Serum hepatitis B core-related antigen predicts hepatocellular carcinoma in hepatitis B e antigen-negative patients.


Journal

Journal of gastroenterology
ISSN: 1435-5922
Titre abrégé: J Gastroenterol
Pays: Japan
ID NLM: 9430794

Informations de publication

Date de publication:
Sep 2020
Historique:
received: 27 04 2020
accepted: 08 06 2020
pubmed: 20 6 2020
medline: 25 2 2023
entrez: 20 6 2020
Statut: ppublish

Résumé

Hepatitis B core-related antigen (HBcrAg) is a novel serum viral marker. Recent studies showed that its level correlates with the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). We aimed to evaluate the accuracy of serum HBsAg and HBcrAg levels at baseline to predict HCC. 1400 CHB patients who received nucleos(t)ide analogues (NA) treatment since December 2005 were included. Their stored serum samples at baseline were retrieved to measure HBsAg and HBcrAg levels. The primary endpoint was the cumulative incidence of HCC. 85 (6.1%) patients developed HCC during a mean (± SD) follow-up duration of 45 ± 20 months. Serum HBcrAg level above 2.9 log10 U/mL at baseline was an independent factor for HCC in hepatitis B e antigen (HBeAg)-negative patients by multivariable analysis (adjusted hazard ratio 2.13, 95% CI 1.10-4.14, P = 0.025). HBcrAg above 2.9 log Serum HBcrAg level predicts the risk of HCC accurately in NA-treated HBeAg-negative CHB patients.

Sections du résumé

BACKGROUND BACKGROUND
Hepatitis B core-related antigen (HBcrAg) is a novel serum viral marker. Recent studies showed that its level correlates with the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). We aimed to evaluate the accuracy of serum HBsAg and HBcrAg levels at baseline to predict HCC.
METHODS METHODS
1400 CHB patients who received nucleos(t)ide analogues (NA) treatment since December 2005 were included. Their stored serum samples at baseline were retrieved to measure HBsAg and HBcrAg levels. The primary endpoint was the cumulative incidence of HCC.
RESULTS RESULTS
85 (6.1%) patients developed HCC during a mean (± SD) follow-up duration of 45 ± 20 months. Serum HBcrAg level above 2.9 log10 U/mL at baseline was an independent factor for HCC in hepatitis B e antigen (HBeAg)-negative patients by multivariable analysis (adjusted hazard ratio 2.13, 95% CI 1.10-4.14, P = 0.025). HBcrAg above 2.9 log
CONCLUSION CONCLUSIONS
Serum HBcrAg level predicts the risk of HCC accurately in NA-treated HBeAg-negative CHB patients.

Identifiants

pubmed: 32556643
doi: 10.1007/s00535-020-01700-z
pii: 10.1007/s00535-020-01700-z
doi:

Substances chimiques

Antiviral Agents 0
Hepatitis B Core Antigens 0
Hepatitis B Surface Antigens 0
Hepatitis B e Antigens 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

899-908

Subventions

Organisme : Health and Medical Research Fund
ID : 15160551

Auteurs

Lilian Yan Liang (LY)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.

Vincent Wai-Sun Wong (VW)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.
State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.

Hidenori Toyoda (H)

Ogaki Municipal Hospital, Ogaki, Gifu, Japan.

Yee-Kit Tse (YK)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.

Terry Cheuk-Fung Yip (TC)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.

Becky Wing-Yan Yuen (BW)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.

Toshifumi Tada (T)

Ogaki Municipal Hospital, Ogaki, Gifu, Japan.

Takashi Kumada (T)

Ogaki Municipal Hospital, Ogaki, Gifu, Japan.

Hye-Won Lee (HW)

Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.

Grace Chung-Yan Lui (GC)

Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.

Henry Lik-Yuen Chan (HL)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong.
State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR.

Grace Lai-Hung Wong (GL)

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR. wonglaihung@cuhk.edu.hk.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, 9/F Prince of Wales Hospital, Shatin, Hong Kong. wonglaihung@cuhk.edu.hk.
State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR. wonglaihung@cuhk.edu.hk.

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Classifications MeSH