[Clinical comparison of endoscopic naso-gallbladder drainage versus percutaneous transhepatic gallbladder drainage for acute cholecystitis].

Early cholecystectomy has become the standard treatment for acute cholecystitis. However, gallbladder drainage is often performed before surgery. In the present study, we compared the clinical outcomes between patients who underwent endoscopic naso-gallbladder drainage (ENGBD) and those who underwent percutaneous transhepatic gallbladder drainage (PTGBD). PTGBD was superior to ENGBD in terms of success rate and procedure time. However, there was no significant difference in the rate of complications, improvement effect on inflammation, the length of hospitalization, the duration from drainage to operation, and operation time. Although PTGBD has become the first choice for cases requiring gallbladder drainage, ENGBD should be considered the most appropriate therapy in cases with a contraindication for PTGBD due to antithrombotic treatment, those associated with choledocholithiasis, and those suspected of gallbladder cancer. The importance of ENGBD is expected to increase in the future.

Adenocarcinoma of the minor duodenal papilla: report of a case.

An 81-year-old male was found to have a duodenal tumor by screening upper gastrointestinal endoscopy. The tumor was located in the minor duodenal papilla. Pathological examination of the biopsy specimen revealed adenocarcinoma, and endoscopic ultrasound showed an elevated hypoechoic mass in the minor duodenal papilla. The preoperative diagnosis was therefore considered to be either adenocarcinoma of the minor duodenal papilla or duodenal cancer. We performed a subtotal stomach-preserving pancreaticoduodenectomy. Histopathological examination of the resected specimen showed the tumor cells to be primarily located in the submucosa of the minor duodenal papilla, with slight invasion into the pancreatic parenchyma through the accessory pancreatic duct. We therefore diagnosed a primary adenocarcima of the minor duodenal papilla. Adenocarcinoma of the minor duodenal papilla is considered to be a rare disease, but it may be underestimated because of the difficulty in distinguishing advanced adenocarcinoma of the minor duodenal papilla from primary duodenal cancer and cancer of the pancreatic head.

[A case of portal vein thrombosis complicating acute cholangitis treated successfully with danaparoid sodium].

An 81-year-old woman was referred to our hospital with a diagnosis of acute cholangitis. Endoscopic retrograde cholangiography revealed a common bile duct (CBD) stone. In addition, CT showed thrombus of the right portal vein. Endoscopic sphincterotomy was performed to remove the CBD stone. Thrombosis was treated successfully with danaparoid sodium. It was speculated that the treatment of the acute cholangitis induced thrombolysis by the auto-fibrinolysis system and danaparoid sodium prevented the development of thrombus formation in this case.

Adrenomedullin antagonist suppresses tumor formation in renal cell carcinoma through inhibitory effects on tumor endothelial cells and endothelial progenitor mobilization.

Adrenomedullin (AM) is a multifunctional 52-amino acid peptide. AM has several effects and acts as a growth factor in several types of cancer cells. Our previous study revealed that an AM antagonist (AMA) suppressed the growth of pancreatic tumors in mice, although its mechanism was not elucidated. In this study, we constructed an AMA expression vector and used it to treat renal cell carcinoma (RCC) in mice. This AMA expression vector significantly reduced tumor growth in mice. In addition, microvessel density was decreased in AMA-treated tumors. To analyze the effect of AMA on tumor angiogenesis in this model, tumor endothelial cells (TECs) were isolated from RCC xenografts. TEC proliferation was stimulated by AM and it was inhibited by AMA significantly. AM induced migration of TECs and it was also blocked by AMA. However, normal ECs (NECs) were not affected by either AM or AMA. These results demonstrate that AMA has inhibitory effects on TECs specifically, not on NEC, thereby inhibiting tumor angiogenesis. Furthermore, we showed that vascular endothelial growth factor-induced mobilization of endothelial progenitor cell (EPC) into circulation was inhibited by AMA. These results suggest that AMA can be considered a good anti-angiogenic reagent that selectively targets TECs and EPC in renal cancer.

A case of polyarteritis nodosa complicated by rectal cancer.

Solid cancers are rarely complicated by the occurrence of polyarteritis nodosa (PN), and most cases diagnosed as PN are, in fact, cases of paraneoplastic vasculitis. Paraneoplastic vasculitis is usually resolved after tumor removal. We present a rare case of a 69-year-old man with PN complicated by rectal cancer, without the occurrence of paraneoplastic vasculitis. Microscopic examination of the resected cancer lesion revealed inflammation of some arteries and neutrophil and lymphocyte infiltration, fibrin deposition, stenosis, and vasodilatation of capillaries caused by congestion in the submucosal layer. It was unclear how these findings exerted influence on the rectal cancer. Although the symptoms of PN did not improve after the patient's tumor was removed surgically, the symptoms improved rapidly after oral treatment with prednisolone and cyclophosphamide.

Neutrophils secrete MIP-1 beta after adhesion to laminin contained in basement membrane of blood vessels.

We have recently demonstrated that granulocyte colony-stimulating factor (G-CSF) stimulated the production of epithelial-cell-derived-neutrophil attractant-78 (ENA-78) by neutrophils and that ENA-78 might promote the accumulation of neutrophils that had migrated from the intravascular space into inflammatory tissues. In this study, we examined whether other chemokines could be secreted by neutrophils that had accumulated after migrating from the intravascular space into the inflammatory tissues. We demonstrated that adhesion to laminin contained in the basement membrane and Matrigel, which is an artificial basement membrane model, induced macrophage inflammatory protein-1 beta (MIP-1 beta) in neutrophils and that MIP-1 beta secreted by neutrophils induced the chemotaxis of dendritic cells. These findings suggest that neutrophils transmigrating through the basement membrane are stimulated to secrete MIP-1 beta by the basement membrane, inducing the transmigration of dendritic cells from the intravascular space into inflammatory tissues. We propose that neutrophils intervene between innate immune response and specific immune response by secreting MIP-1 beta during the transmigration through the basement membrane.