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748
ASSOCIATION BETWEEN PRETREATMENT BASELINE VIRAL
LOAD AND ON-TREATMENT RISK OF HEPATOCELLULAR
CARCINOMA IN CHRONIC HEPATITIS B
Won-Mook Choi1, Gi-Ae Kim2, Jonggi Choi1, Seungbong Han3
and Young-Suk Lim1, (1)Department of Gastroenterology,
Asan Medical Center, University of Ulsan College of Medicine,
(2)Department of Internal Medicine, Kyung Hee University
Hospital, (3)Department of Applied Statistics, Gachon
University
Background: In patients with chronic hepatitis B (CHB),
hepatocellular carcinoma (HCC) risk persists despite antiviral
therapy The association between baseline serum HBV DNA
levels and on-treatment HCC risk remains unclear Methods:
In this multicenter historical cohort study in Korea, HCC risk
was analyzed in 3,541 entecavir- or tenofovir-treated noncirrhotic
adult patients with CHB by Cox proportional-hazards
regression HBV DNA level was analyzed as a categorical
variable Results: During 5 3 years of median follow-up,
100 patients developed HCC (0 50 per 100 person-years)
Baseline HBV DNA level was independently associated with
HCC risk in a non-linear parabolic pattern By multivariable
analysis, HCC risk was highest with HBV DNA levels 5 00–
5 99 log10 IU/mL (adjusted hazard ratio [aHR], 3 50; P<0 001),
followed by 6 00–6 99 log10 IU/mL (aHR, 3 04; P=0 001), and
3 30–4 99 log10 IU/mL (aHR, 1 87; P=0.17), with ≥8.00 log10
IU/mL showing the lowest HCC risk (aHR, 1 00; reference)
When the patients were stratified by FIB-4 index, compared
with baseline HBV DNA levels ≥8.00 log10 IU/mL, aHR for
HCC risk with HBV DNA levels 5 00–5 99 log10 IU/mL was
9 80 (P=0 006) if the patients had FIB-4 index <1 8, while
it was 2 47 (P=0.03) with FIB-4 index ≥1.8. Conclusion:
Pretreatment baseline HBV DNA levels were significantly
associated with HCC risk in a non-linear parabolic pattern in
CHB patients during long-term antiviral treatment, especially
with no significant hepatic fibrosis. Early antiviral intervention
before progressing to moderate viral load, that is associated
with irreversibly increased HCC risk, may optimize HCCpreventive
effect in non-cirrhotic adult CHB patients,
regardless of alanine aminotransferase levels and hepatic
fibrosis.
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