Prevalence and characteristics of familial hepatocellular carcinoma caused by chronic hepatitis B infection in Hong Kong

Chan, Annie On‐On; Yuen, Man‐Fung; Lam, Chi‐Ming; Fong, CY; Wong, Benjamin Chun–Yu; Lai, Ching–Lung

doi:10.1046/j.1365-2036.2004.01855.x

Cited by 6 publications

(4 citation statements)

References 14 publications

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“…Cirrhosis of the liver or HCC occurred earlier in the offspring. Similar results have been described for familial HCC in Hong Kong [Chan et al, ]. These results indicate that unfavorable prognoses (cirrhosis of the liver or HCC) in these families may be associated with genetic defects.…”

Section: Discussionsupporting

confidence: 87%

Hepatitis B virus infection in clustering of infection in families with unfavorable prognoses in northwest China

Yang

Jin

et al. 2013

Journal of Medical Virology

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Hepatitis B virus (HBV) infection and its associated liver diseases have characteristics of familial clustering in China. However, the reasons for this are not understood fully. To address this issue, the prevalence HBV infection and the characteristics of unfavorable prognoses in clustering of infection in families in northwest China were investigated. Families with clustering of infection and unfavorable prognoses were enrolled, and general information and serum samples were collected. The clinical features and sequelae of HBV infection were compared among the blood relatives (including the first-, second-, and third-degree blood relatives) and spouses using the chi-square test or Fisher's exact test. A total of 102 clusterings of infection families with unfavorable prognoses were interviewed. In the first-, second-, and third-degree blood relatives and spouses, the prevalences of cirrhosis of the liver were 29.2%, 11.9%, and 8.7%, respectively, while those of hepatocellular carcinoma (HCC) were 21.8%, 1.4%, and 4.3%, respectively (P<0.05). The mean ages of the onset of cirrhosis of the liver in the first-, second-, and third-degree blood relatives and spouses were 57 ± 9.91, 47 ± 9.96, 38 ± 10.35, and 57 ± 8.49 years, respectively, while the mean ages of the onset of HCC were 60 ± 7.92, 49 ± 8.57, 41 ± 3.54, and 50 ± 0 years, respectively, (P<0.05). The first-, second-, and third-degree blood relatives from clustering of infection in families with unfavorable prognoses had prevalences of cirrhosis or HCC in descending order of relationship. The findings suggest that genetic factors may be associated with a familial tendency for cirrhosis of the liver and HCC.

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Section: Discussionsupporting

confidence: 87%

Hepatitis B virus infection in clustering of infection in families with unfavorable prognoses in northwest China

Yang

Jin

et al. 2013

Journal of Medical Virology

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“…The HBV carrier rate was 17.3% in our cohort, which is higher than in the general population in Hong Kong [31]. There is evidence that HBV infection is more common in patients with lymphoma [32,33].…”

Section: Hbv Reactivation In All Patients With Hbv Infectioncontrasting

confidence: 53%

Clinical outcomes of patients with acute lymphoblastic leukemia receiving the hyper-CVAD regimen and assessment of the risk of hepatitis flares due to hepatitis B virus reactivation after chemotherapy

et al. 2021

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IntroductionHyper-CVAD (hyperfractionated cyclophosphamide, vincristine, doxorubicin and dexamethasone) has become a popular regimen for adults with acute lymphoblastic leukemia (ALL). We assessed the efficacy and tolerability of hyper-CVAD in the treatment of adult ALL.Material and methodsWe retrospectively reviewed ALL patients aged 18 or above receiving the hyper-CVAD regimen. We assessed complete remission rate and overall survival, as well as hepatitis B carrier rate and hepatitis flare due to hepatitis B virus (HBV) reactivation.ResultsFifty-two patients were treated with the hyper-CVAD regimen. The median age at diagnosis was 42 years; 27% of patients were Philadelphia (Ph) chromosome positive. The complete remission (CR) rate was 90.4% after the first cycle of chemotherapy. The induction mortality rate was 1.9%. Three patients required two cycles of hyper-CVAD to achieve CR. The median overall survival was 39.6 months and the 5-year overall survival was 50%. Age over 30 years and white blood cell count of more than 30 × 109/l were found to be prognostic for poor overall survival in multivariate analysis. The hepatitis B carrier rate was 17% in our cohort, and the rate of hepatitis flare due to HBV reactivation was 11% in patients with current infection.ConclusionsHyper-CVAD is feasible and tolerable with a good CR rate in the treatment of adult ALL patients. It is an option for the treatment of ALL. Antiviral prophylaxis should be considered in ALL patients with HBV infection to reduce the risk of HBV reactivation.

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“…16,31–33 Turati et al 18 conducted a case-control study (229 HCC patients vs 431 controls) and showed that the odds ratio of HCC was significantly higher in patients who had a family history of HCC and viral hepatitis B or C. They did not find a multiplicative interaction in their study. However, they did not examine RERI, AP, and SI to assess interaction.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effects of Family History of Hepatocellular Carcinoma and Hepatitis B Virus Infection on Risk for Incident Hepatocellular Carcinoma

Loomba¹,

Liu²,

Yang³

et al. 2013

Clinical Gastroenterology and Hepatology

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BACKGROUND & AIMS Little is known about the effects of family history of hepatocellular carcinoma (HCC) on hepatitis B progression or risk of HCC. We examined how family HCC history and presence or stage of hepatitis B virus (HBV) infection affect risk for HCC. METHODS We performed a population-based cohort study of 22,472 participants from 7 townships in Taiwan who underwent evaluation for liver disease from 1991 through 1992. Those who received a first diagnosis of HCC from January 1, 1991, to December 31, 2008, were identified from the Taiwanese cancer registry. RESULTS There were 374 cases of incident HCC over 362,268 person-years of follow-up evaluation. The cumulative risk of HCC in hepatitis B surface antigen (HBsAg)-seronegative patients without a family history of HCC was 0.62%, in those with a family history of HCC the cumulative risk was 0.65%, in HBsAg-seropositive patients without a family history of HCC the cumulative risk was 7.5%, and in HBsAg-seropositive patients with a family history of HCC the cumulative risk was 15.8% (P < .001). The multivariate-adjusted hazard ratio for HBsAg-seropositive individuals with family history, compared with HBsAg-seronegative individuals without a family history of HCC, was 32.33 (95% confidence interval, 20.8–50.3; P < .001). The relative excess risk owing to interaction was 19, the attributable proportion was 0.59, and the synergy index value was 2.54. These findings indicate synergy between family HCC history and HBsAg serostatus. The synergy between these factors remained significant in stratification analyses by HBeAg serostatus and serum level of HBV DNA. CONCLUSIONS Family history of HCC multiplies the risk of HCC at each stage of HBV infection. Patients with a family history of HCC require more intensive management of HBV infection and surveillance for liver cancer.

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Prevalence and characteristics of familial hepatocellular carcinoma caused by chronic hepatitis B infection in Hong Kong

Cited by 6 publications

References 14 publications

Hepatitis B virus infection in clustering of infection in families with unfavorable prognoses in northwest China

Hepatitis B virus infection in clustering of infection in families with unfavorable prognoses in northwest China

Clinical outcomes of patients with acute lymphoblastic leukemia receiving the hyper-CVAD regimen and assessment of the risk of hepatitis flares due to hepatitis B virus reactivation after chemotherapy

Synergistic Effects of Family History of Hepatocellular Carcinoma and Hepatitis B Virus Infection on Risk for Incident Hepatocellular Carcinoma

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