|
|
Learning Objectives for this Presentation:
By the end of this presentations participants should understand the role of HBV DNA in driving progression to HCC.
Background:
HBV DNA is a marker of efficacy for anti-viral treatment of chronic hepatitis B. We examined the independent effect of HBV DNA on the incidence of HCC in a long-term study.
Methods:
A cohort of 3,851 asymptomatic HBsAg-positive subjects was recruited from 7 townships in Taiwan between 1991 and 1992. Serum samples obtained at enrolment and follow-up examinations were tested for HBsAg, HBeAg, HBV DNA by PCR (LOQ 300 copies/mL), and ALT. The diagnosis of HCC was made through data linkage with profiles of the National Cancer Registry and Death Certification System and confirmed by chart review. Multivariable adjusted relative risks (RRadj) were derived using Cox proportional hazard models.
Results:
During 43,993 person-years of follow-up, 176 subjects were newly diagnosed with HCC. Removing all HCV co-infected subjects, there were 164 HCC cases among 3,653 subjects. In these subjects, the incidence of HCC was strongly linked with increasing HBV DNA level in a dose-response manner (test of trend; P<0.001); incidence of HCC was highest (11.52/1000 PYFU) in subjects with HBV DNA >106 copies/mL. In a Cox regression model, the RRadj (95%CI) was 7.8 (3.7-16.2) for HBV DNA levels >106 copies/ml (reference: HBV DNA < LOQ); in HBeAg negative subjects with normal serum ALT (N=2,966), the RRadj (95%CI) was 18.6 (8.2-42.2) for HBV DNA levels >106 copies/ml.
Conclusions:
Serum HBV DNA can reliably predict the risk of HCC independent of HBeAg status and serum ALT level. Persistent elevation of HBV DNA over time carries the strongest risk of HCC.
See more of Poster Session #1
See more of The 2005 National Viral Hepatitis Prevention Conference