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Title: Schistosomal hepatopathy
Authors: Andrade, Zilton de Araújo
Affilliation: Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.
Abstract: Gross anatomical features and a complex set of vascular changes characterize schistosomal hepatopathy as a peculiar form of chronic liver disease, clinically known as [quot ]hepatosplenic schistosomiasis[quot ]. It differs from hepatic cirrhosis, although clinical and pathological aspects may sometimes induce confusion between these two conditions. Intrahepatic portal vein obstruction and compensatory arterial hypertrophy render the hepatic parenchyma vulnerable to ischemic insult. This may lead to focal necrosis, which may give place to focal post-necrotic scars. These events are of paramount importance for the clinico-pathological evolution of schistosomal hepatopathy. Although portal fibrosis due to schistosomiasis sometimes reveals numerous myofibroblasts, it does not mean that such fibrosis belongs to a peculiar type. Damage to the muscular walls of the portal vein may be followed by dissociation of smooth muscle cells and their transition toward myofibroblasts, which appear only as transient cells in schistosomal portal fibrosis. Studies made with plastic vascular casts, especially those with the murine model of [quot ]pipestem[quot ] fibrosis have helped to reveal the mechanisms involved in systematized portal fibrosis formation. However, the factors involved in the pathogenesis of hepatosplenic disease remain poorly understood. A process of chronic hepatitis is a common accompaniment of portal fibrosis in schistosomiasis. Most of the times it is caused by concomitant viral infection. However, no special interaction seems to exist between schistosomal hepatopathy and viral hepatitis.
Keywords: Schistosomiasis
Schistosoma mansoni
Hepatic fibrosis
Vascular changes
DeCS: Hepatopatias Parasitárias
Esquistossomose mansoni
Issue Date: 2004
Citation: ANDRADE, Z. A. Schistosomal hepatopathy. Memórias do Instituto Oswaldo Cruz, v. 99, p. 51-57, 2004. Suppl 1.
ISSN: 0074-0276
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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