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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Histopathology 13 (1988), S. 0 
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have reviewed 60 liver specimens from 47 patients with the diagnosis of incomplete septal cirrhosis observed between 1968 and 1987. In reaching this diagnosis evaluation of the following histological features appeared to be helpful: parenchymal nodularity, thin incomplete septa, hypoplastic portal tracts, increased number of venous channels, abnormal spacing between portal tracts and veins, crowding of reticulin fibres between adjacent zones of hyperplastic parenchyma, hyperplasia of hepatocytes and dilated sinusoids. These histological features were not specific for incomplete septal cirrhosis as they were also present–although less evident and less frequent–in a series of 87 non-cirrhotic liver specimens. Reticulin stains were an essential adjunct to assess the architectural disturbance, which was often inconspicuous in needle biopsies. Histological features indicating a specific aetiology were lacking in the great majority of cases. On histological and clinical grounds, incomplete septal cirrhosis resembles idiopathic portal hypertension, nodular regenerative hyperplasia and partial nodular transformation; in these entities an obliterative portal venopathy with non-uniformity of portal blood supply to the parenchyma has been suggested as a pathogenic mechanism. In the present study phlebosclerotic lesions of the portal vein were found in only two cases. This might be explained by sampling error or, alternatively, the hypoplastic portal tracts observed might be a functional equivalent of obliterative portal venopathy resulting in a deficient portal blood supply. Non-uniformity of blood supply to the parenchyma may explain the similarities between incomplete septal cirrhosis and the diseases mentioned.
    Type of Medium: Electronic Resource
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