RESUMEN
Hepatic carcinomas were induced with the administration of diethyl-nitrosamine (DEN) in rats. The morphological changes of the liver tissues in the course of carcinogenesis could be divided into 3 successive stages: the nonspecific changes reacting to the drug toxicity, non-cancerous hyperplastic nodules of hepatocytes and ductular cystadenomatous lesions,and the lesions of genuine malignancy including hepatocellular carcinoma and cholangiocarcinoma.The ultrastructural alterations of hepatocellular carcinoma showed a complicate picture and were related to the differentiation of the tumor cells. In one case of cholangiocarcinoma, numerous cytoplasmic dense-core granules similar to the neurosecretary granules seen in apudoma were found in some of the tumor cells, which is postulated to be a special type of cholangiocarcinoma. On the basis of the results, Ihe histogenesis of the neoplasms after DEN administration is considered to originate from hyperplastic nodules of hepatic cells and ductular hyperplasia.
RESUMEN
The report dealt with the pathological changes in the extrahepatic organs from 30 autopsied cases with clinical manifestations of severe viral hepatitis (SAH) . The main findings were epitomized as follows.(1 ) Brain edema with herniation of tonsil cerebelli in 24 (71%) cases among the 27 whose brains were examined. (2) Bilateral pulmonary edema in 20 (43%) cases among the 28 whose lungs were examined. 45% cases of pulmonary edema were complicated by bronchopneumonia, 10% by fungal infection, and 15% by pulmonary hemorrhage. ( 3 ) Cardiac hypertrophy in ( 43% ) cases among the 28 whose hearts were examined. (4) Biliary nephrosis in 22 (92%) cases among the 24 whose kidneys wers examined. ( 5 ) All the 30 cases showed intestinal congestion and edema throughout the 3 laminae of intestinal wall. (6) of 30 cases, 8 (27%) showed esophageal varicosis. Early hepatic cirrhosis was established in half of the cases. (7) of 29 cases, 25 (85%) had ascitis with various amount of transudate ranging from 2000-8000 ml in adults and 300-1500ml in children. (8) of 30 cases, 4 (13%) had subacute phlegmonous colitis. (9) of 30 cases, 3 (10%) were complicated by the generalizad aspergillosis and/or candiasis involving the lungs, brain, heart, kidneys, intestines, et al.It was considered that the alterations in extrahepatic organs should aggravate the primary disease and thus be prone to increase its motality rate. Some of them, such as brain edema might be the direct cause of death. It was thought that two factors might be responsible for the initiation of extrahepatic alterations. ( 1 ) increase in intrahepatic resistance to the portal blood flow which is presumably due to reduction of hepatic microcirculatory beds, and ( 2 ) hypoxemia which is probably due to intrapulmonary vascular shunts in case of hepatic failure. These factors, once established, might in turn trigger off a sequence of pathological events.
RESUMEN
The report deals with autopsies of 30 hospitalized patients with clinical manifestations of severe viral hepatitis (SVH), who died of hepatic failure. Their age ranged from 8-57 years with an average of 27.9. There were 23 males, and 7 females in the group. The duration of the disease varied with different' , individuals, ranging from 1-96 months. Before onset of SVH, 73.3% of the cases had been afflicted with acute hepatitis or CAH. The clinical' course, therefore, was quite different from that .of fulminat variant.The pathological changes in the livers could be classified into 4 different types: subacute necrotic hepatitis (type Ⅰ ), necro-proliferative hepatitis (type Ⅱ), precirrhotic hepatitis (type Ⅲ), and cirrhotic hepatitis (type Ⅳ). Each of the 4types could be delineated with its own morphological features. However, overlaps in between two successional types (e.g. between type Ⅰ -Ⅱ, etc.) existed/morphology. These facts make it reasonable to postulate that each of the 4 types might represent a different stage in the progress of SVH.