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Previous studies have affirmed and denied the importance of obstructive vascular lesions in the pathogenesis of portal hypertension in hepatosplenic schistosomiasis. In addition, the relation between anatomic and hemodynamic alterations has not been adequately explained. In this study, vinylite casts of intrahepatic vessels of cadavers with hepatosplenic schistosomiasis were made and compared with those of cadavers with normal livers and with cirrhosis of the liver. Extensive distortion and obstruction of small portal branches was noted with hepatosplenic schistosomiasis mansoni. These lesions were especially marked in the periphery of the liver, and histological sections from the periphery frequently showed portal tracts in which the portal vein branches were occluded or apparently absent. The rich network of anastamosing venules in the portal spaces was apparently derived from the peribiliary venous plexus. An increase in number and size of intrahepatic arterial branches was marked in cases of hepatosplenic schistosomiasis. Increased arterial supply explains the observed maintenance of normal hepatic blood flow in many patients with this disease. Although the cause of portal hypertension is evident, the pathogenesis of Symmers' clay-pipestem fibrosis of the liver is not. The nearly constant association of Symmers' fibrosis and portal hypertension in schistosomiasis indicates a common, or interrelated, pathogenesis for the obstructive lesions and Symmers' fibrosis.
Formerly Eleanor Roosevelt Cancer Research Fellow, Hospital Prof. Edgard Santos.