Hyperleukocytosis is an emergency of acute leukemia leading to blood hyperviscosity, potentially resulting in life-threatening microvascular obstruction, or leukostasis. Due to the high number of red cells in the circulation, hematocrit/hemoglobin levels (Hct/Hgb) are major drivers of blood viscosity, but how Hct/Hgb mediates hyperviscosity in acute leukemia remains unknown. In vivo hemorheological studies are difficult to conduct and interpret due to issues related to visualizing and manipulating the microvasculature. To that end, a multi-vessel microfluidic device recapitulating the size-scale and geometry of the microvasculature was designed to investigate how Hct/Hgb interacts with acute leukemia to induce “in vitro” leukostasis. Using patient samples and cell lines, the degree of leukostasis was different among leukemia immunophenotypes with respect to white blood cell (WBC) count and Hct/Hgb. Among lymphoid immunophenotypes, severe anemia is protective against in vitro leukostasis and Hct/Hgb thresholds became apparent above which in vitro leukostasis significantly increased, to a greater extent with B-cell acute lymphoblastic leukemia (ALL) versus T-cell ALL. In vitro leukostasis in acute myeloid leukemia was primarily driven by WBC with little interaction with Hct/Hgb. This sets the stage for prospective clinical studies assessing how red cell transfusion may affect leukostasis risk in immunophenotypically different acute leukemia patients.

中文翻译：

---

重新定义急性白血病的高粘血症：对微血管系统中红细胞输注的潜在影响

白细胞增多症是急性白血病的一种紧急情况，会导致血液粘稠度过高，可能导致危及生命的微血管阻塞或白细胞停滞。由于循环中红细胞数量较多，血细胞比容/血红蛋白水平 (Hct/Hgb) 是血液粘度的主要驱动因素，但 Hct/Hgb 如何介导急性白血病的高粘度仍不清楚。由于与微脉管系统的可视化和操作相关的问题，体内血液流变学研究很难进行和解释。为此，设计了一种概括微血管系统的尺寸和几何形状的多血管微流体装置，以研究 Hct/Hgb 如何与急性白血病相互作用以诱导“体外”白细胞停滞。使用患者样本和细胞系，白血病免疫表型之间的白细胞停滞程度在白细胞 (WBC) 计数和 Hct/Hgb 方面有所不同。在淋巴免疫表型中，严重贫血对体外白细胞停滞具有保护作用，Hct/Hgb 阈值变得明显，高于该阈值，体外白细胞停滞显着增加，与 T 细胞 ALL 相比，B 细胞急性淋巴细胞白血病 (ALL) 的程度更大。急性髓性白血病的体外白细胞停滞主要由 WBC 驱动，与 Hct/Hgb 相互作用很少。这为评估红细胞输注如何影响免疫表型不同的急性白血病患者白细胞停滞风险的前瞻性临床研究奠定了基础。