As a result of an increasing number of studies on the surgical treatment of intrahepatic cholangiocarcinoma (ICC), knowledge of its biological characteristics has been accumulating. We analyzed the clinicopathological features and outcome of 36 of 48 surgical patients with histologically proven ICC (75.0%) who underwent hepatic resection between March 1979 and July 1998. According to tumor location, 12 patients had the central type and 24, the peripheral type. The incidence of portal vein tumor thrombus and lymph node metastasis was higher in the central type than in the peripheral type. All 12 patients with the central type had stage IV disease, and none of them underwent complete resection, whereas 12 of the 24 patients with peripheral type tumors had stage IV disease; complete resection was achieved in 12 of the 24 patients with peripheral type tumors (50%). Outcome after resection was significantly poorer in the patients with the central type. The macroscopic type of lesion in the resected specimens was the mass-forming type in 15 patients (41.7%), the mass-forming + periductal-infiltrating type in 15 patients (41.7%), the periductal-infiltrating type in 3 patients (8.3%) and the intraductal growth type in 3 patients (8.3%). The macroscopic tumor type was associated with mode of tumor spread and outcome. All 3 patients with the intraductal growth type are alive without tumor recurrence 26-138 months after surgery. The survival rate was much higher in the patients with the mass-forming type than in those with the mass-forming + periductal-infiltrating type. Importantly, the outcome in the 17 patients who underwent resection for stage IV-B disease and who accounted for 47.2% of patients with resection in the present series was very poor, almost the same as that in the 12 patients who did not undergo resection. By selecting patients based on the biological characteristics of the tumor and taking into account patients' quality of life, complete surgical resection can be performed safely and is associated with long-term survival.
To surgically manage hilar bile duct carcinoma successfully, it is important to be familiar with the principal anatomical variations of the biliary and vascular components of the plate system in the hepatic hilar area, because all the variations in the bile ducts and vessels occur in the plate system. The plate system consists of bile ducts and blood vessels surrounded by a sheath. There are three plates in the hilar area: the hilar plate, the cystic plate, and the umbilical plate. The bile duct and blood vessel branches penetrate the plate system and form Glisson's capsule in all segments of the liver, except for the medial segment. The right hepatic duct is usually (in 53%-72% of individuals) formed by the union of the anterior segmental duct and the posterior segmental duct in the hilar area. However, three other variations have been found in which these segmental ducts do not form the right hepatic duct. Few anatomical variations have been identified in the left hepatic duct, but confusion arises because of the variations in the medial segment ducts (B4) which join the left hepatic duct at different sites. In 35.5% of individuals they join the hepatic duct in the vicinity of the hilar confluence (type I B4 anatomy), and in 64.5% of individuals they join the left hepatic duct some distance away from the confluence (type II B4 anatomy). Because B4 is very close to the hilar confluence in type I, hilar bile duct carcinoma can easily invade B4 and, for that reason, for curative resection of hilar bile duct carcinoma, resection of S4a (the inferior part of the medial segment) should be considered along with the resection of extrahepatic bile duct and caudate lobe. Variations in the portal vein and hepatic artery are found in 16%-26% and 31%-33% of individuals, respectively. Because a considerable number of anatomical variations in the bile ducts and vessels persist in the hilar area, and the reported proportions of the different variations vary, it is necessary to have a good knowledge of the plate system and the variations in the bile ducts and blood vessels in the hilar area to perform safe and curative surgery for hilar bile duct carcinoma.
Recent studies have revealed that bile acids (BAs) are not only facilitators of dietary lipid absorption but also important signaling molecules exerting multiple physiological functions. Some major signaling pathways involving the nuclear BAs receptor farnesoid X receptor and the G protein-coupled BAs receptor TGR5/M-BAR have been identified to be the targets of BAs. BAs regulate their own homeostasis via signaling pathways. BAs also affect diverse metabolic pathways including glucose metabolism, lipid metabolism and energy expenditure. This paper suggests the mechanism of controlling metabolism via BA signaling and demonstrates that BA signaling is an attractive therapeutic target of the metabolic syndrome.
To elucidate the pathogenesis of acute acalculous cholecystitis, the gallbladder was subjected to ischemia-reperfusion by simultaneously occluding the middle hepatic artery and the superior mesenteric vein in dogs, and the degree of inflammation and biochemical changes in the gallbladder mucosa were studied by varying the duration of ischemia or reperfusion. Ischemia alone did not induce cholecystitis either macroscopically and histologically, although it increased phospholipase A2 (PLA2) activity, content of lipid peroxide, and superoxide dismutase (SOD) activity in the mucosa with prolongation of the ischemic time. Cholecystitis was produced in all animals by 45-min ischemia followed by 90-min reperfusion as the shortest ischemia and reperfusion times. In this model, prolongation of the ischemic time increased the area of mucosal inflammation horizontally with increases of the PLA2 activity, content of lipid peroxide, and SOD activity, whereas by prolonging the reperfusion time the inflammation area spread deeper vertically toward the serosal side with significant increase in the mucosal PLA2 activity, content of lipid peroxide, and SOD activity. These results revealed that ischemia-reperfusion plays an important role in the pathogenesis of acute acalculous cholecystitis, causing the generation of free radicals and the activation of membrane-bound PLA2.
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