2018, Number 4
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Ann Hepatol 2018; 17 (4)
Frequency and Characteristics of Occult Hepatitis B Infection Among Hepatocellular Carcinoma Patients in Japan
Muto J, Sugiyama M, Shirabe K, Mukaide M, Kirikae-Muto I, Ikegami T, Yoshizumi T, Yamashita Yo-ichi, Maehara Y, Mizokami M
Language: English
References: 15
Page: 596-603
PDF size: 196.55 Kb.
ABSTRACT
Introduction and aim. Occult hepatitis B virus (HBV) infection (OBI) represents a state without detectable hepatitis B surface
antigen, but positive for HBV DNA. The correlation between OBI and hepatocellular carcinoma (HCC) carcinogenesis is controversial.
We studied the frequency and characteristics of OBI among HCC patients and metastatic liver cancer patients.
Material and
methods. DNA was obtained from tumor and non-tumor tissues from 75 HCC patients (15 chronic hepatitis B (CHB), 39 chronic
hepatitis C (CHC), 21 cryptogenic) and 15 metastatic liver cancer patients who underwent liver resection. HBV DNA and covalentlyclosed
circular (ccc) DNA were detected using real-time polymerase chain reaction (PCR), and four HBV DNA regions were detected
by nested PCR. Clinicopathological factors were compared between patients with and without OBI.
Results. HBV DNA was
detected in 14 (93.3%) CHB, five (22.7%) cryptogenic and four (10.3%) CHC patients. cccDNA was detected in 12 (80.0%) CHB,
three (14.3%) cryptogenic and two (5.1%) CHC patients. All CHB, eight (38.1%) cryptogenic and ten (25.6%) CHC patients tested
positive with nested PCR. No metastatic liver cancer patients were positive for any HBV DNA regions. OBI patients had shorter
prothrombin times (P = 0.0055), and lower inflammation activity score in non-tumor liver (P = 0.0274). There were no differences in
anti-HBV antibodies.
Conclusions. OBI was detected in 38% of cryptogenic and 25.6% of CHC patients. There was no correlation
between OBI and anti-HBV antibodies, but fewer patients with OBI had high inflammatory activity, suggesting that factors other
than inflammation may be involved in HCC carcinogenesis in patients with OBI.
REFERENCES
Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA: a cancer journal for clinicians 2005; 55: 74- 108.
Lai CL, Ratziu V, Yuen MF, Poynard T. Viral hepatitis B. Lancet 2003; 362: 2089-94.
Ikeda K, Marusawa H, Osaki Y, Nakamura T, Kitajima N, Yamashita Y, Kudo M, et al. Antibody to hepatitis B core antigen and risk for hepatitis C-related hepatocellular carcinoma: a prospective study. Annals of internal medicine 2007; 146: 649-56.
Ohki T, Tateishi R, Goto E, Sato T, Masuzaki R, Imamura J, Goto T, et al. Influence of anti-HBc seropositivity on the risk of hepatocellular carcinoma in HCV-infected patients after adjusting for confounding factors. Journal of viral hepatitis 2010; 17: 91-7.
Torbenson M, Thomas DL. Occult hepatitis B. The Lancet infectious diseases 2002; 2: 479-86.
Raimondo G, Pollicino T, Cacciola I, Squadrito G. Occult hepatitis B virus infection. Journal of hepatology 2007; 46: 160-70.
Chang ML, Lin YJ, Chang CJ, Yeh C, Chen TC, Yeh TS, Lee WC, et al. Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma. PloS one 2013; 8: e64891.
Wong DK, Huang FY, Lai CL, Poon RT, Seto WK, Fung J, Hung IF. Occult hepatitis B infection and HBV replicative activity in patients with cryptogenic cause of hepatocellular carcinoma. Hepatology 2011; 54: 829-36.
Pollicino T, Squadrito G, Cerenzia G, Cacciola I, Raffa G, Craxi A, Farinati F. Hepatitis B virus maintains its pro-oncogenic properties in the case of occult HBV infection. Gastroenterology 2004; 126: 102-10.
Squadrito G, Cacciola I, Alibrandi A, Pollicino T, Raimondo G. Impact of occult hepatitis B virus infection on the outcome of chronic hepatitis C. Journal of hepatology 2013; 59: 696-700.
Lok AS, Everhart JE, Di Bisceglie AM, Kim HY, Hussain M, Morgan TR. Occult and previous hepatitis B virus infection are not associated with hepatocellular carcinoma in United States patients with chronic hepatitis C. Hepatology 2011; 54: 434-42.
Kitab B, Ezzikouri S, Alaoui R, Nadir S, Badre W, Trepo C, Chemin I. Occult HBV infection in Morocco: from chronic hepatitis to hepatocellular carcinoma. Liver international: official journal of the International Association for the Study of the Liver 2014.
Fujimoto A, Totoki Y, Abe T, Boroevich KA, Hosoda F, Nguyen HH, Aoki M, Hosono N. Whole-genome sequencing of liver cancers identifies etiological influences on mutation patterns and recurrent mutations in chromatin regulators. Nature genetics 2012; 44: 760-4.
Sung WK, Zheng H, Li S, Chen R, Liu X, Li Y, Lee NP. Genome- wide survey of recurrent HBV integration in hepatocellular carcinoma. Nature genetics 2012; 44: 765-9.
Kim HE, Kim DG, Lee KJ, Son JG, Song MY, Park YM, Kim JJ. Frequent amplification of CENPF, GMNN and CDK13 genes in hepatocellular carcinomas. PloS ONE 2012; 7: e43223.