Tomoyuki Seki

Wegener's Granulomatosis with Onset of Acute Pancreatitis and Rapid Progress

Although Wegener’s granulomatosis is a rare disorder, the clinical and histological characteristics are well known. However, Wegener’s granulomatosis with the onset of acute pancreatitis has rarely been reported. We discuss the case of Wegener’s granulomatosis in a 65-year-old man, presenting with acute pancreatitis and whose disease progressed rapidly.

A case of hemangioma accompanied by inflammatory pseudotumor of the spleen.

Both hemangioma and inflammatory pseudotumor (IPT) of the spleen are rare benign mass lesions. Moreover, a splenic hemangioma accompanied by IPT is extremely rare. A 61-year-old woman who suffered from liver cirrhosis had a splenic cavernous hemangioma surrounded by granuloma. The literature on IPT of the spleen has described several possibilities of its causes; however, it is still unknown. This case was accompanied by portal hypertension due to liver cirrhosis, which may cause microrupture of hemangioma resulting in an IPT.

Different amounts of K-ras mutant epithelial cells in pancreatic carcinoma and mass-forming pancreatitis.

Clinically, differential diagnosis of pancreatic carcinoma (PC) and so-called “mass-forming pancreatitis (MFP)” is difficult. We analyzed the amount, ductal level, and K-ras mutation of ductal hyperplasia and intraductal carcinoma in surgically resected cases of MFP (n = 18) and PC (n = 16). DNAs extracted from microdissected epithelial foci were analyzed for K-ras codon 12 mutation by nested polymerase chain reaction and restriction fragment length polymorphism. The histology of MFP showed severe destruction of exocrine tissue and pancreatic stones and/or protein plugs (72%, 13 of 18 cases) in mostly peripheral ducts. The average basal membrane lengths of nonpapillary and papillary hyperplasia in cases of carcinoma were about 4 and 15 times more than those of MFP, respectively. The frequency of K-ras mutation in hyperplastic foci increased from nonpapillary [six (27%) of 22] to papillary foci [16 (64%) of 25] in K-ras mutant PCs, but there was no difference between nonpapillary [one (6%) of 18] and papillary foci (none of 19) in K-ras wild-type PCs, and also between nonpapillary (none of 24) and papillary foci [one (7%) of 14] in MFPs.

Effect of activin on cell growth in primary cultures of guinea pig gastric epithelial cells

Background: The effect of activin on differentiated cells is known to be different from that on undifferentiated cells. Cultured gastric epithelial cells in complete serum‐free conditions grew into matured mucous cells after treatment with epidermal growth factor (EGF).

Overexpression of cyclin A and p53 in hepatocellular carcinomas. Wild P53 downregurate cyclin a promoter activity

Backround: The p16 INK4a tumor suppressor gene induces a cell cycle G1 arrest. It is the second most commonly inactivated gene identified in human cancers after p53. The p16 gene has been shown to be inactivated in nearly all human colon cancer cell lines and half of colon cancers and adenomas. While the p16 gene has been demonstrated to be inactivated primarily by promoter DNA methylation in hepatocellular carcinomas, there have been no studies examining p16 expression in premalignant liver lesions . Design: 17 macroregenerative and dysplastic nodules and 2 hepatocellular carcinomas from 15 hepatectomy specimens in patients undergoing transplantation for hepatitis C cirrhosis were examined by immunohistochemistry and methylation sensitive polymerase chain reaction (PeR). The nodules were less than 2 cm in diameter and clinically undetected . Sections were stained with anti-human pl6 monoclonal antibody . Human sporadic colon adenocarcinomas served as positive controls . Staining for p16 was considered positive if nuclear staining was greater than cytoplasmic staining. Methylation sensitive PCR was performed on bisulfite-treated DNA extracted from microdissected paraffin sections. Results: No nuclear staining was detected in the macroregenerative or dysplastic nodules. Two nodules demonstrated weak cytoplasmic staining . The surrounding cirrhotic liver showed cytoplasmic and no nuclear staining . Bile ductules at the margins of the nodules showed positive staining and served as internal positive controls. The 2 hepatocellular carcinomas showed a distinct lack of nuclear or cytoplasmic staining. Negative controls lacked cytoplasmic and nuclear staining. One hepatocellular carcinoma and two macroregenerative nodules had methylated p16 gene promoters , while two of the surrounding cirrhotic liver samples had unmethylated pl6 gene promoters. One macroregenerative nodule also showed evidence of both methylated and unmethylated pl6 forms. Conclusions: In patients with hepatitis C, clinically undetected macroregenerative and dysplastic nodules show an absence of pl6 staining. It is likely that pl6 gene methylation is responsible for suppression ofpl6 expression in these nodules. This supports previous observations that a high percentage of hepatocellular carcinomas have inactive p16 genes and suggests that p16 inactivation occurs early in liver tumor progression.

A Case of Chronic Pancreatitis Associated with a Pancreato-gastric Fistula

Abstract: A 51‐year‐old man presented complaining of frequent diarrhea. An ultrasonography and abdominal CT scan revealed a tumor in the tail of the pancreas. An endoscopic retrograde pancreatography revealed contrast medium flowing over the pancreas through the main pancreatic duct. A balloon cathether was then passed into the pancreatic duct, and the scope alone was retracted to the stomach. Maintaining the stomach under endoscopic observation, ICG was injected through the balloon catheter, whereupon it was seen to flow out from two small depressions in the center of a small elevated lesion in the posterior wall of the upper gastric corpus. Based on these endoscopic findings, a diagnosis of chronic pancreatitis with an associated pancreato‐gastric fistula was made.