Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death in the world. The incidence of HCC in India is reportedly low and varies from 0.2 to 1.9 %. Aflatoxins, secondary metabolites produced by Aspergillus flavus and Aspergillus parasiticus, are potent human carcinogens implicated in HCC. The prevalence of aflatoxin B1 (AFB1) as co-carcinogen was analysed using an in-house immunoperoxidase test in 31 liver biopsies and 7 liver-resection specimens from histopathologically proven HCC, and in 15 liver biopsies from cirrhosis patients (control group). Serum was tested for hepatitis B and C serological markers using commercial assays, and for AFB1 using an in-house ELISA with a sensitivity of~1 ng ml "1 for AFB1. In spite of positive AFB1 immunostaining in HCC cases, all serum specimens, from both HCC and the control groups, were AFB1-negative. There were 18 (58.1 %) HCC cases that revealed AFB1 in liver biopsies; 68.8 % (n511) of non-B non-C hepatitis cases with HCC and 46.1 % (n56) of the hepatitis B surface-antigen-positive subjects were positive for AFB1. Out of the two hepatitis B/hepatitis C virus co-infected cases, one was positive for AFB1. Of seven tumour-resection samples, six were positive for AFB1. Only one case revealed AFB1 in the nontumour area of the resected material. Thus AFB1 staining was significantly associated with tumour tissue (P50.03). Aflatoxins proved to have a significant association with HCC in this peninsular part of the subcontinent. The impact seems to be a cumulative process, as revealed by the AFB1 deposits in HCC liver tissue, even though the serum levels were undetectable.

The overall positivity pattern of AFP in HCC does indicate that higher levels of AFP are observed with hepatitis virus positivity, especially with HBV. Further studies must be carried out to correlate the serum levels of AFP with the size, number, and degree of differentiation of HCC nodules.

This report presents the clinical features of 78 cases of the chronic Budd-Chiari syndrome encountered over a period of 13 years. The diagnosis of hepatic venous outflow obstruction was confirmed by venographic studies in all cases. In 20 patients there was hepatic vein occlusion without inferior vena caval (IVC) obstruction (Group A). In 17 patients there was constriction of the IVC above the drainage site of the right hepatic vein which was patent (Group B). In 13 patients there was short segmental obstruction of the hepatic segment of the IVC along with blockage of the hepatic venous orifices (Group C). In 28 patients there was hepatic venous obstruction with long segment involvement of the IVC extending to varying lengths of the infrahepatic segment (Group D). Of particular interest are the operative findings in 12 of 17 patients of Group B of hour glass constriction of the IVC, which can be labelled as 'coarctation of the IVC'. Dorsal cavoatrial bypass using a polytetra fluoroethylene graft has proved useful in Group B. Interesting histopathological findings of the liver in some of the cases are also described; The possible aetiology of the Group B cases is discussed.

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