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Does red blood cell irradiation and/or anemia trigger intestinal injury in premature infants with birth weight?≤?1250?g? An observational birth cohort study

机译:出生体重≤1250?g的早产儿是否会发生红细胞辐射和/或贫血引发肠道损伤?观察性出生队列研究

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Necrotizing enterocolitis (NEC) is a leading cause of neonatal morbidity and mortality in premature infants. To date, no effective biomarkers exist to predict which premature infants will develop NEC, limiting targeted prevention strategies. Multiple observational studies have reported an association between the exposure to red blood cell (RBC) transfusion and/or anemia and the subsequent development of NEC; however, the underlying physiologic mechanisms of how these factors are independently associated with NEC remain unknown. In this paper, we outline our prospective, multicenter observational cohort study of infants with a birth weight?≤?1250?g to investigate the associations between RBC transfusion, anemia, intestinal oxygenation and injury that lead to NEC. Our overarching hypothesis is that irradiation of RBC units followed by longer storage perturbs donor RBC metabolism and function, and these derangements are associated with paradoxical microvascular vasoconstriction and intestinal tissue hypoxia increasing the risk for injury and/or NEC in transfused premature infants with already impaired intestinal oxygenation due to significant anemia. To evaluate these associations, we are examining the relationship between prolonged irradiation storage time (pIST), RBC metabolomic profiles, and anemia on intestinal oxygenation non-invasively measured by near-infrared spectroscopy (NIRS), and the development of NEC in transfused premature infants. Our study will address a critical scientific gap as to whether transfused RBC characteristics, such as irradiation and metabolism, impair intestinal function and/or microvascular circulation. Given the multifactorial etiology of NEC, preventative efforts will be more successful if clinicians understand the underlying pathophysiologic mechanisms and modifiable risk factors influencing the disease. Our study is registered in ClinicalTrials.gov Identifier: NCT02741648 .
机译:坏死性小肠结肠炎(NEC)是早产儿新生儿发病率和死亡率的主要原因。迄今为止,尚无有效的生物标志物来预测哪些早产儿会发展NEC,从而限制了有针对性的预防策略。多项观察性研究报告说,暴露于红细胞(RBC)输血和/或贫血与随后的NEC发展之间存在关联。然而,这些因素如何与NEC独立相关的潜在生理机制仍然未知。在本文中,我们概述了对出生体重≤≤1250μg的婴儿进行的前瞻性,多中心观察性队列研究,以研究RBC输血,贫血,肠道充氧与导致NEC的损伤之间的关系。我们的总体假设是,辐射RBC单位,然后更长的储存时间会扰乱供体的RBC代谢和功能,这些紊乱与矛盾的微血管血管收缩和肠道组织缺氧有关,增加了已经受损肠道的输血早产儿受伤和/或NEC的风险。由于严重贫血而导致充氧。为了评估这些关联,我们正在研究通过近红外光谱法(NIRS)非侵入性测量的延长的辐射储存时间(pIST),RBC代谢组学特征和肠道氧合性贫血与输血早产儿NEC之间的关系。 。我们的研究将解决关于输血RBC特性(例如辐射和代谢),肠功能和/或微血管循环是否受损的重大科学空白。考虑到NEC的病因是多因素的,如果临床医生了解影响该病的潜在病理生理机制和可改变的危险因素,则预防工作将更加成功。我们的研究已在ClinicalTrials.gov标识符中注册:NCT02741648。

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