199 resultados para Portal de Busca Integrada


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FUNDAMENTO: O ecoDopplecardiograma (Eco) tem-se firmado como método não invasivo de excelente acurácia no rastreio de hipertensão portopulmonar (HPP) e pesquisa dos shunts intrapulmonares (SIP) na doença hepática crônica (DHC). Nesta última década, concretizou-se o Eco como de fundamental importância no diagnóstico da cardiomiopatia cirrótica (CMC). OBJETIVO: Realizar uma revisão sistemática envolvendo artigos relevantes sobre a temática: o Eco na DHC. MÉTODOS: Em novembro de 2011, realizou-se uma revisão sistemática a partir das bases de dados da Pubmed, LILACS e SciELO, sendo relatadas as características dos estudos selecionados. RESULTADOS: Foram encontrados 204 artigos a partir da busca de descritores e um termo livre, sendo 179 da Pubmed, 21 da LILACS e 01 da SciELO. Destes, foram selecionados 22 artigos para revisão sistemática, não sendo possível, pois, fazer uma meta-análise devido à heterogeneidade dos mesmos. CONCLUSÃO: O Eco deve fazer parte da estratificação da DHC para o rastreio de HPP, SIP e da CMC, já que a maioria das vezes, o diagnóstico dessas complicações ocorre nos pacientes na fila de transplante hepático.

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In recent years, one of the most significant progress in the understanding of liver diseases was the demonstration that liver fibrosis is a dynamic process resulting from a balance between synthesis and degradation of several matrix components, collagen in particular. Thus, fibrosis has been found to be a very early event during liver diseases, be it of toxic, viral or parasitic origin, and to be spontaneously reversible, either partially or totally. In liver fibrosis cell matrix interactions are dependent on the existence of the many factors (sometimes acting in combination) which produce the same events at the cellular and molecular levels. These events are: (i) the recruitment of fiber-producing cells, (ii) their proliferation, (iii) the secretion of matrix constituents of the extracellular matrix, and (iv) the remodeling and degradation of the newly formed matrix. All these events represent, at least in principle, a target for a therapeutic intervention aimed at influencing the experimentally induced hepatic fibrosis. In this context, hepatosplenic schistosomiasis is of particular interest, being an immune cell-mediated granulomatous disease and a model of liver fibrosis allowing extensive studies in human and animals as well as providing original in vitro models.

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Ultrasonography can reveal most of the manifestations of portal hypertension complicating hepatosplenic, schistosomiasis. However, direct demonstration of gastroesophageal varices by ultrasonography is still very difficult. An attempt was done to correlate sonographic features of portal hypertension with the degree of fibrosis to screen patients having varices and predicting their chance of bleeding. The results obtained were found to be consistent with the esophagogastric endoscopy and with history of hematemesis. Four parameters were used, size of spleen, degree of periportal fibrosis, presence of collaterals and portal vein diameter. A pilot field survey was also done adopting the same principle.

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In heavily infected young patients, there is a "non-congestive" phase of the disease with splenomegaly which can improve after chemoterapy. A strong correlation between hepatosplenic form and worm burden in young patients has been repeatedly shown. The pattern of vascular intrhepatic 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 "functional deviation"of arterial blood to the splenic territory. The best results obtained in treatment of portal hypertension were: esophagogastric desvascularization 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 esophageal varices bleeding are treated by EGDS and, if rebleeding occurs, by sclerosis of the varices.

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There are over 100.000 patients affected by schistosomotic portal hipertension, that may suffer rupture of the esophageal varices. Besides the portal hypertension, local factors must be emphazised as responsible for the three distal centimeters of the esophagus, called "zona vulnerável" (vulnerable zone). The beter liver functional reserve of these schistosomotic patients as compared to the cirrhotic, present two favorable condititions: (1) beter possibility of conservative treatment during acute hemorrhage; (2) elective surgical treatment may be undergo without a mandatory step of large portal descompression. The Author only indicate surgical treatment in patients with hemorrhage antecedence and his preference consist in splenectomy plus obliterative suture of the varices at the "vulnerable zone" and when possible, ligature of left gastric vein also; 358 patients were undergone surgery with operative mortality 3.07%, 347 were followed during 1 to 25 years; late mortality 8.38%; recurrence hemorrage 11.58%; none porto-sustemic encephalopaty was observed.

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In chronic severe infection with Schistosoma mansoni, portal hypertension and related vascular alterations usually develop as a consequence of granulomatous response to eggs. In order to investigate a putative direct effect of worms on the reactivity of their host portal vein, mice infected only with male worms were used in the present study. An higher reactivity to 5-hydroxytryptamine (5-HT) characterized by an increase in the maximal contraction and sensitivity was observed in portal vein from infected mice compared to healthy mice. Blockade of NO-synthase with l-NAME induced a small increase in 5-HT potency in portal vein from non-infected mice without changing the amplitude of the contractions, whereas it did not alter the reactivity of veins from infected mice. The present results show that unisexual infection of mice with male S. mansoni increased the reactivity of the portal vein to 5-HT which seems to be partially related to an alteration in the nitric oxide release by endothelium.

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Myofibroblasts, cells with intermediate features between smooth muscle cells and fibroblasts, have been described as an important cellular component of schistosomal portal fibrosis. The origin, distribution and fate of myofibroblasts were investigated by means of light, fluorescent, immunoenzymatic and ultrastructural techniques in wedge liver biopsies from 68 patients with the hepatosplenic form of schistosomiasis. Results demonstrated that the presence of myofibroblasts varied considerably from case to case and was always related to smooth muscle cell dispersion, which occurred around medium-sized damaged portal vein branches. By sequential observation of several cases, it was evident that myofibroblasts derived by differentiation of vascular smooth muscle and gradually tended to disappear, some of them further differentiating into fibroblasts. Thus, in schistosomal pipestem fibrosis myofibroblasts appear as transient cells, focally accumulated around damaged portal vein branches, and do not seem to have by themselves any important participation in the pathogenesis of hepatosplenic schistosomiasis.

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The study had the objective to evaluate the benefits of surgical indication for portal hypertension in schistosomiasis patients followed from 1985 to 2001. Schistosoma mansoni eggs were confirmed by at least six stool examinations or rectal biopsy. Clinical examination, abdominal ultrasonography, and digestive endoscopy confirmed the diagnosis of esophageal varices. A hundred and two patients, 61.3% male (14-53 years old) were studied. Digestive hemorrhage, hypersplenism, left hypochondrial pain, abdominal discomfort, and hypogonadism were, in a decreasing order, the major signs and symptoms determining surgical indication. Among the surgical techniques employed, either splenectomy associated to splenorenal anastomosis or azigoportal desvascularization, esophageal gastric descompression and esophageal sclerosis were used. Follow-up of patients revealed that, independent on the technique utilized, a 9.9% of death occurred, caused mainly by digestive hemorrhage due to the persistence of post-treatment varices. The authors emphasize the benefits of elective surgical indication allowing a normal active life.

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Portal hypertension is a frequent complication of chronic liver disease, detected not only in schistosomiasis, but also in cirrhosis of any etiology. Vascular alterations in the colonic mucosa are a potential source for acute or chronic bleeding and have been observed in patients with portal hypertension. The purpose of this prospective study was to describe and propose a classification for the vascular alterations of portal hypertension in the colonic mucosa among patients with hepatosplenic schistosomiasis mansoni. One or more alterations of portal colopathy were observed in all patients and they were classified according to their intensity, obeying the classification proposed by the authors. Portal colopathy is an important finding in hepatosplenic schistosomiasis and might be the cause of lower gastrointestinal bleeding in patients with severe portal hypertension.

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Previous studies in mice with hypervitaminosis A have demonstrated that fat-storing cells (hepatic stellate cells-HSCs) participate in schistosomal granuloma fibrogenesis. The origin of such cells in portal areas, away from the Disse spaces, was herein investigated. HSCs were identified in frozen sections of the liver by means of Sudan III staining. They appeared as red-stained cells disposed along the sinusoids of normal mice, but were never found within portal spaces. However, in the chronically inflamed portal spaces of Capillaria hepatica-infected mice, Sudan III-positive cells were frequently present among leukocytes and fibroblast-like cells. Thus, there are no resident HSCs in portal spaces, but their presence there in chronic inflammatory processes indicates that they are able to migrate from peri-sinusoidal areas in order to reach the portal areas.