Antibody To Hepatitis B Core Antigen In Patients With Hepatocellular Carcinoma

Kubo, Yasuhiko; Okuda, Kunio; Hashimoto, Masaharu; Nagasaki, Yoshikazu; Ebata, H; Nakajima, Yutsuki; Musha, Hirotaka; Sakuma, Koshi; Ohtake, Hachiro

doi:10.1016/s0016-5085(77)80014-0

Cited by 63 publications

(8 citation statements)

References 20 publications

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“…Our HCC patients stand at the other extreme, with a much lower frequency of HBsAg positivity (14.7 %), a frequency of anti-HBc positivity three times this, and a mean age of nearly 60. Most of the other published series occupy an intermediate position with respect to these three parameters Omata et af., 1979;Bassendine et al, 1979;Trichopoulis et al, 1978;Kubo et al, 1977), a notable exception being Omata's California series, which has a mean age similar to ours (56.7 years) but close agreement between HBsAg and anti-HBc positivity (26% and 32%) (Omata et al, 1979).…”

Section: Positivesupporting

confidence: 76%

Association of hepatitis b virus infection with hepatocellular carcinoma in american patients

Yarrish

Werner

Blumberg

1980

Intl Journal of Cancer

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Thirty-four patients from the Philadelphia area with hepatocellular carcinoma (HCC) were matched with colon cancer patients, lung cancer patients and blood donors according to age and sex. Sera from the four groups were tested to determine the prevalence of hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), and antibody to hepatitis B core antigen (anti-HBc). Five of the HCC patients (14.7%) and none of the controls were positive for HBsAg. At least one of the three serologic markers of hepatitis B virus (HBV) infection was found in 51.5% of the HCC patients, 5.3% of the colon cancer patients, 11.1% of the lung cancer patients, and 10.7% of the blood donors. Twelve of the seventeen seropositive HCC patients (70.6%) were positive for anti-HBc alone, while all of the seropositive lung cancer patients and donors were positive for anti-HBs alone. Sera positive for any HBV marker were also tested for e antigen (HBeAg) and its antibody (anti-HBe). Four of the HCC patients (23.5% of the seropositives) had anti-HBe, while none of the sera tested had HBeAg. A history of alcoholism did not appear to influence HBV seropositivity in the HCC patients. This study supports the hypothesis that HBV infection is closely associated with HCC even in areas where both conditions are uncommon. The wide disparity between seropositivity for HBsAg and anti-HBc in the HCC patients is an unusual feature, for which an age effect may be the best explanation.

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Section: Positivesupporting

confidence: 76%

Association of hepatitis b virus infection with hepatocellular carcinoma in american patients

Yarrish

Werner

Blumberg

1980

Intl Journal of Cancer

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“…Indeed, patients and controls had a very high rate of exposure to HBV as demonstrated by high rates of seroconversion to anti-HBcAg (96% vs 72.1%, respectively). Except for higher anti-HBcAg responses in our controls, these findings are consistent with those from other investigators (54)(55)(56)(57)(58)(59)(60)(61)(62). The characterization of anti-HBcAg isotypes did not reveal any IgM isotype, suggesting that all our patients were chronically infected with HBV.…”

Section: Discussionsupporting

confidence: 92%

Hepatitis B virus, alpha‐fetoprotein synthesis, and hepatocellular carcinoma in Zaire

Kashala

Conne

Kapançi

et al. 1992

Liver

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ABSTRACT— We investigated the epidemiology of hepatocellular carcinoma (HCC) in Zaire, and evaluated the association between exposure to hepatitis B virus (HBV) and the development of HCC. Two hundred and twenty‐three consecutive cases of HCC diagnosed over 19 years (1966–1985) were reviewed. HCC represented 8.32% of all carcinomas and 5.56% of all cancers. Frequency was higher in males (75.7%) than in females (24.3%); a sex ratio of 3/1. The majority (82.1%o) of patients were aged 14 to 55 years with a peak occurrence in the fourth decade (28.6%). The mean age in males (41.27 ± 17.5 years) and females (37.40 ± 15.16 years) was significantly different (p<0.02). Sera from 40 patients and 68 age and sex‐matched controls were analyzed for markers of HBV infection: patients and controls had comparable rates of exposure (96%) vs 72.1%, respectively). However, patients had significantly higher HBsAg carrier rates (56.7% vs 7.35%; p < 0.001), and lower anti‐HBsAg seroconversion rates (25% vs 63.2%, p < 0.05). Using immunohistochemical analysis, the livers of patients were evaluated for HBsAg and HBcAg. These HBV antigens were more frequent in non‐tumorous hepatocytes (53.3% vs 23.3%, respectively) than in HCC cells (13.3% vs 3.3%). Serum alpha‐fetoprotein (AFP) was abnormal (>20 ng/ml) in 90%) of patients. The geometric mean (GM) AFP was 7273.8 ng/ml. AFP levels were significantly higher in HBsAg‐positive HCC cases (GM: 19 322.6 ng/ml; 95% confidence interval (CI): [3639.2, 102 565.2]) than in antigen negative cases (GM: 1939.5 ng/ml; 95%) CI: [182.8, 19952.6]), but did not correlate with HBV replication. Immunohistochemical detection of AFP revealed a similar correlation between AFP and HBsAg. Neither AFP level nor HBsAg production correlated with cellular atypia or tumor grade.

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“…The frequency of HBV positivity in chronic liver diseases such as chronic hepatitis, liver cirrhosis and HCC in Asia and Africa is about 23%, 35% and 49% respectively and is highest in HCC (Nishioka et al, 1975). The frequency of HBsAg positivity among HCC cases is still higher when anti-HBc in the sera is used as an index (Larouze et al, 1977;Kubo et al, 1977). In particular, the high anti-HBc titer, corresponding to that of chronic persistent HBV infection, is even higher in HCC patients although HBsAg was not detected in the sera (Furuta et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

A prospective study on the development of hepatocellular carcinoma from liver cirrhosis with persistent hepatitis B virus infection

Obata

Hayashi

Motoike

et al. 1980

Intl Journal of Cancer

128

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We made a prospective study on the development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis with hepatitis B virus infection from April, 1973 to December, 1977. Seven out of 30 patients (23%) with hepatitis B surface antigen (HBsAg)-positive cirrhosis developed HCC. On the other hand, only 5.9% of the patients with HBsAg-negative liver cirrhosis developed HCC. These patients were classified into three groups according to their anti-HB core (anti-HBc) titers. When the anti-HBc titer, expressed as a dilution of serum, was 2(10) or more (Group I), 20-24% of the liver cirrhosis patients developed HCC either with or without a detectable amount of HBs Ag present in the sera. When the anti-HBc titer was 2(9) or less (Group II), only 0-5.7% developed HCC. There was no significant difference between this and the anti-HBc and HBsAg-negative group (Group III), which was 4.4%. In five individual cases from group I, HBsAg was detected in serum, and in biopsies of liver cells, before HCC could be detected by angiography and/or rising levels of alphafetoprotein (AFP). In all of these cases, the anti-HBc titer was higher than 2(10) throughout the observation period, even before the development of HCC. These findings indicate that active virus proliferation in chronic hepatitis B virus infection precedes the development of HCC as indicated by a higher anti-HBc titer. Therefore we have prepared these studies to show the pathogenic role of hepatitis B virus in the development of hepatocellular carcinoma.

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Antibody To Hepatitis B Core Antigen In Patients With Hepatocellular Carcinoma

Cited by 63 publications

References 20 publications

Association of hepatitis b virus infection with hepatocellular carcinoma in american patients

Association of hepatitis b virus infection with hepatocellular carcinoma in american patients

Hepatitis B virus, alpha‐fetoprotein synthesis, and hepatocellular carcinoma in Zaire

A prospective study on the development of hepatocellular carcinoma from liver cirrhosis with persistent hepatitis B virus infection

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