ArticleRespiratory research2023
Serum metabolomic signatures of fatty acid oxidation defects differentiate host-response subphenotypes of acute respiratory distress syndrome.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The role of fatty acid metabolism in acute lung injury: a special focus on immunometabolism.Cellular and molecular life sciences : CMLS · 2024Pooled it
- KL-6 assisted subtyping of ARDS: from subtype-specific metabolomics to LPCAT1 as a pathogenic target.Respiratory research · 2026Article
- Clinical Phenotyping in Acute Respiratory Distress Syndrome: Steps Towards Personalized Medicine.Journal of clinical medicine · 2025Article
- Genetic and Multi-Omics Insights Into Monocyte Pantothenate-Mediated Protection in Acute Respiratory Distress Syndrome.Journal of cellular and molecular medicine · 2025Article
- Pulmonary metabolic changes in a rabbit model of Pseudomonas aeruginosa pneumonia: insights from metabolomic analysis.BMC microbiology · 2025Article
- Transgenerational associations between newborn metabolic profiles and bronchopulmonary dysplasia in neonates born to mothers with an obese phenotype.Scientific reports · 2025Article
- Identification of potential biomarkers and pathways involved in high-altitude pulmonary edema using GC-MS and LC-MS metabolomic methods.Scientific reports · 2024Article
- Iridium(III) solvent complex-based electrogenerated chemiluminescence method for the detection of 3-methylhistidine in urine.Analytical and bioanalytical chemistry · 2024Article
- "Now We Got Bad Blood": Beyond Phenotype Labels in an "Era" of Meta-omics in Critical Illness.American journal of respiratory and critical care medicine · 2024Article
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundFatty acid oxidation (FAO) defects have been implicated in experimental models of acute lung injury and associated with poor outcomes in critical illness. In this study, we examined acylcarnitine profiles and 3-methylhistidine as markers of FAO defects and skeletal muscle catabolism, respectively, in patients with acute respiratory failure. We determined whether these metabolites were associated with host-response ARDS subphenotypes, inflammatory biomarkers, and clinical outcomes in acute respiratory failure.
methodsIn a nested case-control cohort study, we performed targeted analysis of serum metabolites of patients intubated for airway protection (airway controls), Class 1 (hypoinflammatory), and Class 2 (hyperinflammatory) ARDS patients (N = 50 per group) during early initiation of mechanical ventilation. Relative amounts were quantified by liquid chromatography high resolution mass spectrometry using isotope-labeled standards and analyzed with plasma biomarkers and clinical data.
resultsOf the acylcarnitines analyzed, octanoylcarnitine levels were twofold increased in Class 2 ARDS relative to Class 1 ARDS or airway controls (P = 0.0004 and < 0.0001, respectively) and was positively associated with Class 2 by quantile g-computation analysis (P = 0.004). In addition, acetylcarnitine and 3-methylhistidine were increased in Class 2 relative to Class 1 and positively correlated with inflammatory biomarkers. In all patients within the study with acute respiratory failure, increased 3-methylhistidine was observed in non-survivors at 30 days (P = 0.0018), while octanoylcarnitine was increased in patients requiring vasopressor support but not in non-survivors (P = 0.0001 and P = 0.28, respectively).
conclusionsThis study demonstrates that increased levels of acetylcarnitine, octanoylcarnitine, and 3-methylhistidine distinguish Class 2 from Class 1 ARDS patients and airway controls. Octanoylcarnitine and 3-methylhistidine were associated with poor outcomes in patients with acute respiratory failure across the cohort independent of etiology or host-response subphenotype. These findings suggest a role for serum metabolites as biomarkers in ARDS and poor outcomes in critically ill patients early in the clinical course.
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