Hepatitis B virus pre-genomic RNA and hepatitis B core-related antigen reductions at week 4 predict favourable hepatitis B surface antigen response upon long-term nucleos(t)ide analogue in chronic hepatitis B.


Journal

Clinical and molecular hepatology
ISSN: 2287-285X
Titre abrégé: Clin Mol Hepatol
Pays: Korea (South)
ID NLM: 101586730

Informations de publication

Date de publication:
01 2023
Historique:
received: 14 06 2022
accepted: 12 08 2022
pubmed: 22 8 2022
medline: 18 1 2023
entrez: 21 8 2022
Statut: ppublish

Résumé

We investigated the dynamics of serum HBV pre-genomic RNA (pgRNA) and hepatitis B core-related antigen (HBcrAg) in patients receiving nucleos(t)ide analogues (NAs) and their predictability for favourable suppression of serum hepatitis B surface antigen (HBsAg). Serum viral biomarkers were measured at baseline, weeks 4, 12, 24, 36, and 48 of treatment. Patients were followed up thereafter and serum HBsAg level was measured at end of follow-up (EOFU). Favourable HBsAg response (FHR) was defined as ≤100 IU/mL or HBsAg seroclearance upon EOFU. Twenty-eight hepatitis B e antigen (HBeAg)-positive and 36 HBeAg-negative patients (median, 38.2 years old; 71.9% male) were recruited with median follow-up duration of 17.1 years (interquartile range, 12.8-18.2). For the entire cohort, 22/64 (34.4%) achieved FHR. For HBeAg-positive patients, serum HBV pgRNA decline at week 4 was significantly greater for patients with FHR compared to non-FHR (5.49 vs. 4.32 log copies/mL, respectively; P=0.016). The area under the receiver-operating-characteristic curve (AUROC) for week 4 HBV pgRNA reduction to predict FHR in HBeAg-positive patients was 0.825 (95% confidence interval [CI], 0.661-0.989). For HBeAg-negative patients, instead of increase in serum HBcrAg in non-FHR patients, FHR patients had median reduction in HBcrAg at week 4 (increment of 1.75 vs. reduction of 2.98 log U/mL; P=0.023). The AUROC for week 4 change of HBcrAg to predict FHR in HBeAg-negative patients was 0.789 (95% CI, 0.596-0.982). Early on-treatment changes of serum HBV pgRNA and HBcrAg at 4 weeks predict HBsAg seroclearance or ≤100 IU/mL in NA-treated CHB patients upon long-term FU.

Sections du résumé

BACKGROUND/AIMS
We investigated the dynamics of serum HBV pre-genomic RNA (pgRNA) and hepatitis B core-related antigen (HBcrAg) in patients receiving nucleos(t)ide analogues (NAs) and their predictability for favourable suppression of serum hepatitis B surface antigen (HBsAg).
METHODS
Serum viral biomarkers were measured at baseline, weeks 4, 12, 24, 36, and 48 of treatment. Patients were followed up thereafter and serum HBsAg level was measured at end of follow-up (EOFU). Favourable HBsAg response (FHR) was defined as ≤100 IU/mL or HBsAg seroclearance upon EOFU.
RESULTS
Twenty-eight hepatitis B e antigen (HBeAg)-positive and 36 HBeAg-negative patients (median, 38.2 years old; 71.9% male) were recruited with median follow-up duration of 17.1 years (interquartile range, 12.8-18.2). For the entire cohort, 22/64 (34.4%) achieved FHR. For HBeAg-positive patients, serum HBV pgRNA decline at week 4 was significantly greater for patients with FHR compared to non-FHR (5.49 vs. 4.32 log copies/mL, respectively; P=0.016). The area under the receiver-operating-characteristic curve (AUROC) for week 4 HBV pgRNA reduction to predict FHR in HBeAg-positive patients was 0.825 (95% confidence interval [CI], 0.661-0.989). For HBeAg-negative patients, instead of increase in serum HBcrAg in non-FHR patients, FHR patients had median reduction in HBcrAg at week 4 (increment of 1.75 vs. reduction of 2.98 log U/mL; P=0.023). The AUROC for week 4 change of HBcrAg to predict FHR in HBeAg-negative patients was 0.789 (95% CI, 0.596-0.982).
CONCLUSION
Early on-treatment changes of serum HBV pgRNA and HBcrAg at 4 weeks predict HBsAg seroclearance or ≤100 IU/mL in NA-treated CHB patients upon long-term FU.

Identifiants

pubmed: 35989092
pii: cmh.2022.0172
doi: 10.3350/cmh.2022.0172
pmc: PMC9845664
doi:

Substances chimiques

Hepatitis B Surface Antigens 0
Hepatitis B Core Antigens 0
Hepatitis B e Antigens 0
RNA 63231-63-0
Antiviral Agents 0
Biomarkers 0
DNA, Viral 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

146-162

Subventions

Organisme : Research Grants Council, The Government of the Hong Kong Special Administrative Region
ID : 17108921

Commentaires et corrections

Type : CommentIn
Type : CommentIn

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Auteurs

Lung-Yi Mak (LY)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.
State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong.

Danny Wong (D)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.
State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong.

Alison Kuchta (A)

Roche Molecular Systems, Inc., Pleasanton, CA, USA.

Martina Hilfiker (M)

Roche Diagnostics Int. AG, Rotkreuz, Switzerland.

Aaron Hamilton (A)

Roche Molecular Systems, Inc., Pleasanton, CA, USA.

Ning Chow (N)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.

XianHua Mao (X)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.

Wai Kay Seto (WK)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.
State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong.

Man-Fung Yuen (MF)

Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Hong Kong.
State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong.

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