Hyperplasia of elastic tissue in hepatic schistosomal fibrosis

Abstract

Elastic tissue hyperplasia, revealed by means of histological, immunocytochemical and ultra-structural methods, appeared as a prominent change in surgical liver biopsies taken from 61 patients with schistosomal periportal and septal fibrosis. Such hyperplasia was absent in experimental murine schistosomiasis, including mice with "pipe-stem" fibrosis. Displaced connective tissue cells in periportal areas, such as smooth muscle cells, more frequently observed in human material, could be the site of excessive elastin synthesis, and could explain the differences observed in human and experimental materials. Elastic tissue, sometimes represented by its microfibrillar components, also appeared to be more condensed in areas of matrix (collagen) degradation, suggesting a participation of this tissue in the remodelling of the extracellular matrix. By its rectratile properties elastic tissue hyperplasia in hepatic schistosomiasis can cause vascular narrowing and thus play a role in the pathogenesis of portal hypertension.

Histopathological study of Schistosoma mansoni infection in the murine model using the PC (Pará) and LILA (Maranhão) strains

“…These were notably absent in the acute and intermediate phases of infection. The results of our studies were similar to those of Andrade and Freitas (1991), namely, with no picture of elastic hyperplasia throughout the experiment. In fact, the involvement of elastic fibers in portal hypertension has not yet been shown with absolute precision in hypertension portal pathogenesis of the murine model.…”

“…In the work published by Andrade and Freitas (1991), the elastic hyperplasia, which is frequently observed in hepatic biopsies of hepatosplenic patients, can play an important role in pathogenesis of portal hypertension and remodeling of the extracellular matrix. This picture differs from that recorded by Silva et al (2000), who were able to detect discrete elastic fibers in some hepatic granulomas of a few infected mice, in the chronic phase of the experiment.…”

Portal hypertension in Williams syndrome: Report of two patients

“…This structural specificity is directed to maintain an open lumen and a large enough blood reservoir to be “filtered” at the liver inspite of the positive intra‐abdominal pressures that would easily lead to venous collapse in the absence of these thick elastic components. Several animal and human studies have described the elastic components of the hepatic and portal vein tissues in normal subjects of different species [Porto et al, 1990] and various types of human liver disease such as schistosomiasis [Andrade and Freitas, 1991], alcoholic liver disease [Porto et al, 1990], liver fibrosis [Sato et al, 2000], and idiopathic portal hypertension [Crissman and Guilford, 1984; Kage et al, 1990]. Primary or idiopathic portal hypertension is characterized by thickening of the venous wall, partly due to excessive proliferation and disorganization of the elastic lamellae.…”

Significance of schistosomal granuloma modulation

“…As a matter of fact, elastic fibers (elastin) were found only in hepatic granulomas, and exclusively during the chronic stage of infection, but that finding was the only one which was qualitatively different from the granulomas formed elsewhere. Although elastic fibers were abundant in portal space fibrosis due to schistosomiasis in man, periovular granulomas were said to be devoid of such fibers (Junqueira et al 1986, Andrade & Freitas 1991. Anyway, quantitatively, the large amount of extracellular matrix found in hepatic granulomas was the main change responsible for the morphologic aspects of modulation.…”