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Periampullary diverticula are associated with dysfunction of the sphincter of Oddi. Papillary dysfunction may allow reflux of pancreatic juice as well as intestinal contents into the common bile duct. We prospectively investigated pancreatobiliary reflux in patients with and without periampullary diverticula.The ductal bile was sampled for amylase concentration during endoscopic retrograde cholangiopancreatography in 47 patients with choledocholithiasis (n = 29; with (n = 14) or without (n = 15) periampullary diverticula) or gallbladder cholesterol polyps (n = 18; with (n = 6) or without (n = 12) diverticula).The amylase concentration within the ductal bile was significantly higher in choledocholithiasis patients with periampullary diverticula (1621 +/- 587 IU/l) than in those without diverticula (1155 +/- 418 IU/l). The amylase concentration tended to be higher in gallbladder polyp patients with diverticula (1087 +/- 275 IU/l) than in those without diverticula (833 +/- 272 IU/l). Irrespective of the presence or absence of diverticula, patients with bile duct stones had significantly higher amylase concentrations than those with gallbladder polyps.Periampullary diverticula cause pancreatobiliary reflux. Further investigation is required to determine the clinical implication of pancreatobiliary reflux.

The high mobility group I (HMGI) family of proteins in mammals belongs to a group of nonhistone nuclear proteins known as architectural transcriptional factors. They function in vivo as both structural components of chromatin and auxiliary gene transcription factors. In an earlier study (N, Abe et nl., Cancer Res., 59: 1169-1174, 1999), we demonstrated that the expression level of the HMGI(Y) gene/proteins was significantly increased in colorectal adenocarcinoma and colorectal adenoma with severe cellular atypia, In the current study, we analyzed HMGI(Y) expression in several human pancreatic lesions to investigate (a) whether HMGI(Y) overexpression is also observed in pancreatic carcinoma, and (b) the role of HMGI(Y) in the diagnosis of pancreatic neoplasms. To this end, HMGI(Y) expression was determined at the protein level by immunohistochemistry using a HMGI(Y)-specific antibody in 6 surgically resected specimens of nonneoplastic tissue (4 specimens of normal pancreatic tissue and 2 specimens of chronic pancreatitis tissue), 8 pancreatic cystic neoplasms (5 intraductal papillary mucinous adenomas, 1 serous cystadenoma, and 2 solid pseudopapillary tumors), and 15 duct cell carcinomas of the pancreas. Immunohistochemical analysis revealed intense nuclear staining in the pancreatic carcinoma cells, whereas only very faint nuclear staining was seen in the nonneoplastic cells. There was a strong correlation between HMGI(Y) protein overexpression and a diagnosis of carcinoma (P = 0.000018). Thus, an increased expression level of the HMGI(Y) proteins was clearly associated with the malignant phenotype in pancreatic tissue. In addition, a low level of protein expression was also apparent in two of the cystic neoplasms that exhibited cellular atypia, but not in those that did not exhibit cellular atypia, Based on these findings, we propose that the HMGI(Y) proteins could be closely associated with tumorigenesis in the pancreas and that HMGI(Y) could serve as a potential diagnostic molecular marker for distinguishing pancreatic malignancies unambiguously from normal tissue or benign lesions.