hepatitis B virus infection. HBeAg loss is an important first stage of viral antigen clearance. We determined the rate and predictors of HBeAg loss in a North American cohort with chronic hepatitis B viral infection (CHB). Among children and adults with CHB and without HIV, HCV or HDV co-infection enrolled in the Hepatitis B Research Network prospective cohort studies, 819 were HBeAg positive at their first assessment (treatment naïve or >24 weeks since treatment). Of these, 577 (200 children, 377 adults) were followed every 24-48 weeks. HBeAg loss was defined as first HBeAg-negative value; sustained HBeAg loss was defined as ≥2 consecutive HBeAg-negative values ≥24 weeks apart. During a median follow-up of 1.8 years, 164 participants experienced HBeAg loss, a rate of 11.4 (95% CI, 9.8-13.3) per 100 person-years. After adjustment for confounders, HBeAg loss rate was significantly higher in males than females, in older than younger individuals, in Whites or Blacks than Asians, in those with genotype A2 or B versus C, and in those with basal core promoter/pre-core mutations versus wild type. Additionally, during follow-up, an ALT flare and a lower quantitative HBsAg, quantitative HBeAg or HBV DNA level predicted higher rates of HBeAg loss. The majority (88%) with HBeAg loss had sustained HBeAg loss. In conclusion, a number of specific demographic, clinical and viral characteristics impacted rate of HBeAg loss and may prove useful in design and interpretation of future therapeutic studies.
Identifiants
pubmed: 34355475
doi: 10.1111/jvh.13591
pmc: PMC8622507
mid: NIHMS1731108
doi:
Substances chimiques
DNA, Viral
0
Hepatitis B Surface Antigens
0
Hepatitis B e Antigens
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1526-1538Subventions
Organisme : NIDDK NIH HHS
ID : U01 DK082872
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK082944
Pays : United States
Investigateurs
Daryl T-Y Lau
(DT)
Raymond T Chung
(RT)
Lewis R Roberts
(LR)
Mohamed A Hassan
(MA)
Sarah Jane Schwarzenberg
(SJ)
Mauricio Lisker-Melman
(M)
Jeffrey Teckman
(J)
David K Wong
(DK)
Joshua Juan
(J)
Colina Yim
(C)
Keyur Patel
(K)
Simon C Ling
(SC)
Robert Perrillo
(R)
Son Do
(S)
Norberto Rodriguez-Baez
(N)
Steven-Huy B Han
(SB)
Tram T Tran
(TT)
Norah A Terrault
(NA)
Mandana Khalili
(M)
Philip Rosenthal
(P)
Anna Suk-Fong Lok
(AS)
Naoky Tsai
(N)
Barak Younoszai
(B)
Andrew Muir
(A)
Donna Evon
(D)
Jama M Darling
(JM)
Robert C Carithers
(RC)
Margaret Shuhart
(M)
Kris V Kowdley
(KV)
Chia C Wang
(CC)
Karen F Murray
(KF)
Velimir A Luketic
(VA)
Kathleen B Schwarz
(KB)
T Jake Liang
(T)
Jay H Hoofnagle
(JH)
Edward Doo
(E)
Kyong-Mi Chang
(KM)
Jang-June Park
(JJ)
Steven H Belle
(SH)
Abdus Wahed
(A)
David Kleiner
(D)
Informations de copyright
© 2021 John Wiley & Sons Ltd.
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