Published online Mar 21, 2021. doi: 10.3748/wjg.v27.i11.1101
Peer-review started: November 20, 2020
First decision: December 17, 2020
Revised: January 7, 2021
Accepted: February 11, 2021
Article in press: February 11, 2021
Published online: March 21, 2021
China is one of the leading countries for hepatitis B virus (HBV) prevalence, but most chronic hepatitis B (CHB) patients do not receive standardized antiviral therapy. There are few relevant reports addressing the outcomes of the large number of CHB patients who do not receive antiviral therapy.
The purpose of this study was to provide clinical evidence on the outcomes of CHB patients without antiviral treatment and evaluate the efficacy of antiviral therapy in the development and progression of CHB.
To observe the outcomes of long-term follow-up of patients with CHB without antiviral treatment.
This study included 362 patients with CHB and 96 with hepatitis B cirrhosis, without antiviral treatment and with only hepatoprotective and anti-inflammatory treatment in 1993-1998. The median follow-up period was 10 and 7 years, respectively. A total of 203 CHB and 129 hepatitis B cirrhosis patients receiving antiviral therapy were selected as the control groups. The median follow-up period was 8 and 7 years, respectively. Kaplan–Meier curves were used to analyze the cumulative incidence of hepatocellular carcinoma (HCC), and the Cox regression model was used to analyze the risk factors of HCC.
Among the patients in the non-antiviral group, 16.9% showed spontaneous decreases in HBV DNA to undetectable levels, and 32.8% showed hepatitis B e antigen (HBeAg) seroconversion. In the antiviral group, 87.2% of patients had undetectable HBV DNA, and 52% showed HBeAg seroconversion. Among CHB and hepatitis B cirrhosis patients, the cumulative incidence rates of HCC were 14.9% and 53.1%, respectively, in the non-antiviral group, and were 10.7% and 31.9%, respectively, in the antiviral group. There was no difference between the two groups CHB, but there was a difference between the groups with hepatitis B cirrhosis. The cumulative incidence rates of HCC were 1.6% and 22.3% in the groups with and without spontaneous HBeAg seroconversion, respectively. The incidence rates of HCC among patients with and without spontaneous declines in HBV DNA to undetectable levels were 1.6% and 19.1%, respectively. There was no difference in the cumulative incidence of HCC between the two groups with drug-resistant CHB, but there was a significant difference between the two groups with cirrhosis. The Cox regression model was used for regression of the corrected REACH-B score, and alanine aminotransferase > 400 U/L, history of diabetes, and family history of liver cancer were risk factors for HCC in men aged > 40 years. Multifactor analysis showed that a family history of HCC among men was a risk factor for HCC.
Antiviral therapy and non-antiviral therapy with hepatoprotective and anti-inflammatory therapy both reduced the risk of HCC. Antiviral therapy may mask the spontaneous serological response of some patients during CHB.
Our study initially verified the outcomes of patients with CHB without antiviral treatment. The effect of early antiviral therapy on reducing the incidence of HCC cannot be overestimated. More evidence-based studies are needed to validate the relationship between HCC incidence and antiviral therapy.