Pappo O, Ramos H, Starzl T E, Fung J J, Demetris A J
Department of Pathology, University of Pittsburgh Medical Center, Pennsylvania 15213.
Am J Surg Pathol. 1995 Feb;19(2):192-206. doi: 10.1097/00000478-199502000-00008.
The clinicopathologic features of liver allograft dysfunction occurring in 51 symptomatic recipients after more than 5 years' survival (mean 7.1 years) with the same hepatic allograft were compared with those of a similar group of 14 asymptomatic patients (mean survival, 9.9 years) who underwent a nonclinically indicated protocol liver biopsy evaluation. Predictably, patients who had clinically indicated biopsies more frequently showed histopathologic alterations (76% versus 36%, p < 0.002). After detailed clinicopathologic correlation, the changes in the symptomatic patients were attributed primarily to definite or presumed viral hepatitis in 17 of 51 (33%) patients, 11 of whom had recurrent viral disease; seven of 51 (14%) had nonviral recurrent original disease, three (6%) had obstructive cholangiopathy, and 11 (22%) had acute and/or chronic rejection. In 13 of 51 (25%) of the symptomatic patients, the clinical and pathologic abnormalities were minimal. Long-term liver allograft survival in nine of 14 (64%) of the asymptomatic patients was associated with minimally abnormal histologic alterations. Two of the asymptomatic patients had obstructive cholangiopathy; two others has recurrence of the original disease and one has possible viral hepatitis. Viral hepatitis types B and C, alcoholic liver disease, autoimmune hepatitis, granulomatous hepatitis (not otherwise specified), and probably primary biliary cirrhosis and primary sclerosing cholangitis were shown to recur after hepatic transplantation. The histopathologic changes associated with acute and chronic rejection frequently overlapped with other syndromes causing late dysfunction, such as chronic viral or autoimmune hepatitis, primary biliary cirrhosis, or primary sclerosing cholangitis; more than one insult could be identified in 15 cases, which made the differential diagnosis of causes of late liver allograft dysfunction much more difficult than early after hepatic transplantation. It is important to correlate the biopsy findings with the liver injury tests, the results of viral and autoimmune antibody serologic studies, and review of previous biopsies and to be aware of the original disease, recent changes in immunosuppression, and results of therapeutic intervention(s) to identify correctly the causes of liver allograft dysfunction in this patient population.
对51例有症状的肝移植受者（平均存活7.1年）在接受同一肝脏移植超过5年后发生的肝移植功能障碍的临床病理特征，与14例无症状患者（平均存活9.9年）组成的类似组进行比较，后者接受了非临床指征的肝脏活检评估。不出所料，有临床指征进行活检的患者更频繁地出现组织病理学改变（76%对36%，p<0.002）。经过详细的临床病理相关性分析，有症状患者的改变主要归因于51例患者中的17例（33%）明确或疑似病毒性肝炎，其中11例有复发性病毒病；51例中的7例（14%）有非病毒性复发性原发病，3例（6%）有阻塞性胆管病，11例（22%）有急性和/或慢性排斥反应。51例有症状患者中的13例（25%）临床和病理异常轻微。14例无症状患者中的9例（64%）长期肝移植存活与组织学改变轻微异常有关。2例无症状患者有阻塞性胆管病；另外2例有原发病复发，1例可能有病毒性肝炎。乙型和丙型病毒性肝炎、酒精性肝病、自身免疫性肝炎、肉芽肿性肝炎（未另作说明），可能还有原发性胆汁性肝硬化和原发性硬化性胆管炎在肝移植后有复发。与急性和慢性排斥反应相关的组织病理学改变经常与导致晚期功能障碍的其他综合征重叠，如慢性病毒性或自身免疫性肝炎、原发性胆汁性肝硬化或原发性硬化性胆管炎；15例中可识别出不止一种损伤，这使得肝移植晚期功能障碍原因的鉴别诊断比肝移植早期困难得多。将活检结果与肝损伤检查、病毒和自身免疫抗体血清学研究结果以及既往活检回顾相关联，并了解原发病、免疫抑制的近期变化以及治疗干预结果，对于正确识别该患者群体肝移植功能障碍的原因很重要。
