A J. Comp. Path. 1998 Vol. 119, 95 110 Pretelangiectasis and Telangiectasis of the Bovine Liver: a Morphological, Immunohistochemical and Ultrastructural Study P. S. Marcato, G. Bettini, L. Della Salda and M. Galeotti* Department of Veterinar~ Public Health and Animal Pathology, University qf Bolo~na and * l)epartrnen! of Animal Production, University of Udine, Italy Summary Forty-five livers from conventionally slaughtered Holstein-Friesian steers with telangiectasis were studied by histochemical methods, immunolabelling for fibronectin, laminin and type IV collagen, and transmission electron micro- scopy. None of the previously described changes in telangiectasis (necrosis, hepatitis, thromboembolism, dilatation of the space of Disse by glycogen extruded from hepatocytes and reduced density of'the perisinusoidat reticulin framework) were evident. Prelelangiectasis (sinusoidal dilatation) and tel- angiectasis (blood-filled cavities) were characterized by sinusoidal barrier alterations, leading to sinusoidal capillarization; and there was progressive tbrmation t)fa true basement membrane and perisinusoidal fibrosis. Com- parison of bovine liver telangiectasis and human peliosis hepatis suggests that they have a similar pathogenesis. It is suggested that a primary alteration of the sinusoidal barrier is responsible tor an increased deposition of basement membrane components (fibronectin, laminin, type IV collagen) in the peri- sinusoidal region, and fibrosis. These are likely to render the exchange of oxygen and substrates between blood and hepatocytes more difiqcuh and to produce haemodynamic imbalances, leading to hepatocyte atrophy and eventually to sinusoidal disruption. 9 1998W.B. Saunders Company Limited Introduction The pathogenesis of telangiectasis, widely regarded as the most common liver lesion in cattle, is still a matter of debate, the various hypotheses being simplistic, inconclusive or unconfirmed. The ectasias ofsinusoids preceding lacunal dilatation (pretelangiectasis) have been hypothesized to be the result of the following phenomena: hepatocellular necrosis (Jaeger, 1907; Monlux and Monlux, 1972); congenital malformation (Dobberstein, 1936) with abnormal branching of central or sublobular veins, or both (Onda et al., 1982); active return to an embryonic lacunal structure (Carta, 1938); focal necrotizing hepatitis (Getty, 1946); disturbance of the circulatory mechanism originating from splenic compression (Cohrs, 1931); hepatocellular extrusion of periodic acid-Schiff-positive material (glycogen) in Correspondence to: P. S. Marcato, Dipartimento di Sanit/t Pubblica Veterinaria e Patologia Animalc, Sezione di Patologia Generale e Anatomia Patologica Veterinaria, Via Tolara di Sopra 50, 1-40064 Ozzano Emilia, Bologna, Italy. 0021 9975/98/060095 + 16 $12.00/0 9 1998 W.B. Saunders Company Limited