University College Dublin, Belfield, Dublin 4, Ireland.
National Maternity Hospital, Holles Street, Dublin 2, Ireland.
Pediatr Res. 2023 Dec;94(6):1973-1977. doi: 10.1038/s41390-023-02731-x. Epub 2023 Jul 13.
Studies have demonstrated increased morbidity and mortality with platelet transfusions in the neonatal period. Platelets are as important for host immunity and inflammation as for hemostasis. Increased inflammation may explain the dose-associated increase in mortality, bleeding, and lung disease.
This study aims to assess if there are any changes in inflammatory cytokines post-platelet transfusion in babies in NICU.
This prospective observational study recruited babies due to receive a non-emergency platelet transfusion. Dried whole blood samples were collected prior to and 2 h post-transfusion. Samples were processed using multiplex immunoassay to enable analysis of tiny blood volumes. Statistical analysis was performed using R.
Seventeen babies underwent 26 platelet transfusions across two centers. Median birthweight was 1545 g (535-3960 g) and median birth gestation was 31 weeks and 1 day (23 + 1 to 40 + 5). Median pre-transfusion platelet count was 19.5 × 10/l. There was a significant increase in levels of CXCL5 (p < 0.001), CD40 (p = 0.001), and TGF-β (p = 0.001) in neonatal blood samples post-platelet transfusion in the study group.
The increase in the cytokines CXCL5, CD40 and TGF-β after platelet transfusion in babies in NICU could potentiate existing inflammation, NEC, lung, or white matter injury. This could potentially explain long-term harm from platelet transfusion in babies.
There is a change in levels of immunomodulatory proteins CXCL5, CD40, and TGF-β after platelet transfusion in babies in NICU. Murine neonatal models have demonstrated an increase in cytokine levels after platelet transfusions. This is the first time that this has been demonstrated in human neonates. The increase in proinflammatory cytokines could potentially explain the long-term harm from platelet transfusion in babies, as they could potentiate existing inflammation, NEC, lung injury, or white matter injury.
研究表明,新生儿期血小板输注会增加发病率和死亡率。血小板对宿主免疫和炎症的重要性不亚于止血。炎症增加可能解释了与剂量相关的死亡率、出血和肺部疾病增加的原因。
本研究旨在评估新生儿重症监护病房(NICU)婴儿血小板输注后炎症细胞因子是否发生变化。
这项前瞻性观察研究招募了因需要接受非紧急血小板输注的婴儿。在输注前和输注后 2 小时采集干全血样本。使用多重免疫分析处理样本,以分析微小的血液量。使用 R 进行统计分析。
17 名婴儿在两个中心接受了 26 次血小板输注。中位出生体重为 1545g(535-3960g),中位出生胎龄为 31 周零 1 天(23+1 至 40+5)。中位输注前血小板计数为 19.5×10/l。研究组新生儿血液样本中,血小板输注后 CXCL5(p<0.001)、CD40(p=0.001)和 TGF-β(p=0.001)水平显著升高。
NICU 婴儿血小板输注后细胞因子 CXCL5、CD40 和 TGF-β 的增加可能加剧现有炎症、NEC、肺或白质损伤。这可能解释了婴儿血小板输注的长期危害。
NICU 婴儿血小板输注后免疫调节蛋白 CXCL5、CD40 和 TGF-β 的水平发生变化。鼠类新生儿模型显示血小板输注后细胞因子水平增加。这是首次在人类新生儿中证明这一点。促炎细胞因子的增加可能解释了婴儿血小板输注的长期危害,因为它们可能加剧现有炎症、NEC、肺损伤或白质损伤。