Background <p>Metabolism is essential for life maintenance, neurological function, and injury repair, yet its role in diffuse axonal injury (DAI) is not fully understood.</p> Methods <p>Thirty patients with DAI and 34 patients without DAI were recruited based on the classification criteria using magnetic resonance imaging within 30 days of admission in this exploratory research. Serum samples and clinical parameters were collected on admission, with the Glasgow Outcome Scale Extended at 6 months after injury used as the neurological functional outcome. We did an untargeted metabolomic analysis using liquid chromatography-mass spectrometry.</p> Results <p>The DAI group and non-DAI group showed significant differences in the expression levels of 27 metabolites in serum, as well as in pupillary light reflex, Glasgow Coma Scale score, and Marshall computed tomography score. Random forest analysis indicated that lysophosphatidylcholine 22:3 sn-2 and carnitine C8:1 greatly contributed to distinguishing patients with DAI from patients without DAI (MeanDecreaseGini: 3.81, 5.16). The combined prediction of DAI using these two metabolites yielded an area under the curve of 0.944, which was higher than the combination of clinical parameters<b>.</b></p> Conclusions <p>The serum metabolomics revealed potential biomarkers for DAI and has significant value for exploring pathogenesis, determining early diagnosis, and improving long-term neurological function.</p>

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Metabolomics Analysis Reveals Potential Biomarkers for Diffuse Axonal Injury Article Category: Original Work

  • Weiliang Chen,
  • Shengwen Li,
  • Jiayi Wu,
  • Chunyu Yao,
  • Wen Su,
  • Lisheng Xu,
  • Guanjun Wang

摘要

Background

Metabolism is essential for life maintenance, neurological function, and injury repair, yet its role in diffuse axonal injury (DAI) is not fully understood.

Methods

Thirty patients with DAI and 34 patients without DAI were recruited based on the classification criteria using magnetic resonance imaging within 30 days of admission in this exploratory research. Serum samples and clinical parameters were collected on admission, with the Glasgow Outcome Scale Extended at 6 months after injury used as the neurological functional outcome. We did an untargeted metabolomic analysis using liquid chromatography-mass spectrometry.

Results

The DAI group and non-DAI group showed significant differences in the expression levels of 27 metabolites in serum, as well as in pupillary light reflex, Glasgow Coma Scale score, and Marshall computed tomography score. Random forest analysis indicated that lysophosphatidylcholine 22:3 sn-2 and carnitine C8:1 greatly contributed to distinguishing patients with DAI from patients without DAI (MeanDecreaseGini: 3.81, 5.16). The combined prediction of DAI using these two metabolites yielded an area under the curve of 0.944, which was higher than the combination of clinical parameters.

Conclusions

The serum metabolomics revealed potential biomarkers for DAI and has significant value for exploring pathogenesis, determining early diagnosis, and improving long-term neurological function.