先天性胆道拡張症における肝組織の病理組織学的検討

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The results of intraoperative liver biopsy performed on 56 clinical cases and the findings of the abnormal pancreatico-choledochal duct junction in 63 expermental canine-models are discussed in this paper. Histopathological findings revealed that fibrosis, small round cell infiltration at the portal area and bile duct proliferation were present in 80% of the patients. Among the 8 infantile patients, giant cells were observed in 2 patients, 1 of them also had cirrhosis. Another of infantile patient also had cirrhosis. Edematous change was present in the jaundiced cases, but marked fibrosis was also seen in the cases without jaundice. In the patients with cystic shape of choledochus, fibrosis was frequently found, while in those with fusiform shape, it was rarely observed. There was no significant correlation between liver pathology and intrahepatic bile duct dilatation or common hepatic duct stenosis. Cases reoperated after cyst-enterostomy had marked lymphocyte infiltration and fibrosis. The second biopsy done after radical operation showed no histological improvement within 1 year, despite the disappearance of clinical symptoms. Among the exprimental canine models, the long time survival cases, especially those which survived more than 5 years, showed slight to moderate lymphocyte infiltration and fibrosis. But no cirrhosis or giant cell formation was observed. Liver damage was considered to be caused by distal bile duct stenosis originating in the abnormal pancreatico-choledochal duct junction and furthermore exacerbated by regurgitated pancreatic juice or infection of the biliary tract. Regurgitated pancreatic juice could bring about moderate fibrosis in the long term, but seems not be able to cause cirrhosis.
日本小児外科学会の論文
1992-02-20

先天性胆道拡張症における肝組織の病理組織学的検討

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