Vik RoseAnn E, Bulle Esther B, Webley Wilmore C, Visintainer Paul, Ramirez Samantha, St Marie Peter, Stec Theresa, O'Hearn Lynne, Andrzejewski Chester, Vlaar Alexander P J
Department of Microbiology, University of Massachusetts Amherst, Amherst, MA.
Department of Intensive Care, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Blood Vessel Thromb Hemost. 2025 Jun 9;2(3):100080. doi: 10.1016/j.bvth.2025.100080. eCollection 2025 Aug.
Transfusion-associated circulatory overload (TACO) is a leading cause of transfusion-associated mortality. TACO is thought to result from hydrostatic forces in the vascular space, leading to transudative pulmonary edema. Recent studies suggest that TACO is not solely a volume overload phenomenon, but may involve inflammatory processes. This study aimed to further explore the presence of inflammation in patients with TACO. We conducted a retrospective study with 3 cohorts receiving red blood cell transfusion: (1) patients having TACO as defined by a national hemovigilance case surveillance classification (conventional TACO [cTACO], n = 33); (2) patients having symptoms consistent with TACO but not completely meeting reporting criteria (institutional TACO [iTACO], n = 33); and (3) a patient cohort who experienced uncomplicated transfusions (n = 6). Samples from before transfusion, after transfusion, and 8 to 36 hours after transfusion were examined. Samples were analyzed for levels of tumor necrosis factor α, interleukin-1α (IL-1α), IL-6, IL-8, IL-10, C-reactive protein, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1, atrial natriuretic peptide, cardiac troponin, and N-terminal pro-B-type natriuretic peptide. Patients with cTACO and iTACO had an elevated body temperature, higher heart rate, and lower oxygen saturation after transfusion, whereas only patients with cTACO had higher blood pressures. Levels of key proinflammatory cytokines, IL-6, and IL-8 were elevated in patients with cTACO and iTACO after transfusion, whereas ICAM-1 was elevated only in patients with iTACO after transfusion. Our results suggest that inflammatory pathways may be invoked in patients with TACO. Patients with iTACO showed a more distinctive inflammatory profile, suggesting a gray area between transfusion-related acute lung injury and TACO.
输血相关循环超负荷（TACO）是输血相关死亡的主要原因。TACO被认为是由血管腔内的流体静力压导致的，进而引起渗出性肺水肿。最近的研究表明，TACO不仅仅是容量超负荷现象，还可能涉及炎症过程。本研究旨在进一步探究TACO患者体内炎症的存在情况。我们对3组接受红细胞输血的队列进行了一项回顾性研究：（1）根据国家血液警戒病例监测分类定义为患有TACO的患者（传统TACO [cTACO]，n = 33）；（2）有与TACO一致的症状但未完全符合报告标准的患者（机构性TACO [iTACO]，n = 33）；以及（3）一组经历了无并发症输血的患者队列（n = 6）。对输血前、输血后以及输血后8至36小时的样本进行了检测。分析样本中肿瘤坏死因子α、白细胞介素-1α（IL-1α）、IL-6、IL-8、IL-10、C反应蛋白、细胞间黏附分子1（ICAM-1）、血管细胞黏附分子1、心房利钠肽、心肌肌钙蛋白和N末端前B型利钠肽的水平。cTACO和iTACO患者输血后体温升高、心率加快且氧饱和度降低，而只有cTACO患者血压升高。cTACO和iTACO患者输血后关键促炎细胞因子IL-6和IL-8水平升高，而ICAM-1仅在iTACO患者输血后升高。我们的结果表明，TACO患者体内可能会激活炎症途径。iTACO患者表现出更独特的炎症特征，表明输血相关急性肺损伤和TACO之间存在灰色地带。
