Tabatabai L, Lewis W D, Gordon F, Jenkins R, Khettry U
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Hum Pathol. 1999 Jan;30(1):39-47. doi: 10.1016/s0046-8177(99)90298-8.
The causes and pathologic changes leading to fibrosis and cirrhosis after orthotopic liver transplantation (OLT) are not fully defined. The computerized pathology files were searched for cases of fibrosis/cirrhosis after OLT. Of 493 grafts from 435 patients, 35 grafts from 32 patients of posttransplantation liver fibrosis/cirrhosis were identified and retrieved (7%). Detailed histopathologic examinations of all post-OLT liver biopsy specimens were performed in conjunction with clinical, virologic, serologic, and molecular diagnostics information. Two cases with subcapsular septa and fibrous tissue close to hilum were excluded as false positives. Fibrosis/cirrhosis was confirmed in the remaining 33 grafts. In 20, the underlying cause was recurrent viral hepatitis, including eight with hepatitis C, 10 with hepatitis B, and two with combined hepatitis C and B. Another two with pretransplantation chronic hepatitis B developed cirrhosis without detectable virologic markers after OLT; these were biliary type secondary to obstruction in one, and chronic changes due to severe graft ischemia in one. Three patients acquired hepatitis C after OLT, with molecular confirmation available in two. In five patients, the underlying causes were Budd-Chiari syndrome and autoimmune hepatitis, recurrent autoimmune hepatitis, recurrent primary biliary cirrhosis, alcohol-induced liver disease, and recurrent bile duct carcinoma. Three cases had centrilobular fibrosis but without bridging septa or cirrhosis as a result of chronic rejection. It was concluded that (1) Cirrhosis after OLT is uncommon (7%). (2) Chronic rejection does not lead to cirrhosis, but it may result in centrilobular fibrosis. (3) In most (70%) cases, cirrhosis after OLT is attributed to recurrent or acquired viral hepatitis.
原位肝移植（OLT）后导致纤维化和肝硬化的原因及病理变化尚未完全明确。检索计算机化病理文件以查找OLT后纤维化/肝硬化病例。在435例患者的493个移植物中，识别并检索出32例患者的35个移植后肝纤维化/肝硬化移植物（7%）。结合临床、病毒学、血清学和分子诊断信息，对所有OLT后肝活检标本进行了详细的组织病理学检查。排除2例包膜下间隔和靠近肝门的纤维组织病例，将其作为假阳性。其余33个移植物确诊为纤维化/肝硬化。其中20例的潜在病因是复发性病毒性肝炎，包括8例丙型肝炎、10例乙型肝炎以及2例丙型和乙型肝炎合并感染。另外2例移植前慢性乙型肝炎患者在OLT后发展为肝硬化，但未检测到病毒学标志物；其中1例为继发于梗阻的胆汁型肝硬化，另1例为严重移植物缺血导致的慢性改变。3例患者在OLT后感染丙型肝炎，其中2例有分子诊断依据。5例患者的潜在病因是布加综合征、自身免疫性肝炎复发、复发性原发性胆汁性肝硬化、酒精性肝病和复发性胆管癌。3例因慢性排斥反应出现中央小叶纤维化，但无桥接间隔或肝硬化。研究得出结论：（1）OLT后肝硬化并不常见（7%）。（2）慢性排斥反应不会导致肝硬化，但可能导致中央小叶纤维化。（3）在大多数（70%）病例中，OLT后肝硬化归因于复发性或获得性病毒性肝炎。
