Küpeli Elif, Ulubay Gaye, Doğrul Ilgaz, Birben Özlem, Seyfettin Pınar, Özsancak Uğurlu Aylin, Öner Eyüboğlu Füsun, Haberal Mehmet
From the Pulmonary Department, Baskent University School of Medicine, Ankara, Turkey.
Exp Clin Transplant. 2015 Apr;13 Suppl 1:223-7.
Solid-organ transplant recipients can develop chronic hypercoagulation that increases the incidence of pulmonary embolism. Here, we evaluate the frequency of pulmonary embolism in solid-organ transplant recipients during the first 10 years after transplantation and evaluate the risk factors for its development.
The medical records of solid-organ transplant recipients who were treated between 2003 and 2013 were retrospectively reviewed. The reviewed data included demographics, type of transplant, comorbidities, procoagulation factors, thromboembolism prophylaxis, and the timing and extent of pulmonary embolism.
In total, 999 solid-organ transplant recipients are included in this study (661 renal and 338 liver transplant recipients) (male: female ratio = 665:334). Twelve renal (1.2%) and 1 liver transplant recipient (0.3%) were diagnosed with pulmonary embolism. Pulmonary embolism developed 1 year after transplantation in 10 patients: 1 patient developed pulmonary embolism < 3 months after transplantation, and the other 9 patients developed pulmonary embolism within 3 to 6 months. No patients had a prior history of deep venous thrombosis or pulmonary embolism. Five patients received tacrolimus, 7 patients received sirolimus, and 1 patient received cyclosporine. Ten patients received prednisolone, and 8 patients received mycophenolate mofetil. All patients were homozygous normal for factor V Leiden and prothrombin genes. One patient was homozygous abnormal, and 1 patient had a heterozygous mutation in the methylenetetrahydrofolate reductase gene. Two patients were treated with low-molecular-weight heparin, while the remaining patients received warfarin. Eight patients were treated for 6 months, and the remainder received longer treatments.
Here, the incidence of pulmonary embolism in solid-organ transplant recipients is 1.2%. Renal transplant recipients are at higher risk of developing pulmonary embolism than liver transplant recipients. The factors that increase the risk of pulmonary embolism in solid-organ transplant recipients appear to be multifactorial and include genetic predisposition.
实体器官移植受者可发生慢性高凝状态，从而增加肺栓塞的发生率。在此，我们评估实体器官移植受者移植后10年内肺栓塞的发生频率，并评估其发生的危险因素。
回顾性分析2003年至2013年期间接受治疗的实体器官移植受者的病历。所回顾的数据包括人口统计学资料、移植类型、合并症、促凝因子、血栓栓塞预防措施以及肺栓塞的发生时间和范围。
本研究共纳入999例实体器官移植受者（661例肾移植受者和338例肝移植受者）（男女比例为665:334）。12例肾移植受者（1.2%）和1例肝移植受者（0.3%）被诊断为肺栓塞。10例患者在移植后1年发生肺栓塞：1例患者在移植后<3个月发生肺栓塞，其他9例患者在3至6个月内发生肺栓塞。所有患者既往均无深静脉血栓形成或肺栓塞病史。5例患者接受他克莫司治疗，7例患者接受西罗莫司治疗，1例患者接受环孢素治疗。10例患者接受泼尼松龙治疗，8例患者接受霉酚酸酯治疗。所有患者的凝血因子V Leiden和凝血酶原基因均为纯合子正常。1例患者为纯合子异常，1例患者亚甲基四氢叶酸还原酶基因存在杂合突变。2例患者接受低分子量肝素治疗，其余患者接受华法林治疗。8例患者接受了6个月的治疗，其余患者接受了更长时间的治疗。
实体器官移植受者中肺栓塞的发生率为1.2%。肾移植受者发生肺栓塞的风险高于肝移植受者。实体器官移植受者发生肺栓塞风险增加的因素似乎是多因素的，包括遗传易感性。
