Browsing by Author "Cheng, Matthew P."

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    Community versus academic hospital community-acquired pneumonia patients: a nested cohort study
    (2024-11-25) Tsang, Jennifer L.; Rego, Kian; Binnie, Alexandra; Lee, Terry; Mccarthy, Anne; Cowan, Juthaporn; Archambault, Patrick; Lellouche, Francois; Turgeon, Alexis F.; Yoon, Jennifer; Lamontagne, Francois; Mcgeer, Allison; Douglas, Josh; Daley, Peter; Fowler, Robert; Maslove, David M.; Winston, Brent W.; Lee, Todd C.; Tran, Karen C.; Cheng, Matthew P.; Vinh, Donald C.; Boyd, John H.; Walley, Keith R.; Singer, Joel; Marshall, John C.; Haljan, Gregory; Jain, Fagun; Russell, James A.
    Abstract Background Most Canadians receive their care in community hospitals, yet most clinical research is conducted in academic hospitals. This study aims to compare patients with community acquired pneumonia (CAP) treated in academic and community hospitals with respect to their demographics, clinical characteristics, treatments and outcomes. Methods This nested observational cohort substudy of the Community Acquired Pneumonia: Toward InnoVAtive Treatment (CAPTIVATE) trial included 1,329 hospitalized adults with CAP recruited between March 1st, 2018 and September 31st, 2023 from 15 Canadian hospitals. Unadjusted and adjusted analyses for age, sex and co-morbidities using logistic, Cox and censored quantile regressions were conducted. Results Patients in community hospitals were older (mean [SD] 75.0 [15.7] years vs. 68.3 [16.2] years; p < 0.001), were more likely to be female (49.7% vs. 41.0%, p = 0.002), and had more comorbidities (75.9% vs. 64.8%, p < 0.001). More patients in community hospitals received corticosteroids (49.2% vs. 37.4%, p < 0.001). Community hospital patients had a higher likelihood of developing acute respiratory distress syndrome (OR 3.13, 95% CI: 1.87, 5.24, p = < 0.001), and acute cardiac injury (OR 2.53, 95% CI: 1.33, 4.83, p = 0.005). In unadjusted and adjusted analyses, 28-day mortality difference did not meet statistical significance (OR 1.43, 95% CI: 0.98, 20.7, p = 0.062 and OR 1.23, 95% CI: 0.81, 1.87, p = 0.332, respective). Conclusion Patients with CAP in Canadian community and academic hospitals differed with respect to their age, clinical characteristics, treatments and outcomes, emphasizing the importance of including more community hospitals in clinical research studies to ensure the generalizability of results.
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    Using a targeted metabolomics approach to explore differences in ARDS associated with COVID-19 compared to ARDS caused by H1N1 influenza and bacterial pneumonia
    (2024-02-27) Lee, Chel H.; Banoei, Mohammad M.; Ansari, Mariam; Cheng, Matthew P.; Lamontagne, Francois; Griesdale, Donald; Lasry, David E.; Demir, Koray; Dhingra, Vinay; Tran, Karen C.; Lee, Terry; Burns, Kevin; Sweet, David; Marshall, John; Slutsky, Arthur; Murthy, Srinivas; Singer, Joel; Patrick, David M.; Lee, Todd C.; Boyd, John H.; Walley, Keith R.; Fowler, Robert; Haljan, Greg; Vinh, Donald C.; Mcgeer, Alison; Maslove, David; Mann, Puneet; Donohoe, Kathryn; Hernandez, Geraldine; Rocheleau, Genevieve; Trahtemberg, Uriel; Kumar, Anand; Lou, Ma; dos Santos, Claudia; Baker, Andrew; Russell, James A.; Winston, Brent W.
    Abstract Rationale Acute respiratory distress syndrome (ARDS) is a life-threatening critical care syndrome commonly associated with infections such as COVID-19, influenza, and bacterial pneumonia. Ongoing research aims to improve our understanding of ARDS, including its molecular mechanisms, individualized treatment options, and potential interventions to reduce inflammation and promote lung repair. Objective To map and compare metabolic phenotypes of different infectious causes of ARDS to better understand the metabolic pathways involved in the underlying pathogenesis. Methods We analyzed metabolic phenotypes of 3 ARDS cohorts caused by COVID-19, H1N1 influenza, and bacterial pneumonia compared to non-ARDS COVID-19-infected patients and ICU-ventilated controls. Targeted metabolomics was performed on plasma samples from a total of 150 patients using quantitative LC–MS/MS and DI-MS/MS analytical platforms. Results Distinct metabolic phenotypes were detected between different infectious causes of ARDS. There were metabolomics differences between ARDSs associated with COVID-19 and H1N1, which include metabolic pathways involving taurine and hypotaurine, pyruvate, TCA cycle metabolites, lysine, and glycerophospholipids. ARDSs associated with bacterial pneumonia and COVID-19 differed in the metabolism of D-glutamine and D-glutamate, arginine, proline, histidine, and pyruvate. The metabolic profile of COVID-19 ARDS (C19/A) patients admitted to the ICU differed from COVID-19 pneumonia (C19/P) patients who were not admitted to the ICU in metabolisms of phenylalanine, tryptophan, lysine, and tyrosine. Metabolomics analysis revealed significant differences between C19/A, H1N1/A, and PNA/A vs ICU-ventilated controls, reflecting potentially different disease mechanisms. Conclusion Different metabolic phenotypes characterize ARDS associated with different viral and bacterial infections.
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    Using a targeted metabolomics approach to explore differences in ARDS associated with COVID-19 compared to ARDS caused by H1N1 influenza and bacterial pneumonia
    (2024-02-27) Lee, Chel H.; Banoei, Mohammad M.; Ansari, Mariam; Cheng, Matthew P.; Lamontagne, Francois; Griesdale, Donald; Lasry, David E.; Demir, Koray; Dhingra, Vinay; Tran, Karen C.; Lee, Terry; Burns, Kevin; Sweet, David; Marshall, John; Slutsky, Arthur; Murthy, Srinivas; Singer, Joel; Patrick, David M.; Lee, Todd C.; Boyd, John H.; Walley, Keith R.; Fowler, Robert; Haljan, Greg; Vinh, Donald C.; Mcgeer, Alison; Maslove, David; Mann, Puneet; Donohoe, Kathryn; Hernandez, Geraldine; Rocheleau, Genevieve; Trahtemberg, Uriel; Kumar, Anand; Lou, Ma; dos Santos, Claudia; Baker, Andrew; Russell, James A.; Winston, Brent W.
    Abstract Rationale Acute respiratory distress syndrome (ARDS) is a life-threatening critical care syndrome commonly associated with infections such as COVID-19, influenza, and bacterial pneumonia. Ongoing research aims to improve our understanding of ARDS, including its molecular mechanisms, individualized treatment options, and potential interventions to reduce inflammation and promote lung repair. Objective To map and compare metabolic phenotypes of different infectious causes of ARDS to better understand the metabolic pathways involved in the underlying pathogenesis. Methods We analyzed metabolic phenotypes of 3 ARDS cohorts caused by COVID-19, H1N1 influenza, and bacterial pneumonia compared to non-ARDS COVID-19-infected patients and ICU-ventilated controls. Targeted metabolomics was performed on plasma samples from a total of 150 patients using quantitative LC–MS/MS and DI-MS/MS analytical platforms. Results Distinct metabolic phenotypes were detected between different infectious causes of ARDS. There were metabolomics differences between ARDSs associated with COVID-19 and H1N1, which include metabolic pathways involving taurine and hypotaurine, pyruvate, TCA cycle metabolites, lysine, and glycerophospholipids. ARDSs associated with bacterial pneumonia and COVID-19 differed in the metabolism of D-glutamine and D-glutamate, arginine, proline, histidine, and pyruvate. The metabolic profile of COVID-19 ARDS (C19/A) patients admitted to the ICU differed from COVID-19 pneumonia (C19/P) patients who were not admitted to the ICU in metabolisms of phenylalanine, tryptophan, lysine, and tyrosine. Metabolomics analysis revealed significant differences between C19/A, H1N1/A, and PNA/A vs ICU-ventilated controls, reflecting potentially different disease mechanisms. Conclusion Different metabolic phenotypes characterize ARDS associated with different viral and bacterial infections.