Geographic correlation between mortality from primary hepatic carcinoma and prevalence of hepatitis B surface antigen in Greece

Trichopoulos, D; Papaevangelou, G.; Violaki, M.; Vissoulis, C.; Sparros, L; Manousos, O. N.

doi:10.1038/bjc.1976.125

Cited by 23 publications

(15 citation statements)

References 16 publications

(17 reference statements)

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“…The numerous case-control studies that indicated a causative role for HBV infection in the development of HCC (Tabor et al, 1977;Maupas et al, 1977;Kubo et al, 1977;Johnson et al, 1978;Trichopoulos et al, 1978;Kew et al, 1979;Omata et al, 1979) have been followed by evidence that suggests that chronic active infection with HBV may be a necessary initial factor in the development of all cases of HCC. A prospective study in Taiwan has indicated a relative risk of over 200 with all but one case occurring among persons who were carriers prior to development of HCC (Beasley et al, 1981) while viral DNA has been found incorporated into the host genome of HCC patients (Shafritz et al, 1981) including those who have no viral markers of HBV infection (Brechot et al, 1982). 1t has also been suggested that chronic HBV infection acting alone could be responsible for the large range of incidence for HCC that exists between different countries and that aflatoxin has little carcinogenic effect on humans (Prince, 1978;Lutwick, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, higher prevalence of HbsAg have been reported from Taiwan both in control populations and among HCC patients (Tong et al, 1971;Sung et al, 1980) than have been found in Mozambique (Bersohn et al, 1974;Kew et al, 1979) and yet the age-standardised incidence for HCC is lower in Taiwan (calculations from data given in Beasley et al, 1981) than in Mozambique. The one clear indication of a geographical association comes from Greece, an area of moderate incidence for HCC, where mortality rates from HCC in different regions showed a correlation with the proportion of army recruits who were positive for HBsAg in both rural and urban areas (Trichopoulos et al, 1976).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei

Rensburg¹,

Cook-Mozaffari²,

Schalkwyk³

et al. 1985

Br J Cancer

291

148

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei

Rensburg¹,

Cook-Mozaffari²,

Schalkwyk³

et al. 1985

Br J Cancer

291

148

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“…Despite the relatively high proportion of HBs antigen-negative patients with liver cirrhosis with hepatocellular cancer in the United States (Dourdourekas et al, 1975) and Great Britain (Fisher et al, 1976), the direct or indirect oncogenic role of ethanol in liver cirrhosis is widely underestimated. The reason may be the fact that all published studies have been carried out in West, East, or South Africa or in the Far East, areas with a known high prevalence of HBs antigen; in these studies a close relationship between the incidence of primary liver cell carcinoma with and without liver cirrhosis on the one hand and HBs antigen on the other hand has been demonstrated (Moertel et al, 1970;Sherlock et al, 1970;Vogel et al, 1970;Tong et al, 1971;Simons et al, 1972;Kew et al, 1974;Prince et al, 1975;Williams, 1975;Trichopoulos et al, 1976;Kubo et al, 1977aKubo et al, , 1977b.…”

Section: Discussionmentioning

confidence: 99%

Etiology of human liver cancer: Controlled prospective study in liver cirrhosis

Lėhmann

Wegener

1979

Journal of Toxicology and Environmental Health

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The incidence of primary liver cell carcinoma was investigated in a prospective study over 6 yr and 5 mo in 403 clinically unselected patients derived from a homogeneous population by means of serial determination of alpha 1-fetoprotein (AFP) by radioimmunoassay. The diagnosis of liver cirrhosis was proved in 90% by laparoscopy and/or histology and/or autopsy. The incidence of primary liver cell carcinoma in liver cirrhosis in the clinically studied patients was 4.47%, significantly lower than in the autopsy material (11.03%; p less than or equal to 0.025). In the follow-up study, all patients with increasing AFP concentrations exhibited a primary liver cell carcinoma. A transitory rise of AFP (higher than 50 ng/ml) was observed in 15.1% of patients with liver cirrhosis without primary liver cell cancer. In contrast to the results of animal experiments, this transitory rise of AFP was not followed by malignant transformation of the cirrhotic tissue. Posthepatitic liver cirrhosis was observed in 21.57%, postalcoholic liver cirrhosis in 42.93%, and cryptogenic liver cirrhosis in 27.30%. Liver cirrhosis of other etiology occurred in 8.19%. The incidences of primary liver cell cancer in these 4 groups were 4.94, 4.62, 5.45, and 0%, respectively. These differences are not statistically significant, although in absolute figures postalcoholic liver cirrhosis is the main cause of primary liver cell carcinoma in this sample from West Germany. HBs antigen-positive liver cirrhosis was more often associated with primary liver cell cancer than HBs antigen-negative liver cirrhosis (6.58 versus 3.96%); this difference also is not statistically significant. Observations of larger groups of patients may show a higher risk of developing primary liver cell carcinoma in those with a combination of alcohol abuse and HBs antigenemia and/or acute hepatitis in the history. Patients without these 2 risk factors had an incidence of primary liver cell carcinoma of 2.61%; those with 1 risk factor, 5.77%; and those with both risk factors, 10.71%.

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“…Numerous studies have shown a highly significant excess of surface antigen, surface antibody, and core antibody in these patients (e.g., see Sherlock et al, 1970;Reed et al, 1973;Nishioka et al, 1975;Prince et al, 1975;Maupas et al, 1975;Larouze et al, 1976;Trichopoulos et al, 1976;Nazarewicz et al, 1977;Tabor et al, 1977).…”

Section: [1o7]mentioning

confidence: 99%

Role of hepatitis b virus in primary liver cancer

Zuckerman

1979

Journal of Toxicology and Environmental Health

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There is an excess prevalence of markers of active infection with hepatitis B virus in patients with primary liver cancer in many parts of the world. Early age of infection with hepatitis B virus is likely to be an important factor, resulting in persistent infection that may progress to chronic liver damage. Results of recent experimental studies are consistent with integration of hepatitis B viral DNA with host cell DNA molecules. It is likely that primary liver cancer is the cumulative result of several cofactors including infection with hepatitis B virus; genetic, immunologic, hormonal, and nutritional factors; and environmental factors including mycotoxins and chemical carcinogens.

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Geographic correlation between mortality from primary hepatic carcinoma and prevalence of hepatitis B surface antigen in Greece

Abstract: Summary.-Average annual age-adjusted mortality rates per 100,000 from primary hepatic carcinoma (PHC) among males for [1971][1972][1973]

Cited by 23 publications

References 16 publications

Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei

Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei

Etiology of human liver cancer: Controlled prospective study in liver cirrhosis

Role of hepatitis b virus in primary liver cancer

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