A case of gastric adenocarcinoma arising from a fundic gland polyp.

A rare case of gastric adenocarcinoma arising on the surface of a fundic gland polyp is reported. A 36-year-old Japanese woman was referred to our hospital for examination and treatment of a polyp that had been detected in another hospital. She did not have a history of familial adenomatous polyposis (FAP). Endoscopic examination revealed a 10-mm-diameter fundic gland polyp in the body of the stomach. The polyp had an irregular depression on its top, suggesting the presence of malignancy. Endoscopic mucosal resection was done to make a histological diagnosis. This revealed a fundic gland polyp with a tiny superficial adenocarcinoma. Atrophic changes of the gastric mucosa were mild, although Helicobacter pylori infection was positive. It is suggested that fundic gland polyps have the potential for malignant transformation.

[A case of H. pylori and API2-MALT1 gene-negative gastric mucosa-associated lymphoid tissue lymphoma with a carcinoma-like signet-ring cell lymphoepithelial lesion].

A 60-year-old woman presented in February 2003 with an ulcer on the lesser curvature of the anglus. The endoscopic biopsy specimens showed epithelial signet-ring cell associated with lymphoid infiltration, suggesting a diagnosis of gastric cancer. Histopathological examination confirmed the diagnosis of low-grade B-cell lymphoma of MALT with epithelial signet-ring cell lymphoepithelial lesion, which was negative for H. pylori and t (11;18) (q21;q21) translocation (API2-MALT1 gene). This case was treated with H. pylori eradication and additional radiation therapy, and the tumor was disappeared.

A case of multiple hepatic peribiliary cysts which contributed to the obstructive jaundice and led to liver failure at the young man with von Recklinghausen's disease.

We treated a young man with obstructive jaundice, in whom multiple hepatic peribiliary cysts were detected at autopsy. He had been diagnosed with von Recklinghausen's disease in early childhood and had undergone surgery for a ventricular septal defect with massive blood transfusion at the age of 4 years. Examination at the age of 21 revealed prominent splenomegaly and a low platelet count. He underwent splenectomy and liver cirrhosis was confirmed by open biopsy of the liver. He was followed up at a local hospital and was admitted several times. When he was 41 years old, he was transferred to our hospital with severe jaundice and hepatic encephalopathy. Computed tomography showed marked dilation of the intrahepatic bile ducts and liver function tests showed that jaundice was mainly due to an increase of direct bilirubin. Despite endoscopic nasobiliary drainage, plasma exchange, and continuous hemodiafiltration, he died of hepatic failure after 5 days. At autopsy, multiple hepatic peribiliary cysts were found. Although peribiliary cysts have generally been considered to cause no symptoms, this report describes a patient with multiple hepatic peribiliary cysts which appear to have been responsible for the progression of obstructive jaundice.

A case of congenital absence of the portal vein.

We experienced a girl with congenital absence of the portal vein. She was examined by computed tomography (CT), three-dimensional computed tomographic angiography (3DCTA), digital subtraction angiography and liver biopsy. Nodular regenerative hyperplasia of the liver was detected, presumably due to an abnormal hepatocellular response to absent portal flow. 3DCTA showed that the splenic vein and superior mesenteric vein joined to form a common trunk, which directly entered the right atrium. 3DCTA may be a valuable noninvasive tool for identifying portal malformations.