我们可以通过一系列的血红蛋白水平来估计晚发性败血症吗?早产新生儿的一项观察研究。

IF 0.7 4区 医学 Q4 PATHOLOGY
Fetal and Pediatric Pathology Pub Date : 2023-10-01 Epub Date: 2023-06-15 DOI:10.1080/15513815.2023.2223308
Gonca Vardar, Turkay Rzayev, Kubra Gokce Tezel, Eren Ozek
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引用次数: 0

摘要

目的:评估早产儿系列高铁血红蛋白(MetHb)水平,作为诊断晚发性败血症(LOS)的一种可能方法。方法:将早产儿分为两组:经培养证实的LOS组和对照组。测量一系列MetHb水平。结果:LOS组的MetHb值明显升高(p  1.75%,优化为81.9%的灵敏度和90%的特异性。抗菌药物治疗后,MetHb值显著下降(p 2%(p 结论:LOS发作时MetHb水平升高,治疗后降低。MetHb可以添加到其他败血症生物标志物中,作为早产儿的快速感染过程指标。MetHb>2%与LOS死亡率相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Can We Estimate Late-Onset Sepsis by Serial Methemoglobin Levels? An Observational Study in Preterm Neonates.

Objective: To assess serial methemoglobin (MetHb) levels in preterm infants as a possible diagnostic method for late-onset sepsis (LOS). Methods: Preterm infants were assigned into two groups: those with culture-proven LOS and controls. Serial MetHb levels were measured. Results: The MetHb values of the LOS group were found to be significantly increased (p < 0.001). The cutoff value for the detection of LOS was calculated as MetHb > 1.75%, optimized for a sensitivity of 81.9% and specificity of 90%. After antimicrobial therapy, MetHb values were found to decrease significantly (p < 0.001). MetHb had an AUC of 0.810 for mortality using the calculated cutoff of >2% (p < 0.005). Conclusions: MetHb levels increase at the onset of LOS and decrease following treatment. MetHb can be added to other sepsis biomarkers as a rapid infectious process indicator for preterm neonates. MetHb > 2% is associated with LOS mortality.

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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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