感染性休克患者血浆维生素C、血糖、氧化应激、内皮功能障碍与预后关系的观察研究

Kondwani G H Katundu, L. Hill, Lester M. Davids, Ivan A Joubert, Malcolm G A Miller, J. L. Piercy, William L Michelle
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引用次数: 5

摘要

背景。感染性休克与内皮功能障碍和氧化应激有关,维生素C对其起保护作用,可能影响临床结果。高血糖会降低维生素c。探讨感染性休克患者血浆维生素C、氧化应激、高血糖、内皮功能障碍与预后的关系。方法。在一项前瞻性观察性研究中,研究人员对25名成人感染性休克患者的血液样本进行了维生素C、硫代巴比妥酸反应物质(TBARS)(氧化应激的生物标志物)、可溶性血管细胞粘附分子-1 (sVCAM-1)和e-选择素(内皮功能障碍的标志物)的分析。监测血糖、顺序器官衰竭评估(SOFA)评分和液体需要量。结果。在整个7天的研究期间,血浆维生素C较低,而血浆TBARS较高。内皮功能障碍标志物(sVCAM-1和e -选择素)在基线时较高。VCAM-1在第1天显著下降,第7天恢复正常。与基线相比,e -选择素在第1天没有变化,但在第7天显著增加。氧化应激和内皮功能障碍与SOFA评分升高有关。氧化应激增加与静脉输液需求增加和血管收缩剂支持持续时间延长有关。9名病人在医院死亡。在基线时,非幸存者的TBARS水平明显高于脓毒性休克幸存者。结论。在感染性休克中,临床相关的氧化应激与内皮功能障碍、低维生素C和高葡萄糖-维生素C比值有关。氧化应激和内皮损伤标志物增加,并与复苏液体需要量、血管收缩剂使用、器官衰竭和死亡率相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An observational study on the relationship between plasma vitamin C, blood glucose, oxidative stress, endothelial dysfunction and outcome in patients with septic shock
Background. Septic shock is associated with endothelial dysfunction and oxidative stress, against which vitamin C plays a protective role, possibly influencing clinical outcome. Hyperglycaemia may lower vitamin C. Objective. To study plasma vitamin C, oxidative stress, hyperglycaemia, endothelial dysfunction and outcome in septic shock. Methods. In a prospective, observational study of 25 adult septic shock patients, serial blood samples were analysed for vitamin C, thiobarbituric acid-reactive substances (TBARS) (a biomarker of oxidative stress), and soluble vascular cell adhesion molecule-1 (sVCAM-1) and E-selectin (markers of endothelial dysfunction). Blood glucose, Sequential Organ Failure Assessment (SOFA) scores and fluid requirements were monitored. Results. Plasma vitamin C was low, while plasma TBARS were high throughout the 7-day study period. Endothelial dysfunction markers (sVCAM-1 and E-selectin) were high at the baseline. VCAM-1 decreased significantly on day 1 and normalised on day 7. E-selectin was unchanged on day 1 compared with baseline, but increased significantly on day 7. Oxidative stress and endothelial dysfunction were associated with increased SOFA score. Increased oxidative stress was associated with increased requirements for intravenous fluids and prolonged duration of vasoconstrictor support. Nine patients died in hospital. At baseline, levels of TBARS were significantly higher in non-survivors than in the survivors of septic shock. Conclusion. In septic shock, clinically relevant oxidative stress was associated with endothelial dysfunction, low vitamin C and high glucoseto- vitamin-C ratios. Markers of oxidative stress and endothelial damage were increased and correlated with resuscitation fluid requirements, vasoconstrictor use, organ failure and mortality.
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