脓毒症患者低镁血症与血清乳酸水平之间的关系:一项回顾性观察研究。

Ken Tonai, Shinshu Katayama, Kansuke Koyama, Hisashi Imahase, Shin Nunomiya
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引用次数: 0

摘要

背景:败血症-3 强调识别败血症引起的细胞代谢异常,并将血清乳酸水平作为细胞代谢异常的生物标志物。镁作为辅助因子在葡萄糖代谢中发挥着重要作用,但目前还不清楚缺镁会导致血清乳酸盐水平升高。此外,镁的状态如何影响血清乳酸水平作为败血症代谢异常标志物的作用,目前仍不清楚。因此,本研究旨在调查脓毒症患者血清镁和乳酸水平之间的关系,并从时间进程和循环异常的角度探讨这种关系:这项回顾性观察研究于2011年6月至2017年12月期间在吉大医科大学附属医院16张病床的重症监护室进行,对象为成年败血症患者。研究人员调查了重症监护室入院 5 天内血清镁和乳酸水平之间的关系。对重症监护室入院期间血清镁和乳酸水平之间的关系进行了多变量逻辑回归分析:结果:在纳入的 759 名患者中,有 105 人在入住重症监护室时患有低镁血症(镁水平为 2.4 mg/dL)。与镁水平正常组和高镁血症组相比(70% vs. 51.6% vs. 50%;P 2 mmol/L(几率比,2.76;95% 置信区间,1.60-4.76;P 结论:低镁血症与乳酸酸中毒有关:低镁血症与败血症早期和复苏后阶段的血清乳酸水平有关。需要进一步的研究来阐明镁的状态是否与败血症引起的细胞和代谢异常有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association between hypomagnesemia and serum lactate levels in patients with sepsis: a retrospective observational study.

Background: Sepsis-3 emphasizes the recognition of sepsis-induced cellular metabolic abnormalities, and utilizes serum lactate level as a biomarker of cellular metabolic abnormalities. Magnesium plays an important role as a cofactor in glucose metabolism, although it is not well known that magnesium deficiency causes elevated serum lactate levels. Additionally, it remains unclear how magnesium status affects the role of serum lactate levels as a marker of metabolic abnormalities in sepsis. Thus, this study aimed to investigate the association between serum magnesium and lactate levels in patients with sepsis and explore this relationship from the perspectives of time course and circulatory abnormalities.

Methods: This retrospective observational study of adult patients with sepsis was performed at the 16-bed intensive care unit of Jichi Medical University Hospital between June 2011 and December 2017. The relationship between serum magnesium and lactate levels for 5 days from intensive care unit admission was investigated along the time course. Multivariate logistic regression analysis was performed to evaluate the association between serum magnesium and lactate levels during intensive care unit admission.

Results: Among 759 patients included, 105 had hypomagnesemia (magnesium level < 1.6 mg/dL), 558 had normal serum magnesium levels (1.6-2.4 mg/dL), and 96 had hypermagnesemia (magnesium level > 2.4 mg/dL) at intensive care unit admission. From intensive care unit admission to day 5, the hypomagnesemia group had higher serum lactate levels and a higher frequency of lactic acidosis than the normal magnesium level and hypermagnesemia groups (70% vs. 51.6% vs. 50%; P < 0.001). Hypomagnesemia at intensive care unit admission was independently associated with lactic acidosis, i.e., lactic acid level > 2 mmol/L (odds ratio, 2.76; 95% confidence interval, 1.60-4.76; P < 0.001).

Conclusions: Hypomagnesemia was associated with serum lactate levels in the early and post-resuscitation phases of sepsis. Further studies are needed to elucidate whether the magnesium status is associated with sepsis-induced cellular and metabolic abnormalities.

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