【Abstract】ObjectiveBy using multidetector row spiral CT (MDCT) to investigate the CT imaging findings of gallbladder abnormalities caused by hepatic parenchymal diseases and those of inflammatory cholecystitis. MethodsCT and clinical data of 80 patients with gallbladder abnormalities were retrospectively reviewed. Fifty patients were in hepatic disease group, including 20 chronic hepatitis, 25 liver cirrhosis, and 5 cirrhosis with hepatocellular carcinoma. Thirty patients were in inflammatory group, including 19 chronic cholecystitis, 6 acute cholecystitis, 3 cholecystitis with acute pancreatitis, 1 gangrenous cholecystitis, and 1 xanthogranulomatous cholecystitis. All patients underwent MDCT plain scan and contrastenhanced dualphase scanning of upper abdomen. ResultsIn hepatic disease group, 48 cases had evenly thickened gallbladder wall (96%) with mean thickness of (3.67±0.49) mm; 38 cases had clear gallbladder outlines (76%); 38 cases had gallbladder wall enhancement of various degree (76%); 14 cases had gallbladder bed edema and localized nondependant pericholecystic fluid collection (28%). In inflammatory cholecystitis group, 28 cases had obscuring gallbladder outlines (93%) ; 26 cases had gallbladder wall evenly thickened (87%), 4 cases showed unevenly thicked wall (13%), the mean thickness being (4.54±1.14) mm; 30 cases had inhomogenous enhancement of the gallbladder wall (100%); 9 cases had highattenuation bile (30%); 4 cases had dependant pericholecystic fluid collection (13%); 5 cases had transient enhancement of adjacent hepatic bed in arterial phase (17%); microabscess and gas in the gallbladder wall was observed in 1 case respectively. ConclusionMDCT can offer imaging findings useful for differentiating abnormal gallbladder changes caused by hepatic parenchymal diseases from those due to inflammatory cholecystitis.
【Abstract】ObjectiveBy using multidetector row spiral CT (MDCT) to investigate the CT imaging findings of gallbladder abnormalities caused by hepatic parenchymal diseases and those of inflammatory cholecystitis. MethodsCT and clinical data of 80 patients with gallbladder abnormalities were retrospectively reviewed. Fifty patients were in hepatic disease group, including 20 chronic hepatitis, 25 liver cirrhosis, and 5 cirrhosis with hepatocellular carcinoma. Thirty patients were in inflammatory group, including 19 chronic cholecystitis, 6 acute cholecystitis, 3 cholecystitis with acute pancreatitis, 1 gangrenous cholecystitis, and 1 xanthogranulomatous cholecystitis. All patients underwent MDCT plain scan and contrastenhanced dualphase scanning of upper abdomen. ResultsIn hepatic disease group, 48 cases had evenly thickened gallbladder wall (96%) with mean thickness of (3.67±0.49) mm; 38 cases had clear gallbladder outlines (76%); 38 cases had gallbladder wall enhancement of various degree (76%); 14 cases had gallbladder bed edema and localized nondependant pericholecystic fluid collection (28%). In inflammatory cholecystitis group, 28 cases had obscuring gallbladder outlines (93%) ; 26 cases had gallbladder wall evenly thickened (87%), 4 cases showed unevenly thicked wall (13%), the mean thickness being (4.54±1.14) mm; 30 cases had inhomogenous enhancement of the gallbladder wall (100%); 9 cases had highattenuation bile (30%); 4 cases had dependant pericholecystic fluid collection (13%); 5 cases had transient enhancement of adjacent hepatic bed in arterial phase (17%); microabscess and gas in the gallbladder wall was observed in 1 case respectively. ConclusionMDCT can offer imaging findings useful for differentiating abnormal gallbladder changes caused by hepatic parenchymal diseases from those due to inflammatory cholecystitis.
ObjectiveTo study the relationship between cholecystectomy and Helicobacter pylori （Hp） infection. MethodsOne hundred and eleven patients with cholecystolithiasis were chosen as the investigation group, while 577 patients with upper digestive tract symptoms without cholecystolithiasis as the control group. All the patients took the 13C breath test to determine whether they were infected by Hp. All the patients with Hp infection continued eradical therapy for Hp infection for one course after cholecystectomy and were followed up on outpatient basis. ResultsThe infection rate in the investigation group was 45.9%, while 27.4% in the control group. During the 3 to 6 months of followup for the patients undergoing eradical therapy for Hp infection, we found no patient complaining of epigastric pain, malaise, belching and nausea. ConclusionThe infection rate of Hp in patients with cholecystolithiasis is high, Hp may be one of the factors causing “postcholecystectomy syndrome”. Eradical therapy for Hp after cholecystectomy will help improve the effects of operation.
bjective To study the change of mucins of expression in lithic cholecystitis and cholecystic adenomatiod polyps. MethodsMUC1 and MUC3 were detected in the mucosa of human normal gallbladders (20 cases, control group), of calcareous cholecystitis (38 cases, calcareous group) and of adenomatoid polyps (18 cases, polyp group) with immunohistochemical stains and Western blotting methods. ResultsThe positive rate and optical density values of MUC1 were increased significantly in calcareous and polyp group vs control group (P＜0.01), otherwise, MUC3 was decreased markedly (P＜0.01). Conclusion The expressions of MUC1, MUC3 were not synchronization in different lesions of cholecyst.
To analyse the causes of biliary injuries and summuarize the experience of prevention of biliary injury during laparoscopic cholecystectomy (LC). Twenty-three patients with biliary duct injury were diagnosed and treated at our center between September 1992 and August 1998. The main causes were either misidentification of the bile duct or aberrant right duct as the cystic or injudicious use of thermal energy (cautery) to dissect, control bleeding, or divide tissue. Conclusion: The causes of biliary duct injury are complex. Training and experience of sugeon, the meticulous dissection of the calot′s triangle and preoperative or operative cholangiography are three key factors in prevention of biliary duct injury during LC.
【Abstract】Objective To study the regulatory ability of peroxisome proliferatoractivated receptor γ(PPARγ) ligands to the inflammatory response in human gallbladder epithelial cells. Methods Culture human gallbladder epithelial cells and identify them . Cells were treated for 24 hours with 0, 10 μmol/L, 20 μmol/L, 30 μmol/L, 50 μmol/L and 100 μmol/L of Ciglitazone during cellular growth peak(5th day), then stimulated them with hIL-1β 5 ng/ml for 2 hours and measured the concentration of IL-6、IL-8 and TNF-α in cellular supernatants by riadioimmunoassay. Results Contrasted with control group, the expression of IL-6 and IL-8 in each test group were inhibited （P＜0.001）. The IL-6 and IL-8 levels were gradually dropped and corelated with the dosage of Cigtitazone, and manifested dosagedependence (P＜0.001). The concentration of TNF-α could not be measured. Conclusion PPARγ ligands can inhibit the expression of IL-6 and IL-8 in human gallbladder epithelial cells and probably produce effect in the regulation of cholecystic inflammation.