ABSTRACT
Introduction
Nucleos(t)ide analogues (NAs) are effective in suppressing the replication of the hepatitis B virus. However, NAs cannot effectively induce hepatitis B surface antigen (HBsAg) seroclearance, which represents the optimal treatment endpoint in chronic hepatitis B (CHB). Hence, most CHB patients are advised for indefinite NA therapy, but recent data has supported the concept of finite NA therapy before HBsAg seroclearance.
Areas covered
This article covered the latest evidence on stopping NAs in CHB, with a focused analysis on international guidelines. Articles were retrieved by a literature search on PubMed with the keywords ‘chronic hepatitis B,’ ‘antiviral therapy,’ ‘nucleos(t)ide analogue,’ ‘cessation,’ ‘stopping’, and ‘finite.’ Studies up till 1 December 2022 were included.
Expert opinion
Finite NA therapy in CHB has the potential in enhancing HBsAg seroclearance, however it also carries rare but potentially severe risks. NA cessation before HBsAg seroclearance is only suitable for a highly selected group of patients, whereas the majority of CHB patients should be treated indefinitely or until HBsAg seroclearance. Current guidelines have provided recommendations on stopping NAs, but further research is required to optimize the monitoring and retreatment protocol after stopping NAs.
Article highlights
Hepatitis B surface antigen (HBsAg) seroclearance is a well-established treatment endpoint for nucleos(t)ide analogue (NA) therapy
NAs cannot effectively induce HBsAg seroclearance, and most patients require indefinite therapy
It is feasible to stop NAs before HBsAg seroclearance in a highly selected group of patients
Finite NA therapy is associated with rare but potentially severe risks
Further research is required on the ideal monitoring and retreatment protocol after NA cessation
Declaration of interest
MF Yuen is an advisor/consultant for AbbVie, Assembly Biosciences, Aligos Therapeutics, Arbutus Biopharma, Bristol Myer Squibb, Clear B Therapeutics, Dicerna Pharmaceuticals, Finch Therapeutics, GlaxoSmithKline, Gilead Sciences, Immunocore, Janssen, Merck Sharp and Dohme, Hoffmann-La Roche and Springbank Pharmaceuticals, Vir Biotechnology and receives grant/research support from Assembly Biosciences, Aligos Therapeutics, Arrowhead Pharmaceuticals, Bristol Myer Squibb, Fujirebio Incorporation, Gilead Sciences, Immunocore, Merck Sharp and Dohme, Hoffmann-La Roche, Springbank Pharmaceuticals, and Sysmex Corporation. WK Seto has received speaker’s fees from AstraZeneca, they are an advisory board member for Abbott, and received research funding from Pfizer, Boehringer Ingelheim, Ribo Life Science, and Alexion Pharmaceuticals. They are an advisory board member and received speaker’s fees and research funding from Gilead Sciences. LY Mak is on the advisory board for Gilead Sciences.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.