Histological study on pathogenesis of sites of isolated islets of Langerhans and their course to the terminal state.

Histological study was performed on the pathogenesis of sites of isolated islets of Langerhans and on their course to the terminal state, using the pancreas of each of 200 randomly selected autopsy cases. With regard to sites of isolated islets, we found an incidence of 26.5% (53/200, 115 sites), which increased with age until subjects were in their 80s. To further our study, we also histologically studied the pancreas in 13 cases with evident obstruction in the lower stream of the main pancreatic ducts due to pancreatic carcinoma (10 cases) and stones (three cases), and one case of mucin-producing intraductal papillary adenocarcinoma in the tail of the pancreas with abundant mucin in the main pancreatic duct. As a result, we believe its pathogenesis to be the obstructive mechanism of pancreatic ductuli, caused by epithelial papillary projection or mucin secreted by epithelial cells of mucinous metaplasia, and that the course to the terminal state of isolated islets is as follows: For the first time, we report that the atrophy and disappearance of acinar cells by obstructive mechanism of ductuli (described above) occur with fibrosis, inflammatory cellular infiltration, and fatty infiltration around the site of isolated islets, accompanied by gathering of islets. This is followed by scarring of the site with further gathering of islets and a decrease in inflammatory cells. Fibrosis is gradually displaced by fatty tissue. Fatty infiltration into the site becomes marked, and gathered islets are found in the fatty tissue.