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Background. Phospholipase A2 (PLA2) may play a central role in the pathogenesis of pancreatic acinar cell necrosis. Several questions, however, are unsolved: Is acinar cell necrosis caused by PLA2 derived from infiltrating leukocytes or from pancreatic PLA2 itself? Does PLA2 cause cellular lysis by the release of lysolecithin from lecithin or by generation of free radicals? The aims of this study were to determine which form of PLA2 is responsible for cellular damage and how to inhibit its action. Methods. Isolated rat pancreatic acini were prepared by collagenase digestion. Newly synthesized proteins were labeled by 35S-methionine. Acini were incubated in buffer to which various factors, such as porcine pancreatic PLA2 or bee venom PLA2, homogenates of either leukocytes or pancreatic homogenates, all with or without lecithin and with or without potential inhibitors (aprotinin, 4-bromophenacylbromide, BM 16.2115, quinacrine, various analogs of arachidonic acid), or free radicals (hydrogen peroxide, xanthine/xanthine oxidase) with or without allo-purinol or dismutase/catalase were added. Cellular destruction was measured by the release of radiolabeled proteins. Results. PLA2 alone, free radicals, and granulocytes were not harmful to acini within 30 min of incubation. Free radicals caused significant release of radiolabeled proteins only after 3 h of incubation; this release could be inhibited by scavengers. Incubation of pancreatic acini with PLA2 in combination with lecithin caused rapid release of radiolabeled proteins. Addition of high concentrations of enterokinase activated pancreatic homogenates both alone and with lecithin caused release of cellular proteins, suggesting that pancreatic PLA2 uses lecithin from pancreatic membranes as substrate. Almost all tested potential inhibitors of PLA2 were unable to prevent the destruction caused by either pancreatic or bee venom PLA2 and lecithin. However, HK 42, a polyunsaturated fatty acid analog, was able to reduce dose dependently the release of acinar proteins caused by pancreatic PLA2 and lecithin. Conclusion. Pancreatic PLA2 and not PLA2 from infiltrating leukocytes may play a role in pancreatic acinar cell necrosis. Cellular lysis is caused upon the action of lysolecithin and probably not via the action of free radicals. [ABSTRACT FROM AUTHOR]

We report a case of bile duct cancer associated with anogenital Paget's disease. The patient was a 80-yr-old Japanese woman whose chief complaint was exanthema from the left vulva to the anus for the previous 4 yr. Histological examination of the skin biopsy of the vulva showed numerous Paget's cells. Resection of the lesion and the rectum were performed, and a permanent colostomy was created. More than 1 month after the operation, the patient suddenly developed obstructive jaundice. Percutaneous transhepatic cholangiography performed simultaneously with endoscopic retrograde cholangiography showed complete obstruction of the middle part of the bile duct. Bile cytology was class V. On the basis of these results, bile duct cancer associated with extramammary Paget's disease IEMPD) was diagnosed. About 5 months after the operation, the patient died of liver failure. Microscopically the tumor in the bile duct was poorly differentiated adenocarcinoma. Although EMPD has a tendency to he associated with underlying internal malignancies, this is the first reported case, to our knowledge, of bile duct cancer associated with EMPD. [ABSTRACT FROM AUTHOR]

Reports the medical case of a 56-year old patient with exocrine pancreatic cancer associated with hypercalcemia due to parathyroid hormone-related protein (PTH-rP). White blood cell count and alkaline phosphatase of the patient according to initial laboratory tests; Findings in which tumor-derived PTH-rP is supposed to be a causative factor of hypercalcemia; Effect of the various standard treatments for humoral hypercalcemia of malignancy.