Ramasubbu K, Mullick T, Koo A, Hussein M, Henderson J M, Mullen K D, Avery R K
Department of Infectious Disease, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Transpl Infect Dis. 2003 Jun;5(2):98-103. doi: 10.1034/j.1399-3062.2003.00019.x.
Thrombotic microangiopathy (TMA) is a rare but potentially lethal complication encountered in solid organ and bone marrow transplant recipients, requiring rapid recognition, diagnosis, and initiation of therapy. Several potential causes have been identified in this setting, including viral infections and medications.
We report a case of TMA in a liver transplant recipient with active cytomegalovirus (CMV) gastritis. A 41-year-old female presented 3 months after liver transplantation with a 5-week history of nausea, vomiting, anorexia, and diarrhea. CMV serology was donor seropositive and recipient seronegative (D+/R-). The immunosuppressive regimen consisted of tacrolimus, mycophenolate mofetil, and prednisone. Evaluation revealed CMV viremia with a high viral load and intravenous ganciclovir was started. A decline in hemoglobin and platelets with an increase in lactate dehydrogenase (LDH) warranted hematologic evaluation, which revealed findings consistent with microangiopathic hemolytic anemia. Ganciclovir and tacrolimus were discontinued. Intravenous immunoglobulin was administered and daily plasmapheresis was initiated. As the patient's blood counts and LDH started to improve, ganciclovir was cautiously reinstituted. The patient's gastrointestinal symptoms gradually resolved and her blood counts continued to improve with prolonged plasmapheresis (a total of 23 plasmapheresis sessions). Tacrolimus and possibly CMV infection were suspected to be the cause for her TMA, and cyclosporine was substituted.
TMA is an important entity in the differential diagnosis of acute hemolytic anemia in liver transplant recipients. Many cases seem to be medication-induced. However, in treatment-resistant or relapsing cases, a possibility of concomitant CMV infection should be considered.
血栓性微血管病（TMA）是实体器官和骨髓移植受者中罕见但可能致命的并发症，需要迅速识别、诊断并开始治疗。在这种情况下已确定了几种潜在病因，包括病毒感染和药物。
我们报告了一例肝移植受者合并活动性巨细胞病毒（CMV）胃炎并发TMA的病例。一名41岁女性在肝移植术后3个月出现，有5周的恶心、呕吐、厌食和腹泻病史。CMV血清学检查显示供体血清阳性而受体血清阴性（D+/R-）。免疫抑制方案包括他克莫司、霉酚酸酯和泼尼松。评估发现CMV病毒血症且病毒载量高，遂开始静脉给予更昔洛韦。血红蛋白和血小板下降，乳酸脱氢酶（LDH）升高，需进行血液学评估，结果显示符合微血管病性溶血性贫血。停用更昔洛韦和他克莫司。给予静脉注射免疫球蛋白并开始每日进行血浆置换。随着患者血细胞计数和LDH开始改善，谨慎重新使用更昔洛韦。患者的胃肠道症状逐渐缓解，通过延长血浆置换（共进行23次血浆置换），其血细胞计数持续改善。怀疑他克莫司以及可能的CMV感染是其TMA的病因，遂改用环孢素。
TMA是肝移植受者急性溶血性贫血鉴别诊断中的一个重要疾病。许多病例似乎是药物诱导的。然而，在治疗抵抗或复发的病例中，应考虑合并CMV感染的可能性。
