Role of serum HBV RNA and hepatitis B surface antigen levels in identifying Asian patients with chronic hepatitis B suitable for entecavir cessation.


Journal

Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R

Informations de publication

Date de publication:
04 2021
Historique:
received: 13 03 2020
revised: 16 06 2020
accepted: 27 06 2020
pubmed: 8 8 2020
medline: 30 11 2021
entrez: 8 8 2020
Statut: ppublish

Résumé

Treatment cessation in chronic HBV infection may be durable in certain patient subgroups before hepatitis B surface antigen (HBsAg) seroclearance. The role of serum HBV RNA in determining treatment cessation suitability has not been well-investigated. Nucleos(t)ide analogue (NUC) treatment was discontinued in non-cirrhotic patients with chronic HBV with serum HBsAg <200 IU/mL and fulfilling internationally recommended criteria for treatment cessation. Patients were monitored till 48 weeks with baseline and serial measurements of serum HBsAg, HBV RNA and hepatitis B core-related antigen. NUCs were resumed when HBV DNA reaches >2000 IU/mL regardless of alanine aminotransferase (ALT) levels. 114 entecavir-treated patients (median age 58.4 years, median serum HBsAg 54.4 IU/mL) with median treatment duration of 6.7 years were recruited. The 48-week cumulative rate of HBV DNA >2000 IU/mL was 58.1%. End-of-treatment serum HBV RNA and off-treatment serial HBV RNA were both independently associated with HBV DNA >2000 IU/mL (HR 2.959, 95% CI 1.776 to 4.926, p<0.001; HR 2.278, 95% CI 1.151 to 4.525, p=0.018, respectively). Patients with HBV RNA ≥44.6 U/mL had a cumulative 48-week rate of 93.2%, while combining HBV RNA undetectability and HBsAg <10 IU/mL had a cumulative 48-week rate of 9.1%. 24 patients (38.7%) developed off-treatment ALT elevation, highest peak ALT was 1515 U/L. 8 patients (median serum HBsAg 2.6 IU/mL) developed HBsAg seroclearance. Serum HBV RNA measurement is essential for deciding on entecavir cessation in patients with chronic HBV, especially with low HBsAg levels. Patients can be stratified on their risk of off-treatment relapse based on both viral determinants. NCT02738554.

Sections du résumé

BACKGROUND
Treatment cessation in chronic HBV infection may be durable in certain patient subgroups before hepatitis B surface antigen (HBsAg) seroclearance. The role of serum HBV RNA in determining treatment cessation suitability has not been well-investigated.
METHODS
Nucleos(t)ide analogue (NUC) treatment was discontinued in non-cirrhotic patients with chronic HBV with serum HBsAg <200 IU/mL and fulfilling internationally recommended criteria for treatment cessation. Patients were monitored till 48 weeks with baseline and serial measurements of serum HBsAg, HBV RNA and hepatitis B core-related antigen. NUCs were resumed when HBV DNA reaches >2000 IU/mL regardless of alanine aminotransferase (ALT) levels.
RESULTS
114 entecavir-treated patients (median age 58.4 years, median serum HBsAg 54.4 IU/mL) with median treatment duration of 6.7 years were recruited. The 48-week cumulative rate of HBV DNA >2000 IU/mL was 58.1%. End-of-treatment serum HBV RNA and off-treatment serial HBV RNA were both independently associated with HBV DNA >2000 IU/mL (HR 2.959, 95% CI 1.776 to 4.926, p<0.001; HR 2.278, 95% CI 1.151 to 4.525, p=0.018, respectively). Patients with HBV RNA ≥44.6 U/mL had a cumulative 48-week rate of 93.2%, while combining HBV RNA undetectability and HBsAg <10 IU/mL had a cumulative 48-week rate of 9.1%. 24 patients (38.7%) developed off-treatment ALT elevation, highest peak ALT was 1515 U/L. 8 patients (median serum HBsAg 2.6 IU/mL) developed HBsAg seroclearance.
CONCLUSION
Serum HBV RNA measurement is essential for deciding on entecavir cessation in patients with chronic HBV, especially with low HBsAg levels. Patients can be stratified on their risk of off-treatment relapse based on both viral determinants.
TRIAL REGISTRATION NUMBER
NCT02738554.

Identifiants

pubmed: 32759300
pii: gutjnl-2020-321116
doi: 10.1136/gutjnl-2020-321116
doi:

Substances chimiques

Antiviral Agents 0
Hepatitis B Surface Antigens 0
RNA, Viral 0
entecavir 5968Y6H45M
Guanine 5Z93L87A1R

Banques de données

ClinicalTrials.gov
['NCT02738554']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

775-783

Commentaires et corrections

Type : CommentIn

Informations de copyright

© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: GC and JG are Abbott Diagnostics employees and hold Abbott stocks. W-KS received speaker’s fees from Mylan, is an advisory board member and received speaker’s fees from AbbVie, and is an advisory board member, received speaker’s fees and researching funding from Gilead Sciences. JF is an advisory board member of Gilead Sciences. M-FY is an advisory board member and/or received research funding from AbbVie, Arbutus Biopharma, Assembly Biosciences, Bristol-Myers Squibb, Dicerna Pharmaceuticals, GlaxoSmithKline, Gilead Sciences, Janssen, Merck Sharp and Dohme, Clear B Therapeutics, Springbank Pharmaceuticals; and received research funding from Arrowhead Pharmaceuticals, Fujirebio Incorporation and Sysmex Corporation. The remaining authors have no conflict of interests.

Auteurs

Wai-Kay Seto (WK)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China wkseto@hku.hk mfyuen@hkucc.hku.hk.
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.
Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Kevin Sh Liu (KS)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

Lung-Yi Mak (LY)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.

Gavin Cloherty (G)

Infectious Disease Research, Abbott Laboratories, Abbott Park, Illinois, USA.

Danny Ka-Ho Wong (DK)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.

Jeffrey Gersch (J)

Infectious Disease Research, Abbott Laboratories, Abbott Park, Illinois, USA.

Yuk-Fai Lam (YF)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

Ka-Shing Cheung (KS)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Ning Chow (N)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

Kwan-Lung Ko (KL)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

Wai-Pan To (WP)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

James Fung (J)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.

Man-Fung Yuen (MF)

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China wkseto@hku.hk mfyuen@hkucc.hku.hk.
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.

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