No abstract

Biliary cystadenocarcinoma with oncocytic differentiation was first reported in 1992. This is a report of a second case. The patient (a 71-year-old man) was admitted to our hospital complaining of abdominal fullness. Multicystic lesions were identified in the left hepatic lobe radiologically. The patient died of peritoneal dissemination of carcinoma 20 months later. At autopsy, the tumor of the left hepatic lobe was found to be composed of adjoining multiple cystic lesions and a solid lesion with infiltration of the hepatic hilus and peritoneal dissemination. Histologically, the multicystic lesions were covered by papillary neoplastic epithelial cells with an eosinophilic granular cytoplasm resembling that of oncocytes and a fine fibrovascular core. The cyst wall was fibrous, but there was no mesenchymal stroma. In the solid lesion and infiltrated areas, acidophilic and granular carcinoma cells formed small glandular or solid cord patterns with much mucin secretion (mucinous carcinoma). Immunohistochemically, carcinoma cells of both components were found to contain many mitochondria and showed the phenotypes of hepatocytes and cholangiocytes. Interestingly, the intrahepatic biliary tree also was invaded by carcinoma cells. This may be a case of intraductal oncocytic papillary neoplasm of the left hepatic lobe followed by secondary cystic dilatation of the affected bile duct.

Aims: In this study, we attempted to define a new histological staging and grading system to provide more information reflecting the clinical laboratory data and prognosis to hepatologists. Methods and Results: First, 17 histological lesions of primary biliary cirrhosis (PBC) were scored in 188 needle liver biopsy specimens. Factor analysis yielded three independent groups of factors: Factor 1 (fibrosis, fibrous piecemeal necrosis, orcein positive granules, bile plugs, Mallory bodies, feathery degeneration, bile duct loss and atypical ductular proliferation); Factor 2 (portal inflammation, eosinophilic infiltration, lymphoid follicle, epithelioid granuloma, interface hepatitis and chronic cholangitis); and Factor 3 (interface hepatitis, lobular hepatitis, acidophilic bodies and pigmented macrophages). Eight findings of Factor 1, but not Factors 2 and 3, were significantly correlated with the clinical laboratory data and scores of Mayo's prognostic model. Factor 1 lesions may reflect the histological progression (staging), while Factor 2 and 3 lesions may relate to necroinflammatory activities (grading). Then, we devised a staging and grading system using three lesions (bile duct loss, fibrosis and orcein positive granules) from Factor 1 and three from Factors 2 and 3 (chronic cholangitis, interface hepatitis and lobular hepatitis). This new system might provide more pathological information of PBC patients to hepatologists. Hiramatsu -4-

Background. Several oncological sterilization methods involving autoclaving, irradiation or