Oya H, Sato Y, Yamamoto S, Nakatsuka H, Kobayashi T, Watanabe T, Kokai H, Hatakeyama K
Division of Digestive and General Surgery, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Transplant Proc. 2008 Oct;40(8):2549-51. doi: 10.1016/j.transproceed.2008.07.117.
Thrombotic microangiopathy (TMA) has rarely been reported in the setting of liver transplantation. Herein we have reported a successful case of TMA after ABO-incompatible living donor liver transplantation (LDLT) treated with plasma exchange and high-dose intravenous gamma-globulin infusion. A 50-year-old woman was diagnosed with hepatitis C virus-related cirrhosis. We performed an ABO-incompatible LDLT (group B to O) with preoperative plasma exchange to reduce the anti-B hemagglutinin titers to 1:8. The immunosuppressants consisted of tacrolimus, mycophenolate mofetil, and steroid. On postoperative day (POD) 8, her anti-B hemagglutinin titer suddenly increased to 1:64. The serum lactate dehydrogenase (LDH) level was grossly elevated (1518 IU/L). On POD 13, we suspected infection of an intra-abdominal hematoma (Serratia marcescens) which was drained surgically. On day 5 after the reoperation, thrombocytopenia developed with a platelet count of 3 x 10(4)/mm3. A peripheral blood film showed severe red blood cell (RBC) fragmentation. Thus, we made a clinical diagnosis of TMA and reduced the tacrolimus dose. We started intensive daily plasma exchange (4 L/d) with fresh frozen plasma and high-dose intravenous gamma-globulin infusions. One week thereafter, thrombocytopenia improved with reduced transfusion requirements. The peripheral blood film showed normal RBC morphology. The serum LDH returned to baseline levels. Four factors were considered to have caused TMA in this case: the prescription of tacrolimus, ABO-incompatible liver transplantation, bacterial infection, and surgical stress. These factors may have all contributed by causing significant endothelial injury and TMA.
血栓性微血管病（TMA）在肝移植患者中鲜有报道。本文报告了1例ABO血型不相容的活体供肝肝移植（LDLT）术后发生TMA的成功治疗病例，治疗方法为血浆置换和大剂量静脉输注丙种球蛋白。一名50岁女性被诊断为丙型肝炎病毒相关性肝硬化。我们进行了ABO血型不相容的LDLT（B型供肝至O型受者），术前进行血浆置换以将抗B血凝素滴度降至1:8。免疫抑制剂包括他克莫司、霉酚酸酯和类固醇。术后第8天，她的抗B血凝素滴度突然升至1:64。血清乳酸脱氢酶（LDH）水平大幅升高（1518 IU/L）。术后第13天，我们怀疑腹腔内血肿感染（粘质沙雷菌），并进行了手术引流。再次手术后第5天，出现血小板减少，血小板计数为3×10⁴/mm³。外周血涂片显示严重的红细胞（RBC）破碎。因此，我们临床诊断为TMA，并降低了他克莫司的剂量。我们开始每天进行强化血浆置换（4 L/d），使用新鲜冰冻血浆，并大剂量静脉输注丙种球蛋白。1周后，血小板减少症有所改善，输血需求减少。外周血涂片显示RBC形态正常。血清LDH恢复至基线水平。该病例中导致TMA的因素有4个：他克莫司的使用、ABO血型不相容的肝移植、细菌感染和手术应激。这些因素可能均通过引起显著的内皮损伤导致了TMA。
