Hepatic mesenchymal cell reaction in liver disease

Conventional light microscopic observation of the mesenchymal cells and of the sinusoidal wall in various types of human liver injury were supplemented by histochemical, electron microscopic, and immunocytochemical investigations. The cells were subdivided into endothelial, phagocytic, protein-forming, fibroblastic, and hematic cells on the basis of structural characteristics. Although transitions between endothelial and phagocytic cells, as well as between protein-forming and phagocytic cells, are suggested, the division presented does not necessarily imply postembryonal derivation from a single precursor reticulum cell but could also be explained by different cell lines proliferating as a result of stimulation. The same types of cells are found in the parenchyma around hepatic necrosis and granulomas as well as in portal tracts and in septa of cirrhosis. The criteria used for phagocytosis were lipofuscin pigment, PAS reaction, acid phosphatase reaction, and phagosomes. For protein formation the criteria were gamma globulin localization and abundant endoplasmic reticulum. For fibroplasia they were electron microscopically characteristic filaments becoming fibers extracellularly. Acute liver cell injury is characterized by proliferation of endothelial and phagocytic cells to which are added protein-forming and fibroblastic cells in chronic injury. Hypergammaglobulinemia and erratic immunologic reactions in cirrhosis were related to activation of the hepatic mesenchyma in chronic liver cell injury. In liver cell injury the tissue space is widened and exhibits accentuated PAS, ATPase, and alkaline phosphatase reaction. Formation of excess fibers in cirrhosis and peripheral “piecemeal” necrosis is eventually followed by formation of a basement membrane in the hepatic sinusoids closing the previously open circulation. The reduced permeability of the sinusoidal wall resulting from an increase in cells and a fibrous barrier with a basement membrane, together with alterations of the hepatocellular microvilli, increases hepatic insufficiency.