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Difference between revisions of "Talk:Medical liver disease"
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Talk:Medical liver disease (view source)
Revision as of 23:03, 27 January 2011
, 23:03, 27 January 2011→Glycogen storage disease: new section
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====Comment==== | ====Comment==== | ||
The histomorphologic findings (cholestasis, fibrosis and steatosis) are compatible changes seen in total parenteral nutrition (TPN). | The histomorphologic findings (cholestasis, fibrosis and steatosis) are compatible changes seen in total parenteral nutrition (TPN). | ||
== Glycogen storage disease == | |||
===Microscopic description=== | |||
The sections show hepatocytes with moderate enlargement and pale cytoplasm diffusely, with cobweb-like cytoplasmic material. Focally, hepatocytes have marked enlargement with pynotic nuclei. There are ten portal tracts present in the specimen. | |||
There is minimal focal portal inflammation and moderate inflammation of the lobule, characterized by eosinophils and neutrophils, with focal hepatocyte necrosis. There is no inflammation at the interface. The Laennec inflammation grade is I-II/IV. There is significant fibrosis, which includes the presence of portal expansion and septa; the Laennec fibrosis stage is II / IV. | |||
There is no cholestasis, no iron deposition, no bile duct injury and no copper deposition. PAS staining is equivocal for glycogen deposition. PAS-D marks scattered, predominantly periportal, macrophages. | |||
Electron microscopy demonstrates electron dense material consistent with glycogen that is not membrane bound. | |||
===Final diagnosis=== | |||
Liver, core biopsy - <br> | |||
i) Changes consistent with glycogen storage disease, see comment.<br> | |||
ii) Fibrotic portal expansion and focal septa (Laennec fibrosis stage II / IV). | |||
====Comment==== | |||
The periportal predominant fibrosis, diffuse hepatocyte distension with whispy and pale cytoplasm, and non-membrane bound electron dense (glycogen-like) material, are suggestive of glycogen storage disease type III (Cori disease). | |||