Browsing by Author "Patrick, David M."

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    Quality of antibiotic prescribing for pediatric community-acquired Pneumonia in outpatient care
    (2023-10-28) Saatchi, Ariana; Haverkate, Manon R.; Reid, Jennifer N.; Shariff, Salimah Z.; Povitz, Marcus; Patrick, David M.; Silverman, Michael; Morris, Andrew M.; McCormack, James; Marra, Fawziah
    Abstract Background Antibiotics remain the primary treatment for community acquired pneumonia (CAP), however rising rates of antimicrobial resistance may jeopardize their future efficacy. With higher rates of disease reported in the youngest populations, effective treatment courses for pediatric pneumonia are of paramount importance. This study is the first to examine the quality of pediatric antibiotic use by agent, dose and duration. Methods A retrospective cohort study included all outpatient/primary care physician visits for pediatric CAP (aged < 19 years) between January 1 2014 to December 31 2018. Relevant practice guidelines were identified, and treatment recommendations extracted. Amoxicillin was the primary first-line agent for pediatric CAP. Categories of prescribing included: guideline adherent, effective but unnecessary (excess dose and/or duration), under treatment (insufficient dose and/or duration), and not recommended. Proportions of attributable-antibiotic use were examined by prescribing category, and then stratified by age and sex. Result(s) A total of 42,452 episodes of pediatric CAP were identified. Of those, 31,347 (76%) resulted in an antibiotic prescription. Amoxicillin accounted for 51% of all prescriptions. Overall, 27% of prescribing was fully guideline adherent, 19% effective but unnecessary, 10% under treatment, and 44% not recommended by agent. Excessive duration was the hallmark of effective but unnecessary prescribing (97%) Macrolides accounted for the majority on non-first line agent use, with only 32% of not recommended prescribing preceded by a previous course of antibiotics. Conclusion(s) This study is the first in Canada to examine prescribing quality for pediatric CAP by agent, dose and duration. Utilizing first-line agents, and shorter-course treatments are targets for stewardship.
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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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    ItemOpen Access
    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.