Histologic Observations in Human Hepatitis Non-A, Non-B

Abstract

Specimens from 57 patients with acute or chronic hepatitis non-A, non-B (HNANB), mostly mild to moderate, were studied by light and, in 22 instances, by electron microscopy. They were compared to specimens of hepatitis A and hepatitis B on file or obtained simultaneously with the HNANB cases. In the HNANB material, two types of light-microscopic lesions were noted in the lobular parenchyma singly or in combination. One was an eosinophilic alteration of the hepatocytic cytoplasm associated with many acidophilic bodies. Conspicuous alteration were often accompanied by microvesicular steatosis. This lesion was associated with nuclear particles detectable by electron microscopy. The second lesion consisted of sinusoidal cell activation which was prominent in some cases. From experiences with chimpanzees, these features were tentatively considered to be stages of the same process. Both lesions were associated with portal and usually mild periportal inflammation which was not related to the degree and type of parenchymal reaction. They were also observed in chronic stages, making the differentiation between acute and chronic HNANB difficult. Active hepatitis B seems to differ from HNANB primarily by the conspicuous presence of lymphocytes in the lobular parenchyma often in contact with hepatocytes, acidophilic bodies, and a more uniform portal inflammatory reaction. In hepatitis A, hepatocellular injury was conspicuously periportal. In HNANB, a cytopathic effect rather than lymphocytic immune attack appears to be of greater significance than in the other forms of viral hepatitis. The recurrence of lobular mainly eosinophilic changes may explain chronicity.

Abnormalities of lipid metabolism in hepatitis C virus infection

“…If all these factors of fatty liver are excluded, the prevalence of steatosis in chronic hepatitis C is still approximately 40%—that is, about a twofold increase compared with chronic hepatitis B 66 67. This suggests that HCV may directly cause fatty liver, at least in a subgroup of patients with chronic hepatitis C. Indeed, the association is so strong that in the pre-serology era it was used as a diagnostic tool to identify patients with chronic non-A, non-B hepatitis 68 69…”

Significance of apoptotic cell death in systemic complications with severe acute pancreatitis

“…26 The increase of serum lactate dehydrogenase in severe acute pancreatitis suggests latent liver damage and was reported to correlate with mortality. 27 Hepatocyte apoptosis has been observed in various disease conditions, such as viral or chemical hepatitis, 28 allograft rejection, 29 portal vein ligation, 30 and ischemic-reperfusion injury. 31 In particular, Bohlinger et al 11 reported that hepatocyte apoptosis was induced in mice with endotoxin shock.…”

Hepatitis C Virus, Cholesterol and Lipoproteins — Impact for the Viral Life Cycle and Pathogenesis of Liver Disease

“…Most notably, the accumulation of neutral lipids in cytosolic lipid droplets in hepatocytes was defined as a pathologic hallmark of hepatitis C virus infection [8]. Early biophysical characterizations of virus particles in patient serum also revealed the virus to be highly heterogenous in buoyant density due to association with host lipoproteins [9,10].…”