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Hepatocellular Hyalin in Cholestasis and Cirrhosis: Its Diagnostic Significance

  • Michael A. Gerber
    Correspondence
    Address requests for reprints to: Dr. Michael A. Gerber, Department of Pathology, Mount Sinai Hospital, 100th Street and Fifth Avenue, New York, New York 10029.
    Affiliations
    The Stratton Laboratory for the Study of Liver Disease, Department of Pathology Mount Sinai School of Medicine of The City University of New York, New York, New York
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  • William Orr
    Affiliations
    The Stratton Laboratory for the Study of Liver Disease, Department of Pathology Mount Sinai School of Medicine of The City University of New York, New York, New York
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  • Helmut Denk
    Affiliations
    The Stratton Laboratory for the Study of Liver Disease, Department of Pathology Mount Sinai School of Medicine of The City University of New York, New York, New York
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  • Fenton Schaffner
    Affiliations
    The Stratton Laboratory for the Study of Liver Disease, Department of Pathology Mount Sinai School of Medicine of The City University of New York, New York, New York
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  • Hans Popper
    Affiliations
    The Stratton Laboratory for the Study of Liver Disease, Department of Pathology Mount Sinai School of Medicine of The City University of New York, New York, New York
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      Liver tissue of patients with various stages of alcoholic liver injury, with cholestatic liver diseases and with various types of cirrhosis, were examined for the presence of hyalin, mainly by light microscopy and, in selected instances, also by electron microscopy. Hyalin was detected in alcoholic liver disease and in prolonged cholestasis, mainly in primary biliary cirrhosis. It was not found in diseases in which cholestasis was of shorter duration and was predominantly central in location. Electron microscopically, hyalin was identical in alcoholic hepatitis and in primary biliary cirrhosis, although the pattern of injury of hepatocytic organelles was different in these diseases. A morphologic relation between hyalin and cholestasis or any other hepatocellular abnormalities could not be detected. Hyalin was also found in advanced nonalcoholic cirrhosis, in Wilson's disease, and in Indian childhood cirrhosis, and with the exception of the last, it was always associated with peripheral cholestasis. Centrolobular hyalin in specimens with intact lobular architecture is diagnostic for alcoholic liver injury. Peripheral hyalin in the absence of cirrhosis favors primary biliary cirrhosis over extrahepatic biliary obstruction. Hyalin throughout nodules in advanced cirrhosis does not necessarily indicate alcoholic liver disease, Wilson's disease, or Indian childhood cirrhosis, but also occurs in “cryptogenic” cirrhosis.

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