Ammonia Metabolism and Hepatic Coma in Hepatosplenic Schistosomiasis

Abstract

Hepatosplenic schistosomiasis, a widespread disease syndrome in large areas of the tropics, is a relatively unique clinical and pathophysiological entity. Extensive portal-systemic collateral circulation in the presence of only minimal liver parenchymal damage is frequently encountered (1-4). Other forms of chronic intrahepatic liver disease are more complicated, in that they are a combination of both circulatory derangements and hepatocellular malfunction (5). Clinical investigation of patients with hepatosplenic schistosomiasis should offer an opportunity to dissociate the effects of collateral circulation and parenchymal damage and thus elucidate some of the physiological and biochemical problems that are encountered in chronic liver disease. The