Pathogenesis of schistosomal hepatic fibrosis ("pipestem" fibrosis of the
liver) was investigated by means of the murine model. Although worm load
appears as the main pathogenetic factor, alone it is not sufficient to
produce that characteristic lesion. By comparing the findings in animals
with heavy and prolonged Schistosoma mansoni infection, which developed or
not "pipestem" fibrosis, it was observed that the lesion was more frequent
in intact animals than in the splenectomized one. However, the size of the
spleen, the number of recovered worms, the number of eggs per gram of liver
tissue, the level of serum idiotype and anti-idiotype antibodies, the size
and volume of periovular granulomas formed in the liver, all that failed to
show statistically significant differences between the two groups. After
analysing all these data, other factors, that apparently have been hitherto
negleted, rested to explain the findings. Among them, the timing and
sequence of the egg-induced intrahepatic vascular changes seemed crucial.
The sequential development of intrahepatic portal vein obstruction,
followed by the opening of periportal collateral veins and the continous
arrival of schistosome eggs going to be lodged into the latter, appeared as
essential steps in the pathogenesis of "pipestem" fibrosis.
