RESUMO
1. The single leading cause of death among 81 autopsied cases of parasitic cirrhosis caused by Schistosoma Japonica was massive upper gastrointestinal hemorrhage from ruptured gastroesophageal varices. Only one patient died from hepatic insufficiency. The changes seen in the liver of autopsy were those of fibrosis of the portal tracts, with very minimal parenchymal damage and distortion of the lobular architecture2. The clinical features, liver function tests, hepatic wedge and splenic pulp pressures, splenoportography, and liver biopsies of 16 patients with parasitic cirrhosis secondary to Schistosoma Japonica were reviewed. Clinically, these patients presented the problem of portal hypertension. Standard liver function tests revealed very insignificant impairment of parenchymal hepatic function. The wedged hepatic vein pressures were found to be normal, while the splenic pulp pressures were markedly elevated. A significant pressure gradient between the splenic pulp and hepatic wedge pressures was demonstrated. Splenoportography revealed evidences of portal hypertension, with no obstruction of the extrahepatic portal venous system. Liver biopsy showed deposition of Schistosoma ova with varying degrees of portal and periportal fibrosis3. A correlation between the clinical, hemodynamic and morphologic changes in parasitic cirrhosis was made. The morphologic aberration in parasitic cirrhosis was demonstrated to be fibrosis of the intrahepatic radicles of the portal vein, resulting in intrahepatic presinusoidal portal hypertension. There was very minimal damage to the liver cells, and hence hepatic perenchymal function remained essentially intact. (Summary)