Detectable HBV DNA during nucleos(t)ide analogues stratifies predictive hepatocellular carcinoma risk score

Abstract

Nucleos(t)ide analogs (NA) suppress hepatitis B virus (HBV) replication and reduce the risk of hepatocellular carcinoma (HCC). However, NA cannot suppress carcinogenesis completely in patients with chronic hepatitis B. The aims of this study were to identify risk factors for HCC and develop a refined carcinogenesis prediction model. Patients receiving NA therapy (n = 1,183) were recruited retrospectively from the 16 hospitals. All patients had been receiving NA continuously for more than 1 year until the end of the follow-up. During a median follow-up of 4.9 (1.0-12.9) years, 52 (4.4%) patients developed HCC. A multivariate analysis revealed that male gender, older age, lower platelet counts at the baseline, and detectable HBV DNA during NA therapy were independent predictive factors of HCC development. The PAGE-B score was calculated by using these factors. 240 (20.3%), 661 (55.9%), and 282 (23.8%) patients were classified into low-, intermediate-, and high-risk groups, respectively. In the intermediate-and high-risk group, detectable HBV DNA was significantly associated with a higher risk of HCC development compared with continuously undetectable HBV DNA, respectively (HR 3.338; 95%

Dynamic evaluation of hepatocellular carcinoma prediction models in patients with chronic hepatitis B receiving nucleotide/nucleoside analogue treatment

“…In the time of NA administration was an excellent predictive model for carcinogenesis in Japanese population. 18 In the present study, the utility of these scores as a real-time monitor was verified by exam- We previously reported that undetectable HBV DNA during NA treatment is a predictive factor for HCC development, 19 and it was also confirmed in this cohort (data was not shown). Therefore, undetectable HBV DNA may be used as a factor constituting a predictive model for HCC development.…”

“…Therefore, it is necessary to develop a model that reflects treatment response, and some factors may improve the predictability of HCC during NA treatment by combining PAGE‐B. We previously reported that undetectable HBV DNA during NA treatment is a predictive factor for HCC development, 19 and it was also confirmed in this cohort (data was not shown). Therefore, undetectable HBV DNA may be used as a factor constituting a predictive model for HCC development.…”

“…Therefore, undetectable HBV DNA may be used as a factor constituting a predictive model for HCC development. Furthermore, previous reports showed that HBsAg, [20][21][22] HBcrAg, [21][22][23] HBV DNA level, 19,24 liver stiffness 25 and M2BPGi [26][27][28][29][30] during treatment were useful for stratification of carcinogenic risk. Future studies are required to determine whether a more accurate carcinogenic risk prediction model could be constructed by combining these scores with PAGE-B.…”

Hepatocellular carcinoma progression in hepatitis B virus-related cirrhosis patients receiving nucleoside (acid) analogs therapy: A retrospective cross-sectional study

“…In our study of patients treated with antiviral therapy for more than 6 mo, the number of HBV DNA-negative patients in the HCC group was lower than that in the No-HCC group. Many studies have found a correlation between serum HBV DNA levels and the occurrence of HCC in patients with hepatitis B. Kaneko et al [ 39 ] reported that detectable HBV DNA was significantly associated with a higher risk of HCC development compared with continuously undetectable HBV DNA. Chen et al [ 40 ] found that the incidence of HCC increased with serum HBV DNA level at study entry in a dose-response relationship ranging from 108/100,000 person-years for an HBV DNA level of < 300 copies/mL to 1152/100,000 person-years for an HBV DNA level of 1 million copies/mL or more.…”

Stratification of Hepatocellular Carcinoma Risk Following HCV Eradication or HBV Control

“…This classification achieved a negative predictive value of 99.5% in excluding patients without HCC development at 5 years. However, the persistent presence of detectable HBV DNA during NUC therapy is associated with HCC development [ 71 ], leading to the development of the new PAGE-B-DNA score. The latter combines features of the PAGE-B algorithm with the level of detected HBV DNA and has proven to be efficient in refining HCC risk stratification.…”