The structural basis of altered hepatic function in viral hepatitis

Abstract

The electron microscopic study of liver tissue in viral hepatitis has yielded greater understanding of the light microscopic changes and has permitted some extrapolation to provide a morphologic basis of altered hepatic function; this, despite the fact that electron microscopic findings in viral hepatitis are less striking than those of light microscopy. The decrease in hepatic function is less the result of a decrease in the mass of functioning hepatic tissue, but rather more the result of impaired and ineffective function of surviving cells. Most responsible for reduced hepatic function are injury to the hepatocellular endoplasmic reticulum and impaired blood exchange in the liver, partly because of a larger barrier between the blood and the liver cells, partly because of impaired blood flow owing to the presence of inflammatory cells in and around sinusoids. Cholestasis is a factor leading to jaundice. The etiologic agent has not been identified in the liver, but the description of hepatitis-associated antigen an the finding of unidentified particles in nuclei may be the keys to the riddle of the etiology of the disease. The electron microscope has also provided evidence that all is not viral hepatitis that looks like it with the light microscope. The electron microscopic study of liver tissue in viral hepatitis has yielded greater understanding of the light microscopic changes and has permitted some extrapolation to provide a morphologic basis of altered hepatic function; this, despite the fact that electron microscopic findings in viral hepatitis are less striking than those of light microscopy. The decrease in hepatic function is less the result of a decrease in the mass of functioning hepatic tissue, but rather more the result of impaired and ineffective function of surviving cells. Most responsible for reduced hepatic function are injury to the hepatocellular endoplasmic reticulum and impaired blood exchange in the liver, partly because of a larger barrier between the blood and the liver cells, partly because of impaired blood flow owing to the presence of inflammatory cells in and around sinusoids. Cholestasis is a factor leading to jaundice. The etiologic agent has not been identified in the liver, but the description of hepatitis-associated antigen an the finding of unidentified particles in nuclei may be the keys to the riddle of the etiology of the disease. The electron microscope has also provided evidence that all is not viral hepatitis that looks like it with the light microscope.