PDF(Pubmed)
Abstract：
Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the common causes of cirrhosis and hepatocellular carcinoma (HCC) and is a leading indication for liver transplantation (LT). Patients with NAFLD-related cirrhosis and HCC are at high risk for the development of recurrent NAFLD after LT. NAFLD can also develop de novo post-transplantation in patients subjected to LT for other indications. Besides the pretransplant presence of various components of metabolic syndrome (MS) use of immunosuppressive agents in the post-LT setting forms one of the major drivers for the development of post-LT NAFLD. Individual components of conventional immunosuppressive regimens (corticosteroids, calcineurin inhibitors, and m-TOR inhibitors) are all implicated in the development of post-LT metabolic derangement and follow unique mechanisms of action and degree of disturbances. The development of cardiovascular risk is associated with post-LT NAFLD, although graft outcomes do not seem to be influenced only by the presence of post-LT NAFLD. Measures in consonance with the management of NAFLD, in general, including lifestyle modifications and control of metabolic risk factors, hold true for post-LT NAFLD. Tailoring immunosuppression strategies with early corticosteroid withdrawal and calcineurin inhibitor minimization balancing against the risk of graft rejection constitutes important nuances in the individualized management of post-LT NAFLD.
摘要：
非酒精性脂肪性肝病（NAFLD）已成为肝硬化和肝细胞癌（HCC）的常见原因之一，是肝移植（LT）的主要指征。NAFLD相关性肝硬化和HCC患者在LT后发生复发性NAFLD的风险很高。NAFLD还可以在接受LT治疗的患者中在移植后从头发展为其他适应症。除了移植前存在代谢综合征（MS）的各种成分外，在LT后环境中使用免疫抑制剂也是LT后NAFLD发展的主要驱动因素之一。常规免疫抑制方案的个体成分（皮质类固醇，钙调磷酸酶抑制剂，和m-TOR抑制剂）都与LT后代谢紊乱的发展有关，并遵循独特的作用机制和紊乱程度。心血管风险的发展与LT后NAFLD有关，尽管移植物结局似乎不仅受LT后NAFLD的影响。与NAFLD管理相一致的措施，总的来说,包括改变生活方式和控制代谢危险因素，适用于LT后NAFLD。调整免疫抑制策略与早期皮质类固醇戒断和钙调磷酸酶抑制剂最小化与移植物排斥风险的平衡构成了LT后NAFLD个体化管理的重要细微差别。
