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Contributed
by Randall G. Lee, M.D.
Comment:
The histologic changes do no definitively point to a
particular etiology, but the degree of inflammatory activity, the presence of
focal confluent parenchymal collapse, and the plasma cell-rich infiltrate all
suggest the possibility of autoimmune hepatitis. Other causes of chronic
hepatitis such as the hepatitis viruses and drugs should also be considered,
however.
Previous Biopsies on this Patient:
None
TPIS Related Resources:
Liver
Transplant Topics
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The liver biopsy shows generally intact lobular landmarks, but there is considerable portal expansion and inflammation with zones of bridging fibrosis. In one portion of the biopsy there has been apparent panlobular parenchymal collapse with fibrosis. The portal areas contain a moderate predominantly mononuclear infiltrate containing numerous scattered and clustered plasma cells. This is associated with obvious piecemeal necrosis of moderate degree. Bile ductular proliferation is patchy and minor and there are a few associated neutrophils and eosinophils. Intralobular bile ducts are intact and show mild focal injury, but no florid duct lesions or granulomatous cholangitis is seen. The parenchyma demonstrates mild mononuclear infiltrate associated with focal necroses and a more diffusely distributed liver cell swelling. There is mild macrovesicular steatosis and occasional hepatocytes contain glycogenated nuclei. The architectural distortion is well demonstrated in trichrome and reticulin stains. The PAS stain is not diastase pretreated, but appears to show no positive staining globules. The iron stain demonstrates a few kupffer cells with positive staining, but no significant hepatocellular accumulation. No ground glass hepatocytes, viral inclusions or other pigment deposition is seen.
Overall, the changes are those a active chronic hepatitis that has progressed with piecemeal and confluent necrosis to bridging fibrosis. Early architectural distortion has appeared but cirrhosis has not yet developed. Several of the findings in the biopsy suggest autoimmune hepatitis as the underlying cause of the chronic hepatitis. This should be correlated with serologic and laboratory data. In addition, of course, other causes of chronic hepatitis such as hepatitis viruses, drugs should be excluded. The histologic activity index is assessed as follows:
| KNODELL'S HISTOLOGY ACTIVITY INDEX | ||
|---|---|---|
| Feature | RANGE | SCORE |
| Periportal and bridging necrosis | (0-10) | 5 |
| Intralobular degeneration and necrosis | (0-4) | 3 |
| Portal inflammation | (0-4) | 3 |
| Fibrosis | (0-4) | 3 |
| TOTAL | (0-22) | 14/22 |
The numerical scoring system of histologic activity index (HAI) has been developed to grade the liver biopsies of chronic active hepatitis. This is based on four categories of periportal and bridging necrosis, intralobular degeneration and necrosis, portal inflammation and fibrosis, with total score of up to 22. This scoring system is correlated well with the severity of disease. A copy of the original paper published by the American Association for the Study of Liver Disease [Hepatology 1:431, 1981] is available at the Department of Pathology upon request.