Cases reported "Liver Cirrhosis"

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1/4. Hepatic hypervitaminosis a: a familial observation.

    Four siblings with hepatic fibrosis are described. The liver damage in these patients was secondary to chronic ingestion of massive doses of vitamin a for congenital ichthyosis. Although the extrahepatic manifestations were helpful in the diagnosis of hypervitaminosis a, the distinctive features of hepatic histopathology were confirmatory. The plasma concentrations of vitamin a and retinol-binding protein were misleading. The recovery from the liver damage in these patients was slow despite a complete withdrawal of the vitamin a intake. These cases show the importance of hepatic vitamin a assessment in the diagnosis of hepatic fibrosis.
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2/4. Hepatic and dermatologic manifestations of chronic hypervitaminosis a in adults. Report of two cases.

    Chronic hypervitaminosis a in adults is a clinical syndrome that can develop over varying periods of time depending on the average daily intake of vitamin a. Two adult cases of chronic hypervitaminosis a are described and illustrate this diverse dosage-duration relationship. Hepatic cirrhosis developed as a manifestation of vitamin a toxicity in one of the patients; this appears to be the first reported case of chronic hypervitaminosis a in an adult induced by the long-term frequent ingestion of beef liver.
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3/4. Chance discovery of hepatic fibrosis in patient with asymptomatic hypervitaminosis a.

    A liver biopsy specimen was obtained from a 50-year-old patient whose clinical and functional liver tests showed no abnormalities but who had for some time a high vitamin a intake (109 X 10(6) IU over four years). liver architecture was normal. Sinusoids were slightly dilated in zone 2. Perisinusoidal cells were numerous and enlarged. On Sirius red staining, there was mild fibrosis of the central veins, portal tracts, and terminal portal venules and perisinusoidal fibrosis in zone 1 of the acinus. liver vitamin a level was increased. By electron microscopy, perisinusoidal cells filled with numerous lipid droplets had slightly dilated rough endoplasmic reticulum, numerous minute filament condensations below the plasma membrane, and stellate-shaped processes giving them the appearance of fibroblast-myofibroblast-like cells. Numerous collagen bundles, fibrils, amorphous material, and fragments of basement membrane-like material were identified in Disse's space. Immunocytochemistry showed increased amounts of collagen types I, III, IV, laminin, and fibronectin. This observation suggests that vitamin a per se, and not the cellular damage often seen in hypervitaminosis a, is responsible for fibrosis.
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4/4. Chronic hypervitaminosis a.

    A case of chronic hypervitaminosis a in a 51-year-old female is discussed. The patient was ingesting 27,500--35,000 international units of vitamin a daily for 30 years. The patient displayed the classic symptoms of the disease, including skin and hair changes, esophageal varices and extensive liver disease. vitamin a products were discontinued and the patient's dietary intake of the vitamin was minimized. Previous reports and studies of hypervitaminosis a are reviewed. Social factors causing increased consumption of vitamin a and regulations governing the sale of vitamin a are discussed. By being aware of the factors influencing vitamin a consumption, hypervitaminosis a can be detected and prevented more readily.
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