No abstract

A Chinese patient with documented hepatocellular carcinoma (HCC) satisfied the criteria of Everson and Cole4 for spontaneous regression of malignant tumors. Subsequently he survived a tumor‐free period of at least 13 years. During the period of regression, shrinkage of liver coincided with a rise of SGOT to a level comparable to that reported for patients with liver cancer during hepatic arterial ligation and cytotoxic therapy. Postregression liver biopsy from the site of the previous tumor revealed relatively uninflamed HBsAg‐positive tissue without dysplasia. The case provided the positive end of the survival spectrum in HCC, evidence that regression of HCC might occur by involution rather than maturation, and histologic data suggesting that regressed HCC might be replaced by surrounding tissue instead of leaving behind dysplasia.

A 54‐year‐old Chinese patient with a slowly growing hepatocellular carcinoma developed persistent hypoglycemia and received continuous dextrose infusion for some 5 months before death. In contrast to all save 1 previously reported patients, the blood glucose response to intravenous glucagon was normal. At necropsy the liver appeared to consist almost entirely of tumor. Histologically, the well‐differentiated malignant cells were loaded with fat, and on chemical analysis the lipid content was 475 mg per gm of tumor tissue. The glycogen content was not increased and was reduced by 23% after storage at 37°C for 4 hours. Enzyme studies of the tumor showed reduced activities of glucose‐6‐phosphatase, fructose‐1, 6‐diphosphatase, pyruvate carbox‐ylase, and phosphoenolpyruvate carboxykinase. There was increased activity of glucose‐6‐phosphate dehydrogenase. Phosphorylase activity was recorded only upon addition of adenylic acid. These findings were similar to those of tumors of patients who did not have hypoglycemia. The small amount of normal residual liver available for examination showed similar enzyme changes. In the residual liver of nonhypoglycemic patients the rate‐limiting enzymes for gluconeogenesis were normal. It is postulated that the main factors responsible for the development of early hypoglycemia and lipid accumulation in the tumor were the diversion of the substrates of the Krebs cycle from gluconeogenesis towards lipogenesis and the failure of lipolysis in the tumor. It is considered probable that the slow rate of growth of the tumor and the prolonged dextrose infusion contributed towards lipogenesis. The same abnormalities were probably present, but to a lesser extent, in the residual liver.