Biomarkers of endothelial cell dysfunction persist beyond resuscitation in patients with hemorrhagic shock.
Biomarkers of endothelial cell dysfunction persist beyond resuscitation in patients with hemorrhagic shock.
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DOI：
10.1097/ta.0000000000003758
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发表时间：
2022-11-01
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已经显示，microRNA-19 b（miRNA-19 b）在出血性休克（HS）后结合并降解多配体蛋白聚糖-1，并在体外和体内促成内皮功能障碍。本研究的目的是评估HS患者中miRNA-19 b和syndecan-1的纵向变化。在入院时、止血完成时和24小时后收集HS患者的血液样品（血压<90 mmHg和≥2单位血液）用于miRNA-19 b（RT-qPCR）和syndecan-1（ELISA），并与对照和最小损伤（损伤严重程度评分ISS≤9）进行比较。测量炎性细胞因子（Luminex）。syndecan-1，miRNA-19 b，炎症标志物和患者预后之间的相关性进行了研究。Logistic回归模型的结果。研究了34例HS患者：年龄46岁（19-89岁），82%为男性，35%为穿透性，ISS 24±10，24小时血制品21±19单位。miRNA-19 b在到达时增加，并随着时间的推移进一步增加：4.6 -> 6.7 -> 24.1倍变化，相比之下，轻微损伤患者和对照组分别为0.1和1.2倍。多配体蛋白聚糖-1随时间增加至42.6 -> 50 -> 51.5ng/ml，相比之下，轻微损伤和对照组分别为14.7和23.5。两种生物标志物的值在24小时内保持显著增加，并且与炎性细胞因子的持续增加相关。入院syndecan-1显著预测死亡率、凝血功能障碍和大量输血。我们首次证明miR-19 b和syndecan-1是不依赖于复苏的内皮功能障碍的生物标志物。miR-19 b与syndecan-1和结局均无强相关性。然而，入院syndecan-1仍然是一个强有力的预后标志物，但其随时间的升高表明出血性休克后的多功能作用，需要进一步研究。II -前瞻性
It has been shown that microRNA-19b (miRNA-19b) binds to and degrades syndecan-1 after hemorrhagic shock (HS) and contributes to endothelial dysfunction in-vitro and in-vivo. The objective of the current study was to assess longitudinal changes in miRNA-19b and syndecan-1 in HS patients. Blood samples from HS patients (blood pressure<90mmHg and ≥2 units blood) were collected upon admission, completion of hemostasis, and after 24 hours for miRNA-19b (RT-qPCR) and syndecan-1 (ELISA) and compared to controls and minimally injured (Injury severity score ISS≤9). Inflammatory cytokines were measured (Luminex). Correlations between syndecan-1, miRNA-19b, inflammatory markers, and patient outcomes were performed. Logistic regression models were developed for outcomes. Thirty-four HS patients were studied: age 46 (19–89), 82% male, 35% penetrating, ISS 24±10, and blood products at 24 hours 21±19 units. MiRNA-19b was increased upon arrival and further increased over time: 4.6 -> 6.7 -> 24.1 fold change compared to 0.1 and 1.2 for minimally injured patients and controls, respectively. Syndecan-1 was increased to 42.6 -> 50 -> 51.5ng/ml over time compared to 14.7 and 23.5 for minimally-injured and controls, respectively. Values for both biomarkers remained significantly increased through 24 hours and were associated with a persistent increase in inflammatory cytokines. Admission syndecan-1 significantly predicted mortality, coagulopathy, and massive transfusion. We have shown for the first time that miR-19b and syndecan-1 were biomarkers for endothelial dysfunction independent of resuscitation. MiR-19b did not demonstrate a strong correlation with syndecan-1 nor outcomes. Admission syndecan-1, however, remains a strong prognostic marker but its elevation over time suggests a versatile role following hemorrhagic shock that requires further investigation. II – Prospective