Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy

Abstract Chronic hepatitis B virus (HBV) infection is the leading risk factor for hepatocellular carcinoma (HCC). The aim of this study was to explore the incidence of HCC in a cohort of subjects with HBV and correlate with HBV treatment current guidance. We identified 2846 subjects with HBV over th...

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Main Authors: Omar Alshuwaykh, Tami Daugherty, Amanda Cheung, Aparna Goel, Renumathy Dhanasekaran, T. Tara Ghaziani, Aijaz Ahmed, Deepti Dronamraju, Radhika Kumari, Allison Kwong, Mindie Nguyen, W. Ray Kim, Paul Yien Kwo
Format: Article
Language:English
Published: Wolters Kluwer Health/LWW 2022-11-01
Series:Hepatology Communications
Online Access:https://doi.org/10.1002/hep4.2064
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author Omar Alshuwaykh
Tami Daugherty
Amanda Cheung
Aparna Goel
Renumathy Dhanasekaran
T. Tara Ghaziani
Aijaz Ahmed
Deepti Dronamraju
Radhika Kumari
Allison Kwong
Mindie Nguyen
W. Ray Kim
Paul Yien Kwo
author_facet Omar Alshuwaykh
Tami Daugherty
Amanda Cheung
Aparna Goel
Renumathy Dhanasekaran
T. Tara Ghaziani
Aijaz Ahmed
Deepti Dronamraju
Radhika Kumari
Allison Kwong
Mindie Nguyen
W. Ray Kim
Paul Yien Kwo
author_sort Omar Alshuwaykh
collection DOAJ
description Abstract Chronic hepatitis B virus (HBV) infection is the leading risk factor for hepatocellular carcinoma (HCC). The aim of this study was to explore the incidence of HCC in a cohort of subjects with HBV and correlate with HBV treatment current guidance. We identified 2846 subjects with HBV over the study period. HCC was diagnosed in 386 of 2846 (14%) subjects; 209 of 386 (54%) were on nucleos(t)ide analogue (NA) therapy at time of HCC diagnosis, and 177 of 386 (46%) were not on NA therapy. Of the 177 subjects not on NAs who developed HCC during follow‐up, 153 of 177 (86%) had cirrhosis. Within the 177 subjects not on NAs, 158 of 177 (89%) had undetectable HBV DNA, 10 of 177 (6%) had detectable HBV DNA < 2000 IU/L, and 9 of 177 (5%) had HBV DNA > 2000 IU/L. Of those with cirrhosis and undetectable HBV DNA, 115 of 141 had compensated cirrhosis, and 26 of 141 had decompensated cirrhosis. Significant predictors of HCC on time to event analysis included cirrhosis (hazard ratio [HR] 10, 95% confidence interval [CI] 5.8–17.5; p < 0.001), alanine aminotransferase level (HR 1.004, 95% CI 1.002–1.006; p < 0.001), age (HR 1.04, 95% CI 1.03–1.06; p < 0.001), (HR 1.9, 95% CI 1.2–3.1; p 0.007), and nonalcoholic fatty liver disease (HR 1.7, 95% CI 1.1–2.8; p 0.02). Kaplan–Meier analysis demonstrated the cumulative incidence of HCC in subjects with compensated cirrhosis receiving NA therapy was significantly lower compared to subjects with compensated cirrhosis outside current HBV treatment practice guidance (undetectable HBV DNA) (32% vs. 51%; p < 0.001). Conclusion: Those with untreated compensated cirrhosis with undetectable HBV DNA who do not meet current guidance for treatment had higher rates of HCC than those with compensated cirrhosis and suppressed HBV DNA by NA therapy. This study highlights the need for earlier diagnosis and treatment of HBV.
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spelling doaj.art-3adeae4f48864b8ca84f80d8786246df2023-08-02T08:27:28ZengWolters Kluwer Health/LWWHepatology Communications2471-254X2022-11-016113052306110.1002/hep4.2064Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapyOmar Alshuwaykh0Tami Daugherty1Amanda Cheung2Aparna Goel3Renumathy Dhanasekaran4T. Tara Ghaziani5Aijaz Ahmed6Deepti Dronamraju7Radhika Kumari8Allison Kwong9Mindie Nguyen10W. Ray Kim11Paul Yien Kwo12Division of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USADivision of Gastroenterology and Hepatology Stanford University Medical Center Stanford California USAAbstract Chronic hepatitis B virus (HBV) infection is the leading risk factor for hepatocellular carcinoma (HCC). The aim of this study was to explore the incidence of HCC in a cohort of subjects with HBV and correlate with HBV treatment current guidance. We identified 2846 subjects with HBV over the study period. HCC was diagnosed in 386 of 2846 (14%) subjects; 209 of 386 (54%) were on nucleos(t)ide analogue (NA) therapy at time of HCC diagnosis, and 177 of 386 (46%) were not on NA therapy. Of the 177 subjects not on NAs who developed HCC during follow‐up, 153 of 177 (86%) had cirrhosis. Within the 177 subjects not on NAs, 158 of 177 (89%) had undetectable HBV DNA, 10 of 177 (6%) had detectable HBV DNA < 2000 IU/L, and 9 of 177 (5%) had HBV DNA > 2000 IU/L. Of those with cirrhosis and undetectable HBV DNA, 115 of 141 had compensated cirrhosis, and 26 of 141 had decompensated cirrhosis. Significant predictors of HCC on time to event analysis included cirrhosis (hazard ratio [HR] 10, 95% confidence interval [CI] 5.8–17.5; p < 0.001), alanine aminotransferase level (HR 1.004, 95% CI 1.002–1.006; p < 0.001), age (HR 1.04, 95% CI 1.03–1.06; p < 0.001), (HR 1.9, 95% CI 1.2–3.1; p 0.007), and nonalcoholic fatty liver disease (HR 1.7, 95% CI 1.1–2.8; p 0.02). Kaplan–Meier analysis demonstrated the cumulative incidence of HCC in subjects with compensated cirrhosis receiving NA therapy was significantly lower compared to subjects with compensated cirrhosis outside current HBV treatment practice guidance (undetectable HBV DNA) (32% vs. 51%; p < 0.001). Conclusion: Those with untreated compensated cirrhosis with undetectable HBV DNA who do not meet current guidance for treatment had higher rates of HCC than those with compensated cirrhosis and suppressed HBV DNA by NA therapy. This study highlights the need for earlier diagnosis and treatment of HBV.https://doi.org/10.1002/hep4.2064
spellingShingle Omar Alshuwaykh
Tami Daugherty
Amanda Cheung
Aparna Goel
Renumathy Dhanasekaran
T. Tara Ghaziani
Aijaz Ahmed
Deepti Dronamraju
Radhika Kumari
Allison Kwong
Mindie Nguyen
W. Ray Kim
Paul Yien Kwo
Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
Hepatology Communications
title Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
title_full Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
title_fullStr Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
title_full_unstemmed Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
title_short Incidence of hepatocellular carcinoma in chronic hepatitis B virus infection in those not meeting criteria for antiviral therapy
title_sort incidence of hepatocellular carcinoma in chronic hepatitis b virus infection in those not meeting criteria for antiviral therapy
url https://doi.org/10.1002/hep4.2064
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