Early alcoholic liver injury: changes of the Disse space in acinar zone 3
Thomas Horn, Jette Junge, Per Christoffersen
Abstract
Thomas Horn, Jette Junge, Per Christoffersen
Abstract
One hundred and twelve consecutive liver biopsies were studied by transmission electron microscopy. In 18 out of 23 biopsies from chronic alcoholics showing preserved architecture by light microscopy, basal laminas were found in acinar zone 3 applied to endothelial cells as well as to hepatocytes. Basal laminas occurred independently of Mallory bodies and lipogranulomas, and were observed even in cases where light microscopy showed no fibrosis in zone 3. In addition to basal laminas, deposition of collagen and defenestration of the endothelial cells were observed. Basal laminas were seen only rarely in biopsies from non-alcoholics. We suggest that basal lamina formation in acinar zone 3 is initiated by changes in the perisinusoidal space and that it may contribute to impaired liver cell function and possibly initiate liver cell necrosis.
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One hundred and twelve consecutive liver biopsies were studied by transmission electron microscopy. In 18 out of 23 biopsies from chronic alcoholics showing preserved architecture by light microscopy, basal laminas were found in acinar zone 3 applied to endothelial cells as well as to hepatocytes. Basal laminas occurred independently of Mallory bodies and lipogranulomas, and were observed even in cases where light microscopy showed no fibrosis in zone 3. In addition to basal laminas, deposition of collagen and defenestration of the endothelial cells were observed. Basal laminas were seen only rarely in biopsies from non-alcoholics. We suggest that basal lamina formation in acinar zone 3 is initiated by changes in the perisinusoidal space and that it may contribute to impaired liver cell function and possibly initiate liver cell necrosis.
Key concepts: Perisinusoidal space, Basal lamina, Pathology, Basal (medicine), Sinusoid, Fibrosis, Alcoholic liver disease, Lobules of liver