Multidimensional metabolic profiling in carbon monoxide poisoning: acid-base disturbances correlate with neurological severity.

IF 1.9 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Biomarkers Pub Date : 2025-09-04 DOI:10.1080/1354750X.2025.2551303

Weiguang Wang, Huihua Huang, Xianwei Xiong, Changsheng Ye, Jin Huang, Yong Ai Ling

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引用次数: 0

Abstract

Background: Acute carbon monoxide poisoning triggers complex metabolic derangements including acidosis and alkalosis, but their correlation with neurological injury severity remains insufficiently characterized clinically.

Methods: Consecutive poisoning patients (age ≥14) admitted between January 2019 and February 2025 were classified by neurological impairment severity. Acid-base parameters were analysed using Kruskal-Wallis tests, Spearman's correlation, and principal component analysis with varimax rotation.

Results: Among 940 patients (37.2% male), participants were categorized into three groups by neurological impairment severity: Mild (n = 597), moderate (n = 225), and severe (n = 118). Severe cases showed lower pH (7.39 vs. 7.41), reduced PaCO₂ (34.5 vs. 38.2 mmHg), greater base excess deficit -3.3 vs. 0.4), and higher lactate (3.7 vs. 1.6 mmol/L) (all p < 0.001). Neurological severity positively correlated with lactate (rho = 0.338) and inversely with base excess (rho = -0.268). Principal component analysis identified two components: Factor Component 1 (FAC1) (metabolic compensation, 47-65% variance) and FAC2 (respiratory regulation, 26-41% variance), with FAC1 inversely correlating with severity (rho = -0.319, p < 0.001).

Conclusions: Neurological impairment severity shows dose-dependent correlation with metabolic dysfunction (lactate accumulation, mixed metabolic acidosis-respiratory alkalosis). FAC1 (metabolic compensation) is a strong prognostic biomarker in acute carbon monoxide poisoning.

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一氧化碳中毒的多维代谢谱分析：酸碱紊乱与神经系统严重程度相关。

背景：急性一氧化碳中毒可引起复杂的代谢紊乱，包括酸中毒和碱中毒，但其与神经损伤严重程度的相关性在临床上尚不充分。方法：对2019年1月至2025年2月住院的连续中毒患者（年龄≥14岁）按神经功能损害程度进行分类。酸碱参数分析采用Kruskal-Wallis检验、Spearman相关检验和主成分分析。结果：在940例患者中（37.2%为男性），参与者根据神经损伤严重程度分为三组：轻度（n = 597），中度（n = 225）和重度（n = 118）。重度患者pH值较低（7.39 vs 7.41）， PaCO2降低（34.5 vs 38.2 mmHg），碱基过剩缺陷较大（-3.3 vs 0.4），乳酸含量较高（3.7 vs 1.6 mmol/L）（均为P P）。结论：神经损伤严重程度与代谢功能障碍（乳酸积累，混合性代谢性酸中毒-呼吸性碱中毒）呈剂量依赖性相关。因子成分1（代谢代偿）是急性一氧化碳中毒的一个强有力的预后生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biomarkers 医学-毒理学

CiteScore

5.00

自引率

3.80%

发文量

140

审稿时长

3 months

期刊介绍： The journal Biomarkers brings together all aspects of the rapidly growing field of biomarker research, encompassing their various uses and applications in one essential source. Biomarkers provides a vital forum for the exchange of ideas and concepts in all areas of biomarker research. High quality papers in four main areas are accepted and manuscripts describing novel biomarkers and their subsequent validation are especially encouraged: • Biomarkers of disease • Biomarkers of exposure • Biomarkers of response • Biomarkers of susceptibility Manuscripts can describe biomarkers measured in humans or other animals in vivo or in vitro. Biomarkers will consider publishing negative data from studies of biomarkers of susceptibility in human populations.