Soriano-López D P, Alcántar-Fierros J M, Hernández-Plata J A, González-Jorge A L, Velázquez-Ramos S, Flores-Hernández M A, Fuentes V, Castañeda P, Nieto J, Sánchez J L, López B, Valencia-Mayoral P, Varela-Fascinetto G
Department of Transplantation, Hospital Infantil de México Federico Gómez, México City, México.
Department of Anesthesiology, Hospital Infantil de México Federico Gómez, México City, México.
Transplant Proc. 2016 Mar;48(2):654-7. doi: 10.1016/j.transproceed.2016.02.031.
This is a cohort, retrospective, comparative study of all liver transplant recipients from a single center, from May 1998 to July 2015. Patients were divided into two groups according to the type of Epstein-Barr viral load monitoring. For group I (1998-2007), polymerase chain reaction (PCR) was not available or it was only qualitative with limited access. For group II (2008-2015), we used periodically scheduled quantitative PCR in plasma and leukocytes, with aggressive tapering of immunosuppression as soon as viral replication was detected. Ninety-eight recipients were included, 41 (41.8%) were Epstein-Barr virus (EBV) - seronegative before liver transplantation (LT). EBV replication was confirmed in 74 patients (75.5%), being more frequent in seronegative (87.8%) than seropositive patients (66.6%). Eight recipients (8.1%) developed post-transplantation lymphoproliferative disorder (PTLD) on average at 14.3 months post-LT, seven of eight were <3 years at LT, four of eight were D+/R- for EBV, and all had post-LT EBV replication confirmed by PCR. PTLD was classified as lymphoma (n = 4), polymorphic polyclonal (n = 3), and lymphoid hyperplasia (n = 1). Five patients died, and three cleared PTLD after immunosuppression tapering or interruption. There were no significant differences in the etiology, age at LT (5.6 vs. 7.3 years, P = .069), patients <4 years (53.2% vs. 35.3%, P = .103), or EBV seronegative recipients (44.7% vs. 37.3%, P = .54); however, the incidence of PTLD decreased from 14.9% to 1.9% (P = .026), and graft rejection from 51.1% to 29.4% (P = .039). One- and 5-year patient survival rates were 94.7% and 85%, respectively, with no differences between groups. This strategy dramatically decreased the incidence of PTLD (14.9% vs. 1.9%), without increasing the incidence of rejection; therefore, we recommend that it should be used in the follow-up of all pediatric LT recipients.
这是一项针对1998年5月至2015年7月期间来自单一中心的所有肝移植受者的队列回顾性比较研究。根据爱泼斯坦-巴尔病毒载量监测类型将患者分为两组。对于第一组(1998 - 2007年),聚合酶链反应(PCR)不可用或仅为定性检测且获取有限。对于第二组(2008 - 2015年),我们在血浆和白细胞中定期进行定量PCR检测,一旦检测到病毒复制就积极逐渐减少免疫抑制剂用量。共纳入98名受者,41名(41.8%)在肝移植(LT)前为爱泼斯坦-巴尔病毒(EBV)血清阴性。74名患者(75.5%)证实有EBV复制,血清阴性患者(87.8%)的EBV复制比血清阳性患者(66.6%)更常见。8名受者(8.1%)在肝移植后平均14.3个月发生移植后淋巴组织增生性疾病(PTLD),8名中有7名肝移植时年龄小于3岁,8名中有4名EBV为D + /R -,且所有患者肝移植后经PCR证实有EBV复制。PTLD分为淋巴瘤(n = 4)、多形性多克隆(n = 3)和淋巴样增生(n = 1)。5名患者死亡,3名患者在免疫抑制剂减量或停用后PTLD消退。在病因、肝移植时年龄(5.6岁对7.3岁,P = 0.069)、年龄小于4岁的患者(53.2%对35.3%,P = 0.103)或EBV血清阴性受者(44.7%对37.3%,P = 0.54)方面无显著差异;然而,PTLD的发生率从14.9%降至1.9%(P = 0.026),移植物排斥发生率从51.1%降至29.4%(P = 0.039)。1年和5年患者生存率分别为94.7%和85%,两组间无差异。该策略显著降低了PTLD的发生率(14.9%对1.9%),且未增加排斥发生率;因此,我们建议在所有小儿肝移植受者的随访中采用该策略。