Histopathology of cholestasis.

摘要: Abstract Cholestasis may be extrahepatic or intrahepatic in origin. The block bile secretion complete incomplete to variable extent. Complete cholestasis occurs case of primary parenchymal disease (intrahepatic cholestasis) total obstruction ducts (extrahepatic cholestasis). Incomplete is due intra- (intra- both). Histologically, it useful distinguish between bilirubionstasis and cholate-stasis. secretory causes as early changers: bilirubinostasis (in hepatocytes, canaliculi Kupffer cells) acinar zone 3, "ductular reaction" 1. latter refers an increase periportal ductular profiles, associated with neutrophil infiltration. With longer duration cholestasis, further lesions ensue: feathery degeneration hepatocytes retention detergent acids, cholestatic liver cell rosettes representing a shift from hepatocellular biliary differentiation, xanthomatous cells reflecting hyperlipidemia, cholate stasis 1 overload membrane-damaging eventually paraportal infarcts, progressive reaction. multiplication pre-existing ductules, metaplasia activation progenitor cells. It invariably periductular fibrosis: the pacemaker for increasing matrix deposition, resulting fibrosis true cirrhosis. (e.g. PBC, PSC) characterized by absence during long periods time, whereas afore mentioned features chronic do appear. Hence follows that most reliable markers are stasis, Bilirubinostasis only late often ominous sign.