In a consecutive series of 35 cases of HCC, 21 (60%) had a habitual alcoholic intake of greater than 80 g/die and 26 (74.2%) were positive for at least one HBV serum marker. At tissue level, HBsAg was positive in non-tumoral tissue in 8 cases (22.9%) and HBcAg in 6 cases (17.1%) in non-neoplastic tissue and in 3 cases (8.6%) in neoplastic tissue with focal type positivity. The positivity of HBsAg presented at cytoplasmatic level and that of HBcAg almost exclusively at nuclear level. The comparatively low expression of HBV antigens at tissue level can be explained by the integration of viral DNA in the host genome which probably took place in many of these cases. Cirrhosis was associated with HCC in 23 cases (65.7%). In 9 (25.7%) cirrhosis was macronodular, in 4 (11.4%) micronodular and in 10 (28.6%) it was mixed. 18 cases (51.4%) presented an association of significant alcoholic consumption and positivity of at least one HBV marker. In 19 cases (54.3%), cirrhosis was associated with positivity of at least one HBV marker. Finally, in 14 cases (40%) there was an association of cirrhosis, alcohol and positivity of at least one HBV marker. These results suggest a multifactorial aetiology of HCC in our geographic area, identifying the factors in question in cirrhosis of the liver, independently of its aetiology (through the hyperplastic-regenerative process that characterises it) in HBV and in alcohol (with direct and independent pathogenetic mechanisms known only in part, or mediated by cirrhosis of which HBV and alcohol represent the two main aetiological agents). In cases in which more than one of the aetiological factors considered was observed, it is legitimate to admit a cocarcinogenic perhaps synergistic hypothesis of this cancer.
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