Diagnostic Use of Endoscopic Ultrasonography in the Evaluation of Common Bile Duct Dilatation / 대한소화기내시경학회지

BACKGROUND/AIMS: The aim of this study was to assess the diagnostic use of endoscopic ultrasonograpy (EUS) in detecting the cause of common bile duct (CBD) dilatation in patients in whom abdominal ultrasonography or abdominal CT scan could not identify the cause of dilatation. METHODS: Thirty-seven patients (23 men, 14 women, mean age 62.2 years) with uncertain causes of CBD dilatation on abdominal sonogram and CT scan between October 1999 and November 2003 were enrolled. All patients were evaluated by EUS and endoscopic retrograde cholangiopancreatography (ERCP). Final diagnosis were determined by ERCP, surgical exploration and clinical follow-up. RESULTS: The following diagnosis were made by EUS: choledocholithiasis in 11 patients, CBD dilatation only in 12, benign stricture of distal CBD in 8, periampullary tumor in 6. The definitive diagnosis of choledocholithiasis (n=11), benign stricture of distal CBD (n=10), ampullary tumor (n= 5) were determined by ERCP with or without sphincterotomy and surgical exploration. EUS provided the accurate explanation for CBD dilatation in 32 of the 37 patients (86%). CONCLUSIONS: When the diagnosis of biliary obstruction remains obscure on abdominal sonography or CT scan, EUS may be useful.

Pathologic Findings in the Liver of Hepatitis B Virus X Transgenic Mice

BACKGROUND: The aim of this study was to investigate the hepatic pathology of HBx transgenic mice. METHODS: The gross and histological examinations were done in 125 HBx transgenic mice and 34 non-transgenic littermates. RESULTS: The incidence of a hepatic tumor was in-creased in the HBx transgenic mice older than 7 months and the overall incidence of a hepatic tumor was 62.2% (51/82) in the 13-18 months group of the HBx transgenic mice. The size of the hepatic tumor was 2.06+/-.92 mm in the 7-12 months group and 4.94+/-.05 mm in the 13-18 months group of HBx transgenic mice. All hepatic tumors were hepatocellular carcinomas and the histological patterns of hepatocellular carcinoma were either solid (84.2%, 48/57) or trabecular (15.8%, 9/57). Dysplastic changes in the hepatocytes were evident in 59.2% (74/125) of the HBx transgenic mice. There was lymphocyte infiltration, necrosis, fatty metamorphosis in both the dysplastic and tumor areas of the HBx transgenic mice. Vascular ectasia was identified in the tumor area of the HBx transgenic mice. CONCLUSIONS: The pathological findings of the HBx transgenic mice were dysplastic changes in the hepatocytes and development of a hepatocellular carcinoma associated with lymphocyte infiltration, necrosis, fatty metamorphosis in the dysplastic area and tumor area of the HBx transgenic mice.

A Study on the Expression of Proliferating Cell Nuclear Antigen and Apoptosis of the Hepatocellular Carcinoma in Human and Hepatitis B Virus X Transgenic Mice

BACKGROUND: This experiment was designed to study the cell kinetics of hepatocellular carcinoma (HCC) in both hepatitis B virus X (HBx) transgenic mice and humans. METHODS: The immunohistochemical stain of proliferating cell nuclear antigen (PCNA) and TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay of apoptosis were used on formalin fixed-paraffin embedded tissues. RESULTS: PCNA labeling indices (PCNA-LI) in the liver of HBx transgenic mice were markedly increased in HCC (11.3%) compare to the dysplastic areas (1.3%) and in the liver of non-transgenic littermates (0.1%). There was no significant difference of PCNA-LI in the dysplastic areas between HCC developed mice and non-HCC developed mice. Apoptosis labeling indices (Apoptosis-LI) in both the dysplastic areas and HCC of HBx transgenic mice were similar to those of non-transgenic littermates. PCNA-LI was markedly increased in human HCC (28.9%) compare to the background of HCC (2.9%) and the control liver (2.9%). Apoptosis-LI was decreased in human HCC (0.3%) compare to the background of HCC (0.4%) and the control liver (1.0%). Conclusion : There is a marked increase of cell proliferating activity in human HCC and in HCC of HBx transgenic mice, and there is a decrease of apoptosis in human HCC, but not in HCC of HBx transgenic mice.