Abstract

Septal fibrosis is a common form of hepatic fibrosis, but its etiology and pathogenesis are poorly understood. Rats infected with the helminth Capillaria hepatica constitute a good experimental model of such fibrosis. To investigate the pathogenetic contribution of the several parasitic factors involved, the following procedures were performed in rats: a) regarding the role of eggs, these were isolated and injected either into the peritoneal cavity or directly into the liver parenchyma; b) for worms alone, 15-day-old infection was treated with mebendazole, killing the parasites before oviposition started; c) for both eggs and worms, rats at the 30th day of infection were treated with either mebendazole or ivermectin. Eggs only originated focal fibrosis from cicatricial granulomas, but no septal fibrosis. Worms alone induced a mild degree of perifocal septal fibrosis. Systematized septal fibrosis of the liver, similar to that observed in the infected controls, occurred only in the rats treated with mebendazole or ivermectin, with dead worms and immature eggs in their livers. Thus, future search for fibrogenic factors associated with C. hepatica infection in rats should consider lesions with both eggs and worms.

Highlights

  • Septal fibrosis is a common form of hepatic fibrosis, but its etiology and pathogenesis are poorly understood

  • Immature eggs of C. hepatica injected into the inflammation and fibrosis, involving the mesenteric peritoneal cavity caused local chronic granulomatous fatty tissue

  • A small degree of septal fibrosis formed around dead worm lesions in the liver of animals treated with mebendazole before oviposition

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Summary

Introduction

Septal fibrosis is a common form of hepatic fibrosis, but its etiology and pathogenesis are poorly understood. Septal fibrosis of the liver is characterized by formation of long and thin fibrous septa along the acinar zone III, connecting central veins between them and, later on, to portal spaces, forming bridges It is a peculiar type of hepatic fibrosis, that usually occurs as a mild and nonspecific change in most examples of chronic liver diseases of man, but that may assume prominence and diagnostic significance in cases of incomplete septal cirrhosis[2 10] and chronic septal hepatitis[7]. In 1993, Ferreira and Andrade[5] observed that rats infected with the helminth Capillaria hepatica regularly developed septal fibrosis of the liver, exhibiting a picture similar to that obtained with repeated pig-serum administration. When all worms are dead and disintegrating and the focal encapsulated lesions are undergoing resorption, septal fibrosis starts its progressive course, eventually evolving toward cirrhosis

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