PORTAL-HYPERTENSION IN SCHISTOSOMIASIS - PATHOPHYSIOLOGY AND TREATMENT
PORTAL-HYPERTENSION IN SCHISTOSOMIASIS - PATHOPHYSIOLOGY AND TREATMENT
复制标题
DOI:
10.1590/s0074-02761992000800028
复制
发表时间:
1992-01-01
影响因子:
2.8
通讯作者:
DASILVA, LC
中科院分区:
文献类型:
--
作者:
DASILVA, LC
In heavily infected young patients, there is a ''non-congestive'' phase of the disease with splenomegaly which can improve after chemotherapy. A strong correlation between hepatosplenic form and worm burden in young patients has been repeatedly shown. The pattern of vascular intrahepatic lesions, seems to depend on two mechanisms: (a) egg embolization, with a partial blocking of the portal vasculature; (b) the appearance of small portal collaterals along the intrahepatic portal sistem. The role played by hepatitis B virus (HBV) and C virus infections in the pathogenesis of liver lesions is variably considered. Selective arteriography shows a reduced diameter of hepatic artery with thin and arched branches outlining vascular gaps. A rich arterial network, as described in autopsy cases, is usually not seen in vivo, except after splenectomy or shunt surgery. An augmented hepatic arterial flow was demonstrated in infected animals. These facts suggest that the poor intrahepatic arterial vascularization demonstrated by selective arteriography in humans is due to a ''funtional deviation'' of arterial blood to the splenic territory.The best results obtained in treatment of portal hypertension were: esophagogastric devascularization and splenectomy (EGDS), although risk of rebleeding persists; classical (proximal) splenorenal shunt (SRS) should be abandoned; distal splenorenal shunt may complicate with hepatic encephalopaty, although later and in a lower percentage than in SRS. Propranolol is currently under investigation. In our Department, schistosomotic patients with esophagoal varices bleeding are treated by EGDS and, if rebleeding occurs, by sclerosis of the varices.