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  • Title: [Clinical manifestation and patho-typing of biliary cast syndrome in patients after orthotopic liver transplantation].
    Author: Zhu XD, Shen ZY, Chen XG, Zang YJ.
    Journal: Zhonghua Wai Ke Za Zhi; 2008 May 15; 46(10):728-32. PubMed ID: 18953924.
    Abstract:
    OBJECTIVE: To summarize the Patho-typing and the clinical manifestation of biliary cast syndrome (BCS) in patients after orthotopic liver transplantation. METHODS: The clinical manifestation, findings,therapeutic means and efficacy of 103 patients with biliary cast syndrome after orthotopic liver transplantation were retrospectively analyzed. According to the injury level of biliary duct epithelium, patients were divided into different groups. All cases were followed up for twelve months. The place, degree and time after operation would be recorded when non-anastomotic biliary stricture was found. RESULTS: There were 59 BCS cases in the general hospital of armed police force of China. The incidence rate of BCS was 9.1%. Many BCS patients showed symptoms such as jaundice, deep urine color, gray stools, itch of skin and fever. Some were asymptomatic. In laboratory test, the liver functional enzyme in serum were increased, the total white cell count in peripheral blood was increased either. Cholangiography via T tube of biliary tract might show filling defect. According to the change degree of the biliary tract tree, there were four types filling defect concluded from all the presentation in BCS patients. Solid obturation of biliary tract were found by the check with optical fiber choledochoscope in all BCS patients, necrosis of biliary tract epithelium were observed in partial BCS patients. According to the injury level of biliary duct epithelium (gradually aggravated), BCS patients were divided into six groups (type I, type II, type III, type IV, type V and type VI). Fourteen cases were found in type I and 18 in type II. No clinical symptom was found in these two groups, a few indicators in serum (alanine aminotransferase ALT, total bilirubin TBIL, direct bilirubin DBIL) were in normal range, and others (gamma-glutamyl transferase GGT, alkaline phosphatase ALP) were heightened in 5 patients. There was no biliary cast (BC) found anymore in the period of follow-up in two groups. No stricture was found in both group. Twenty-seven cases in type III and 23 cases in type IV, it was found there were about 33.4% patients accompanied with fever and 25.9% accompanied with jaundice in type III. Paralleled,there were about 30.4% and 34.8% patients in type IV. The liver functional enzyme in serum were found increased in both type. After supporting treatment for 3-6 months,there were 5 and 3 patients present as mild non-anastomotic biliary stricture in type III and type IV group. In the group type V, there were 13 patients. The detected liver functional indicators in serum were increased. After supporting treatment for 6-12 months,there were 4 patients present as moderate non-anastomotic biliary stricture in this group. There were 18 patients in type VI group, all indicators of the liver functional enzyme in serum before the treatment were elevated conspicuously. All patients in this group were found serious stricture up to three places that have not been sustained in the period of follow-up. Nine died of MOSF, 1 died of AOSC, 8 had undergone retransplantation. In the retransplantation patients, 4 died of post operation MOSF, 3 recovered to normal, 1 patient was found BCS once more 15 d after the retransplantation and the third-transplantation was performed 7 months after the second transplantation, no BCS was found again. The deaths total rate was 13.6%, death rate of retransplantation was 44.0%, total cure rate was 54.0%, total improvement rate was 71.0% and total stenosis rate was 29.0%. CONCLUSIONS: (1) According to the check with optical fiber choledochoscope, there are 6 types of patho-typing in BCS patients. The clinical manifestation includes jaundice and fever. The filling defect of the biliary tract tree might showed 4 appearances. (2)The patho-typing contributes to the clinical manifestation and the filling defect of the biliary tract tree.
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