Abstract
We investigated the long-term risk of hepatocellular carcinoma (HCC) in dual-infected hepatitis B and C patients after eradication of hepatitis C virus (HCV). A total of 164 (62% male, median age, 50.5 years) hepatitis B and C dual-infected patients who achieved HCV sustained virological response were recruited. Half the patients were HCV genotype 1 with a median viral load of 5.5 log10 IU/mL, and 22.6%had an HBV DNA level ≥ 2000 IU/mL before therapy. HCC developed in 14 patients (8.5%), with an annual incidence of 1.38% per person-year. The 3-year, 5-year, 10-year, and 15-year cumulative probabilities were 2.5%, 5.1%, 12.6%, and 22.7%, respectively. Six months after treatment, a Cox regression hazard analysis revealed platelet level (HR: 0.98, 95% CI: 0.957–0.999, P = 0.038) and AFP level (HR: 1.20, 95% CI: 1.031–1.400, P = 0.019) to be independent factors in HCC. A higher 10-year cumulative risk of HCC was detected in patients with 6-month post-treatment AFP levels > 5.0 ng/mL and platelet levels < 130 x1000/µL (54.9%), compared to patients with neither (8.6%). Although the risk of HCC is low, surveillance of HCC is encouraged in dual-infected patients after eradication of HCV. Post-treatment AFP and platelet levels predict HCC development.
Highlights
A dual infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) is not uncommon in the AsiaPacific region, a high endemic area for both HBV and HCV [1]
After adjusting for the pre treatment and post-treatment significant factors, we found the 6month post-treatment platelet level (HR: 0.98, 95% CI: 0.957–0.999, P = 0.038) and alpha fetoprotein (AFP) level (HR: 1.20, 95% CI: 1.031–1.400, P = 0.019) were independent factors correlated with hepatocellular carcinoma (HCC) development (Table 3)
We further identified that AFP and platelet levels at 6 months after treatment were the independent predictive factors of HCC
Summary
A dual infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) is not uncommon in the AsiaPacific region, a high endemic area for both HBV and HCV [1]. Dual infection with the two viruses indicates patients who are at a high risk for disease aggravation and progression compared with patients with mono-infection [5, 6]. Whether the risk of HCC is higher in dual-infected patients has been studied. The investigators concluded that the risk of HCC in HBV/HCV dual-infection patients is not greater than the risk of HCC in HBV or HCV mono-infection patients. A study that investigated the clinical outcomes of HBV co-infection in a United States cohort reported that patients with documented HBV viremia were at a higher risk for HCC compared with HCV monoinfected patients [8]. A study from Taiwan concluded that HCV co-infection is an independent risk factor for HCC [9]
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