Objective To investigate the recurrence of hepatolithiasis and reoperation and their relation to the location of intrahepatic stone. MethodsTwo hundred and twentysix patients of hepatolithiasis operated upon in the period of 1990-1995 were retrospectively analysed.ResultsAmong those patients, there were 101 patients (44.7%) had previous operation for the gallstones diseases including cholecystectomy for gallbladder stones (n=21, 20.8%), choledocholithotomy (n=72, 71.3%),liver segmentectomy (n=6， 5.9%), and choledochojejunostomy (n=2, 2.0%). The operative mortality was 5.0% for the reoperation group and none for the first time operation for hepatolithiasis.Conclusion Although the liver resection is an ideal surgical method to eradicate the diseased lesion and to minimize the malignant changes especially in primary hepatolithiasis (type I, or IE)， choledochojejunostomy is only recommended for the secondary type (type IE or IE) where possible. In the management of hepatolithiasis, the complete information of biliary tract is needed for the choice of surgical methods.
The mumber of Polymorphonuclear leukocyte (PMN) in hepatic tissue increased in the rats with cholangitis, PMN infiltration was mainly in the hepatic sinus in the early stage; and PMN infiltration presented around the hepatocytes 12 hours after infection. Degeneration and necrosis of the hepatic cells was also observed in the rats with acute cholangitis. Only 40 percent of the rats survived 24 hours after infection. Depletion of circulating PMN decreased the damage and necrosis of hepatocytes and improving the survival rate of the infected rats. The results suggest that PMN infiltration plays an important role in hepatic damage in acute cholangitis.
To evaluate the effect of intercellular adhesiveness molecule-1 (ICAM-1), E-selectin on hepatic microcirculation in acute cholangitis. The Changes of hepatic tissue, content of blood flow and Evan′s blue (EB) in hepatic tissue in acute cholangitis were determinated. Results: The number of PMN in hepatic tissue and sinusin increased, degenaration and necrosis of the hepatic cells and hepatic sinusoidal endothelial cells and content of blood flow in liver were reduced, and content of EB in hepatic tissue increased remarkbly in the rats with acute cholangitis. Pretreatment of anti ICAM-1 and E-selectin mAb reduced the damage of hepatic microcirculation. Conclusion: ICAM-1 and E-selectin may play an important role in damage to hepatic microcirculation in acute cholangitis.
The contents of lipid peroxides(LPO)and vitamin E(V.E)and some functional index and histologic changes in the lungs from the the rabbit models of acute cholangitis of severe type(ACST)were measured dynamically.The results revealed that the V.E content decreased strikingly from 6 hours and the LPO level increased progressivelg from 12 hours in the lungs.Simultanuosly,the congestion and neutrophil infiltreation in the lung mesenchyme,and the endothelial cell damage and thrombosis in the lung blood capillaries had been observed.These suggest that acute lung injury induced by ACST is referable to the lipid peroxidation damage to the lung blood capillaries which is due to increased LPO and decreased antioxidants including V.E.
The authors observed the progressive changes of the platelet activity in 25 cases of acute cholangitis severe type(ASCT)within 2 weeks of pre-and-post-operation.The results revealed that there are signficant changes of the platelet activity in ASCT.The levels of the platelet activity were proportional to the severity of disease and degree of biliary duct obstruction.Persistency of abnormality of platelet activity may predict the worse of disease and bad prognosis.The results are useful to understand the complex changes of pathophysiology in ACST,to the mechanism of multiple organic failure.
31 cases of iatrogenic cholangic injury reported. 28 cases followed from 9 months to 6 years. iatrogenic cholangic injury is not an uncommon occurence main cases are inregular procedures, and carelessness in this group, only 9 cases were found intraoperatively. The main manifestations after injury were aggravating jaundice and/or bilious peritonitis. Symptoms, signs, B-type ultrsound and sometimes ERCP were used for diagnosis. Once the injury ascertained ends are the best treatment, an alternative Roux-Y Cholangiojejunostomy was also commonly used. In this group, 4 cases received the first methos and all with good results; 23 patients treated by the second methos, 17 were uneventful, 4 experienced more or less abdomenal pain, 2 suffered difinite repeated cholangitis and another 1 died.
ObjectiveTo investigate the effectiveness of epidermal growth factor receptor antagonist (AG-1478) on chronic proliferative cholangitis (CPC), so as to investigate new treatment approach for hepatolithiasis associated with CPC. MethodsForty-six SD rats were divided into 5 groups: CPC model group (n=10), only made models. AG-1478 treatment group (divided into 3 mg/kg， 6 mg/kg， and 12 mg/kg groups, n=10 per group), the common bile ducts in CPC animal model received an intralumenal administration of AG-1478 at the meantime of modeling, followed by intraperitoneal AG-1478 injection of 1.5 mg/(kg·d) for 7 days. Sham operation group (SO group, n=6). Subsequently, histopathological observation, immunohistochemistry, real time PCR， and Western blot were used to evaluate the mRNA expression and influence of AG-1478 on the hyperplasia （EGFR， ki-67， BrdU， collagen Ⅰ protein） and lithogenic potential (Mucin 5AC) of CPC. ResultsCompared with CPC model group, the expressions of EGFR, ki-67， and BrdU were obviously decreased in the AG-1478 treatment group. Also, the inhibition of hyperplasia of biliary epithelium and collagen fibers were confirmed by histopathological observation. Additionally, the expressions of Mucin 5AC mRNA and collagen Ⅰ protein remarkable decreased in the AG-1478 treatment group (Plt;0.05). Conclusions EGFR inhibitor (AG-1478) could shows inhibitory effectivenss on the CPC-mediated hyperplasia and lithogenic potential, and therefore holds promise as the new treatment approach for CPC.
Objective To investigate the phenotypic change and proliferation of fibroblasts in human inflammatory strictured bile duct wall. Methods We observed the density and ultrastructure of fibroblasts, and the histologic structure in human normal bile duct wall and inflammatory strictured bile duct wall by light and electron microscope.Results The results showed that fibroblasts were the main source of extracellular matrix production in bile duct wall. The phenotype of fibroblasts in inflammatory strictured bile duct wall changed obviously, quiescent fibroblasts were activated and transformed to myofibroblasts, with massive proliferation. Conclusion These data suggest that massive proliferation of activated fibroblasts and myofibroblasts is the main source of extracellular matrix overproduction which results in inflammatory bile duct stricture.