Ludwig J, Batts K P, MacCarty R L
Section of Medical Pathology, Mayo Clinic, Rochester, MN 55905.
Mayo Clin Proc. 1992 Jun;67(6):519-26. doi: 10.1016/s0025-6196(12)60457-1.
In this report, our objectives are to introduce the term "ischemic cholangitis" as an etiologic designation and to describe its manifestations. Herein we use the label "ischemic cholangitis" as a collective term for ischemic bile duct necrosis, cholangitis caused by ischemia but without necrosis, and biliary fibrosis as a manifestation of ischemic damage. The condition was observed in 12 allografts, either at the time of retransplantation (9 cases) or at autopsy (3 cases). Ischemic cholangitis involved primarily perihilar extrahepatic and intrahepatic bile ducts. The findings included duct necroses (eight cases), strictures (four cases), and cholangiectases (four cases); some of these features coexisted. In addition, complicating ascending cholangitis and cholangitic abscesses were noted in three cases. Ischemic cholangitis was caused by hepatic artery thrombosis (in nine patients) or stenosis (in one) or by occlusion of parabiliary arteries by fibrointimal proliferations, probably attributable to old thromboses (in two, in conjunction with associated foam cell arteriopathy in one). Biopsy specimens before retransplantation or autopsy were obtained in 11 patients, only 1 of whom had an infarct as direct evidence of ischemia. Nine patients had evidence of biliary obstruction or bile flow impairment; in two cases, specimens were normal or nondiagnostic relative to cholangitis. Features of cellular rejection associated with the manifestations of bile flow impairment and ischemia were noted in five cases. Thus, biopsy features that suggest biliary obstruction, with or without cellular rejection, may be a manifestation of ischemic cholangitis. We conclude that ischemic cholangitis is an important cause of cholestatic graft failure but that this type of cholangitis is difficult to diagnose because of its misleading biopsy manifestations.
在本报告中，我们的目的是引入“缺血性胆管炎”这一病因学名称并描述其表现。在此，我们将“缺血性胆管炎”这一标签用作缺血性胆管坏死、缺血所致但无坏死的胆管炎以及作为缺血性损伤表现的胆管纤维化的统称。在12例同种异体移植中观察到了这种情况，其中9例是在再次移植时发现，3例是在尸检时发现。缺血性胆管炎主要累及肝门部肝外胆管和肝内胆管。所见包括胆管坏死（8例）、狭窄（4例）和胆管扩张（4例）；其中一些特征并存。此外，3例出现了并发的上行性胆管炎和胆管脓肿。缺血性胆管炎是由肝动脉血栓形成（9例患者）或狭窄（1例），或由纤维内膜增生导致的胆管旁动脉闭塞（2例，其中1例伴有相关的泡沫细胞动脉病变）引起的。11例患者在再次移植或尸检前获取了活检标本，其中只有1例有梗死作为缺血的直接证据。9例患者有胆管梗阻或胆汁流动受损的证据；2例患者的标本相对于胆管炎而言正常或无法诊断。5例患者出现了与胆汁流动受损及缺血表现相关的细胞排斥特征。因此，提示胆管梗阻的活检特征，无论有无细胞排斥，都可能是缺血性胆管炎的一种表现。我们得出结论，缺血性胆管炎是胆汁淤积性移植物功能衰竭的一个重要原因，但由于其活检表现具有误导性，这种类型的胆管炎难以诊断。
