ESQUISTOSSOMOSE MANSONI

Abstract

The author reports 28 cases of schistosomiasis mansoni with liver and spleen involvement and reviews the clinicai and the laboratory data. He emphasizes particularly the results of the liver function tests, serum protein and its fractions - albumin and globulin and the hematological findings. Special references were made regarding the radiological and esophagoscopic examinations for esophageal varices and be pointed out that sometimes contradictory results were obtained 16 patients were submitted to splenectomy and 12 to splenectomy plus splenorenal anastomosis. The A. tried to correlate the portal hypertension, measured during the opera tive act and the clinicai findings: esophageal varices, hematemesis, ascitis, hypoproteinemia; he studied ais o the degree of portal hypertension and the size of the spleen and the degree of histopathological alterations of liver ( operatory biopsy) and spleen.In his final considerations the A. states. The 28 cases studied represent the average of cases of schistosomiasis mansoni with liver and spleen involvement. They show hence what fundamental the disease of Manson-Pirajá da Silva with spleen and liver involvement has on its clinicai, functional pathogenical and histopathological aspects. The liver and spleen enlargement, the past and present intestinal symptoms, the functional involvement of the liver as indicated by the laboratory tests, the portal hypertension and its after effects, the hyper splenism caracterized not only by the enlargement of the spleen but mainly by the blood citopenias (and bone marrow picture as we demonstrated earlier) and corrected as known by splenectomy, the histopathological lesions of the liver and the spleen, emphasize the multiple elements that caracterize the schistosomiasis mansoni with liver and spleen involvement. The analysis of the above data in the 28 cases studied furnished the elements for a tentative pathogenical interpretation of the role of the liver and spleen in this clinicai variety of schistosomosis mansoni and confirmed conclusions of a former study which is referred to later in this summary. The study of the histopathological alterations of the liver in the schistosomiasis mansoni, in vivo, by means of operatory liver biopsy permited the A. to appreciate the biology of the lesions course from the early through the final stages, anel to correlate them with the clinicai manifestations of the disease. In many instances there is no corresponelence between the liver histological picture anel the degree of portal hypertension, anel on the other hand the lesions in certain cases are limiteel to some circunscribeel hepatic fibrosis ( precirrhosis) while the alterations in the spleen are much aelvanced(in its late stage it is called chronic sclero congestive splenomegaly), being impossible in an unselecteel case to preelict with certainty the elegree of splenomegaly by the microscopic examination of the liver. The A. suggest the following anatomico-clinical phases of the disease:1) hepato-lienal fibrosis, the anatomico-clinical picture being one of hepatic splenomegalic cirrhosis.2) fibrocongestive splenomegaly with discrete hepatic lesions of the precirrhosis type ( precirrhotic Banti'sinelrome).3) the terminal picture of the schistosomiasis mansoni with liver and spleen involvement represents the last phase of a long anel progressive process with clinicai manifestations comparable to the cirrhosis of the portal type. Clinically the hepatolienal phase proceeeling the terminal perioel of the disease is already anel early hepatic cirrhosis of the portal type associated with splenopathy although from the histopathological point of view the hepatic lesions do not correspond to the clear cut lesions of liver cirrhosis but to the picture of precirrhosis or incipient cirrhosis. 4) the degree anel the extension o f the hepatic lesions do not expia in all the cases of schistosomiasis splenomegaly. 5) in certa in cases portal hypertension may occur with no hepatic lesions anel presumably be able to originate portal intra hepatic obstacle according to the current accepted histopathological knowledge. These cases may indicate a possible genesis of the splenomegaly as a functional disturbance of the regulactions flow of the blood in and out the spleen causing the portal hypertension. 6) it may be found splenomegaly fibrocongestive type without portal hypertension.7) in every case of schistosomiasis splenomegaly we found the existence of hepatic lesions although they may be discrete (precirrhosis). 8) the schistosomiasis splenomegaly is secondary or concomitant to the hepatic lesion and also it may occur with celular infiltration of the liver without any obstructive vascular lesion. The splenopathy features may nevertheless predominate in the anatomico-clinical picture of hepatolienal schistosomiasis mansoni. 9) one must admit that in the mechanism of the hepatosplenopaty in the schistosomiasis mansoni plays three orders of factors, considering the phisiopathology unity of the two organs involved: a) schistosomiasis hepatic lesions causing spleen alteration through portal hypertension. b) schistosomiasis hepatic Jesions causing spleen alterations presumably through disturbances of the regulation flow of blood in and out of the spleen. c) a toxin action of Schistosoma IIUlnsoni directly on the spleen probably disturbing its caudal circulation. These factors vary in individual cases and adding action of the three factors may be present in advanced stages of the disease. 10) when portal hypertension coexist with fibrocongestive splenic Jesion with hepatic lesion of the infiltration type without obstructive vascular lesion one must admit a splenic origin for the portal hypertension through an unknown mechanism but in which may participate the vascular connective structures of the spleen damaged by noxious substances of a by-product of the helminths.