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Biomarker use in ARDS resulting from COVID-19 infection
There is renewed interest in the use of immunomodulator therapies in patients with acute hypoxemic respiratory failure.
Beyond COVID-19, studies have also shown corticosteroid therapy improves clinical outcomes in patients with severe community-acquired pneumonia.3 However, the overwhelming majority of studies identifying plasma biomarkers that are associated with clinical outcomes in severe lung injury predate the routine use of corticosteroids.4 Two investigators at Massachusetts General Hospital, Jehan W. Alladina, MD, and George A. Alba, MD, performed a study to assess whether plasma biomarkers previously associated with clinical outcomes in ARDS maintained their predictive value in the setting of widespread immunomodulator therapy in the ICU. Drs. Alladina and Alba are physician-scientists and codirectors of the Program for Advancing Critical Care Translational Science at Massachusetts General Hospital in Boston.
In a study published in CHEST®Critical Care earlier this year, they prospectively enrolled patients with ARDS due to confirmed SARS-CoV-2 infection during the second wave of the COVID-19 pandemic from December 31, 2020, to March 31, 2021, at Massachusetts General Hospital.5 Plasma samples were collected within 24 hours of intubation for mechanical ventilation for protein analysis in 69 patients. Baseline demographics included a mean age of 62 plus or minus 15 years and a BMI of 31 plus or minus 8, and 45% were female. The median PaO2 to FiO2 ratio was 174 mm Hg, consistent with moderate ARDS, and the median duration of ventilation was 17 days. The patients had a median modified sequential organ failure assessment score of 8.5, and in-hospital mortality was 44% by 60 days. Notably, all patients in this cohort received steroids during their ICU stay.
Interestingly, the study investigators found no association between clinical outcomes and circulating proteins implicated in inflammation (eg, interleukin [IL]-6, IL-8), epithelial injury (eg, soluble receptor for advanced glycation end products, surfactant protein D), or coagulation (eg, D-dimer, tissue factor). However, four endothelial biomarkers—von Willebrand factor A2 domain; angiopoietin-2; syndecan-1; and neural precursor cell expressed, developmentally downregulated 9 (NEDD9)—were associated with 60-day mortality after adjusting for age, sex, and severity of illness. A sensitivity analysis, in which patients treated with the IL-6 inhibitor tocilizumab (n=4) were excluded, showed similar results.
Of the endothelial proteins, NEDD9 demonstrated the greatest effect size in its association with mortality in patients with ARDS due to COVID-19 who were treated with immunomodulators. NEDD9 is a scaffolding protein highly expressed in the pulmonary vascular endothelium, but its role in ARDS is not well known. In pulmonary vascular disease, plasma levels are associated with adverse pulmonary hemodynamics and clinical outcomes. Pulmonary artery endothelial NEDD9 is upregulated by cellular hypoxia and can mediate platelet-endothelial adhesion by interacting with P-selectin on the surface of activated platelets.6 Additionally, there is evidence of increased pulmonary endothelial NEDD9 expression and colocalization with fibrin within pulmonary arteries in lung tissue of patients who died from ARDS due to COVID-19.7 Thus, NEDD9 may be an important mediator of pulmonary vascular dysfunction observed in ARDS and could be a novel biomarker for patient subphenotyping and prognostication of clinical outcomes.
In summary, in a cohort of patients with COVID-19 ARDS uniformly treated with corticosteroids, plasma biomarkers of inflammation, coagulation, and epithelial injury were not associated with clinical outcomes, but endothelial biomarkers remained prognostic. It is biologically plausible that immunomodulators could attenuate the association between inflammatory biomarkers and patient outcomes. The findings of this study highlight the association of endothelial biomarkers with clinical outcomes in patients with COVID-19 ARDS treated with immunomodulators and warrant prospective validation, especially with the increasing evidence-based use of antiinflammatory therapy in acute lung injury. However, there are several important limitations to consider, including a small sample size from a single institution that precludes any definitive conclusions regarding any negative associations. Moreover, the single time point studied (the day of initiation of mechanical ventilation) and absence of a comparator group do not allow a comprehensive evaluation of the impact of antiinflammatory therapies across the trajectory of disease. Whether the findings are generalizable to all patients with ARDS treated with immunomodulators also remains unknown.
Overall, these data suggest that circulating signatures previously associated with ARDS, particularly those related to systemic inflammation, may have limited prognostic utility in the era of increasing immunomodulator use in critical illness. A deeper understanding of the pathobiology of ARDS, including the complex interplay with systemic immunomodulation, is needed to identify prognostic biomarkers and targeted therapies that improve patient outcomes.
Both authors work in the Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, in Boston.
References
1. Horby P, Lim WS, Emberson JR, et al; RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with Covid-19. N Engl J Med. 2021;384(8):693-704.
2. Tomazini BM, Maia IS, Cavalcanti AB, et al. Effect of dexamethasone on days alive and ventilator-free in patients with moderate or severe acute respiratory distress syndrome and COVID-19. JAMA. 2020;324(13):1-11.
3. Dequin P-F, Meziani F, Quenot J-P, et al. Hydrocortisone in severe community-acquired pneumonia. N Engl J Med. 2023;388(21):1931-1941.
4. Del Valle DM, Kim-Schulze S, Huang H-H, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med. 2020;26(10):1636-1643.
5. Alladina JW, Giacona FL, Haring AM, et al. Circulating biomarkers of endothelial dysfunction associated with ventilatory ratio and mortality in ARDS resulting from SARS-CoV-2 infection treated with antiinflammatory therapies. CHEST Crit Care. 2024;2(2):100054.
6. Alba GA, Samokhin AO, Wang R-S, et al. NEDD9 is a novel and modifiable mediator of platelet-endothelial adhesion in the pulmonary circulation. Am J Respir Crit Care Med. 2021;203(12):1533-1545.
7. Alba GA, Samokhin AO, Wang R-S, et al. Pulmonary endothelial NEDD9 and the prothrombotic pathophenotype of acute respiratory distress syndrome due to SARS‐CoV‐2 infection. Pulm Circ. 2022;12(2):e12071.
There is renewed interest in the use of immunomodulator therapies in patients with acute hypoxemic respiratory failure.
Beyond COVID-19, studies have also shown corticosteroid therapy improves clinical outcomes in patients with severe community-acquired pneumonia.3 However, the overwhelming majority of studies identifying plasma biomarkers that are associated with clinical outcomes in severe lung injury predate the routine use of corticosteroids.4 Two investigators at Massachusetts General Hospital, Jehan W. Alladina, MD, and George A. Alba, MD, performed a study to assess whether plasma biomarkers previously associated with clinical outcomes in ARDS maintained their predictive value in the setting of widespread immunomodulator therapy in the ICU. Drs. Alladina and Alba are physician-scientists and codirectors of the Program for Advancing Critical Care Translational Science at Massachusetts General Hospital in Boston.
In a study published in CHEST®Critical Care earlier this year, they prospectively enrolled patients with ARDS due to confirmed SARS-CoV-2 infection during the second wave of the COVID-19 pandemic from December 31, 2020, to March 31, 2021, at Massachusetts General Hospital.5 Plasma samples were collected within 24 hours of intubation for mechanical ventilation for protein analysis in 69 patients. Baseline demographics included a mean age of 62 plus or minus 15 years and a BMI of 31 plus or minus 8, and 45% were female. The median PaO2 to FiO2 ratio was 174 mm Hg, consistent with moderate ARDS, and the median duration of ventilation was 17 days. The patients had a median modified sequential organ failure assessment score of 8.5, and in-hospital mortality was 44% by 60 days. Notably, all patients in this cohort received steroids during their ICU stay.
Interestingly, the study investigators found no association between clinical outcomes and circulating proteins implicated in inflammation (eg, interleukin [IL]-6, IL-8), epithelial injury (eg, soluble receptor for advanced glycation end products, surfactant protein D), or coagulation (eg, D-dimer, tissue factor). However, four endothelial biomarkers—von Willebrand factor A2 domain; angiopoietin-2; syndecan-1; and neural precursor cell expressed, developmentally downregulated 9 (NEDD9)—were associated with 60-day mortality after adjusting for age, sex, and severity of illness. A sensitivity analysis, in which patients treated with the IL-6 inhibitor tocilizumab (n=4) were excluded, showed similar results.
Of the endothelial proteins, NEDD9 demonstrated the greatest effect size in its association with mortality in patients with ARDS due to COVID-19 who were treated with immunomodulators. NEDD9 is a scaffolding protein highly expressed in the pulmonary vascular endothelium, but its role in ARDS is not well known. In pulmonary vascular disease, plasma levels are associated with adverse pulmonary hemodynamics and clinical outcomes. Pulmonary artery endothelial NEDD9 is upregulated by cellular hypoxia and can mediate platelet-endothelial adhesion by interacting with P-selectin on the surface of activated platelets.6 Additionally, there is evidence of increased pulmonary endothelial NEDD9 expression and colocalization with fibrin within pulmonary arteries in lung tissue of patients who died from ARDS due to COVID-19.7 Thus, NEDD9 may be an important mediator of pulmonary vascular dysfunction observed in ARDS and could be a novel biomarker for patient subphenotyping and prognostication of clinical outcomes.
In summary, in a cohort of patients with COVID-19 ARDS uniformly treated with corticosteroids, plasma biomarkers of inflammation, coagulation, and epithelial injury were not associated with clinical outcomes, but endothelial biomarkers remained prognostic. It is biologically plausible that immunomodulators could attenuate the association between inflammatory biomarkers and patient outcomes. The findings of this study highlight the association of endothelial biomarkers with clinical outcomes in patients with COVID-19 ARDS treated with immunomodulators and warrant prospective validation, especially with the increasing evidence-based use of antiinflammatory therapy in acute lung injury. However, there are several important limitations to consider, including a small sample size from a single institution that precludes any definitive conclusions regarding any negative associations. Moreover, the single time point studied (the day of initiation of mechanical ventilation) and absence of a comparator group do not allow a comprehensive evaluation of the impact of antiinflammatory therapies across the trajectory of disease. Whether the findings are generalizable to all patients with ARDS treated with immunomodulators also remains unknown.
Overall, these data suggest that circulating signatures previously associated with ARDS, particularly those related to systemic inflammation, may have limited prognostic utility in the era of increasing immunomodulator use in critical illness. A deeper understanding of the pathobiology of ARDS, including the complex interplay with systemic immunomodulation, is needed to identify prognostic biomarkers and targeted therapies that improve patient outcomes.
Both authors work in the Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, in Boston.
References
1. Horby P, Lim WS, Emberson JR, et al; RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with Covid-19. N Engl J Med. 2021;384(8):693-704.
2. Tomazini BM, Maia IS, Cavalcanti AB, et al. Effect of dexamethasone on days alive and ventilator-free in patients with moderate or severe acute respiratory distress syndrome and COVID-19. JAMA. 2020;324(13):1-11.
3. Dequin P-F, Meziani F, Quenot J-P, et al. Hydrocortisone in severe community-acquired pneumonia. N Engl J Med. 2023;388(21):1931-1941.
4. Del Valle DM, Kim-Schulze S, Huang H-H, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med. 2020;26(10):1636-1643.
5. Alladina JW, Giacona FL, Haring AM, et al. Circulating biomarkers of endothelial dysfunction associated with ventilatory ratio and mortality in ARDS resulting from SARS-CoV-2 infection treated with antiinflammatory therapies. CHEST Crit Care. 2024;2(2):100054.
6. Alba GA, Samokhin AO, Wang R-S, et al. NEDD9 is a novel and modifiable mediator of platelet-endothelial adhesion in the pulmonary circulation. Am J Respir Crit Care Med. 2021;203(12):1533-1545.
7. Alba GA, Samokhin AO, Wang R-S, et al. Pulmonary endothelial NEDD9 and the prothrombotic pathophenotype of acute respiratory distress syndrome due to SARS‐CoV‐2 infection. Pulm Circ. 2022;12(2):e12071.
There is renewed interest in the use of immunomodulator therapies in patients with acute hypoxemic respiratory failure.
Beyond COVID-19, studies have also shown corticosteroid therapy improves clinical outcomes in patients with severe community-acquired pneumonia.3 However, the overwhelming majority of studies identifying plasma biomarkers that are associated with clinical outcomes in severe lung injury predate the routine use of corticosteroids.4 Two investigators at Massachusetts General Hospital, Jehan W. Alladina, MD, and George A. Alba, MD, performed a study to assess whether plasma biomarkers previously associated with clinical outcomes in ARDS maintained their predictive value in the setting of widespread immunomodulator therapy in the ICU. Drs. Alladina and Alba are physician-scientists and codirectors of the Program for Advancing Critical Care Translational Science at Massachusetts General Hospital in Boston.
In a study published in CHEST®Critical Care earlier this year, they prospectively enrolled patients with ARDS due to confirmed SARS-CoV-2 infection during the second wave of the COVID-19 pandemic from December 31, 2020, to March 31, 2021, at Massachusetts General Hospital.5 Plasma samples were collected within 24 hours of intubation for mechanical ventilation for protein analysis in 69 patients. Baseline demographics included a mean age of 62 plus or minus 15 years and a BMI of 31 plus or minus 8, and 45% were female. The median PaO2 to FiO2 ratio was 174 mm Hg, consistent with moderate ARDS, and the median duration of ventilation was 17 days. The patients had a median modified sequential organ failure assessment score of 8.5, and in-hospital mortality was 44% by 60 days. Notably, all patients in this cohort received steroids during their ICU stay.
Interestingly, the study investigators found no association between clinical outcomes and circulating proteins implicated in inflammation (eg, interleukin [IL]-6, IL-8), epithelial injury (eg, soluble receptor for advanced glycation end products, surfactant protein D), or coagulation (eg, D-dimer, tissue factor). However, four endothelial biomarkers—von Willebrand factor A2 domain; angiopoietin-2; syndecan-1; and neural precursor cell expressed, developmentally downregulated 9 (NEDD9)—were associated with 60-day mortality after adjusting for age, sex, and severity of illness. A sensitivity analysis, in which patients treated with the IL-6 inhibitor tocilizumab (n=4) were excluded, showed similar results.
Of the endothelial proteins, NEDD9 demonstrated the greatest effect size in its association with mortality in patients with ARDS due to COVID-19 who were treated with immunomodulators. NEDD9 is a scaffolding protein highly expressed in the pulmonary vascular endothelium, but its role in ARDS is not well known. In pulmonary vascular disease, plasma levels are associated with adverse pulmonary hemodynamics and clinical outcomes. Pulmonary artery endothelial NEDD9 is upregulated by cellular hypoxia and can mediate platelet-endothelial adhesion by interacting with P-selectin on the surface of activated platelets.6 Additionally, there is evidence of increased pulmonary endothelial NEDD9 expression and colocalization with fibrin within pulmonary arteries in lung tissue of patients who died from ARDS due to COVID-19.7 Thus, NEDD9 may be an important mediator of pulmonary vascular dysfunction observed in ARDS and could be a novel biomarker for patient subphenotyping and prognostication of clinical outcomes.
In summary, in a cohort of patients with COVID-19 ARDS uniformly treated with corticosteroids, plasma biomarkers of inflammation, coagulation, and epithelial injury were not associated with clinical outcomes, but endothelial biomarkers remained prognostic. It is biologically plausible that immunomodulators could attenuate the association between inflammatory biomarkers and patient outcomes. The findings of this study highlight the association of endothelial biomarkers with clinical outcomes in patients with COVID-19 ARDS treated with immunomodulators and warrant prospective validation, especially with the increasing evidence-based use of antiinflammatory therapy in acute lung injury. However, there are several important limitations to consider, including a small sample size from a single institution that precludes any definitive conclusions regarding any negative associations. Moreover, the single time point studied (the day of initiation of mechanical ventilation) and absence of a comparator group do not allow a comprehensive evaluation of the impact of antiinflammatory therapies across the trajectory of disease. Whether the findings are generalizable to all patients with ARDS treated with immunomodulators also remains unknown.
Overall, these data suggest that circulating signatures previously associated with ARDS, particularly those related to systemic inflammation, may have limited prognostic utility in the era of increasing immunomodulator use in critical illness. A deeper understanding of the pathobiology of ARDS, including the complex interplay with systemic immunomodulation, is needed to identify prognostic biomarkers and targeted therapies that improve patient outcomes.
Both authors work in the Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, in Boston.
References
1. Horby P, Lim WS, Emberson JR, et al; RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with Covid-19. N Engl J Med. 2021;384(8):693-704.
2. Tomazini BM, Maia IS, Cavalcanti AB, et al. Effect of dexamethasone on days alive and ventilator-free in patients with moderate or severe acute respiratory distress syndrome and COVID-19. JAMA. 2020;324(13):1-11.
3. Dequin P-F, Meziani F, Quenot J-P, et al. Hydrocortisone in severe community-acquired pneumonia. N Engl J Med. 2023;388(21):1931-1941.
4. Del Valle DM, Kim-Schulze S, Huang H-H, et al. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med. 2020;26(10):1636-1643.
5. Alladina JW, Giacona FL, Haring AM, et al. Circulating biomarkers of endothelial dysfunction associated with ventilatory ratio and mortality in ARDS resulting from SARS-CoV-2 infection treated with antiinflammatory therapies. CHEST Crit Care. 2024;2(2):100054.
6. Alba GA, Samokhin AO, Wang R-S, et al. NEDD9 is a novel and modifiable mediator of platelet-endothelial adhesion in the pulmonary circulation. Am J Respir Crit Care Med. 2021;203(12):1533-1545.
7. Alba GA, Samokhin AO, Wang R-S, et al. Pulmonary endothelial NEDD9 and the prothrombotic pathophenotype of acute respiratory distress syndrome due to SARS‐CoV‐2 infection. Pulm Circ. 2022;12(2):e12071.
Improved CHEST Physician® coming in 2025
FROM THE CHEST PHYSICIAN EDITORIAL BOARD – There will be some exciting changes happening at the CHEST Physician publication in 2025. We’re building on nearly three decades as a leading source of news and clinical commentary in pulmonary and critical care medicine to roll out several notable improvements.
First, the CHEST Physician website, chestphysician.org, will undergo a complete transformation. With an improved user experience, you’ll be able to more easily find content relevant to your interests and specialties.
Second, a brand-new email newsletter will hit your inbox twice a month, starting in January 2025. These emails will give you a quick look into timely content that may interest you and affect your daily practice. Additionally, this digital-first approach will get you the news and research you rely on sooner.
Lastly, the redesigned CHEST Physician print issue will now be produced and delivered on a quarterly basis. The first issue will arrive in March 2025. These special issues will feature print-exclusive content and graphics, as well as offer a deeper dive into the most relevant news stories from recent months.
Notably, all new CHEST Physician content published in the new year will be tailored to our audience and readership, and it will address the issues and topics that matter to you most as health care providers.
As the CHEST Physician publication undergoes this transformation, we want to hear from you. What topics do you want more of? How can CHEST continue to best serve the chest medicine community? Email chestphysiciannews@chestnet.org to share your ideas.
Thank you for being a loyal CHEST Physician reader. We look forward to bringing you elevated content and an enhanced reader experience in the new year.
FROM THE CHEST PHYSICIAN EDITORIAL BOARD – There will be some exciting changes happening at the CHEST Physician publication in 2025. We’re building on nearly three decades as a leading source of news and clinical commentary in pulmonary and critical care medicine to roll out several notable improvements.
First, the CHEST Physician website, chestphysician.org, will undergo a complete transformation. With an improved user experience, you’ll be able to more easily find content relevant to your interests and specialties.
Second, a brand-new email newsletter will hit your inbox twice a month, starting in January 2025. These emails will give you a quick look into timely content that may interest you and affect your daily practice. Additionally, this digital-first approach will get you the news and research you rely on sooner.
Lastly, the redesigned CHEST Physician print issue will now be produced and delivered on a quarterly basis. The first issue will arrive in March 2025. These special issues will feature print-exclusive content and graphics, as well as offer a deeper dive into the most relevant news stories from recent months.
Notably, all new CHEST Physician content published in the new year will be tailored to our audience and readership, and it will address the issues and topics that matter to you most as health care providers.
As the CHEST Physician publication undergoes this transformation, we want to hear from you. What topics do you want more of? How can CHEST continue to best serve the chest medicine community? Email chestphysiciannews@chestnet.org to share your ideas.
Thank you for being a loyal CHEST Physician reader. We look forward to bringing you elevated content and an enhanced reader experience in the new year.
FROM THE CHEST PHYSICIAN EDITORIAL BOARD – There will be some exciting changes happening at the CHEST Physician publication in 2025. We’re building on nearly three decades as a leading source of news and clinical commentary in pulmonary and critical care medicine to roll out several notable improvements.
First, the CHEST Physician website, chestphysician.org, will undergo a complete transformation. With an improved user experience, you’ll be able to more easily find content relevant to your interests and specialties.
Second, a brand-new email newsletter will hit your inbox twice a month, starting in January 2025. These emails will give you a quick look into timely content that may interest you and affect your daily practice. Additionally, this digital-first approach will get you the news and research you rely on sooner.
Lastly, the redesigned CHEST Physician print issue will now be produced and delivered on a quarterly basis. The first issue will arrive in March 2025. These special issues will feature print-exclusive content and graphics, as well as offer a deeper dive into the most relevant news stories from recent months.
Notably, all new CHEST Physician content published in the new year will be tailored to our audience and readership, and it will address the issues and topics that matter to you most as health care providers.
As the CHEST Physician publication undergoes this transformation, we want to hear from you. What topics do you want more of? How can CHEST continue to best serve the chest medicine community? Email chestphysiciannews@chestnet.org to share your ideas.
Thank you for being a loyal CHEST Physician reader. We look forward to bringing you elevated content and an enhanced reader experience in the new year.
Our Biggest Turnout Ever for Advocacy Day!
That’s why we gathered our leaders from across the United States in Washington, DC, to meet with congressional offices during our annual Advocacy Day.
GIs from California to Massachusetts and many states in between met with House and Senate offices to educate members of Congress and their staff about the most critical policy issues impacting you and your patients. In total, 28 states were represented and we attended more than 100 meetings in 64 different districts, which was a mix of both Republican and Democratic offices.
For the second year in a row, we were fortunate to be joined by GI patient advocates as well, who shared personal stories about the challenges they encountered in the health care system, and the negative effects to their well-being and quality of life because of red tape caused by prior authorization and step therapy.
The in-person advocacy of our members and patient advocates makes a difference. In one of AGA President Dr. Maria Abreu’s meetings, the congressional staffer remembered that he met with her, Dr. Mel Wilcox, and a patient advocate during 2023’s Advocacy Day and recounted the impact of their conversation about delays to timely access to care for inflammatory bowel disease medication.
Numerous GIs had similar experiences on Advocacy Day and recounted the benefits of being able to walk into House and Senate offices and educate congressional staff on the issues they’re experiencing in their clinic or lab.
Being able to start these conversations about health care and GI and build these relationships showcases the value of Advocacy Day, and demonstrates how AGA works with members to make it easy to advocate for the issues important to them. We were able to have a full day of constructive meetings with lawmakers and their staff thanks to members and patient advocates. Thank you for being engaged and using your voices to protect GI patient care!
That’s why we gathered our leaders from across the United States in Washington, DC, to meet with congressional offices during our annual Advocacy Day.
GIs from California to Massachusetts and many states in between met with House and Senate offices to educate members of Congress and their staff about the most critical policy issues impacting you and your patients. In total, 28 states were represented and we attended more than 100 meetings in 64 different districts, which was a mix of both Republican and Democratic offices.
For the second year in a row, we were fortunate to be joined by GI patient advocates as well, who shared personal stories about the challenges they encountered in the health care system, and the negative effects to their well-being and quality of life because of red tape caused by prior authorization and step therapy.
The in-person advocacy of our members and patient advocates makes a difference. In one of AGA President Dr. Maria Abreu’s meetings, the congressional staffer remembered that he met with her, Dr. Mel Wilcox, and a patient advocate during 2023’s Advocacy Day and recounted the impact of their conversation about delays to timely access to care for inflammatory bowel disease medication.
Numerous GIs had similar experiences on Advocacy Day and recounted the benefits of being able to walk into House and Senate offices and educate congressional staff on the issues they’re experiencing in their clinic or lab.
Being able to start these conversations about health care and GI and build these relationships showcases the value of Advocacy Day, and demonstrates how AGA works with members to make it easy to advocate for the issues important to them. We were able to have a full day of constructive meetings with lawmakers and their staff thanks to members and patient advocates. Thank you for being engaged and using your voices to protect GI patient care!
That’s why we gathered our leaders from across the United States in Washington, DC, to meet with congressional offices during our annual Advocacy Day.
GIs from California to Massachusetts and many states in between met with House and Senate offices to educate members of Congress and their staff about the most critical policy issues impacting you and your patients. In total, 28 states were represented and we attended more than 100 meetings in 64 different districts, which was a mix of both Republican and Democratic offices.
For the second year in a row, we were fortunate to be joined by GI patient advocates as well, who shared personal stories about the challenges they encountered in the health care system, and the negative effects to their well-being and quality of life because of red tape caused by prior authorization and step therapy.
The in-person advocacy of our members and patient advocates makes a difference. In one of AGA President Dr. Maria Abreu’s meetings, the congressional staffer remembered that he met with her, Dr. Mel Wilcox, and a patient advocate during 2023’s Advocacy Day and recounted the impact of their conversation about delays to timely access to care for inflammatory bowel disease medication.
Numerous GIs had similar experiences on Advocacy Day and recounted the benefits of being able to walk into House and Senate offices and educate congressional staff on the issues they’re experiencing in their clinic or lab.
Being able to start these conversations about health care and GI and build these relationships showcases the value of Advocacy Day, and demonstrates how AGA works with members to make it easy to advocate for the issues important to them. We were able to have a full day of constructive meetings with lawmakers and their staff thanks to members and patient advocates. Thank you for being engaged and using your voices to protect GI patient care!
An Investment in the Future of GI: The AGA Research Foundation
What will the practice of gastroenterology look like in 20 years? It is our hope that physicians have an abundance of new tools and treatments to care for their patients suffering from digestive disorders.
How will we get there? New treatments and devices are the result of years of research.
To help make this dream a reality, AGA — through the AGA Research Foundation — has made a commitment to support investigators in GI and hepatology with its Research Awards Program.
These diverse researchers range from young investigators to more seasoned leaders in GI, all embarking on novel research projects that will advance our understanding of digestive conditions and pave the way for future discoveries in the field.
To our AGA Research Foundation donors, we sincerely thank you for your gifts.
We invite the GI community to join others in supporting and helping spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.
Make your tax-deductible gift today at www.gastro.org/donateonline.
What will the practice of gastroenterology look like in 20 years? It is our hope that physicians have an abundance of new tools and treatments to care for their patients suffering from digestive disorders.
How will we get there? New treatments and devices are the result of years of research.
To help make this dream a reality, AGA — through the AGA Research Foundation — has made a commitment to support investigators in GI and hepatology with its Research Awards Program.
These diverse researchers range from young investigators to more seasoned leaders in GI, all embarking on novel research projects that will advance our understanding of digestive conditions and pave the way for future discoveries in the field.
To our AGA Research Foundation donors, we sincerely thank you for your gifts.
We invite the GI community to join others in supporting and helping spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.
Make your tax-deductible gift today at www.gastro.org/donateonline.
What will the practice of gastroenterology look like in 20 years? It is our hope that physicians have an abundance of new tools and treatments to care for their patients suffering from digestive disorders.
How will we get there? New treatments and devices are the result of years of research.
To help make this dream a reality, AGA — through the AGA Research Foundation — has made a commitment to support investigators in GI and hepatology with its Research Awards Program.
These diverse researchers range from young investigators to more seasoned leaders in GI, all embarking on novel research projects that will advance our understanding of digestive conditions and pave the way for future discoveries in the field.
To our AGA Research Foundation donors, we sincerely thank you for your gifts.
We invite the GI community to join others in supporting and helping spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.
Make your tax-deductible gift today at www.gastro.org/donateonline.
Gastro Journal Club: Proximal Cancers in FIT-Positive Patients
For our next installment of the Gastro Journal Club, They are joined by fellows from the Icahn School of Medicine at Mount Sinai in New York City for a discussion of the article “Risk of Cancers Proximal to the Colon in Fecal Immunochemical Test Positive Screenees in a Colorectal Cancer Screening Program,” published in the September 2024 issue of Gastroenterology .
Visit our YouTube Channel (youtube.com/@AmerGastroAssn) to watch the session.
The Gastro Journal Club is by and for fellows and residents. During these sessions, fellows and residents have the opportunity to ask authors questions about their recently published work in Gastroenterology. If you are interested in arranging a Gastro Journal Club session at your institution, please contact mpogachar@gastro.org.
For our next installment of the Gastro Journal Club, They are joined by fellows from the Icahn School of Medicine at Mount Sinai in New York City for a discussion of the article “Risk of Cancers Proximal to the Colon in Fecal Immunochemical Test Positive Screenees in a Colorectal Cancer Screening Program,” published in the September 2024 issue of Gastroenterology .
Visit our YouTube Channel (youtube.com/@AmerGastroAssn) to watch the session.
The Gastro Journal Club is by and for fellows and residents. During these sessions, fellows and residents have the opportunity to ask authors questions about their recently published work in Gastroenterology. If you are interested in arranging a Gastro Journal Club session at your institution, please contact mpogachar@gastro.org.
For our next installment of the Gastro Journal Club, They are joined by fellows from the Icahn School of Medicine at Mount Sinai in New York City for a discussion of the article “Risk of Cancers Proximal to the Colon in Fecal Immunochemical Test Positive Screenees in a Colorectal Cancer Screening Program,” published in the September 2024 issue of Gastroenterology .
Visit our YouTube Channel (youtube.com/@AmerGastroAssn) to watch the session.
The Gastro Journal Club is by and for fellows and residents. During these sessions, fellows and residents have the opportunity to ask authors questions about their recently published work in Gastroenterology. If you are interested in arranging a Gastro Journal Club session at your institution, please contact mpogachar@gastro.org.
Top reads from the CHEST journal portfolio
Explore articles on PAP adherence, plasma biomarkers in ARDS, and airways disorders hospitalizations during wildfire season
Journal CHEST®
Association Between Healthy Behaviors and Health Care Resource Use With Subsequent Positive Airway Pressure Therapy Adherence in OSA
By Launois, MD, PhD, and colleagues
One of the pitfalls in the interpretation of the effect of treatment adherence on health outcomes is the healthy-adherer effect (HAE) bias. Healthy-adherer bias occurs when patients who are treatment-adherent tend to actively seek out preventative care and engage in other healthy behaviors. Incomplete adjustment for such behaviors can lead to spurious inferences regarding study outcomes because healthy behaviors are associated with a reduced risk of many poor health outcomes.
This study demonstrates that HAE proxies (adherence to CV active drugs, no history of smoking, or sleepiness-related car accidents) were associated with subsequent PAP adherence after adjustment for confounders. PAP-adherent patients used less health care resources before PAP initiation. Unfortunately, the study did not measure other healthy behaviors (nutrition, physical activity, psychosocial support) that could also potentially explain HAE. Until the HAE associated with PAP adherence is better understood, clinicians should use caution when interpreting the association of PAP adherence with CV health outcomes and health care resource use.
– Commentary by Sai Venkateshiah, MD, FCCP, Member of the CHEST Physician Editorial Board
CHEST® Critical Care
Circulating Biomarkers of Endothelial Dysfunction Associated With Ventilatory Ratio and Mortality in ARDS Resulting From SARS-CoV-2 Infection Treated With Anti-inflammatory Therapies
By Alladina, MD, and colleagues
Practitioners in the intensive care unit have become increasingly aware that the population of patients with ARDS is highly heterogenous not only in terms of the inciting factors of their condition but also in terms of their respiratory physiology. Calfee and co-workers opened new horizons for us with their 2014 descriptions of two phenotypes of ARDS based upon biological markers that had different clinical outcome profiles. The work by Alladina et al adds to this body of knowledge by studying biomarkers from patients with COVID-ARDS who were receiving anti-inflammatory therapies. These researchers demonstrated that in such patients, endothelial biomarkers, particularly NEDD9, were associated with 60-day mortality. Increased understanding of biologic phenotypes in ARDS patients may facilitate the application of precision medicine to patients with this condition, improving outcome prediction and allowing practitioners to target specific treatments to selected patients.
– Commentary by Daniel R. Ouellette, MD, FCCP, Critical Care Commentary Editor of CHEST Physician
CHEST® Pulmonary
Association of Short-Term Increases in Ambient Fine Particulate Matter With Hospitalization for Asthma or COPD During Wildfire Season and Other Time Periods
By Horne, PhD, MStat, MPH, and colleagues
Trigger avoidance is one the most important interventions in the control of symptoms and prevention of exacerbations in chronic airways diseases. Nevertheless, trigger avoidance is at times not possible. This is the case with wildfire smoke and other environmental irritants—an increasing global health problem. Using data from 11 hospitals along the Utah’s Wasatch Front, the study by Horne and colleagues shows a clear association between a short-term increase in ambient fine particulate matter exposure resulting from wildfires and a surge in asthma exacerbations. This effect was also seen in patients with COPD but to a lesser degree. The study is limited by its observational design and because measurements of pollution levels were performed regionally and not at individual patient level. Yet this study offers valuable insights on the effects of environmental exposures in patients with chronic airways diseases and the consequences to our health care systems. Futures studies are still needed to assess the long-term consequences of sustained exposures to these irritants in patients with respiratory conditions.
– Commentary by Diego J. Maselli, MD, FCCP, Member of the CHEST Physician Editorial Board
Explore articles on PAP adherence, plasma biomarkers in ARDS, and airways disorders hospitalizations during wildfire season
Explore articles on PAP adherence, plasma biomarkers in ARDS, and airways disorders hospitalizations during wildfire season
Journal CHEST®
Association Between Healthy Behaviors and Health Care Resource Use With Subsequent Positive Airway Pressure Therapy Adherence in OSA
By Launois, MD, PhD, and colleagues
One of the pitfalls in the interpretation of the effect of treatment adherence on health outcomes is the healthy-adherer effect (HAE) bias. Healthy-adherer bias occurs when patients who are treatment-adherent tend to actively seek out preventative care and engage in other healthy behaviors. Incomplete adjustment for such behaviors can lead to spurious inferences regarding study outcomes because healthy behaviors are associated with a reduced risk of many poor health outcomes.
This study demonstrates that HAE proxies (adherence to CV active drugs, no history of smoking, or sleepiness-related car accidents) were associated with subsequent PAP adherence after adjustment for confounders. PAP-adherent patients used less health care resources before PAP initiation. Unfortunately, the study did not measure other healthy behaviors (nutrition, physical activity, psychosocial support) that could also potentially explain HAE. Until the HAE associated with PAP adherence is better understood, clinicians should use caution when interpreting the association of PAP adherence with CV health outcomes and health care resource use.
– Commentary by Sai Venkateshiah, MD, FCCP, Member of the CHEST Physician Editorial Board
CHEST® Critical Care
Circulating Biomarkers of Endothelial Dysfunction Associated With Ventilatory Ratio and Mortality in ARDS Resulting From SARS-CoV-2 Infection Treated With Anti-inflammatory Therapies
By Alladina, MD, and colleagues
Practitioners in the intensive care unit have become increasingly aware that the population of patients with ARDS is highly heterogenous not only in terms of the inciting factors of their condition but also in terms of their respiratory physiology. Calfee and co-workers opened new horizons for us with their 2014 descriptions of two phenotypes of ARDS based upon biological markers that had different clinical outcome profiles. The work by Alladina et al adds to this body of knowledge by studying biomarkers from patients with COVID-ARDS who were receiving anti-inflammatory therapies. These researchers demonstrated that in such patients, endothelial biomarkers, particularly NEDD9, were associated with 60-day mortality. Increased understanding of biologic phenotypes in ARDS patients may facilitate the application of precision medicine to patients with this condition, improving outcome prediction and allowing practitioners to target specific treatments to selected patients.
– Commentary by Daniel R. Ouellette, MD, FCCP, Critical Care Commentary Editor of CHEST Physician
CHEST® Pulmonary
Association of Short-Term Increases in Ambient Fine Particulate Matter With Hospitalization for Asthma or COPD During Wildfire Season and Other Time Periods
By Horne, PhD, MStat, MPH, and colleagues
Trigger avoidance is one the most important interventions in the control of symptoms and prevention of exacerbations in chronic airways diseases. Nevertheless, trigger avoidance is at times not possible. This is the case with wildfire smoke and other environmental irritants—an increasing global health problem. Using data from 11 hospitals along the Utah’s Wasatch Front, the study by Horne and colleagues shows a clear association between a short-term increase in ambient fine particulate matter exposure resulting from wildfires and a surge in asthma exacerbations. This effect was also seen in patients with COPD but to a lesser degree. The study is limited by its observational design and because measurements of pollution levels were performed regionally and not at individual patient level. Yet this study offers valuable insights on the effects of environmental exposures in patients with chronic airways diseases and the consequences to our health care systems. Futures studies are still needed to assess the long-term consequences of sustained exposures to these irritants in patients with respiratory conditions.
– Commentary by Diego J. Maselli, MD, FCCP, Member of the CHEST Physician Editorial Board
Journal CHEST®
Association Between Healthy Behaviors and Health Care Resource Use With Subsequent Positive Airway Pressure Therapy Adherence in OSA
By Launois, MD, PhD, and colleagues
One of the pitfalls in the interpretation of the effect of treatment adherence on health outcomes is the healthy-adherer effect (HAE) bias. Healthy-adherer bias occurs when patients who are treatment-adherent tend to actively seek out preventative care and engage in other healthy behaviors. Incomplete adjustment for such behaviors can lead to spurious inferences regarding study outcomes because healthy behaviors are associated with a reduced risk of many poor health outcomes.
This study demonstrates that HAE proxies (adherence to CV active drugs, no history of smoking, or sleepiness-related car accidents) were associated with subsequent PAP adherence after adjustment for confounders. PAP-adherent patients used less health care resources before PAP initiation. Unfortunately, the study did not measure other healthy behaviors (nutrition, physical activity, psychosocial support) that could also potentially explain HAE. Until the HAE associated with PAP adherence is better understood, clinicians should use caution when interpreting the association of PAP adherence with CV health outcomes and health care resource use.
– Commentary by Sai Venkateshiah, MD, FCCP, Member of the CHEST Physician Editorial Board
CHEST® Critical Care
Circulating Biomarkers of Endothelial Dysfunction Associated With Ventilatory Ratio and Mortality in ARDS Resulting From SARS-CoV-2 Infection Treated With Anti-inflammatory Therapies
By Alladina, MD, and colleagues
Practitioners in the intensive care unit have become increasingly aware that the population of patients with ARDS is highly heterogenous not only in terms of the inciting factors of their condition but also in terms of their respiratory physiology. Calfee and co-workers opened new horizons for us with their 2014 descriptions of two phenotypes of ARDS based upon biological markers that had different clinical outcome profiles. The work by Alladina et al adds to this body of knowledge by studying biomarkers from patients with COVID-ARDS who were receiving anti-inflammatory therapies. These researchers demonstrated that in such patients, endothelial biomarkers, particularly NEDD9, were associated with 60-day mortality. Increased understanding of biologic phenotypes in ARDS patients may facilitate the application of precision medicine to patients with this condition, improving outcome prediction and allowing practitioners to target specific treatments to selected patients.
– Commentary by Daniel R. Ouellette, MD, FCCP, Critical Care Commentary Editor of CHEST Physician
CHEST® Pulmonary
Association of Short-Term Increases in Ambient Fine Particulate Matter With Hospitalization for Asthma or COPD During Wildfire Season and Other Time Periods
By Horne, PhD, MStat, MPH, and colleagues
Trigger avoidance is one the most important interventions in the control of symptoms and prevention of exacerbations in chronic airways diseases. Nevertheless, trigger avoidance is at times not possible. This is the case with wildfire smoke and other environmental irritants—an increasing global health problem. Using data from 11 hospitals along the Utah’s Wasatch Front, the study by Horne and colleagues shows a clear association between a short-term increase in ambient fine particulate matter exposure resulting from wildfires and a surge in asthma exacerbations. This effect was also seen in patients with COPD but to a lesser degree. The study is limited by its observational design and because measurements of pollution levels were performed regionally and not at individual patient level. Yet this study offers valuable insights on the effects of environmental exposures in patients with chronic airways diseases and the consequences to our health care systems. Futures studies are still needed to assess the long-term consequences of sustained exposures to these irritants in patients with respiratory conditions.
– Commentary by Diego J. Maselli, MD, FCCP, Member of the CHEST Physician Editorial Board
Advocating for diversity in medical education
Earlier this year,
If enacted, the EDUCATE Act would cut off federal funding to medical schools that force students or faculty to adopt specific beliefs; discriminate based on race or ethnicity; or have diversity, equity, and inclusion (DEI) offices or any functional equivalent. The bill would also require accreditation agencies to check that their standards do not push these practices, while still allowing instruction about health issues tied to race or collecting data for research.
In response to the introduction of this act, CHEST published a statement in support of DEI practices and their necessary role within the practice of health care and medical training programs.
It is our belief that health care requires a solid patient-provider therapeutic alliance to achieve successful outcomes, and decades of scientific research have shown that a lack of clinician diversity worsens health disparities. For patients from historically underserved communities, having clinicians who share similar lived experiences almost always leads to significant improvements in patient outcomes. If identity concordance is not feasible, clinicians with considerable exposure to diverse patient populations, equitable approaches to care, and inclusive perspectives on health gained through continuing, comprehensive medical education and professional training can also positively impact outcomes.
Research indicates that a diverse medical workforce improves cultural competence and can help clinicians better meet the needs of patients from diverse backgrounds and ethnicities and that the benefits of diverse learning environments enhance the educational experience of all participants. Racial and ethnic health inequities illuminate the greatest gaps and worst patient outcomes, especially when compounded by disparities related to gender identity, ability, language, immigration status, sexual orientation, age, socioeconomics, and other social drivers of health. Research also shows that nearly one-fifth of Latine Americans avoid medical care due to concern about experiencing discrimination, Black Americans have significantly lower life expectancies, and Asian Americans are the only racial group to experience cancer as a leading cause of death. It is also well documented that communities experiencing disproportionately high rates of COVID-19 infection, hospitalization, and mortality when compared with White Americans include Black, Latine, Asian, Native Hawaiian, and Native Americans.
“In 2023, the CHEST organization shared its organizational values: community, inclusivity, innovation, advocacy, and integrity,” said CHEST President, Jack D. Buckley, MD, MPH, FCCP. “In strong accordance with these values and with our mission to champion the prevention, diagnosis, and treatment of chest diseases and advance the best patient outcomes, CHEST is firmly committed to the necessity of diversity, equity, and inclusion in health care research, education, and delivery.”
Guided by our core values, CHEST is relentlessly committed to improving the professional’s experience and patient outcomes equally. This commitment compels us to work toward eliminating disparities in the medical field. According to the most recent US Census projections, by 2045, White Americans will no longer be considered a racial majority, with Black, Latine, and Asian Americans continuing to rise. It is incumbent upon us to ensure that our clinician workforce reflects the diversity of its local and national communities.
The underrepresentation of physicians from racially diverse backgrounds is factually clear. Black physicians comprise 5% of the current physician workforce despite Black Americans representing 13% of the population.1 Similarly, while Native Americans comprise 3% of the United States population, Native American physicians account for less than 1% of the physician workforce, with less than 10% of medical schools reporting total enrollment of more than four Native American students.2 Where gender is concerned, women make up about 36% of the physician workforce, a professional disparity that is further exacerbated given the intersections of race and gender, resulting in a significant impact on the current workforce.3 Allowing disinformation to influence the future of medical education and patient care directly contradicts our mission as clinicians dedicated to improving the health of all people.
If physician representation and patient outcomes are linked, as research shows, the lack of diverse medical school representation has dire consequences for matriculation, job recruitment, retention, and promotion. Without supportive policies, programs, and equity-focused curriculums in medical education, we will never close the gap on professional disparities, which means we will similarly never close the gap on health disparities.
Our commitment to our members, all health care professionals, and the field of medicine means that we will stand firm in our defense of DEI today and every day until we have achieved optimal, equitable health for all people in all places. CHEST is committed to an intersectional approach to equitable health care education and delivery. We strive to design solutions that center the most impacted and radiate support outward, ensuring our interventions benefit all others experiencing discrimination.
Read more about CHEST’s commitment to diversity and other advocacy work on the CHEST website.
References
1. AAMC. Figure 18. Percentage of all active physicians by race/ethnicity, 2018. AAMC; 2019. https://www.aamc.org/data-reports/workforce/data/figure-18-percentage-all-active-physicians-race/ethnicity-2018#:~:text=Diversity%20in%20Medicine%3A%20Facts%20and%20Figures%202019,-Diversity%20in%20Medicine&text=Among%20active%20physicians%2C%2056.2%25%20identified,as%20Black%20or%20African%20American
2. Murphy B. New effort to help Native American pre-meds pursue physician dreams. AMA. January 13, 2022. https://www.ama-assn.org/education/medical-school-diversity/new-effort-help-native-american-pre-meds-pursue-physician-dreams
3. AAMC. U.S. Physician Workforce Data Dashboard. AAMC; 2023. https://www.aamc.org/data-reports/report/us-physician-workforce-data-dashboard
Earlier this year,
If enacted, the EDUCATE Act would cut off federal funding to medical schools that force students or faculty to adopt specific beliefs; discriminate based on race or ethnicity; or have diversity, equity, and inclusion (DEI) offices or any functional equivalent. The bill would also require accreditation agencies to check that their standards do not push these practices, while still allowing instruction about health issues tied to race or collecting data for research.
In response to the introduction of this act, CHEST published a statement in support of DEI practices and their necessary role within the practice of health care and medical training programs.
It is our belief that health care requires a solid patient-provider therapeutic alliance to achieve successful outcomes, and decades of scientific research have shown that a lack of clinician diversity worsens health disparities. For patients from historically underserved communities, having clinicians who share similar lived experiences almost always leads to significant improvements in patient outcomes. If identity concordance is not feasible, clinicians with considerable exposure to diverse patient populations, equitable approaches to care, and inclusive perspectives on health gained through continuing, comprehensive medical education and professional training can also positively impact outcomes.
Research indicates that a diverse medical workforce improves cultural competence and can help clinicians better meet the needs of patients from diverse backgrounds and ethnicities and that the benefits of diverse learning environments enhance the educational experience of all participants. Racial and ethnic health inequities illuminate the greatest gaps and worst patient outcomes, especially when compounded by disparities related to gender identity, ability, language, immigration status, sexual orientation, age, socioeconomics, and other social drivers of health. Research also shows that nearly one-fifth of Latine Americans avoid medical care due to concern about experiencing discrimination, Black Americans have significantly lower life expectancies, and Asian Americans are the only racial group to experience cancer as a leading cause of death. It is also well documented that communities experiencing disproportionately high rates of COVID-19 infection, hospitalization, and mortality when compared with White Americans include Black, Latine, Asian, Native Hawaiian, and Native Americans.
“In 2023, the CHEST organization shared its organizational values: community, inclusivity, innovation, advocacy, and integrity,” said CHEST President, Jack D. Buckley, MD, MPH, FCCP. “In strong accordance with these values and with our mission to champion the prevention, diagnosis, and treatment of chest diseases and advance the best patient outcomes, CHEST is firmly committed to the necessity of diversity, equity, and inclusion in health care research, education, and delivery.”
Guided by our core values, CHEST is relentlessly committed to improving the professional’s experience and patient outcomes equally. This commitment compels us to work toward eliminating disparities in the medical field. According to the most recent US Census projections, by 2045, White Americans will no longer be considered a racial majority, with Black, Latine, and Asian Americans continuing to rise. It is incumbent upon us to ensure that our clinician workforce reflects the diversity of its local and national communities.
The underrepresentation of physicians from racially diverse backgrounds is factually clear. Black physicians comprise 5% of the current physician workforce despite Black Americans representing 13% of the population.1 Similarly, while Native Americans comprise 3% of the United States population, Native American physicians account for less than 1% of the physician workforce, with less than 10% of medical schools reporting total enrollment of more than four Native American students.2 Where gender is concerned, women make up about 36% of the physician workforce, a professional disparity that is further exacerbated given the intersections of race and gender, resulting in a significant impact on the current workforce.3 Allowing disinformation to influence the future of medical education and patient care directly contradicts our mission as clinicians dedicated to improving the health of all people.
If physician representation and patient outcomes are linked, as research shows, the lack of diverse medical school representation has dire consequences for matriculation, job recruitment, retention, and promotion. Without supportive policies, programs, and equity-focused curriculums in medical education, we will never close the gap on professional disparities, which means we will similarly never close the gap on health disparities.
Our commitment to our members, all health care professionals, and the field of medicine means that we will stand firm in our defense of DEI today and every day until we have achieved optimal, equitable health for all people in all places. CHEST is committed to an intersectional approach to equitable health care education and delivery. We strive to design solutions that center the most impacted and radiate support outward, ensuring our interventions benefit all others experiencing discrimination.
Read more about CHEST’s commitment to diversity and other advocacy work on the CHEST website.
References
1. AAMC. Figure 18. Percentage of all active physicians by race/ethnicity, 2018. AAMC; 2019. https://www.aamc.org/data-reports/workforce/data/figure-18-percentage-all-active-physicians-race/ethnicity-2018#:~:text=Diversity%20in%20Medicine%3A%20Facts%20and%20Figures%202019,-Diversity%20in%20Medicine&text=Among%20active%20physicians%2C%2056.2%25%20identified,as%20Black%20or%20African%20American
2. Murphy B. New effort to help Native American pre-meds pursue physician dreams. AMA. January 13, 2022. https://www.ama-assn.org/education/medical-school-diversity/new-effort-help-native-american-pre-meds-pursue-physician-dreams
3. AAMC. U.S. Physician Workforce Data Dashboard. AAMC; 2023. https://www.aamc.org/data-reports/report/us-physician-workforce-data-dashboard
Earlier this year,
If enacted, the EDUCATE Act would cut off federal funding to medical schools that force students or faculty to adopt specific beliefs; discriminate based on race or ethnicity; or have diversity, equity, and inclusion (DEI) offices or any functional equivalent. The bill would also require accreditation agencies to check that their standards do not push these practices, while still allowing instruction about health issues tied to race or collecting data for research.
In response to the introduction of this act, CHEST published a statement in support of DEI practices and their necessary role within the practice of health care and medical training programs.
It is our belief that health care requires a solid patient-provider therapeutic alliance to achieve successful outcomes, and decades of scientific research have shown that a lack of clinician diversity worsens health disparities. For patients from historically underserved communities, having clinicians who share similar lived experiences almost always leads to significant improvements in patient outcomes. If identity concordance is not feasible, clinicians with considerable exposure to diverse patient populations, equitable approaches to care, and inclusive perspectives on health gained through continuing, comprehensive medical education and professional training can also positively impact outcomes.
Research indicates that a diverse medical workforce improves cultural competence and can help clinicians better meet the needs of patients from diverse backgrounds and ethnicities and that the benefits of diverse learning environments enhance the educational experience of all participants. Racial and ethnic health inequities illuminate the greatest gaps and worst patient outcomes, especially when compounded by disparities related to gender identity, ability, language, immigration status, sexual orientation, age, socioeconomics, and other social drivers of health. Research also shows that nearly one-fifth of Latine Americans avoid medical care due to concern about experiencing discrimination, Black Americans have significantly lower life expectancies, and Asian Americans are the only racial group to experience cancer as a leading cause of death. It is also well documented that communities experiencing disproportionately high rates of COVID-19 infection, hospitalization, and mortality when compared with White Americans include Black, Latine, Asian, Native Hawaiian, and Native Americans.
“In 2023, the CHEST organization shared its organizational values: community, inclusivity, innovation, advocacy, and integrity,” said CHEST President, Jack D. Buckley, MD, MPH, FCCP. “In strong accordance with these values and with our mission to champion the prevention, diagnosis, and treatment of chest diseases and advance the best patient outcomes, CHEST is firmly committed to the necessity of diversity, equity, and inclusion in health care research, education, and delivery.”
Guided by our core values, CHEST is relentlessly committed to improving the professional’s experience and patient outcomes equally. This commitment compels us to work toward eliminating disparities in the medical field. According to the most recent US Census projections, by 2045, White Americans will no longer be considered a racial majority, with Black, Latine, and Asian Americans continuing to rise. It is incumbent upon us to ensure that our clinician workforce reflects the diversity of its local and national communities.
The underrepresentation of physicians from racially diverse backgrounds is factually clear. Black physicians comprise 5% of the current physician workforce despite Black Americans representing 13% of the population.1 Similarly, while Native Americans comprise 3% of the United States population, Native American physicians account for less than 1% of the physician workforce, with less than 10% of medical schools reporting total enrollment of more than four Native American students.2 Where gender is concerned, women make up about 36% of the physician workforce, a professional disparity that is further exacerbated given the intersections of race and gender, resulting in a significant impact on the current workforce.3 Allowing disinformation to influence the future of medical education and patient care directly contradicts our mission as clinicians dedicated to improving the health of all people.
If physician representation and patient outcomes are linked, as research shows, the lack of diverse medical school representation has dire consequences for matriculation, job recruitment, retention, and promotion. Without supportive policies, programs, and equity-focused curriculums in medical education, we will never close the gap on professional disparities, which means we will similarly never close the gap on health disparities.
Our commitment to our members, all health care professionals, and the field of medicine means that we will stand firm in our defense of DEI today and every day until we have achieved optimal, equitable health for all people in all places. CHEST is committed to an intersectional approach to equitable health care education and delivery. We strive to design solutions that center the most impacted and radiate support outward, ensuring our interventions benefit all others experiencing discrimination.
Read more about CHEST’s commitment to diversity and other advocacy work on the CHEST website.
References
1. AAMC. Figure 18. Percentage of all active physicians by race/ethnicity, 2018. AAMC; 2019. https://www.aamc.org/data-reports/workforce/data/figure-18-percentage-all-active-physicians-race/ethnicity-2018#:~:text=Diversity%20in%20Medicine%3A%20Facts%20and%20Figures%202019,-Diversity%20in%20Medicine&text=Among%20active%20physicians%2C%2056.2%25%20identified,as%20Black%20or%20African%20American
2. Murphy B. New effort to help Native American pre-meds pursue physician dreams. AMA. January 13, 2022. https://www.ama-assn.org/education/medical-school-diversity/new-effort-help-native-american-pre-meds-pursue-physician-dreams
3. AAMC. U.S. Physician Workforce Data Dashboard. AAMC; 2023. https://www.aamc.org/data-reports/report/us-physician-workforce-data-dashboard
Pseudomonas infection in patients with noncystic fibrosis bronchiectasis
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Sleep and athletic performance
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
The gas stove: Friend or foe?
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.