Belhaj Asmae, Boven Carine, Dewachter Laurence, Ruiz Patino Maria, Sokolow Youri, Rondelet Benoît
Department of Cardio-Vascular, Thoracic Surgery and Lung Transplantation, CHU UcL Namur, Catholic University of Louvain, Yvoir, Belgium.
Laboratory of Physiology and Pharmacology, Faculty of Medicine, Free University of Brussels, Brussels, Belgium.
Ann Transplant. 2017 Jun 16;22:361-369. doi: 10.12659/aot.903313.
BACKGROUND Primary graft dysfunction (PGD) is responsible of high early mortality in lung transplanted patients. We measured the rate of surfactant proteins in the organ donor, and we observed the occurrence of lung PGD in the recipient. The co-relation between these two parameters was evaluated. MATERIAL AND METHODS In this pilot study, we prospectively collected blood samples and lung biopsies in thirteen donors at the time of recovery of organs before preservation. Gene expression of SP-A, SP-B, SP-D, and CC16 was evaluated by real-time quantitative PCR. Surfactant proteins plasma levels were evaluated by ELISA. Post-transplant assessments included hemodynamic, arterial blood gas measurements, and radiographic evaluation to determine PGD and lung biopsies. RESULTS Nine of the thirteen recipients (69%) developed lung infiltrates and four (31%) developed PGD at either stages 2 or 3. SP-A and SP-B expressions were dramatically reduced in lung allografts of these patients, while lung expression of SP-D and CC16 remained unchanged. Plasma levels of SP-A, SP-B, SP-D, and CC16 did not differ. CONCLUSIONS Primary graft dysfunction may be initiated in the donor. Lung allografts with low lung SP-A and SP-B gene expression prior to implantation are associated with increased incidence of lung infiltrates after transplantation.
背景 原发性移植肺功能障碍(PGD)是肺移植患者早期高死亡率的原因。我们测量了器官供体中表面活性物质蛋白的水平,并观察了受体中肺PGD的发生情况。评估了这两个参数之间的相关性。材料与方法 在这项初步研究中,我们前瞻性地在13名供体器官保存前回收时采集了血样和肺活检样本。通过实时定量PCR评估SP-A、SP-B、SP-D和CC16的基因表达。通过ELISA评估表面活性物质蛋白的血浆水平。移植后评估包括血流动力学、动脉血气测量以及影像学评估以确定PGD和肺活检。结果 13名受体中有9名(69%)出现肺部浸润,4名(31%)在2期或3期出现PGD。这些患者的同种异体肺移植中SP-A和SP-B的表达显著降低,而SP-D和CC16的肺表达保持不变。SP-A、SP-B、SP-D和CC16的血浆水平没有差异。结论 原发性移植肺功能障碍可能在供体中就已启动。植入前肺SP-A和SP-B基因表达低的同种异体肺移植与移植后肺部浸润发生率增加相关。