Shah Janak N, Haigh W Geoffrey, Lee Sum P, Lucey Michael R, Brensinger Colleen M, Kochman Michael L, Long William B, Olthoff Kim, Shaked Abraham, Ginsberg Gregory G
Division of Gastroenterology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Am J Gastroenterol. 2003 Aug;98(8):1861-7. doi: 10.1111/j.1572-0241.2003.07617.x.
Biliary casts develop in up to 18% of liver transplant recipients. Casts are associated with morbidity, graft failure, need for retransplantation, and mortality. Proposed etiological mechanisms include acute cellular rejection, ischemia, infection, and biliary obstruction. We aimed to identify clinical features associated with biliary cast formation, review treatments, and analyze the biochemical composition of casts at a single, large, liver transplant center.
Patient records were reviewed retrospectively to identify patients who developed casts. Data were collected with attention to ischemia, rejection, obstruction, infection, immunosuppression, postoperative biliary drain use, and cast-directed management, and were compared with data from controls. Cast specimens, retrieved at cholangiography, were analyzed with chromatography techniques.
Ischemic factors were noted in 70% (7/10) of cast patients versus 15% (6/40) of controls (OR = 13.2; 95% CI = 2.7-66.0; p = 0.001). Biliary strictures were present in 50% of cast patients versus 10% of controls (OR = 9.0; 95% CI = 1.8-45.2; p = 0.01). Differences in cold ischemia time, acute cellular rejection, cyclosporin use, infection, and postoperative biliary drain use were not significant. Casts were successfully treated by endoscopic and percutaneous methods in 60% of patients. One patient died of cast-related complications (mortality 10%). Four casts were in satisfactory condition for biochemical analysis. Bilirubin was the main component ( approximately 10-50%). Bile acid synthesis products and cholesterol comprised smaller percentages, and protein comprised only 5-10%.
Biliary casts are more likely to develop in the setting of hepatic ischemia and biliary strictures. Endoscopic and percutaneous cast extraction might achieve favorable results and should be attempted before surgical therapy.
高达18%的肝移植受者会出现胆泥。胆泥与发病率、移植物衰竭、再次移植需求及死亡率相关。推测的病因机制包括急性细胞排斥反应、缺血、感染及胆道梗阻。我们旨在确定与胆泥形成相关的临床特征，回顾治疗方法，并分析一家大型肝移植中心胆泥的生化成分。
回顾性分析患者记录以确定出现胆泥的患者。收集有关缺血、排斥反应、梗阻、感染、免疫抑制、术后胆道引流使用及针对胆泥的处理的数据，并与对照组数据进行比较。在胆管造影时获取的胆泥标本采用色谱技术进行分析。
70%（7/10）的胆泥患者存在缺血因素，而对照组为15%（6/40）（比值比=13.2；95%置信区间=2.7-66.0；p=0.001）。50%的胆泥患者存在胆道狭窄，而对照组为10%（比值比=9.0；95%置信区间=1.8-45.2；p=0.01）。冷缺血时间、急性细胞排斥反应、环孢素使用、感染及术后胆道引流使用方面的差异无统计学意义。60%的患者通过内镜和经皮方法成功治疗了胆泥。1例患者死于胆泥相关并发症（死亡率10%）。4份胆泥标本状况良好，可用于生化分析。胆红素是主要成分（约10%-50%）。胆汁酸合成产物和胆固醇占比更小，蛋白质仅占5%-10%。
在肝缺血和胆道狭窄情况下更易形成胆泥。内镜和经皮胆泥清除术可能取得良好效果，应在手术治疗前尝试。
