Total pancreatectomy for metastatic renal cell carcinoma with marked extension into the main pancreatic duct.

A 59-year-old man who had undergone left nephrectomy for renal cell carcinoma (RCC) 14 years previously was admitted for the treatment of obstructive jaundice. Imaging studies showed head-to-tail dilation of the main pancreatic duct (MPD) and a few ring-shaped enhanced nodules. Main duct-type intraductal papillary mucinous neoplasm was suspected and total pancreatectomy was performed. Pathologically, the entire length of MPD was filled with tumor. It consisted mainly of necrotic material, but included some clear cell carcinoma; the final diagnosis was metastatic RCC of the pancreas. This is an extremely rare case of pancreatic metastasis from RCC, with marked extension into MPD.

[One case of pancreatic mucinous carcinoma discovered due to acute pancreatitis].

The patient was a woman, aged 69, diagnosed with acute pancreatitis by a local physician; simultaneously, with US, a low-echo tumor was indicated in the pancreas' uncinate process. Diagnosis was made of acute pancreatitis resulting from a pancreatic IPMN, and the patient was referred. Ultrasound showed hypoechoic tumor images accompanied by posterior echo enhancement. With radiography-CT, from the pancreas parenchymal phase, the peripheral portion was densely stained, while internally, images showed densely stained dendriforms towards the equilibrium phase. With MRI T1-weighted images, there was appearance at low intensity, and with T2-weighted images, there was appearance at high intensity; with MRCP, there was depiction at relatively high intensity. In the final pathological diagnosis, there was prominent formation of mucinous nodules, and mucinous carcinoma including large quantity of mucous.

Surgical treatment of pT2 gallbladder carcinoma: a reevaluation of the therapeutic effect of hepatectomy and extrahepatic bile duct resection based on the long-term outcome.

BACKGROUND: The clinical indications for hepatectomy and extrahepatic bile duct resection (EBDR) for pT2 gallbladder carcinoma (GBC) remains controversial. The aim of this study is to elucidate the therapeutic effect of hepatectomy and extrahepatic bile duct resection on the surgical treatment of pT2 GBC. METHODS: Ninety-four patients with pT2 GBC who underwent a potentially curative resection were retrospectively analyzed regarding their pathological findings, surgical procedures, and survival. RESULTS: The most powerful predicting factor for the survival is the nodal status. The 5-year survival rate was 87.1% for the pN0 patients and 55.7% for the pN1 patients. With respect to surgical procedures, the 5-year survival rate was 73.3% for the 51 patients with hepatectomy, and 87.2% for the 43 patients without hepatectomy. In addition, the 5-year survival rate was 66.7% for the 11 patients with EBDR, and 81.1% for the 83 patients without EBDR. When restricting the patients to those with pN1 disease, the 5-year survival rate of the patients who received these procedures did not surpass that of the patients who did not. CONCLUSION: There is no positive therapeutic effect besides providing surgical margins in hepatectomy and EBDR in the surgical treatment of pT2 GBC whereas lymph node dissection is most effective procedure for improving survival. Provided that the negative surgical margins are secured, a hepatectomy and an EBDR can therefore be withheld in the surgical treatment for the pT2 GBC.

Glutamine-dependent inhibition of pial arteriolar dilation to acetylcholine with and without hyperammonemia in the rat.

Glutamine has been shown to influence endothelial-dependent relaxation and nitric oxide production in vitro, possibly by limiting arginine availability, but its effects in vivo have not been well studied. Hyperammonemia is a pathophysiological condition in which glutamine is elevated and contributes to depressed CO(2) reactivity of cerebral arterioles. We tested the hypothesis that acute hyperammonemia decreases pial arteriolar dilation to acetylcholine in vivo and that this decrease could be prevented by inhibiting glutamine synthetase with L-methionine-S-sulfoximine (MSO) or by intravenous infusion of L-arginine. Pial arteriolar diameter responses to topical superfusion of acetylcholine were measured in anesthetized rats before and at 6 h of infusion of either sodium or ammonium acetate. Ammonium acetate infusion increased plasma ammonia concentration from approximately 30 to approximately 600 microM and increased cerebral glutamine concentration fourfold. Arteriolar dilation to acetylcholine was intact after infusion of sodium acetate in groups pretreated with vehicle or with MSO plus methionine, which was coadministered to prevent MSO-induced seizures. In contrast, dilation in response to acetylcholine was completely blocked in hyperammonemic groups pretreated with vehicle or methionine alone. However, MSO plus methionine administration before hyperammonemia, which maintained cerebral glutamine concentration at control values, preserved acetylcholine dilation. Intravenous infusion of L-arginine during the last 2 h of the ammonium acetate infusion partially restored dilation to acetylcholine without reducing cerebral glutamine accumulation. Superfusion of 1 or 2 mM L-glutamine through the cranial window for 1 h in the absence of hyperammonemia attenuated acetylcholine dilation but had no effect on endothelial-independent dilation to nitroprusside. We conclude that 1) hyperammonemia reduces acetylcholine-evoked dilation in cerebral arterioles, 2) this reduction depends on increased glutamine rather than ammonium ions, and 3) increasing arginine partially overcomes the inhibitory effect of glutamine.