Immunohistochemical localization of collagen type III and type IV, laminin, tenascin and alpha-smooth muscle actin (alphaSMA) in the human liver in peliosis.

The expression of collagen types III and IV, laminin, tenascin, and hepatic stellate cells (HSCs) activation marker alphaSMA was evaluated immunohistochemically in the liver of three patients with non-bacilar peliosis. Peliosis was attributed to tuberculosis, endometriosis treated with anabolic androgenic steroids, and to pheochromocytoma. Ultrastructural examination of the lesions of the liver revealed cavities that were sometimes lined with sinusoidal endothelial cells or hepatocytic microvilli. In liver sinusoids around cavities, cystic dilatation of the space of Disse and an abundance of amorphous matrix were observed. At this location, HSCs were transformed into transitional cells or myofibroblasts. Extracellular matrix proteins (ECM) were increased in the dilated sinusoids around cavities perisinusoidally and in the wall of cavities themselves. AlphaSMA was also increased. Ultrastructural immunohistochemistry revealed strong intracellular deposits of collagen type IV, laminin, and alphaSMA in HSCs. Laminin immunoreactivity was also noted in the endocytic vesicles in the cytoplasm of a monocyte. These findings suggest that enhanced ECM accumulation and the transformation of HSCs into myofibroblasts constitute a secondary event in peliosis and an attempt of the liver to restrict and remove sinusoidal dilatation.