T. Wakatsuki

Resected case of hepatocellular carcinoma associated with lupoid hepatitis

Abstract A 65 year old woman with lupoid hepatitis developed hepatocellular carcinoma which was diagnosed at an early stage. She had no history of blood transfusion and serum hepatitis B virus markers were negative. Prednisolone and 6‐mercaptopurine were administered for the treatment of lupoid hepatitis. A hepatocellular carcinoma was detected by the elevation of serum α‐fetoprotein and imaging studies. A tumour, 1.4 cm in diameter, was located in the lateral segment of the left hepatic lobe. It was resected by hepatic subsegmentectomy. Histological study showed a hepatocellular carcinoma of Edmondson type II against a background of posthepatitic cirrhosis. The patient was in good condition 2.5 years after the operation.

The clinical and histological studies on subacute hepatitis (II)

We previously reported tha t the values of the ratios of the mesenchymal areas, which were stained in blue in the s taining sections of the liver specimens with azan, to the total areas (M/ T) were all above 17.3% in 17 pat ients of subacute hepatit is diagnosed according to the criteria of Tisdale, and were significantly higher tean those in acute hepatit is or chronic hepatitis. The M/T ratio of the patients died of hepatic coma were all above 71.6% and were significantly higher than those of the survived cases. Severe clinical signs, such as prolonged jaundice, ascites, edema, neurological findings and gastrointest inal bleeding tended to be found more frequently in the cases showing the larger M/T ratios among the survived cases. However, the development of hepatic cirrhosis was not correlated to the area ratios in the initial biopsy specimens. The resul ts indicated tha t the quant i ty of the initial destruction in the hepatocytes was closely related to the fatality or the development of the servere clinical s igns in the relatively early stage. However, the prognosis in the late stage, which means the development of hepatic cirrhosis, may be influenced by the reaction in the host following the hepatocytic destruct ion ra ther than the quant i ty of the hepatocellular damage.