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Piecemeal necrosis

1. Hepatocyte cytoplasme ingestion

Piecemeal necrosis, currently called interface hepatitis, is a feature of viral hepatitis as well as
autoimmune hepatitis and steatohepatitis.
The mechanism of liver cell loss and piecemeal necrosis needs to be determined…. We hypothesize that
piecemeal necrosis in hepatitis is due to a piecemeal removal of hepatocyte cytoplasm by lymphocytic
ingestion.
To test this hypothesis, 61 consecutive liver biopsies were examined by light microscopy, by
immunohistochemistry and by electron microscopy, and the lymphocytic-hepatocytic interaction was
morphologically assessed.
In cases of hepatitis C, hepatitis B, autoimmune hepatitis, primary biliary cirrhosis, and
steatohepatitis, piecemeal necrosis was found.
Using cytokeratin stains, it was apparent that
1. the lymphocyte-hepatocyte interaction and piecemeal necrosis leads first to binding of the
lymphocyte to hepatocyte plasma membrane
2. and then blebbing or indentation of the hepatocyte by the lymphocyte,
3. followed by endocytosis of liver cell cellular components and digestion in the lymphocyte lysosomes.
4. This process is repeated while the cytoplasm and the nucleus of the hepatocyte disappear bite by
bite, and only nubbins of residual hepatocytic cytoplasm remain, either attached to intact hepatocytes
or surrounded and sequestered within scar tissue and lymphocytes.
We conclude that piecemeal necrosis is a gradual disappearance of hepatocytes as a result of
lymphocyte-hepatocyte binding and ligand internalization of liver surface molecules by the lymphocyte.
This gradual process leads to a slow reduction of hepatocyte size and eventual disappearance at the
interface between the lobule and portal tracts.
To term this new kind of necrosis, we propose the name troxis necrosis, after the Greek noun meaning
"nibbling."
Copyright 2001 , Academic Press.

2. Apoptotic theory

On the basis of histological studies, it is proposed that the type of liver-cell death in piecemeal
necrosis is apoptosis.
The characteristic inconspicuousness of apoptosis explains why the mode of hepatocyte elimination in
piecemeal necrosis has hitherto remained obscure.
Cell-mediated immune attack induces apoptosis, not classical necrosis, and the occurrence of apoptosis
in piecemeal necrosis links the observed morphological changes in chronic active hepatitis with the other
evidence for an autoimmune pathogenesis.
It is significant that apoptosis does not evoke inflammation or fibroplasia. In attempting to elucidate
the cause of the fibrosis that accompanies progression to cirrhosis in chronic hepatitis, it may thus be
more relevant to study the effect on fibroblasts of substances liberated during lymphocyte-hepatocyte
interactions than the death of the hepatocytes.