We prospectively monitored 140 cirrhotic patients for the development of hepatocellular carcinoma for 6 yr, using periodical screening by high-resolution convex-array ultrasonography and alpha-fetoprotein. Twenty-eight patients were positive for HBs antigen, 26 patients had received blood transfusions and were negative for HBs antigen and 26 patients had a history of heavy drinking. We detected hepatocellular carcinoma in 40 patients during this period. The overall cumulative incidence of hepatocellular carcinoma in the 6 yr was 39%; the cumulative incidence was 59% in patients with HBsAg, 53% in patients who had had blood transfusions and were negative for HBsAg and 22% in patients who had a history of heavy drinking and who were without HBsAg. Detection of the carcinoma in 85% of these 40 patients was based on results of ultrasonography. Twenty-six of the patients (65%) had a small hepatocellular carcinoma of 2 cm or less. alpha-Fetoprotein levels were lower than 100 ng/ml in 56% of these 40 patients. Patients with cirrhosis are at high risk of developing hepatocellular carcinoma, especially patients with HBsAg or with a history of blood transfusion who are negative for HBsAg. Periodic monitoring by use of ultrasonography in particular is recommended for early detection of hepatocellular carcinoma.

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This is the first report to document pit cells in the human liver. These cells were identified by characteristic electron-dense granules and rod-cored vesicles. The granules of human pit cells were smaller in number and size than those of the rat. In the present case of autoimmune hepatitis, pit cells and conventional agranular lymphocytes migrated into hepatic parenchyma and contacted degenerating and immature hepatocytes. Pit cells show natural killer activity (Kaneda et al., 1983), and may participate in development of lesions and cellular damage.

Of 34 solitary small hepatocellular carcinomas (HCC) 2 cm in diameter or less, 13 with hyperechoic lesions were observed serially by sonography, and 11 of these were examined histologically. Serial examination showed that hypoechoic areas appeared at the periphery of or within, the hyperechoic tumor, and that these areas expanded more with tumor growth than the hyperechoic areas as if compressing or displacing the existing hyperechoic areas. Histologically, the hyperechoic lesions were composed mostly of well-differentiated cancer cells containing fat droplets, whereas the hypoechoic lesions were composed of cancer cells without fat droplets. In the two tumors that were formed almost completely of cancer cells showing fatty metamorphosis, cancer cells without fat droplets proliferated mainly in the periphery of the tumor. These findings suggest that, in hyperechoic HCC, cancer cells with fat droplets appear in the early stage of HCC, and probably change into concer cells without fat droplets by the time that a certain tumor size is reached, with gradual displacement by the latter type of cell during tumor growth.