The following is a summary of “Using a targeted metabolomics approach to explore differences in ARDS associated with COVID-19 compared to ARDS caused by H1N1 influenza and bacterial pneumonia,” published in the February 2024 issue of Critical Care by Lee et al.
Acute respiratory distress syndrome (ARDS), a severe lung complication linked to infections, is actively researched for better treatments and ways to dampen inflammation and heal lungs.
Researchers conducted a retrospective study comparing metabolic profiles of ARDS caused by various infections, aiming to understand the underlying metabolic mechanisms of the disease.
They analyzed metabolic phenotypes across three distinct cohorts of ARDS stemming from COVID-19, H1N1 influenza, and bacterial pneumonia, juxtaposed against non-ARDS COVID-19-infected individuals and ICU-ventilated controls. Utilizing targeted metabolomics, plasma samples from 150 patients underwent quantitative assessment through LC-MS/MS and DI-MS/MS analytical platforms.
The results showed that distinct metabolic phenotypes were identified among various infectious causes of ARDS. Metabolomic disparities between ARDS cases associated with COVID-19 and H1N1 were evident, encompassing metabolic pathways related to taurine and hypotaurine, pyruvate, TCA cycle metabolites, lysine, and glycerophospholipids. Metabolic variances between ARDS linked to bacterial pneumonia and COVID-19 were observed in D-glutamine and D-glutamate, arginine, proline, histidine, and pyruvate metabolism. Notably, the metabolic profile of patients admitted to ICU with COVID-19 ARDS (C19/A) differed from COVID-19 pneumonia (C19/P) patients not requiring ICU admission, particularly in the metabolisms of phenylalanine, tryptophan, lysine, and tyrosine. Metabolomics analysis indicated significant variations between C19/A, H1N1/A, and PNA/A compared to ICU-ventilated controls, suggesting potential distinctions in underlying disease mechanisms.
Investigators concluded that viral and bacterial infections in ARDS showed unique metabolic profiles, suggesting distinct pathways involved in the disease process.
Source: ccforum.biomedcentral.com/articles/10.1186/s13054-024-04843-0
