Pulmonology

Now is the time for pulmonary clinicians to become comfortable counseling patients about and treating obesity. By 2030, half of the US population will have obesity, a quarter of which will be severe (Ward et al. NEJM. 2019;2440-2450).

Many pulmonary diseases, including asthma, COPD, and interstitial pulmonary fibrosis (IPF) are linked to and made worse by obesity with increased exacerbations, patient-reported decreased quality of life, and resistance to therapy (Ray et al. Am Rev Respir Dis. 1983;501-6). Asthma is even recognized as an obesity-related comorbid condition by both the American Society Metabolic and Bariatric Surgery (ASMBS) and the American Association of Clinical Endocrinologists (AACE) when considering indications for early or more aggressive treatment of obesity (Eisenberg et al. Obesity Surg. 2023;3-14) (Garvey et al. Endocr Pract. 2016;1-203).

Obesity has multiple negative effects on pulmonary function due to the physical forces of extra weight on the lungs and inflammation related to adipose tissue (see Figure 1) (Zerah et al. Chest. 1993;1470-6).

CHEST

Obesity-related respiratory changes include reduced lung compliance, functional residual capacity (FRC), and expiratory reserve volume (ERV). These changes lead to peripheral atelectasis and V/Q mismatch and increased metabolic demands placed on the respiratory system (Parameswaran et al. Can Respir J. 2006;203-10). The increased weight supported by the thoracic cage alters the equilibrium between the chest wall and lung tissue decreasing FRC and ERV. This reduces lung compliance and increases stiffness by promoting areas of atelectasis and increased alveolar surface tension (Dixon et al. Expert Rev Respir Med. 2018;755-67).

CHEST

Another biomechanical cost of obesity on respiratory function is the increased consumption of oxygen to sustain ventilation at rest (Koenig SM, Am J Med Sci. 2001;249-79). This can lead to early respiratory muscle fatigue when respiratory rate and tidal volume increase with activity. Patients with obesity are more likely to develop obstructive sleep apnea and obesity hypoventilation syndrome. The resulting alveolar hypoxemia is thought to contribute to the increase in pulmonary hypertension observed in patients with obesity (Shah et al. Breathe. 2023;19[1]). In addition to the biomechanical consequences of obesity, increased adipose tissue can lead to chronic, systemic inflammation that can exacerbate or unmask underlying respiratory disease. Increased leptin and downregulation of adiponectin have been shown to increase systemic cytokine production (Ray et al. Am Rev Respir Dis. 1983;501-6). This inflammatory process contributes to increased airway resistance and an altered response to corticosteroids (inhaled or systemic) in obese patients treated for bronchial hyperresponsiveness. This perhaps reflects the Th2-low phenotype seen in patients with obesity and metabolic syndrome-related asthma (Shah et al. Breathe. 2023;19[1]) (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812).

CHEST

Multiple studies have demonstrated weight loss through lifestyle changes, medical therapy, and obesity surgery result benefits pulmonary disease (Forno et al. PloS One. 2019;14[4]) (Ardila-Gatas et al. Surg Endosc. 2019;1952-8). Benefits include decreased exacerbation frequency, improved functional testing, and improved patient-reported quality of life. Pulmonary clinicians should be empowered to address obesity as a comorbid condition and treat with appropriate referrals for obesity surgery and initiation of medications when indicated.
 

GLP-1 receptor agonists

In the past year, glucagon-like peptide receptor agonists (GLP-1RAs) have garnered attention in the medical literature and popular news outlets. GLP-1RAs, including semaglutide, liraglutide, and tirzepatide, are currently FDA approved for the treatment of obesity in patients with a body mass index (BMI) greater than or equal to 30 or a BMI greater than or equal to 27 in the setting of an obesity-related comorbidity, including asthma.

This class of medications acts by increasing the physiologic insulin response to a glucose load, delaying gastric emptying, and reducing production of glucagon. In a phase III study, semaglutide resulted in greater than 15% weight reduction from baseline (Wadden et al. JAMA. 2021;1403-13). In clinical trials, these medications have not only resulted in significant, sustained weight loss but also improved lipid profiles, decreased A1c, and reduced major cardiovascular events (Lincoff et al. N Engl J Med. 2023;389[23]:2221-32) (Verma et al. Circulation. 2018;138[25]:2884-94).
 

GLP-1RAs and lung disease

GLP-1RAs are associated with ranges of weight loss that lead to symptom improvement. Beyond the anticipated benefits for pulmonary health, there is interest in whether GLP-1RAs may improve specific lung diseases. GLP-1 receptors are found throughout the body (eg, gastrointestinal tract, kidneys, and heart) with the largest proportion located in the lungs (Wu AY and Peebles RS. Expert Rev Clin Immunol. 2021;1053-7). In addition to their known effect on insulin response, GLP-1RAs are hypothesized to reduce proinflammatory cytokine signaling and alter surfactant production potentially improving both airway resistance and lung compliance (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Animal models suggest an antifibrotic effect with delay in the endothelial-mesenchymal transition. If further substantiated, this could impact both acute and chronic lung injury.

Early clinical studies of GLP-1RAs in patients with respiratory diseases have demonstrated improved symptoms and pulmonary function (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Even modest weight loss (2.5 kg in a year) with GLP-1RAs leads to improved symptoms and a reduction in asthma exacerbations. Other asthma literature shows GLP-1RAs improve symptoms and reduce exacerbations independent of changes in weight, supporting the hypothesis that the benefit of GLP-1RAs may be more than biomechanical improvement from weight loss alone (Foer et al. Am J Respir Crit Care Med. 2021;831-40).

GLP-1RAs reduce the proinflammatory cytokine signaling in both TH2-high and TH2-low asthma phenotypes and alter surfactant production, airway resistance, and perhaps even pulmonary vascular resistance (Altintas Dogan et al. Int J Chron Obstruct Pulmon Dis. 2022,405-14). GATA-3 is an ongoing clinical trial examining whether GLP-1RAs reduce airway inflammation via direct effects on of the respiratory tract (NCT05254314).

Drugs developed to treat one condition are often found to impact others during validation studies or postmarketing observation. Some examples are aspirin, sildenafil, minoxidil, hydroxychloroquine, and SGLT-2 inhibitors. Will GLP-1RAs be the latest medication to affect a broad array of physiologic process and end up improving not just metabolic but also lung health?

Now is the time for pulmonary clinicians to become comfortable counseling patients about and treating obesity. By 2030, half of the US population will have obesity, a quarter of which will be severe (Ward et al. NEJM. 2019;2440-2450).

Many pulmonary diseases, including asthma, COPD, and interstitial pulmonary fibrosis (IPF) are linked to and made worse by obesity with increased exacerbations, patient-reported decreased quality of life, and resistance to therapy (Ray et al. Am Rev Respir Dis. 1983;501-6). Asthma is even recognized as an obesity-related comorbid condition by both the American Society Metabolic and Bariatric Surgery (ASMBS) and the American Association of Clinical Endocrinologists (AACE) when considering indications for early or more aggressive treatment of obesity (Eisenberg et al. Obesity Surg. 2023;3-14) (Garvey et al. Endocr Pract. 2016;1-203).

Obesity has multiple negative effects on pulmonary function due to the physical forces of extra weight on the lungs and inflammation related to adipose tissue (see Figure 1) (Zerah et al. Chest. 1993;1470-6).

CHEST

Obesity-related respiratory changes include reduced lung compliance, functional residual capacity (FRC), and expiratory reserve volume (ERV). These changes lead to peripheral atelectasis and V/Q mismatch and increased metabolic demands placed on the respiratory system (Parameswaran et al. Can Respir J. 2006;203-10). The increased weight supported by the thoracic cage alters the equilibrium between the chest wall and lung tissue decreasing FRC and ERV. This reduces lung compliance and increases stiffness by promoting areas of atelectasis and increased alveolar surface tension (Dixon et al. Expert Rev Respir Med. 2018;755-67).

CHEST

Another biomechanical cost of obesity on respiratory function is the increased consumption of oxygen to sustain ventilation at rest (Koenig SM, Am J Med Sci. 2001;249-79). This can lead to early respiratory muscle fatigue when respiratory rate and tidal volume increase with activity. Patients with obesity are more likely to develop obstructive sleep apnea and obesity hypoventilation syndrome. The resulting alveolar hypoxemia is thought to contribute to the increase in pulmonary hypertension observed in patients with obesity (Shah et al. Breathe. 2023;19[1]). In addition to the biomechanical consequences of obesity, increased adipose tissue can lead to chronic, systemic inflammation that can exacerbate or unmask underlying respiratory disease. Increased leptin and downregulation of adiponectin have been shown to increase systemic cytokine production (Ray et al. Am Rev Respir Dis. 1983;501-6). This inflammatory process contributes to increased airway resistance and an altered response to corticosteroids (inhaled or systemic) in obese patients treated for bronchial hyperresponsiveness. This perhaps reflects the Th2-low phenotype seen in patients with obesity and metabolic syndrome-related asthma (Shah et al. Breathe. 2023;19[1]) (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812).

CHEST

Multiple studies have demonstrated weight loss through lifestyle changes, medical therapy, and obesity surgery result benefits pulmonary disease (Forno et al. PloS One. 2019;14[4]) (Ardila-Gatas et al. Surg Endosc. 2019;1952-8). Benefits include decreased exacerbation frequency, improved functional testing, and improved patient-reported quality of life. Pulmonary clinicians should be empowered to address obesity as a comorbid condition and treat with appropriate referrals for obesity surgery and initiation of medications when indicated.
 

GLP-1 receptor agonists

In the past year, glucagon-like peptide receptor agonists (GLP-1RAs) have garnered attention in the medical literature and popular news outlets. GLP-1RAs, including semaglutide, liraglutide, and tirzepatide, are currently FDA approved for the treatment of obesity in patients with a body mass index (BMI) greater than or equal to 30 or a BMI greater than or equal to 27 in the setting of an obesity-related comorbidity, including asthma.

This class of medications acts by increasing the physiologic insulin response to a glucose load, delaying gastric emptying, and reducing production of glucagon. In a phase III study, semaglutide resulted in greater than 15% weight reduction from baseline (Wadden et al. JAMA. 2021;1403-13). In clinical trials, these medications have not only resulted in significant, sustained weight loss but also improved lipid profiles, decreased A1c, and reduced major cardiovascular events (Lincoff et al. N Engl J Med. 2023;389[23]:2221-32) (Verma et al. Circulation. 2018;138[25]:2884-94).
 

GLP-1RAs and lung disease

GLP-1RAs are associated with ranges of weight loss that lead to symptom improvement. Beyond the anticipated benefits for pulmonary health, there is interest in whether GLP-1RAs may improve specific lung diseases. GLP-1 receptors are found throughout the body (eg, gastrointestinal tract, kidneys, and heart) with the largest proportion located in the lungs (Wu AY and Peebles RS. Expert Rev Clin Immunol. 2021;1053-7). In addition to their known effect on insulin response, GLP-1RAs are hypothesized to reduce proinflammatory cytokine signaling and alter surfactant production potentially improving both airway resistance and lung compliance (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Animal models suggest an antifibrotic effect with delay in the endothelial-mesenchymal transition. If further substantiated, this could impact both acute and chronic lung injury.

Early clinical studies of GLP-1RAs in patients with respiratory diseases have demonstrated improved symptoms and pulmonary function (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Even modest weight loss (2.5 kg in a year) with GLP-1RAs leads to improved symptoms and a reduction in asthma exacerbations. Other asthma literature shows GLP-1RAs improve symptoms and reduce exacerbations independent of changes in weight, supporting the hypothesis that the benefit of GLP-1RAs may be more than biomechanical improvement from weight loss alone (Foer et al. Am J Respir Crit Care Med. 2021;831-40).

GLP-1RAs reduce the proinflammatory cytokine signaling in both TH2-high and TH2-low asthma phenotypes and alter surfactant production, airway resistance, and perhaps even pulmonary vascular resistance (Altintas Dogan et al. Int J Chron Obstruct Pulmon Dis. 2022,405-14). GATA-3 is an ongoing clinical trial examining whether GLP-1RAs reduce airway inflammation via direct effects on of the respiratory tract (NCT05254314).

Drugs developed to treat one condition are often found to impact others during validation studies or postmarketing observation. Some examples are aspirin, sildenafil, minoxidil, hydroxychloroquine, and SGLT-2 inhibitors. Will GLP-1RAs be the latest medication to affect a broad array of physiologic process and end up improving not just metabolic but also lung health?

Now is the time for pulmonary clinicians to become comfortable counseling patients about and treating obesity. By 2030, half of the US population will have obesity, a quarter of which will be severe (Ward et al. NEJM. 2019;2440-2450).

Many pulmonary diseases, including asthma, COPD, and interstitial pulmonary fibrosis (IPF) are linked to and made worse by obesity with increased exacerbations, patient-reported decreased quality of life, and resistance to therapy (Ray et al. Am Rev Respir Dis. 1983;501-6). Asthma is even recognized as an obesity-related comorbid condition by both the American Society Metabolic and Bariatric Surgery (ASMBS) and the American Association of Clinical Endocrinologists (AACE) when considering indications for early or more aggressive treatment of obesity (Eisenberg et al. Obesity Surg. 2023;3-14) (Garvey et al. Endocr Pract. 2016;1-203).

Obesity has multiple negative effects on pulmonary function due to the physical forces of extra weight on the lungs and inflammation related to adipose tissue (see Figure 1) (Zerah et al. Chest. 1993;1470-6).

CHEST

Obesity-related respiratory changes include reduced lung compliance, functional residual capacity (FRC), and expiratory reserve volume (ERV). These changes lead to peripheral atelectasis and V/Q mismatch and increased metabolic demands placed on the respiratory system (Parameswaran et al. Can Respir J. 2006;203-10). The increased weight supported by the thoracic cage alters the equilibrium between the chest wall and lung tissue decreasing FRC and ERV. This reduces lung compliance and increases stiffness by promoting areas of atelectasis and increased alveolar surface tension (Dixon et al. Expert Rev Respir Med. 2018;755-67).

CHEST

Another biomechanical cost of obesity on respiratory function is the increased consumption of oxygen to sustain ventilation at rest (Koenig SM, Am J Med Sci. 2001;249-79). This can lead to early respiratory muscle fatigue when respiratory rate and tidal volume increase with activity. Patients with obesity are more likely to develop obstructive sleep apnea and obesity hypoventilation syndrome. The resulting alveolar hypoxemia is thought to contribute to the increase in pulmonary hypertension observed in patients with obesity (Shah et al. Breathe. 2023;19[1]). In addition to the biomechanical consequences of obesity, increased adipose tissue can lead to chronic, systemic inflammation that can exacerbate or unmask underlying respiratory disease. Increased leptin and downregulation of adiponectin have been shown to increase systemic cytokine production (Ray et al. Am Rev Respir Dis. 1983;501-6). This inflammatory process contributes to increased airway resistance and an altered response to corticosteroids (inhaled or systemic) in obese patients treated for bronchial hyperresponsiveness. This perhaps reflects the Th2-low phenotype seen in patients with obesity and metabolic syndrome-related asthma (Shah et al. Breathe. 2023;19[1]) (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812).

CHEST

Multiple studies have demonstrated weight loss through lifestyle changes, medical therapy, and obesity surgery result benefits pulmonary disease (Forno et al. PloS One. 2019;14[4]) (Ardila-Gatas et al. Surg Endosc. 2019;1952-8). Benefits include decreased exacerbation frequency, improved functional testing, and improved patient-reported quality of life. Pulmonary clinicians should be empowered to address obesity as a comorbid condition and treat with appropriate referrals for obesity surgery and initiation of medications when indicated.
 

GLP-1 receptor agonists

In the past year, glucagon-like peptide receptor agonists (GLP-1RAs) have garnered attention in the medical literature and popular news outlets. GLP-1RAs, including semaglutide, liraglutide, and tirzepatide, are currently FDA approved for the treatment of obesity in patients with a body mass index (BMI) greater than or equal to 30 or a BMI greater than or equal to 27 in the setting of an obesity-related comorbidity, including asthma.

This class of medications acts by increasing the physiologic insulin response to a glucose load, delaying gastric emptying, and reducing production of glucagon. In a phase III study, semaglutide resulted in greater than 15% weight reduction from baseline (Wadden et al. JAMA. 2021;1403-13). In clinical trials, these medications have not only resulted in significant, sustained weight loss but also improved lipid profiles, decreased A1c, and reduced major cardiovascular events (Lincoff et al. N Engl J Med. 2023;389[23]:2221-32) (Verma et al. Circulation. 2018;138[25]:2884-94).
 

GLP-1RAs and lung disease

GLP-1RAs are associated with ranges of weight loss that lead to symptom improvement. Beyond the anticipated benefits for pulmonary health, there is interest in whether GLP-1RAs may improve specific lung diseases. GLP-1 receptors are found throughout the body (eg, gastrointestinal tract, kidneys, and heart) with the largest proportion located in the lungs (Wu AY and Peebles RS. Expert Rev Clin Immunol. 2021;1053-7). In addition to their known effect on insulin response, GLP-1RAs are hypothesized to reduce proinflammatory cytokine signaling and alter surfactant production potentially improving both airway resistance and lung compliance (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Animal models suggest an antifibrotic effect with delay in the endothelial-mesenchymal transition. If further substantiated, this could impact both acute and chronic lung injury.

Early clinical studies of GLP-1RAs in patients with respiratory diseases have demonstrated improved symptoms and pulmonary function (Kanwar et al. Cureus. 2022 Oct 28. doi: 10.7759/cureus.30812). Even modest weight loss (2.5 kg in a year) with GLP-1RAs leads to improved symptoms and a reduction in asthma exacerbations. Other asthma literature shows GLP-1RAs improve symptoms and reduce exacerbations independent of changes in weight, supporting the hypothesis that the benefit of GLP-1RAs may be more than biomechanical improvement from weight loss alone (Foer et al. Am J Respir Crit Care Med. 2021;831-40).

GLP-1RAs reduce the proinflammatory cytokine signaling in both TH2-high and TH2-low asthma phenotypes and alter surfactant production, airway resistance, and perhaps even pulmonary vascular resistance (Altintas Dogan et al. Int J Chron Obstruct Pulmon Dis. 2022,405-14). GATA-3 is an ongoing clinical trial examining whether GLP-1RAs reduce airway inflammation via direct effects on of the respiratory tract (NCT05254314).

Drugs developed to treat one condition are often found to impact others during validation studies or postmarketing observation. Some examples are aspirin, sildenafil, minoxidil, hydroxychloroquine, and SGLT-2 inhibitors. Will GLP-1RAs be the latest medication to affect a broad array of physiologic process and end up improving not just metabolic but also lung health?

Children and adolescents ages 5-17 who received a bivalent COVID-19 mRNA vaccine were less likely to become infected with SARS-CoV-2 compared with those who were unvaccinated or received only the monovalent COVID-19 vaccine, according to new data published February 6 in JAMA.

“All eligible children and adolescents should remain up to date with recommended COVID-19 vaccinations,” wrote the authors, led by Leora R. Feldstein, PhD, with the US Centers for Disease Control and Prevention (CDC) in Atlanta.

By the end of 2023, at least 911 youths ages 5-17 had died from COVID-related causes.

Researchers found that compared with participants who did not receive the COVID-19 vaccine or got monovalent-only doses 180 days or more before, the adjusted vaccine effectiveness of a bivalent COVID-19 vaccine dose against SARS-CoV-2 infection was 51.3% (95% confidence interval [CI], 23.6%-71.9%) 7-60 days after vaccination. Relative effectiveness was 62.4% (95% CI, 38.5%-81.1%) 61-150 days after vaccination. The researchers said the confidence intervals were wide because of the small sample size.

The information can help inform public health strategies, the authors noted, especially as new variants emerge.
 

Bivalent Dose Recommended in Fall of 2022

Bivalent mRNA COVID vaccines were recommended in the United States for children and adolescents ages 12 years or older on Sept. 1, 2022, and for children ages 5-11 on Oct. 12, 2022, when Omicron BA.4/5 types were the predominant circulating variant.

The study included 2,959 participants who completed periodic surveys (answering questions on demographics, household details, chronic medical conditions, and COVID-19 symptoms) and submitted weekly self-collected nasal swabs (whether or not they had symptoms). Those in the study submitted additional nasal swabs if they developed any symptoms.

Median adherence to weekly upper respiratory specimen swabbing was high throughout the study period at 93.8%.

Data from Sept. 4, 2022, to Jan. 31, 2023, were combined from three prospective US cohort studies at six sites. In addition to the surveys, researchers used information from state immunization information systems and electronic medical records.
 

Most of the Infected Were Unvaccinated or Had Monovalent Vax

Of the 426 participants (14.4% of the combined cohorts) infected with SARS-CoV-2, 383 (89.9%) were either unvaccinated or received monovalent vaccine doses only.

Calculations were adjusted for age, sex, race, ethnicity, health conditions, prior SARS-CoV-2 infections, geographic location, proportion of circulating variants by site, and local virus prevalence.

Participants living in Oregon, for example, had the highest uptake of bivalent COVID-19 vaccine (56.2%), whereas those in Texas had the lowest (2.4%). Participants reporting Hispanic ethnicity had lower bivalent uptake (17.1%) compared with non-Hispanic participants of all races (27.1%).

Of the 2,207 participants who did not receive a bivalent dose, 24.2% were unvaccinated and 1,672 (75.8%) received at least 1 monovalent dose.

The researchers said they saw no sign of waning effectiveness 61-150 days (the limit for this analysis) after receipt of the bivalent COVID-19 vaccine.

They wrote that continuation of the cohorts will allow study of waning patterns, which could help inform vaccine recommendations.

Among the limitations of the study are that testing methods and the COVID-19 symptoms surveyed varied among the three cohorts, so there may be some differences in defining infection or symptomatic COVID. In addition, the researchers were not able to account for the social vulnerability index and immunocompromised status, which could have affected vaccine uptake and risk of SARS-CoV-2 infection.

This study was supported by the National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, and by the National Institute of Allergy and Infectious Diseases. Coauthor Dr. Caban-Martinez reported grants from the Florida Firefighter Cancer Initiative and the Florida Department of Health. Coauthors Dr. Chu, Dr. Englund, Dr. Martin, and Dr. Monto reported receiving personal fees or grants from multiple pharmaceutical companies. Dr. Hegmann reported being the editor of the American College of Occupational and Environmental Medicine practice guidelines. Coauthor Dr. Gaglani reported serving as cochair of the infectious diseases and immunization committee and the respiratory syncytial virus task force lead for the Texas Pediatric Society and the Texas Chapter of the American Academy of Pediatrics. No other disclosures were reported.

Children and adolescents ages 5-17 who received a bivalent COVID-19 mRNA vaccine were less likely to become infected with SARS-CoV-2 compared with those who were unvaccinated or received only the monovalent COVID-19 vaccine, according to new data published February 6 in JAMA.

“All eligible children and adolescents should remain up to date with recommended COVID-19 vaccinations,” wrote the authors, led by Leora R. Feldstein, PhD, with the US Centers for Disease Control and Prevention (CDC) in Atlanta.

By the end of 2023, at least 911 youths ages 5-17 had died from COVID-related causes.

Researchers found that compared with participants who did not receive the COVID-19 vaccine or got monovalent-only doses 180 days or more before, the adjusted vaccine effectiveness of a bivalent COVID-19 vaccine dose against SARS-CoV-2 infection was 51.3% (95% confidence interval [CI], 23.6%-71.9%) 7-60 days after vaccination. Relative effectiveness was 62.4% (95% CI, 38.5%-81.1%) 61-150 days after vaccination. The researchers said the confidence intervals were wide because of the small sample size.

The information can help inform public health strategies, the authors noted, especially as new variants emerge.
 

Bivalent Dose Recommended in Fall of 2022

Bivalent mRNA COVID vaccines were recommended in the United States for children and adolescents ages 12 years or older on Sept. 1, 2022, and for children ages 5-11 on Oct. 12, 2022, when Omicron BA.4/5 types were the predominant circulating variant.

The study included 2,959 participants who completed periodic surveys (answering questions on demographics, household details, chronic medical conditions, and COVID-19 symptoms) and submitted weekly self-collected nasal swabs (whether or not they had symptoms). Those in the study submitted additional nasal swabs if they developed any symptoms.

Median adherence to weekly upper respiratory specimen swabbing was high throughout the study period at 93.8%.

Data from Sept. 4, 2022, to Jan. 31, 2023, were combined from three prospective US cohort studies at six sites. In addition to the surveys, researchers used information from state immunization information systems and electronic medical records.
 

Most of the Infected Were Unvaccinated or Had Monovalent Vax

Of the 426 participants (14.4% of the combined cohorts) infected with SARS-CoV-2, 383 (89.9%) were either unvaccinated or received monovalent vaccine doses only.

Calculations were adjusted for age, sex, race, ethnicity, health conditions, prior SARS-CoV-2 infections, geographic location, proportion of circulating variants by site, and local virus prevalence.

Participants living in Oregon, for example, had the highest uptake of bivalent COVID-19 vaccine (56.2%), whereas those in Texas had the lowest (2.4%). Participants reporting Hispanic ethnicity had lower bivalent uptake (17.1%) compared with non-Hispanic participants of all races (27.1%).

Of the 2,207 participants who did not receive a bivalent dose, 24.2% were unvaccinated and 1,672 (75.8%) received at least 1 monovalent dose.

The researchers said they saw no sign of waning effectiveness 61-150 days (the limit for this analysis) after receipt of the bivalent COVID-19 vaccine.

They wrote that continuation of the cohorts will allow study of waning patterns, which could help inform vaccine recommendations.

Among the limitations of the study are that testing methods and the COVID-19 symptoms surveyed varied among the three cohorts, so there may be some differences in defining infection or symptomatic COVID. In addition, the researchers were not able to account for the social vulnerability index and immunocompromised status, which could have affected vaccine uptake and risk of SARS-CoV-2 infection.

This study was supported by the National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, and by the National Institute of Allergy and Infectious Diseases. Coauthor Dr. Caban-Martinez reported grants from the Florida Firefighter Cancer Initiative and the Florida Department of Health. Coauthors Dr. Chu, Dr. Englund, Dr. Martin, and Dr. Monto reported receiving personal fees or grants from multiple pharmaceutical companies. Dr. Hegmann reported being the editor of the American College of Occupational and Environmental Medicine practice guidelines. Coauthor Dr. Gaglani reported serving as cochair of the infectious diseases and immunization committee and the respiratory syncytial virus task force lead for the Texas Pediatric Society and the Texas Chapter of the American Academy of Pediatrics. No other disclosures were reported.

Children and adolescents ages 5-17 who received a bivalent COVID-19 mRNA vaccine were less likely to become infected with SARS-CoV-2 compared with those who were unvaccinated or received only the monovalent COVID-19 vaccine, according to new data published February 6 in JAMA.

“All eligible children and adolescents should remain up to date with recommended COVID-19 vaccinations,” wrote the authors, led by Leora R. Feldstein, PhD, with the US Centers for Disease Control and Prevention (CDC) in Atlanta.

By the end of 2023, at least 911 youths ages 5-17 had died from COVID-related causes.

Researchers found that compared with participants who did not receive the COVID-19 vaccine or got monovalent-only doses 180 days or more before, the adjusted vaccine effectiveness of a bivalent COVID-19 vaccine dose against SARS-CoV-2 infection was 51.3% (95% confidence interval [CI], 23.6%-71.9%) 7-60 days after vaccination. Relative effectiveness was 62.4% (95% CI, 38.5%-81.1%) 61-150 days after vaccination. The researchers said the confidence intervals were wide because of the small sample size.

The information can help inform public health strategies, the authors noted, especially as new variants emerge.
 

Bivalent Dose Recommended in Fall of 2022

Bivalent mRNA COVID vaccines were recommended in the United States for children and adolescents ages 12 years or older on Sept. 1, 2022, and for children ages 5-11 on Oct. 12, 2022, when Omicron BA.4/5 types were the predominant circulating variant.

The study included 2,959 participants who completed periodic surveys (answering questions on demographics, household details, chronic medical conditions, and COVID-19 symptoms) and submitted weekly self-collected nasal swabs (whether or not they had symptoms). Those in the study submitted additional nasal swabs if they developed any symptoms.

Median adherence to weekly upper respiratory specimen swabbing was high throughout the study period at 93.8%.

Data from Sept. 4, 2022, to Jan. 31, 2023, were combined from three prospective US cohort studies at six sites. In addition to the surveys, researchers used information from state immunization information systems and electronic medical records.
 

Most of the Infected Were Unvaccinated or Had Monovalent Vax

Of the 426 participants (14.4% of the combined cohorts) infected with SARS-CoV-2, 383 (89.9%) were either unvaccinated or received monovalent vaccine doses only.

Calculations were adjusted for age, sex, race, ethnicity, health conditions, prior SARS-CoV-2 infections, geographic location, proportion of circulating variants by site, and local virus prevalence.

Participants living in Oregon, for example, had the highest uptake of bivalent COVID-19 vaccine (56.2%), whereas those in Texas had the lowest (2.4%). Participants reporting Hispanic ethnicity had lower bivalent uptake (17.1%) compared with non-Hispanic participants of all races (27.1%).

Of the 2,207 participants who did not receive a bivalent dose, 24.2% were unvaccinated and 1,672 (75.8%) received at least 1 monovalent dose.

The researchers said they saw no sign of waning effectiveness 61-150 days (the limit for this analysis) after receipt of the bivalent COVID-19 vaccine.

They wrote that continuation of the cohorts will allow study of waning patterns, which could help inform vaccine recommendations.

Among the limitations of the study are that testing methods and the COVID-19 symptoms surveyed varied among the three cohorts, so there may be some differences in defining infection or symptomatic COVID. In addition, the researchers were not able to account for the social vulnerability index and immunocompromised status, which could have affected vaccine uptake and risk of SARS-CoV-2 infection.

This study was supported by the National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, and by the National Institute of Allergy and Infectious Diseases. Coauthor Dr. Caban-Martinez reported grants from the Florida Firefighter Cancer Initiative and the Florida Department of Health. Coauthors Dr. Chu, Dr. Englund, Dr. Martin, and Dr. Monto reported receiving personal fees or grants from multiple pharmaceutical companies. Dr. Hegmann reported being the editor of the American College of Occupational and Environmental Medicine practice guidelines. Coauthor Dr. Gaglani reported serving as cochair of the infectious diseases and immunization committee and the respiratory syncytial virus task force lead for the Texas Pediatric Society and the Texas Chapter of the American Academy of Pediatrics. No other disclosures were reported.

TOPLINE:

Gabapentinoid use significantly increased the risk for exacerbations in adults with chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• Previous research has prompted warnings from North American and European health agencies of severe exacerbations associated with gabapentinoid use by patients with COPD.
• The researchers compared data from patients with COPD in Canadian databases between 1994 and 2015 who were new to gabapentinoids and matched them to patients who did not use gabapentinoids.
• The primary outcome was exacerbation of COPD that required hospitalization in a propensity score-matched study. 

TAKEAWAY:

• The study population included 356 epilepsy patients, 9411 neuropathic pain patients, and 3737 patients with other chronic pain.
• Use of gabapentinoids was significantly associated with an overall increased risk for severe COPD exacerbation (hazard ratio, 1.49) compared with nonuse.
• Gabapentinoid use was associated with a significantly increased COPD exacerbation risk for each group of users compared with nonusers, with hazard ratios of 1.58, 1.35, and 1.49 for epilepsy, neuropathic pain, and other chronic pain, respectively.

IN PRACTICE:

“This study supports the warnings from regulatory agencies and highlights the importance of considering this potential risk when prescribing gabapentin and pregabalin to patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Alvi A. Rahman, MSc, of Jewish General Hospital, Montreal. The study was published online on January 16, 2024, in Annals of Internal Medicine. 

LIMITATIONS:

A lack of data on smoking status and other residual confounding factors limited the study findings. 

DISCLOSURES:

The study was supported by the Canadian Institutes of Health Research and the Canadian Lung Association. Mr. Rahman had no financial conflicts to disclose, but some coauthors disclosed consulting and advisory relationships with various companies, including Merck, Pfizer, Seqirus, Boehringer-Ingelheim, and Novartis outside of the current work.

A version of this article appeared on Medscape.com.

TOPLINE:

Gabapentinoid use significantly increased the risk for exacerbations in adults with chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• Previous research has prompted warnings from North American and European health agencies of severe exacerbations associated with gabapentinoid use by patients with COPD.
• The researchers compared data from patients with COPD in Canadian databases between 1994 and 2015 who were new to gabapentinoids and matched them to patients who did not use gabapentinoids.
• The primary outcome was exacerbation of COPD that required hospitalization in a propensity score-matched study. 

TAKEAWAY:

• The study population included 356 epilepsy patients, 9411 neuropathic pain patients, and 3737 patients with other chronic pain.
• Use of gabapentinoids was significantly associated with an overall increased risk for severe COPD exacerbation (hazard ratio, 1.49) compared with nonuse.
• Gabapentinoid use was associated with a significantly increased COPD exacerbation risk for each group of users compared with nonusers, with hazard ratios of 1.58, 1.35, and 1.49 for epilepsy, neuropathic pain, and other chronic pain, respectively.

IN PRACTICE:

“This study supports the warnings from regulatory agencies and highlights the importance of considering this potential risk when prescribing gabapentin and pregabalin to patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Alvi A. Rahman, MSc, of Jewish General Hospital, Montreal. The study was published online on January 16, 2024, in Annals of Internal Medicine. 

LIMITATIONS:

A lack of data on smoking status and other residual confounding factors limited the study findings. 

DISCLOSURES:

The study was supported by the Canadian Institutes of Health Research and the Canadian Lung Association. Mr. Rahman had no financial conflicts to disclose, but some coauthors disclosed consulting and advisory relationships with various companies, including Merck, Pfizer, Seqirus, Boehringer-Ingelheim, and Novartis outside of the current work.

A version of this article appeared on Medscape.com.

TOPLINE:

Gabapentinoid use significantly increased the risk for exacerbations in adults with chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• Previous research has prompted warnings from North American and European health agencies of severe exacerbations associated with gabapentinoid use by patients with COPD.
• The researchers compared data from patients with COPD in Canadian databases between 1994 and 2015 who were new to gabapentinoids and matched them to patients who did not use gabapentinoids.
• The primary outcome was exacerbation of COPD that required hospitalization in a propensity score-matched study. 

TAKEAWAY:

• The study population included 356 epilepsy patients, 9411 neuropathic pain patients, and 3737 patients with other chronic pain.
• Use of gabapentinoids was significantly associated with an overall increased risk for severe COPD exacerbation (hazard ratio, 1.49) compared with nonuse.
• Gabapentinoid use was associated with a significantly increased COPD exacerbation risk for each group of users compared with nonusers, with hazard ratios of 1.58, 1.35, and 1.49 for epilepsy, neuropathic pain, and other chronic pain, respectively.

IN PRACTICE:

“This study supports the warnings from regulatory agencies and highlights the importance of considering this potential risk when prescribing gabapentin and pregabalin to patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Alvi A. Rahman, MSc, of Jewish General Hospital, Montreal. The study was published online on January 16, 2024, in Annals of Internal Medicine. 

LIMITATIONS:

A lack of data on smoking status and other residual confounding factors limited the study findings. 

DISCLOSURES:

The study was supported by the Canadian Institutes of Health Research and the Canadian Lung Association. Mr. Rahman had no financial conflicts to disclose, but some coauthors disclosed consulting and advisory relationships with various companies, including Merck, Pfizer, Seqirus, Boehringer-Ingelheim, and Novartis outside of the current work.

A version of this article appeared on Medscape.com.

Sirolimus may be an effective treatment for patients with persistent cutaneous sarcoidosis.

In a small clinical trial, 7 of 10 patients treated with sirolimus via oral solution had improvements in skin lesions after 4 months, which was sustained for up to 2 years after the study concluded.

The results suggested that mechanistic target of rapamycin (mTOR) inhibition is a potential therapeutic avenue for sarcoidosis, which the authors said should be explored in larger clinical trials. 

In the past decade, there has been a growing amount of evidence suggesting mTOR’s role in sarcoidosis. In 2017, researchers showed that activation of mTOR in macrophages could cause progressive sarcoidosis in mice. In additional studies, high levels of mTOR activity were detected in human sarcoidosis granulomas in various organs, including the skin, lung, and heart.

Three case reports also documented using the mTOR inhibitor sirolimus to effectively treat systemic sarcoidosis.

“Although all reports observed improvement of the disease following the treatment, no clinical trial investigating the efficacy and safety of sirolimus in patients with sarcoidosis had been published” prior to this study, wrote senior author Georg Stary, MD, of the Medical University of Vienna and the Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria, and colleagues. 

The findings were published in the The Lancet Rheumatology.

For the study, researchers recruited 16 individuals with persistent and glucocorticoid-refractory cutaneous sarcoidosis between September 2019 and June 2021. A total of 14 participants were randomly assigned to the topical phase of the study, whereas two immediately received systemic treatment. All treatment was conducted at Vienna General Hospital.

In the placebo-controlled, double-blinded topical treatment arm, patients received either 0.1% topical sirolimus in Vaseline or Vaseline alone (placebo) twice daily for 2 months. After a 1-month washout period, participants were switched to the alternate treatment arm for an additional 2 months.

Following this topical phase and an additional 1-month washout period, all remaining participants received systemic sirolimus via a 1-mg/mL solution, starting with a 6-mg loading dose and continuing with 2 mg once daily for 4 months. The primary outcome was change in Cutaneous Sarcoidosis Activity and Morphology Index (CSAMI) from baseline, with decrease of more than five points representing a response to treatment.

A total of 10 patients completed the trial.

There was no change in CSAMI in either topical treatment groups. In the systemic group, 70% of patients had clinical improvement in skin lesions, with three responders in this group having complete resolution of skin lesions. The median change in CSAMI was −7.0 points (P = .018). 

This improvement persisted for 2 months following study conclusion, with more pronounced improvement from baseline after 2 years of drug-free follow-up (−11.5 points).

There were no serious adverse events reported during the study, but 42% of patients treated with systemic sirolimus reported mild skin reactions, such as acne and eczema. Other related adverse events were hypertriglyceridemia (17%), hyperglycemia (17%), and proteinuria (8%).

Compared with clinical outcomes with tofacitinib and tumor necrosis factor (TNF) inhibitors, “the strength of our study lies in the sustained treatment effect after drug withdrawal among all responders. This prolonged effect has not yet been explored with tofacitinib, whereas with TNF inhibitors disease relapse was seen in more than 50% of patients at 3-8 months,” the authors wrote.

The researchers also analyzed participants’ skin biopsies to gain a better understanding of how mTOR inhibition affected granuloma structures. They found that, at baseline, mTOR activity was significantly lower in the fibroblasts of treatment nonresponders than in responders. They speculated that lower expression of mTOR could make these granuloma-associated cells resistant to systemic sirolimus.

These promising findings combine “clinical response with a molecular analysis,” Avrom Caplan, MD, co-director of the Sarcoidosis Program at NYU Langone in New York City, told this news organization. He was not involved with the research. Adding molecular information to clinical outcome data “helps solidify that [the mTOR] pathway has relevance in the sarcoid granuloma formation.”

The study had a limited sample size — a challenge for many clinical trials of rare diseases, Dr. Caplan said. Larger clinical trials are necessary to explore mTOR inhibition in sarcoidosis, both he and the authors agreed. A larger trial could also include greater heterogeneity of patients, including varied sarcoid presentation and demographics, Dr. Caplan noted. In this study, all but one participants were White individuals, and 63% of participants were female.

Larger studies could also address important questions on ideal length of therapy, dosing, and where this therapy “would fall within the therapeutic step ladder,” Dr. Caplan continued. 

Whether mTOR inhibition could be effective at treating individuals with sarcoidosis in other organs beyond the skin is also unknown. 

“If the pathogenesis of sarcoid granuloma formation does include mTOR upregulation, which they are showing here…then you could hypothesize that, yes, using this therapy could benefit other organs,” he said. “But that has to be investigated in larger trials.”

The study was funded in part by a Vienna Science and Technology Fund project. Several authors report receiving grants from the Austrian Science Fund and one from the Ann Theodore Foundation Breakthrough Sarcoidosis Initiative. Dr. Caplan reported no relevant financial relationships.

A version of this article appeared on Medscape.com .

Sirolimus may be an effective treatment for patients with persistent cutaneous sarcoidosis.

In a small clinical trial, 7 of 10 patients treated with sirolimus via oral solution had improvements in skin lesions after 4 months, which was sustained for up to 2 years after the study concluded.

The results suggested that mechanistic target of rapamycin (mTOR) inhibition is a potential therapeutic avenue for sarcoidosis, which the authors said should be explored in larger clinical trials. 

In the past decade, there has been a growing amount of evidence suggesting mTOR’s role in sarcoidosis. In 2017, researchers showed that activation of mTOR in macrophages could cause progressive sarcoidosis in mice. In additional studies, high levels of mTOR activity were detected in human sarcoidosis granulomas in various organs, including the skin, lung, and heart.

Three case reports also documented using the mTOR inhibitor sirolimus to effectively treat systemic sarcoidosis.

“Although all reports observed improvement of the disease following the treatment, no clinical trial investigating the efficacy and safety of sirolimus in patients with sarcoidosis had been published” prior to this study, wrote senior author Georg Stary, MD, of the Medical University of Vienna and the Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria, and colleagues. 

The findings were published in the The Lancet Rheumatology.

For the study, researchers recruited 16 individuals with persistent and glucocorticoid-refractory cutaneous sarcoidosis between September 2019 and June 2021. A total of 14 participants were randomly assigned to the topical phase of the study, whereas two immediately received systemic treatment. All treatment was conducted at Vienna General Hospital.

In the placebo-controlled, double-blinded topical treatment arm, patients received either 0.1% topical sirolimus in Vaseline or Vaseline alone (placebo) twice daily for 2 months. After a 1-month washout period, participants were switched to the alternate treatment arm for an additional 2 months.

Following this topical phase and an additional 1-month washout period, all remaining participants received systemic sirolimus via a 1-mg/mL solution, starting with a 6-mg loading dose and continuing with 2 mg once daily for 4 months. The primary outcome was change in Cutaneous Sarcoidosis Activity and Morphology Index (CSAMI) from baseline, with decrease of more than five points representing a response to treatment.

A total of 10 patients completed the trial.

There was no change in CSAMI in either topical treatment groups. In the systemic group, 70% of patients had clinical improvement in skin lesions, with three responders in this group having complete resolution of skin lesions. The median change in CSAMI was −7.0 points (P = .018). 

This improvement persisted for 2 months following study conclusion, with more pronounced improvement from baseline after 2 years of drug-free follow-up (−11.5 points).

There were no serious adverse events reported during the study, but 42% of patients treated with systemic sirolimus reported mild skin reactions, such as acne and eczema. Other related adverse events were hypertriglyceridemia (17%), hyperglycemia (17%), and proteinuria (8%).

Compared with clinical outcomes with tofacitinib and tumor necrosis factor (TNF) inhibitors, “the strength of our study lies in the sustained treatment effect after drug withdrawal among all responders. This prolonged effect has not yet been explored with tofacitinib, whereas with TNF inhibitors disease relapse was seen in more than 50% of patients at 3-8 months,” the authors wrote.

The researchers also analyzed participants’ skin biopsies to gain a better understanding of how mTOR inhibition affected granuloma structures. They found that, at baseline, mTOR activity was significantly lower in the fibroblasts of treatment nonresponders than in responders. They speculated that lower expression of mTOR could make these granuloma-associated cells resistant to systemic sirolimus.

These promising findings combine “clinical response with a molecular analysis,” Avrom Caplan, MD, co-director of the Sarcoidosis Program at NYU Langone in New York City, told this news organization. He was not involved with the research. Adding molecular information to clinical outcome data “helps solidify that [the mTOR] pathway has relevance in the sarcoid granuloma formation.”

The study had a limited sample size — a challenge for many clinical trials of rare diseases, Dr. Caplan said. Larger clinical trials are necessary to explore mTOR inhibition in sarcoidosis, both he and the authors agreed. A larger trial could also include greater heterogeneity of patients, including varied sarcoid presentation and demographics, Dr. Caplan noted. In this study, all but one participants were White individuals, and 63% of participants were female.

Larger studies could also address important questions on ideal length of therapy, dosing, and where this therapy “would fall within the therapeutic step ladder,” Dr. Caplan continued. 

Whether mTOR inhibition could be effective at treating individuals with sarcoidosis in other organs beyond the skin is also unknown. 

“If the pathogenesis of sarcoid granuloma formation does include mTOR upregulation, which they are showing here…then you could hypothesize that, yes, using this therapy could benefit other organs,” he said. “But that has to be investigated in larger trials.”

The study was funded in part by a Vienna Science and Technology Fund project. Several authors report receiving grants from the Austrian Science Fund and one from the Ann Theodore Foundation Breakthrough Sarcoidosis Initiative. Dr. Caplan reported no relevant financial relationships.

A version of this article appeared on Medscape.com .

Sirolimus may be an effective treatment for patients with persistent cutaneous sarcoidosis.

In a small clinical trial, 7 of 10 patients treated with sirolimus via oral solution had improvements in skin lesions after 4 months, which was sustained for up to 2 years after the study concluded.

The results suggested that mechanistic target of rapamycin (mTOR) inhibition is a potential therapeutic avenue for sarcoidosis, which the authors said should be explored in larger clinical trials. 

In the past decade, there has been a growing amount of evidence suggesting mTOR’s role in sarcoidosis. In 2017, researchers showed that activation of mTOR in macrophages could cause progressive sarcoidosis in mice. In additional studies, high levels of mTOR activity were detected in human sarcoidosis granulomas in various organs, including the skin, lung, and heart.

Three case reports also documented using the mTOR inhibitor sirolimus to effectively treat systemic sarcoidosis.

“Although all reports observed improvement of the disease following the treatment, no clinical trial investigating the efficacy and safety of sirolimus in patients with sarcoidosis had been published” prior to this study, wrote senior author Georg Stary, MD, of the Medical University of Vienna and the Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria, and colleagues. 

The findings were published in the The Lancet Rheumatology.

For the study, researchers recruited 16 individuals with persistent and glucocorticoid-refractory cutaneous sarcoidosis between September 2019 and June 2021. A total of 14 participants were randomly assigned to the topical phase of the study, whereas two immediately received systemic treatment. All treatment was conducted at Vienna General Hospital.

In the placebo-controlled, double-blinded topical treatment arm, patients received either 0.1% topical sirolimus in Vaseline or Vaseline alone (placebo) twice daily for 2 months. After a 1-month washout period, participants were switched to the alternate treatment arm for an additional 2 months.

Following this topical phase and an additional 1-month washout period, all remaining participants received systemic sirolimus via a 1-mg/mL solution, starting with a 6-mg loading dose and continuing with 2 mg once daily for 4 months. The primary outcome was change in Cutaneous Sarcoidosis Activity and Morphology Index (CSAMI) from baseline, with decrease of more than five points representing a response to treatment.

A total of 10 patients completed the trial.

There was no change in CSAMI in either topical treatment groups. In the systemic group, 70% of patients had clinical improvement in skin lesions, with three responders in this group having complete resolution of skin lesions. The median change in CSAMI was −7.0 points (P = .018). 

This improvement persisted for 2 months following study conclusion, with more pronounced improvement from baseline after 2 years of drug-free follow-up (−11.5 points).

There were no serious adverse events reported during the study, but 42% of patients treated with systemic sirolimus reported mild skin reactions, such as acne and eczema. Other related adverse events were hypertriglyceridemia (17%), hyperglycemia (17%), and proteinuria (8%).

Compared with clinical outcomes with tofacitinib and tumor necrosis factor (TNF) inhibitors, “the strength of our study lies in the sustained treatment effect after drug withdrawal among all responders. This prolonged effect has not yet been explored with tofacitinib, whereas with TNF inhibitors disease relapse was seen in more than 50% of patients at 3-8 months,” the authors wrote.

The researchers also analyzed participants’ skin biopsies to gain a better understanding of how mTOR inhibition affected granuloma structures. They found that, at baseline, mTOR activity was significantly lower in the fibroblasts of treatment nonresponders than in responders. They speculated that lower expression of mTOR could make these granuloma-associated cells resistant to systemic sirolimus.

These promising findings combine “clinical response with a molecular analysis,” Avrom Caplan, MD, co-director of the Sarcoidosis Program at NYU Langone in New York City, told this news organization. He was not involved with the research. Adding molecular information to clinical outcome data “helps solidify that [the mTOR] pathway has relevance in the sarcoid granuloma formation.”

The study had a limited sample size — a challenge for many clinical trials of rare diseases, Dr. Caplan said. Larger clinical trials are necessary to explore mTOR inhibition in sarcoidosis, both he and the authors agreed. A larger trial could also include greater heterogeneity of patients, including varied sarcoid presentation and demographics, Dr. Caplan noted. In this study, all but one participants were White individuals, and 63% of participants were female.

Larger studies could also address important questions on ideal length of therapy, dosing, and where this therapy “would fall within the therapeutic step ladder,” Dr. Caplan continued. 

Whether mTOR inhibition could be effective at treating individuals with sarcoidosis in other organs beyond the skin is also unknown. 

“If the pathogenesis of sarcoid granuloma formation does include mTOR upregulation, which they are showing here…then you could hypothesize that, yes, using this therapy could benefit other organs,” he said. “But that has to be investigated in larger trials.”

The study was funded in part by a Vienna Science and Technology Fund project. Several authors report receiving grants from the Austrian Science Fund and one from the Ann Theodore Foundation Breakthrough Sarcoidosis Initiative. Dr. Caplan reported no relevant financial relationships.

A version of this article appeared on Medscape.com .

UPDATE: On March 29, 2024, the authors of this study published in JAMA Internal Medicine issued a formal retraction of their article. "Unfortunately, we have found significant coding errors that are difficult to rectify," the author wrote. "We also discovered discrepancies in the calculation process that cast doubt on the accuracy and reliability of the reported findings." The CHEST Physician® Editorial Board apologizes for any confusion this may have caused.

TOPLINE:

Among adults motivated to quit smoking, electronic cigarettes are more effective than nicotine chewing gum and as effective as varenicline in achieving sustained abstinence at 6 months, a randomized trial found. Questions about the long-term safety of e-cigarettes remain, however, according to the researchers. 

METHODOLOGY:

• The study included 1068 participants in China who were smoking at least 10 cigarettes per day.
• They were randomly assigned to undergo 12 weeks of treatment with a cartridge-based e-cigarette, varenicline, or nicotine chewing gum.

TAKEAWAY: 

• At 6 months, the biochemically validated rate of quitting was 15.7% for those who received e-cigarettes, 14.2% for those who received varenicline, and 8.8% for those who chewed nicotine gum.
• At 6 months, 62.8% of participants in the e-cigarette arm were still using the devices, whereas those in the other study arms had not continued their treatments.
• Adverse reactions with e-cigarettes and nicotine chewing gum included irritation of the throat and mouth, which occurred in 7%-8% of participants.
• In the varenicline group, 8.8% experienced nausea.
• No serious adverse events were reported.

IN PRACTICE:

“A moderate approach would be to recommend approved medications as the first step and, if that fails, then inform the patient of the evidence regarding the use of electronic cigarettes as a possible approach, acknowledging all its caveats,” Dorothy K. Hatsukami, PhD, with the University of Minnesota in Minneapolis, and Judith J. Prochaska, PhD, MPH, with Stanford (California) University, wrote in an invited commentary. 

SOURCE:

Zhao Liu, PhD, with the China-Japan Friendship Hospital in Beijing, was the corresponding author for the study. The study was published online on January 29, 2024, in JAMA Internal Medicine. 

LIMITATIONS:

The trial had an open-label design, so participants’ expectations about their assigned treatment may have influenced the results.

The study did not include participants older than 45 years, so it is unclear how the results apply to older populations.

More studies are needed to see whether continued use of e-cigarettes is beneficial or harmful, the researchers wrote.

Combining forms of nicotine replacement therapy, such as gum plus a patch, may be more effective than a single form, but the trial did not assess a combined approach, the commentary authors noted. The dose of nicotine gum for some participants may have been suboptimal, they added.

DISCLOSURES:

The study was supported by the Scientific Research Project Fund of China-Japan Friendship Hospital. The researchers had no conflict of interest disclosures. Dr. Prochaska disclosed receiving fees from Achieve Life Sciences, OneLeaf, and attorneys who are involved in litigation against tobacco companies.

A version of this article appeared on Medscape.com.

UPDATE: On March 29, 2024, the authors of this study published in JAMA Internal Medicine issued a formal retraction of their article. "Unfortunately, we have found significant coding errors that are difficult to rectify," the author wrote. "We also discovered discrepancies in the calculation process that cast doubt on the accuracy and reliability of the reported findings." The CHEST Physician® Editorial Board apologizes for any confusion this may have caused.

TOPLINE:

Among adults motivated to quit smoking, electronic cigarettes are more effective than nicotine chewing gum and as effective as varenicline in achieving sustained abstinence at 6 months, a randomized trial found. Questions about the long-term safety of e-cigarettes remain, however, according to the researchers. 

METHODOLOGY:

• The study included 1068 participants in China who were smoking at least 10 cigarettes per day.
• They were randomly assigned to undergo 12 weeks of treatment with a cartridge-based e-cigarette, varenicline, or nicotine chewing gum.

TAKEAWAY: 

• At 6 months, the biochemically validated rate of quitting was 15.7% for those who received e-cigarettes, 14.2% for those who received varenicline, and 8.8% for those who chewed nicotine gum.
• At 6 months, 62.8% of participants in the e-cigarette arm were still using the devices, whereas those in the other study arms had not continued their treatments.
• Adverse reactions with e-cigarettes and nicotine chewing gum included irritation of the throat and mouth, which occurred in 7%-8% of participants.
• In the varenicline group, 8.8% experienced nausea.
• No serious adverse events were reported.

IN PRACTICE:

“A moderate approach would be to recommend approved medications as the first step and, if that fails, then inform the patient of the evidence regarding the use of electronic cigarettes as a possible approach, acknowledging all its caveats,” Dorothy K. Hatsukami, PhD, with the University of Minnesota in Minneapolis, and Judith J. Prochaska, PhD, MPH, with Stanford (California) University, wrote in an invited commentary. 

SOURCE:

Zhao Liu, PhD, with the China-Japan Friendship Hospital in Beijing, was the corresponding author for the study. The study was published online on January 29, 2024, in JAMA Internal Medicine. 

LIMITATIONS:

The trial had an open-label design, so participants’ expectations about their assigned treatment may have influenced the results.

The study did not include participants older than 45 years, so it is unclear how the results apply to older populations.

More studies are needed to see whether continued use of e-cigarettes is beneficial or harmful, the researchers wrote.

Combining forms of nicotine replacement therapy, such as gum plus a patch, may be more effective than a single form, but the trial did not assess a combined approach, the commentary authors noted. The dose of nicotine gum for some participants may have been suboptimal, they added.

DISCLOSURES:

The study was supported by the Scientific Research Project Fund of China-Japan Friendship Hospital. The researchers had no conflict of interest disclosures. Dr. Prochaska disclosed receiving fees from Achieve Life Sciences, OneLeaf, and attorneys who are involved in litigation against tobacco companies.

A version of this article appeared on Medscape.com.

UPDATE: On March 29, 2024, the authors of this study published in JAMA Internal Medicine issued a formal retraction of their article. "Unfortunately, we have found significant coding errors that are difficult to rectify," the author wrote. "We also discovered discrepancies in the calculation process that cast doubt on the accuracy and reliability of the reported findings." The CHEST Physician® Editorial Board apologizes for any confusion this may have caused.

TOPLINE:

Among adults motivated to quit smoking, electronic cigarettes are more effective than nicotine chewing gum and as effective as varenicline in achieving sustained abstinence at 6 months, a randomized trial found. Questions about the long-term safety of e-cigarettes remain, however, according to the researchers. 

METHODOLOGY:

• The study included 1068 participants in China who were smoking at least 10 cigarettes per day.
• They were randomly assigned to undergo 12 weeks of treatment with a cartridge-based e-cigarette, varenicline, or nicotine chewing gum.

TAKEAWAY: 

• At 6 months, the biochemically validated rate of quitting was 15.7% for those who received e-cigarettes, 14.2% for those who received varenicline, and 8.8% for those who chewed nicotine gum.
• At 6 months, 62.8% of participants in the e-cigarette arm were still using the devices, whereas those in the other study arms had not continued their treatments.
• Adverse reactions with e-cigarettes and nicotine chewing gum included irritation of the throat and mouth, which occurred in 7%-8% of participants.
• In the varenicline group, 8.8% experienced nausea.
• No serious adverse events were reported.

IN PRACTICE:

“A moderate approach would be to recommend approved medications as the first step and, if that fails, then inform the patient of the evidence regarding the use of electronic cigarettes as a possible approach, acknowledging all its caveats,” Dorothy K. Hatsukami, PhD, with the University of Minnesota in Minneapolis, and Judith J. Prochaska, PhD, MPH, with Stanford (California) University, wrote in an invited commentary. 

SOURCE:

Zhao Liu, PhD, with the China-Japan Friendship Hospital in Beijing, was the corresponding author for the study. The study was published online on January 29, 2024, in JAMA Internal Medicine. 

LIMITATIONS:

The trial had an open-label design, so participants’ expectations about their assigned treatment may have influenced the results.

The study did not include participants older than 45 years, so it is unclear how the results apply to older populations.

More studies are needed to see whether continued use of e-cigarettes is beneficial or harmful, the researchers wrote.

Combining forms of nicotine replacement therapy, such as gum plus a patch, may be more effective than a single form, but the trial did not assess a combined approach, the commentary authors noted. The dose of nicotine gum for some participants may have been suboptimal, they added.

DISCLOSURES:

The study was supported by the Scientific Research Project Fund of China-Japan Friendship Hospital. The researchers had no conflict of interest disclosures. Dr. Prochaska disclosed receiving fees from Achieve Life Sciences, OneLeaf, and attorneys who are involved in litigation against tobacco companies.

A version of this article appeared on Medscape.com.

Some Robitussin cough syrup products are being recalled nationwide due to potentially deadly microbial contamination. 

The company that makes Robitussin syrups did not specify which microorganisms may be in the products. The recall announcement from the global consumer health products company Haleon stated that the contamination could lead to fungal infections or the presence of fungi or yeasts in a person’s blood. So far, the company has not received any reports of people being sickened by the recalled products.

The recall applies to bottles of Robitussin Honey CF Max Day and Robitussin Honey CF Max Nighttime. Both varieties are for adults. Affected products were sold nationwide and have specific lot numbers printed at the bottom of the back of the bottles. Consumers can view the lot numbers on the FDA’s recall webpage.

People with weakened immune systems have a higher risk of life-threatening health problems due to the cough syrup, the company warned.

“In non-immunocompromised consumers, the population most likely to use the product, life-threatening infections are not likely to occur,” the recall notice from Haleon stated. “However, the occurrence of an infection that may necessitate medical intervention cannot be completely ruled out.”

People who have affected products should stop using them immediately. The company asked that anyone with the products email Haleon at mystory.us@haleon.com, or call the company at 800-245-1040 Monday through Friday from 8 a.m. to 6 p.m. Eastern time. 
 

A version of this article appeared on WebMD.com.

Some Robitussin cough syrup products are being recalled nationwide due to potentially deadly microbial contamination. 

The company that makes Robitussin syrups did not specify which microorganisms may be in the products. The recall announcement from the global consumer health products company Haleon stated that the contamination could lead to fungal infections or the presence of fungi or yeasts in a person’s blood. So far, the company has not received any reports of people being sickened by the recalled products.

The recall applies to bottles of Robitussin Honey CF Max Day and Robitussin Honey CF Max Nighttime. Both varieties are for adults. Affected products were sold nationwide and have specific lot numbers printed at the bottom of the back of the bottles. Consumers can view the lot numbers on the FDA’s recall webpage.

People with weakened immune systems have a higher risk of life-threatening health problems due to the cough syrup, the company warned.

“In non-immunocompromised consumers, the population most likely to use the product, life-threatening infections are not likely to occur,” the recall notice from Haleon stated. “However, the occurrence of an infection that may necessitate medical intervention cannot be completely ruled out.”

People who have affected products should stop using them immediately. The company asked that anyone with the products email Haleon at mystory.us@haleon.com, or call the company at 800-245-1040 Monday through Friday from 8 a.m. to 6 p.m. Eastern time. 
 

A version of this article appeared on WebMD.com.

Some Robitussin cough syrup products are being recalled nationwide due to potentially deadly microbial contamination. 

The company that makes Robitussin syrups did not specify which microorganisms may be in the products. The recall announcement from the global consumer health products company Haleon stated that the contamination could lead to fungal infections or the presence of fungi or yeasts in a person’s blood. So far, the company has not received any reports of people being sickened by the recalled products.

The recall applies to bottles of Robitussin Honey CF Max Day and Robitussin Honey CF Max Nighttime. Both varieties are for adults. Affected products were sold nationwide and have specific lot numbers printed at the bottom of the back of the bottles. Consumers can view the lot numbers on the FDA’s recall webpage.

People with weakened immune systems have a higher risk of life-threatening health problems due to the cough syrup, the company warned.

“In non-immunocompromised consumers, the population most likely to use the product, life-threatening infections are not likely to occur,” the recall notice from Haleon stated. “However, the occurrence of an infection that may necessitate medical intervention cannot be completely ruled out.”

People who have affected products should stop using them immediately. The company asked that anyone with the products email Haleon at mystory.us@haleon.com, or call the company at 800-245-1040 Monday through Friday from 8 a.m. to 6 p.m. Eastern time. 
 

A version of this article appeared on WebMD.com.

Emergencies happen anywhere and anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

A week earlier I’d had a heart surgery and was heading out for a post-op appointment when I saw it: I had a flat tire. It didn’t make sense. The tire was brand new, and there was no puncture. But it was flat.

I swapped out the flat for the spare and went off base to a tire shop. While I was there, my surgeon’s office called and rescheduled my appointment for a couple of hours later. That was lucky because by the time the tire was fixed, I had just enough time to get there.

The hospital is right near I-35 in San Antonio, Texas. I got off the freeway and onto the access road and paused to turn into the parking lot. That’s when I heard an enormous crash.

I saw a big poof of white smoke, and a car barreled off the freeway and came rolling down the embankment.

When the car hit the access road, I saw a woman ejected through the windshield. She bounced and landed in the road about 25 feet in front of me.

I put my car in park, grabbed my face mask and gloves, and started running toward her. But another vehicle — a truck towing a trailer — came from behind to drive around me. The driver didn’t realize what had happened and couldn’t stop in time…

The trailer ran over her.

I didn’t know if anyone could’ve survived that, but I went to her. I saw several other bystanders, but they were frozen in shock. I was praying, dear God, if she’s alive, let me do whatever I need to do to save her life.

It was a horrible scene. This poor lady was in a bloody heap in the middle of the road. Her right arm was twisted up under her neck so tightly, she was choking herself. So, the first thing I did was straighten her arm out to protect her airway.

I started yelling at people, “Call 9-1-1! Run to the hospital! Let them know there’s an accident out here, and I need help!”

The woman had a pulse, but it was super rapid. On first glance, she clearly had multiple fractures and a bad head bleed. With the sheer number of times she’d been injured, I didn’t know what was going on internally, but it was bad. She was gargling on her own blood and spitting it up. She was drowning.

A couple of technicians from the hospital came and brought me a tiny emergency kit. It had a blood pressure cuff and an oral airway. All the vital signs indicated the lady was going into shock. She’d lost a lot of blood on the pavement.

I was able to get the oral airway in. A few minutes later, a fire chief showed up. By now, the traffic had backed up so badly, the emergency vehicles couldn’t get in. But he managed to get there another way and gave me a cervical collar (C collar) and an Ambu bag.

I was hyper-focused on what I could do at that moment and what I needed to do next. Her stats were going down, but she still had a pulse. If she lost the pulse or went into a lethal rhythm, I’d have to start cardiopulmonary resuscitation (CPR). I asked the other people, but nobody else knew CPR, so I wouldn’t have help.

I could tell the lady had a pelvic fracture, and we needed to stabilize her. I directed people how to hold her neck safely and log-roll her flat on the ground. I also needed to put pressure on the back of her head because of all the bleeding. I got people to give me their clothes and tried to do that as I was bagging her.

The windows of her vehicle had all been blown out. I asked somebody to go find her purse with her ID. Then I noticed something …

My heart jumped into my stomach.

A car seat. There was an empty child’s car seat in the back of the car.

I started yelling at everyone, “Look for a baby! Go up and down the embankment and across the road. There might have been a baby in the car!”

But there wasn’t. Thank God. She hadn’t been driving with her child.

At that point, a paramedic came running from behind all the traffic. We did life support together until the ambulance finally arrived.

Emergency medical services got an intravenous line in and used medical anti-shock trousers. Thankfully, I already had the C collar on, and we’d been bagging her, so they could load her very quickly.

I got rid of my bloody gloves. I told a police officer I would come back. And then I went to my doctor’s appointment.

The window at my doctor’s office faced the access road, so the people there had seen all the traffic. They asked me what happened, and I said, “It was me. I saw it happen. I tried to help.” I was a little frazzled.

When I got back to the scene, the police and the fire chief kept thanking me for stopping. Why wouldn’t I stop? It was astounding to realize that they imagined somebody wouldn’t stop in a situation like this.

They told me the lady was alive. She was in the intensive care unit in critical condition, but she had survived. At that moment, I had this overwhelming feeling: God had put me in this exact place at the exact time to save her life.

Looking back, I think about how God ordered my steps. Without the mysterious flat tire, I would’ve gone to the hospital earlier. If my appointment hadn’t been rescheduled, I wouldn’t have been on the access road. All those events brought me there.

Several months later, the woman’s family contacted me and asked if we could meet. I found out more about her injuries. She’d had multiple skull fractures, facial fractures, and a broken jaw. Her upper arm was broken in three places. Her clavicle was broken. She had internal bleeding, a pelvic fracture, and a broken leg. She was 28 years old.

She’d had multiple surgeries, spent 2 months in the ICU, and another 3 months in intensive rehab. But she survived. It was incredible.

We all met up at a McDonald’s. First, her little son — who was the baby I thought might have been in the car — ran up to me and said, “Thank you for saving my mommy’s life.”

Then I turned, and there she was — a beautiful lady looking at me with awe and crying, saying, “It’s me.”

She obviously had gone through a transformation from all the injuries and the medications. She had a little bit of a speech delay, but mentally, she was there. She could walk.

She said, “You’re my angel. God put you there to save my life.” Her family all came up and hugged me. It was so beautiful.

She told me about the accident. She’d been speeding that day, zigzagging through lanes to get around the traffic. And she didn’t have her seatbelt on. She’d driven onto the shoulder to try to pass everyone, but it started narrowing. She clipped somebody’s bumper, went into a tailspin, and collided with a second vehicle, which caused her to flip over and down the embankment.

“God’s given me a new lease on life,” she said, “a fresh start. I will forever wear my seatbelt. And I’m going to do whatever I can to give back to other people because I don’t even feel like I deserve this.”

I just cried.

I’ve been a nurse for 29 years, first on the civilian side and later in the military. I’ve led codes and responded to trauma in a hospital setting or a deployed environment. I was well prepared to do what I did. But doing it under such stress with adrenaline bombarding me ... I’m amazed. I just think God’s hand was on me.

At that time, I was personally going through some things. After my heart surgery, I was in an emotional place where I didn’t feel loved or valued. But when I had that realization — when I knew that I was meant to be there to save her life, I also got the very clear message that I was valued and loved so much.

I know I have a very strong purpose. That day changed my life.
 

US Air Force Lt. Col. Anne Staley is the officer in charge of the Military Training Network, a division of the Defense Health Agency Education and Training Directorate in San Antonio, Texas.

A version of this article appeared on Medscape.com.

Emergencies happen anywhere and anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

A week earlier I’d had a heart surgery and was heading out for a post-op appointment when I saw it: I had a flat tire. It didn’t make sense. The tire was brand new, and there was no puncture. But it was flat.

I swapped out the flat for the spare and went off base to a tire shop. While I was there, my surgeon’s office called and rescheduled my appointment for a couple of hours later. That was lucky because by the time the tire was fixed, I had just enough time to get there.

The hospital is right near I-35 in San Antonio, Texas. I got off the freeway and onto the access road and paused to turn into the parking lot. That’s when I heard an enormous crash.

I saw a big poof of white smoke, and a car barreled off the freeway and came rolling down the embankment.

When the car hit the access road, I saw a woman ejected through the windshield. She bounced and landed in the road about 25 feet in front of me.

I put my car in park, grabbed my face mask and gloves, and started running toward her. But another vehicle — a truck towing a trailer — came from behind to drive around me. The driver didn’t realize what had happened and couldn’t stop in time…

The trailer ran over her.

I didn’t know if anyone could’ve survived that, but I went to her. I saw several other bystanders, but they were frozen in shock. I was praying, dear God, if she’s alive, let me do whatever I need to do to save her life.

It was a horrible scene. This poor lady was in a bloody heap in the middle of the road. Her right arm was twisted up under her neck so tightly, she was choking herself. So, the first thing I did was straighten her arm out to protect her airway.

I started yelling at people, “Call 9-1-1! Run to the hospital! Let them know there’s an accident out here, and I need help!”

The woman had a pulse, but it was super rapid. On first glance, she clearly had multiple fractures and a bad head bleed. With the sheer number of times she’d been injured, I didn’t know what was going on internally, but it was bad. She was gargling on her own blood and spitting it up. She was drowning.

A couple of technicians from the hospital came and brought me a tiny emergency kit. It had a blood pressure cuff and an oral airway. All the vital signs indicated the lady was going into shock. She’d lost a lot of blood on the pavement.

I was able to get the oral airway in. A few minutes later, a fire chief showed up. By now, the traffic had backed up so badly, the emergency vehicles couldn’t get in. But he managed to get there another way and gave me a cervical collar (C collar) and an Ambu bag.

I was hyper-focused on what I could do at that moment and what I needed to do next. Her stats were going down, but she still had a pulse. If she lost the pulse or went into a lethal rhythm, I’d have to start cardiopulmonary resuscitation (CPR). I asked the other people, but nobody else knew CPR, so I wouldn’t have help.

I could tell the lady had a pelvic fracture, and we needed to stabilize her. I directed people how to hold her neck safely and log-roll her flat on the ground. I also needed to put pressure on the back of her head because of all the bleeding. I got people to give me their clothes and tried to do that as I was bagging her.

The windows of her vehicle had all been blown out. I asked somebody to go find her purse with her ID. Then I noticed something …

My heart jumped into my stomach.

A car seat. There was an empty child’s car seat in the back of the car.

I started yelling at everyone, “Look for a baby! Go up and down the embankment and across the road. There might have been a baby in the car!”

But there wasn’t. Thank God. She hadn’t been driving with her child.

At that point, a paramedic came running from behind all the traffic. We did life support together until the ambulance finally arrived.

Emergency medical services got an intravenous line in and used medical anti-shock trousers. Thankfully, I already had the C collar on, and we’d been bagging her, so they could load her very quickly.

I got rid of my bloody gloves. I told a police officer I would come back. And then I went to my doctor’s appointment.

The window at my doctor’s office faced the access road, so the people there had seen all the traffic. They asked me what happened, and I said, “It was me. I saw it happen. I tried to help.” I was a little frazzled.

When I got back to the scene, the police and the fire chief kept thanking me for stopping. Why wouldn’t I stop? It was astounding to realize that they imagined somebody wouldn’t stop in a situation like this.

They told me the lady was alive. She was in the intensive care unit in critical condition, but she had survived. At that moment, I had this overwhelming feeling: God had put me in this exact place at the exact time to save her life.

Looking back, I think about how God ordered my steps. Without the mysterious flat tire, I would’ve gone to the hospital earlier. If my appointment hadn’t been rescheduled, I wouldn’t have been on the access road. All those events brought me there.

Several months later, the woman’s family contacted me and asked if we could meet. I found out more about her injuries. She’d had multiple skull fractures, facial fractures, and a broken jaw. Her upper arm was broken in three places. Her clavicle was broken. She had internal bleeding, a pelvic fracture, and a broken leg. She was 28 years old.

She’d had multiple surgeries, spent 2 months in the ICU, and another 3 months in intensive rehab. But she survived. It was incredible.

We all met up at a McDonald’s. First, her little son — who was the baby I thought might have been in the car — ran up to me and said, “Thank you for saving my mommy’s life.”

Then I turned, and there she was — a beautiful lady looking at me with awe and crying, saying, “It’s me.”

She obviously had gone through a transformation from all the injuries and the medications. She had a little bit of a speech delay, but mentally, she was there. She could walk.

She said, “You’re my angel. God put you there to save my life.” Her family all came up and hugged me. It was so beautiful.

She told me about the accident. She’d been speeding that day, zigzagging through lanes to get around the traffic. And she didn’t have her seatbelt on. She’d driven onto the shoulder to try to pass everyone, but it started narrowing. She clipped somebody’s bumper, went into a tailspin, and collided with a second vehicle, which caused her to flip over and down the embankment.

“God’s given me a new lease on life,” she said, “a fresh start. I will forever wear my seatbelt. And I’m going to do whatever I can to give back to other people because I don’t even feel like I deserve this.”

I just cried.

I’ve been a nurse for 29 years, first on the civilian side and later in the military. I’ve led codes and responded to trauma in a hospital setting or a deployed environment. I was well prepared to do what I did. But doing it under such stress with adrenaline bombarding me ... I’m amazed. I just think God’s hand was on me.

At that time, I was personally going through some things. After my heart surgery, I was in an emotional place where I didn’t feel loved or valued. But when I had that realization — when I knew that I was meant to be there to save her life, I also got the very clear message that I was valued and loved so much.

I know I have a very strong purpose. That day changed my life.
 

US Air Force Lt. Col. Anne Staley is the officer in charge of the Military Training Network, a division of the Defense Health Agency Education and Training Directorate in San Antonio, Texas.

A version of this article appeared on Medscape.com.

Emergencies happen anywhere and anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

A week earlier I’d had a heart surgery and was heading out for a post-op appointment when I saw it: I had a flat tire. It didn’t make sense. The tire was brand new, and there was no puncture. But it was flat.

I swapped out the flat for the spare and went off base to a tire shop. While I was there, my surgeon’s office called and rescheduled my appointment for a couple of hours later. That was lucky because by the time the tire was fixed, I had just enough time to get there.

The hospital is right near I-35 in San Antonio, Texas. I got off the freeway and onto the access road and paused to turn into the parking lot. That’s when I heard an enormous crash.

I saw a big poof of white smoke, and a car barreled off the freeway and came rolling down the embankment.

When the car hit the access road, I saw a woman ejected through the windshield. She bounced and landed in the road about 25 feet in front of me.

I put my car in park, grabbed my face mask and gloves, and started running toward her. But another vehicle — a truck towing a trailer — came from behind to drive around me. The driver didn’t realize what had happened and couldn’t stop in time…

The trailer ran over her.

I didn’t know if anyone could’ve survived that, but I went to her. I saw several other bystanders, but they were frozen in shock. I was praying, dear God, if she’s alive, let me do whatever I need to do to save her life.

It was a horrible scene. This poor lady was in a bloody heap in the middle of the road. Her right arm was twisted up under her neck so tightly, she was choking herself. So, the first thing I did was straighten her arm out to protect her airway.

I started yelling at people, “Call 9-1-1! Run to the hospital! Let them know there’s an accident out here, and I need help!”

The woman had a pulse, but it was super rapid. On first glance, she clearly had multiple fractures and a bad head bleed. With the sheer number of times she’d been injured, I didn’t know what was going on internally, but it was bad. She was gargling on her own blood and spitting it up. She was drowning.

A couple of technicians from the hospital came and brought me a tiny emergency kit. It had a blood pressure cuff and an oral airway. All the vital signs indicated the lady was going into shock. She’d lost a lot of blood on the pavement.

I was able to get the oral airway in. A few minutes later, a fire chief showed up. By now, the traffic had backed up so badly, the emergency vehicles couldn’t get in. But he managed to get there another way and gave me a cervical collar (C collar) and an Ambu bag.

I was hyper-focused on what I could do at that moment and what I needed to do next. Her stats were going down, but she still had a pulse. If she lost the pulse or went into a lethal rhythm, I’d have to start cardiopulmonary resuscitation (CPR). I asked the other people, but nobody else knew CPR, so I wouldn’t have help.

I could tell the lady had a pelvic fracture, and we needed to stabilize her. I directed people how to hold her neck safely and log-roll her flat on the ground. I also needed to put pressure on the back of her head because of all the bleeding. I got people to give me their clothes and tried to do that as I was bagging her.

The windows of her vehicle had all been blown out. I asked somebody to go find her purse with her ID. Then I noticed something …

My heart jumped into my stomach.

A car seat. There was an empty child’s car seat in the back of the car.

I started yelling at everyone, “Look for a baby! Go up and down the embankment and across the road. There might have been a baby in the car!”

But there wasn’t. Thank God. She hadn’t been driving with her child.

At that point, a paramedic came running from behind all the traffic. We did life support together until the ambulance finally arrived.

Emergency medical services got an intravenous line in and used medical anti-shock trousers. Thankfully, I already had the C collar on, and we’d been bagging her, so they could load her very quickly.

I got rid of my bloody gloves. I told a police officer I would come back. And then I went to my doctor’s appointment.

The window at my doctor’s office faced the access road, so the people there had seen all the traffic. They asked me what happened, and I said, “It was me. I saw it happen. I tried to help.” I was a little frazzled.

When I got back to the scene, the police and the fire chief kept thanking me for stopping. Why wouldn’t I stop? It was astounding to realize that they imagined somebody wouldn’t stop in a situation like this.

They told me the lady was alive. She was in the intensive care unit in critical condition, but she had survived. At that moment, I had this overwhelming feeling: God had put me in this exact place at the exact time to save her life.

Looking back, I think about how God ordered my steps. Without the mysterious flat tire, I would’ve gone to the hospital earlier. If my appointment hadn’t been rescheduled, I wouldn’t have been on the access road. All those events brought me there.

Several months later, the woman’s family contacted me and asked if we could meet. I found out more about her injuries. She’d had multiple skull fractures, facial fractures, and a broken jaw. Her upper arm was broken in three places. Her clavicle was broken. She had internal bleeding, a pelvic fracture, and a broken leg. She was 28 years old.

She’d had multiple surgeries, spent 2 months in the ICU, and another 3 months in intensive rehab. But she survived. It was incredible.

We all met up at a McDonald’s. First, her little son — who was the baby I thought might have been in the car — ran up to me and said, “Thank you for saving my mommy’s life.”

Then I turned, and there she was — a beautiful lady looking at me with awe and crying, saying, “It’s me.”

She obviously had gone through a transformation from all the injuries and the medications. She had a little bit of a speech delay, but mentally, she was there. She could walk.

She said, “You’re my angel. God put you there to save my life.” Her family all came up and hugged me. It was so beautiful.

She told me about the accident. She’d been speeding that day, zigzagging through lanes to get around the traffic. And she didn’t have her seatbelt on. She’d driven onto the shoulder to try to pass everyone, but it started narrowing. She clipped somebody’s bumper, went into a tailspin, and collided with a second vehicle, which caused her to flip over and down the embankment.

“God’s given me a new lease on life,” she said, “a fresh start. I will forever wear my seatbelt. And I’m going to do whatever I can to give back to other people because I don’t even feel like I deserve this.”

I just cried.

I’ve been a nurse for 29 years, first on the civilian side and later in the military. I’ve led codes and responded to trauma in a hospital setting or a deployed environment. I was well prepared to do what I did. But doing it under such stress with adrenaline bombarding me ... I’m amazed. I just think God’s hand was on me.

At that time, I was personally going through some things. After my heart surgery, I was in an emotional place where I didn’t feel loved or valued. But when I had that realization — when I knew that I was meant to be there to save her life, I also got the very clear message that I was valued and loved so much.

I know I have a very strong purpose. That day changed my life.
 

US Air Force Lt. Col. Anne Staley is the officer in charge of the Military Training Network, a division of the Defense Health Agency Education and Training Directorate in San Antonio, Texas.

A version of this article appeared on Medscape.com.

When the American Cancer Society recently unveiled changes to its lung cancer screening guidance, the aim was to remove barriers to screening and catch more cancers in high-risk people earlier.

Although the lung cancer death rate has declined significantly over the past few decades, lung cancer remains the leading cause of cancer deaths worldwide.

Detecting lung cancer early is key to improving survival. Still, lung cancer screening rates are poor. In 2021, the American Lung Association estimated that 14 million US adults qualified for lung cancer screening, but only 5.8% received it.

Smokers or former smokers without symptoms may forgo regular screening and only receive their screening scan after symptoms emerge, explained Janani S. Reisenauer, MD, Division Chair of Thoracic Surgery at Mayo Clinic, Rochester, Minnesota. But by the time symptoms develop, the cancer is typically more advanced, and treatment options become more limited.

The goal of the new American Cancer Society guidelines, published in early November 2023 in CA: A Cancer Journal for Physicians, is to identify lung cancers at earlier stages when they are easier to treat.

The new guidelines, which update a 2013 version, expand the eligibility age for screening and the pool of current and former smokers who qualify for annual screening with low-dose CT. Almost 5 million more high-risk people will now qualify for regular lung cancer screening, the guideline authors estimated.

But will expanding screening help reduce deaths from lung cancer? And perhaps just as important, will the guidelines move the needle on the “disappointingly low” lung cancer screening rates up to this point?

“I definitely think it’s a step in the right direction,” said Lecia V. Sequist, MD, MPH, clinical researcher and lung cancer medical oncologist, Massachusetts General Hospital Cancer Center, Boston, Massachusetts.

The new guidelines lowered the age for annual lung cancer screening among asymptomatic former or current smokers from 55-74 years to 50-80 years. The update also now considers a high-risk person anyone with a 20-pack-year history, down from a 30-pack-year history, and removes the requirement that former smokers must have quit within 15 years to be eligible for screening.

As people age, their risk for lung cancer increases, so it makes sense to screen all former smokers regardless of when they quit, explained Kim Lori Sandler, MD, from Vanderbilt University Medical Center, Nashville, Tennessee, and cochair of the American College of Radiology’s Lung Cancer Screening Steering Committee.

“There’s really nothing magical or drastic that happens at the 15-year mark,” Dr. Sequist agreed. For “someone who quit 14 years ago versus 16 years ago, it is essentially the same risk, and so scientifically it doesn’t really make sense to impose an artificial cut-off where no change in risk exists.”

The latest evidence reviewed in the new guidelines shows that expanding the guidelines would identify more early-stage cancers and potentially save lives. The authors modeled the benefits and harms of lung cancer screening using several scenarios.

Moving the start age from 55 to 50 years would lead to a 15% reduction in lung cancer mortality in men aged 50-54 years, the model suggested.

Removing the 15-year timeline for quitting smoking also would also improve outcomes. Compared with scenarios that included the 15-year quit timeline for former smokers, those that removed the limit would result in a 37.3% increase in screening exams, a 21% increase in would avert lung cancer deaths, and offer a 19% increase in life-years gained per 100,000 population.

Overall, the evidence indicates that, “if fully implemented, these recommendations have a high likelihood of significantly reducing death and suffering from lung cancer in the United States,” the guideline authors wrote.

But screening more people also comes with risks, such as more false-positive findings, which could lead to extra scans, invasive tests for tissue sampling, or even procedures for benign disease, Dr. Sandler explained. The latter “is what we really need to avoid.”

Even so, Dr. Sandler believes the current guidelines show that the benefit of screening “is great enough that it’s worth including these additional individuals.”
 

Guidelines Are Not Enough

But will expanding the screening criteria prompt more eligible individuals to receive their CT scans?

Simply expanding the eligibility criteria, by itself, likely won’t measurably improve screening uptake, said Paolo Boffetta, MD, MPH, of Stony Brook Cancer Center, Stony Brook, New York.

Healthcare and insurance access along with patient demand may present the most significant barriers to improving screening uptake.

The “issue is not the guideline as much as it’s the healthcare system,” said Otis W. Brawley, MD, professor of oncology at the Johns Hopkins University School of Medicine, Baltimore, Maryland.

Access to screening at hospitals with limited CT scanners and staff could present one major issue.

When Dr. Brawley worked at a large inner-city safety net hospital in Atlanta, patients with lung cancer frequently had to wait over a week to use one of the four CT scanners, he recalled. Adding to these delays, we didn’t have enough people to read the screens or enough people to do the diagnostics for those who had abnormalities, said Dr. Brawley.

To increase lung cancer screening in this context would increase the wait time for patients who do have cancer, he said.

Insurance coverage could present a roadblock for some as well. While the 2021 US Preventive Services Task Force (USPSTF) recommendations largely align with the new ones from the American Cancer Society, there’s one key difference: The USPSTF still requires former smokers to have quit within 15 years to be eligible for annual screening.

Because the USPSTF recommendations dictate insurance coverage, some former smokers — those who quit more than 15 years ago — may not qualify for coverage and would have to pay out-of-pocket for screening.

Dr. Sequist, however, had a more optimistic outlook about screening uptake.

The American Cancer Society guidelines should remove some of the stigma surrounding lung cancer screening. Most people, when asked a lot of questions about their tobacco use and history, tend to downplay it because there’s shame associated with smoking, Dr. Sequist said. The new guidelines limit the information needed to determine eligibility.

Dr. Sequist also noted that the updated American Cancer Society guideline would improve screening rates because it simplifies the eligibility criteria and makes it easier for physicians to determine who qualifies.

The issue, however, is that some of these individuals — those who quit over 15 years ago — may not have their scan covered by insurance, which could preclude lower-income individuals from getting screened.

The American Cancer Society guidelines” do not necessarily translate into a change in policy,” which is “dictated by the USPSTF and payors such as Medicare,” explained Peter Mazzone, MD, MPH, director of the Lung Cancer Program and Lung Cancer Screening Program for the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio.

On the patient side, Dr. Brawley noted, “we don’t yet have a large demand” for screening.

Many current and former smokers may put off lung cancer screening or not seek it out. Some may be unaware of their eligibility, while others may fear the outcome of a scan. Even among eligible individuals who do receive an initial scan, most — more than 75% — do not return for their next scan a year later, research showed.

Enhancing patient education and launching strong marketing campaigns would be a key element to encourage more people to get their annual screening and reduce the stigma associated with lung cancer as a smoker’s disease.

“Primary care physicians are integral in ensuring all eligible patients receive appropriate screening for lung cancer,” said Steven P. Furr, MD, president of the American Academy of Family Physicians and a family physician in Jackson, Alabama. “It is imperative that family physicians encourage screening in at-risk patients and counsel them on the importance of continued screening, as well as smoking cessation, if needed.”

Two authors of the new guidelines reported financial relationships with Seno Medical Instruments, the Genentech Foundation, Crispr Therapeutics, BEAM Therapeutics, Intellia Therapeutics, Editas Medicine, Freenome, and Guardant Health.

A version of this article appeared on Medscape.com.

When the American Cancer Society recently unveiled changes to its lung cancer screening guidance, the aim was to remove barriers to screening and catch more cancers in high-risk people earlier.

Although the lung cancer death rate has declined significantly over the past few decades, lung cancer remains the leading cause of cancer deaths worldwide.

Detecting lung cancer early is key to improving survival. Still, lung cancer screening rates are poor. In 2021, the American Lung Association estimated that 14 million US adults qualified for lung cancer screening, but only 5.8% received it.

Smokers or former smokers without symptoms may forgo regular screening and only receive their screening scan after symptoms emerge, explained Janani S. Reisenauer, MD, Division Chair of Thoracic Surgery at Mayo Clinic, Rochester, Minnesota. But by the time symptoms develop, the cancer is typically more advanced, and treatment options become more limited.

The goal of the new American Cancer Society guidelines, published in early November 2023 in CA: A Cancer Journal for Physicians, is to identify lung cancers at earlier stages when they are easier to treat.

The new guidelines, which update a 2013 version, expand the eligibility age for screening and the pool of current and former smokers who qualify for annual screening with low-dose CT. Almost 5 million more high-risk people will now qualify for regular lung cancer screening, the guideline authors estimated.

But will expanding screening help reduce deaths from lung cancer? And perhaps just as important, will the guidelines move the needle on the “disappointingly low” lung cancer screening rates up to this point?

“I definitely think it’s a step in the right direction,” said Lecia V. Sequist, MD, MPH, clinical researcher and lung cancer medical oncologist, Massachusetts General Hospital Cancer Center, Boston, Massachusetts.

The new guidelines lowered the age for annual lung cancer screening among asymptomatic former or current smokers from 55-74 years to 50-80 years. The update also now considers a high-risk person anyone with a 20-pack-year history, down from a 30-pack-year history, and removes the requirement that former smokers must have quit within 15 years to be eligible for screening.

As people age, their risk for lung cancer increases, so it makes sense to screen all former smokers regardless of when they quit, explained Kim Lori Sandler, MD, from Vanderbilt University Medical Center, Nashville, Tennessee, and cochair of the American College of Radiology’s Lung Cancer Screening Steering Committee.

“There’s really nothing magical or drastic that happens at the 15-year mark,” Dr. Sequist agreed. For “someone who quit 14 years ago versus 16 years ago, it is essentially the same risk, and so scientifically it doesn’t really make sense to impose an artificial cut-off where no change in risk exists.”

The latest evidence reviewed in the new guidelines shows that expanding the guidelines would identify more early-stage cancers and potentially save lives. The authors modeled the benefits and harms of lung cancer screening using several scenarios.

Moving the start age from 55 to 50 years would lead to a 15% reduction in lung cancer mortality in men aged 50-54 years, the model suggested.

Removing the 15-year timeline for quitting smoking also would also improve outcomes. Compared with scenarios that included the 15-year quit timeline for former smokers, those that removed the limit would result in a 37.3% increase in screening exams, a 21% increase in would avert lung cancer deaths, and offer a 19% increase in life-years gained per 100,000 population.

Overall, the evidence indicates that, “if fully implemented, these recommendations have a high likelihood of significantly reducing death and suffering from lung cancer in the United States,” the guideline authors wrote.

But screening more people also comes with risks, such as more false-positive findings, which could lead to extra scans, invasive tests for tissue sampling, or even procedures for benign disease, Dr. Sandler explained. The latter “is what we really need to avoid.”

Even so, Dr. Sandler believes the current guidelines show that the benefit of screening “is great enough that it’s worth including these additional individuals.”
 

Guidelines Are Not Enough

But will expanding the screening criteria prompt more eligible individuals to receive their CT scans?

Simply expanding the eligibility criteria, by itself, likely won’t measurably improve screening uptake, said Paolo Boffetta, MD, MPH, of Stony Brook Cancer Center, Stony Brook, New York.

Healthcare and insurance access along with patient demand may present the most significant barriers to improving screening uptake.

The “issue is not the guideline as much as it’s the healthcare system,” said Otis W. Brawley, MD, professor of oncology at the Johns Hopkins University School of Medicine, Baltimore, Maryland.

Access to screening at hospitals with limited CT scanners and staff could present one major issue.

When Dr. Brawley worked at a large inner-city safety net hospital in Atlanta, patients with lung cancer frequently had to wait over a week to use one of the four CT scanners, he recalled. Adding to these delays, we didn’t have enough people to read the screens or enough people to do the diagnostics for those who had abnormalities, said Dr. Brawley.

To increase lung cancer screening in this context would increase the wait time for patients who do have cancer, he said.

Insurance coverage could present a roadblock for some as well. While the 2021 US Preventive Services Task Force (USPSTF) recommendations largely align with the new ones from the American Cancer Society, there’s one key difference: The USPSTF still requires former smokers to have quit within 15 years to be eligible for annual screening.

Because the USPSTF recommendations dictate insurance coverage, some former smokers — those who quit more than 15 years ago — may not qualify for coverage and would have to pay out-of-pocket for screening.

Dr. Sequist, however, had a more optimistic outlook about screening uptake.

The American Cancer Society guidelines should remove some of the stigma surrounding lung cancer screening. Most people, when asked a lot of questions about their tobacco use and history, tend to downplay it because there’s shame associated with smoking, Dr. Sequist said. The new guidelines limit the information needed to determine eligibility.

Dr. Sequist also noted that the updated American Cancer Society guideline would improve screening rates because it simplifies the eligibility criteria and makes it easier for physicians to determine who qualifies.

The issue, however, is that some of these individuals — those who quit over 15 years ago — may not have their scan covered by insurance, which could preclude lower-income individuals from getting screened.

The American Cancer Society guidelines” do not necessarily translate into a change in policy,” which is “dictated by the USPSTF and payors such as Medicare,” explained Peter Mazzone, MD, MPH, director of the Lung Cancer Program and Lung Cancer Screening Program for the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio.

On the patient side, Dr. Brawley noted, “we don’t yet have a large demand” for screening.

Many current and former smokers may put off lung cancer screening or not seek it out. Some may be unaware of their eligibility, while others may fear the outcome of a scan. Even among eligible individuals who do receive an initial scan, most — more than 75% — do not return for their next scan a year later, research showed.

Enhancing patient education and launching strong marketing campaigns would be a key element to encourage more people to get their annual screening and reduce the stigma associated with lung cancer as a smoker’s disease.

“Primary care physicians are integral in ensuring all eligible patients receive appropriate screening for lung cancer,” said Steven P. Furr, MD, president of the American Academy of Family Physicians and a family physician in Jackson, Alabama. “It is imperative that family physicians encourage screening in at-risk patients and counsel them on the importance of continued screening, as well as smoking cessation, if needed.”

Two authors of the new guidelines reported financial relationships with Seno Medical Instruments, the Genentech Foundation, Crispr Therapeutics, BEAM Therapeutics, Intellia Therapeutics, Editas Medicine, Freenome, and Guardant Health.

A version of this article appeared on Medscape.com.

When the American Cancer Society recently unveiled changes to its lung cancer screening guidance, the aim was to remove barriers to screening and catch more cancers in high-risk people earlier.

Although the lung cancer death rate has declined significantly over the past few decades, lung cancer remains the leading cause of cancer deaths worldwide.

Detecting lung cancer early is key to improving survival. Still, lung cancer screening rates are poor. In 2021, the American Lung Association estimated that 14 million US adults qualified for lung cancer screening, but only 5.8% received it.

Smokers or former smokers without symptoms may forgo regular screening and only receive their screening scan after symptoms emerge, explained Janani S. Reisenauer, MD, Division Chair of Thoracic Surgery at Mayo Clinic, Rochester, Minnesota. But by the time symptoms develop, the cancer is typically more advanced, and treatment options become more limited.

The goal of the new American Cancer Society guidelines, published in early November 2023 in CA: A Cancer Journal for Physicians, is to identify lung cancers at earlier stages when they are easier to treat.

The new guidelines, which update a 2013 version, expand the eligibility age for screening and the pool of current and former smokers who qualify for annual screening with low-dose CT. Almost 5 million more high-risk people will now qualify for regular lung cancer screening, the guideline authors estimated.

But will expanding screening help reduce deaths from lung cancer? And perhaps just as important, will the guidelines move the needle on the “disappointingly low” lung cancer screening rates up to this point?

“I definitely think it’s a step in the right direction,” said Lecia V. Sequist, MD, MPH, clinical researcher and lung cancer medical oncologist, Massachusetts General Hospital Cancer Center, Boston, Massachusetts.

The new guidelines lowered the age for annual lung cancer screening among asymptomatic former or current smokers from 55-74 years to 50-80 years. The update also now considers a high-risk person anyone with a 20-pack-year history, down from a 30-pack-year history, and removes the requirement that former smokers must have quit within 15 years to be eligible for screening.

As people age, their risk for lung cancer increases, so it makes sense to screen all former smokers regardless of when they quit, explained Kim Lori Sandler, MD, from Vanderbilt University Medical Center, Nashville, Tennessee, and cochair of the American College of Radiology’s Lung Cancer Screening Steering Committee.

“There’s really nothing magical or drastic that happens at the 15-year mark,” Dr. Sequist agreed. For “someone who quit 14 years ago versus 16 years ago, it is essentially the same risk, and so scientifically it doesn’t really make sense to impose an artificial cut-off where no change in risk exists.”

The latest evidence reviewed in the new guidelines shows that expanding the guidelines would identify more early-stage cancers and potentially save lives. The authors modeled the benefits and harms of lung cancer screening using several scenarios.

Moving the start age from 55 to 50 years would lead to a 15% reduction in lung cancer mortality in men aged 50-54 years, the model suggested.

Removing the 15-year timeline for quitting smoking also would also improve outcomes. Compared with scenarios that included the 15-year quit timeline for former smokers, those that removed the limit would result in a 37.3% increase in screening exams, a 21% increase in would avert lung cancer deaths, and offer a 19% increase in life-years gained per 100,000 population.

Overall, the evidence indicates that, “if fully implemented, these recommendations have a high likelihood of significantly reducing death and suffering from lung cancer in the United States,” the guideline authors wrote.

But screening more people also comes with risks, such as more false-positive findings, which could lead to extra scans, invasive tests for tissue sampling, or even procedures for benign disease, Dr. Sandler explained. The latter “is what we really need to avoid.”

Even so, Dr. Sandler believes the current guidelines show that the benefit of screening “is great enough that it’s worth including these additional individuals.”
 

Guidelines Are Not Enough

But will expanding the screening criteria prompt more eligible individuals to receive their CT scans?

Simply expanding the eligibility criteria, by itself, likely won’t measurably improve screening uptake, said Paolo Boffetta, MD, MPH, of Stony Brook Cancer Center, Stony Brook, New York.

Healthcare and insurance access along with patient demand may present the most significant barriers to improving screening uptake.

The “issue is not the guideline as much as it’s the healthcare system,” said Otis W. Brawley, MD, professor of oncology at the Johns Hopkins University School of Medicine, Baltimore, Maryland.

Access to screening at hospitals with limited CT scanners and staff could present one major issue.

When Dr. Brawley worked at a large inner-city safety net hospital in Atlanta, patients with lung cancer frequently had to wait over a week to use one of the four CT scanners, he recalled. Adding to these delays, we didn’t have enough people to read the screens or enough people to do the diagnostics for those who had abnormalities, said Dr. Brawley.

To increase lung cancer screening in this context would increase the wait time for patients who do have cancer, he said.

Insurance coverage could present a roadblock for some as well. While the 2021 US Preventive Services Task Force (USPSTF) recommendations largely align with the new ones from the American Cancer Society, there’s one key difference: The USPSTF still requires former smokers to have quit within 15 years to be eligible for annual screening.

Because the USPSTF recommendations dictate insurance coverage, some former smokers — those who quit more than 15 years ago — may not qualify for coverage and would have to pay out-of-pocket for screening.

Dr. Sequist, however, had a more optimistic outlook about screening uptake.

The American Cancer Society guidelines should remove some of the stigma surrounding lung cancer screening. Most people, when asked a lot of questions about their tobacco use and history, tend to downplay it because there’s shame associated with smoking, Dr. Sequist said. The new guidelines limit the information needed to determine eligibility.

Dr. Sequist also noted that the updated American Cancer Society guideline would improve screening rates because it simplifies the eligibility criteria and makes it easier for physicians to determine who qualifies.

The issue, however, is that some of these individuals — those who quit over 15 years ago — may not have their scan covered by insurance, which could preclude lower-income individuals from getting screened.

The American Cancer Society guidelines” do not necessarily translate into a change in policy,” which is “dictated by the USPSTF and payors such as Medicare,” explained Peter Mazzone, MD, MPH, director of the Lung Cancer Program and Lung Cancer Screening Program for the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio.

On the patient side, Dr. Brawley noted, “we don’t yet have a large demand” for screening.

Many current and former smokers may put off lung cancer screening or not seek it out. Some may be unaware of their eligibility, while others may fear the outcome of a scan. Even among eligible individuals who do receive an initial scan, most — more than 75% — do not return for their next scan a year later, research showed.

Enhancing patient education and launching strong marketing campaigns would be a key element to encourage more people to get their annual screening and reduce the stigma associated with lung cancer as a smoker’s disease.

“Primary care physicians are integral in ensuring all eligible patients receive appropriate screening for lung cancer,” said Steven P. Furr, MD, president of the American Academy of Family Physicians and a family physician in Jackson, Alabama. “It is imperative that family physicians encourage screening in at-risk patients and counsel them on the importance of continued screening, as well as smoking cessation, if needed.”

Two authors of the new guidelines reported financial relationships with Seno Medical Instruments, the Genentech Foundation, Crispr Therapeutics, BEAM Therapeutics, Intellia Therapeutics, Editas Medicine, Freenome, and Guardant Health.

A version of this article appeared on Medscape.com.

When clinicians suspect lung fibrosis and particularly its most devastating form, idiopathic pulmonary fibrosis (IPF), a noninvasive artificial intelligence (AI)-driven digital diagnostic tool may identify subtype classifications facilitating proper treatment at earlier disease stages. On January 16, 2024, the tool, Fibresolve, developed and produced by the digital biomarker company IMVARIA Inc., received the first-ever US Food and Drug Administration (FDA) marketing authorization of a Breakthrough Designated AI diagnostic tool. Simultaneously, the American Medical Association adopted relevant CPT [Current Procedural Terminology] billing codes, according to an IMVARIA Inc. press release.

Diagnosis and treatment of the lung inflammation and fibrosis that drive IPF lung function decline are often long delayed, Joshua Reicher, MD, CEO of IMVARIA Inc. and an adjunct clinical professor at Stanford (California) University said in an interview for CHEST Physician.

“There are multiple challenges with this somewhat uncommon condition. Part of the frequent delays in diagnosis is the lack of access to local experts. Another part is vague presenting symptoms like general fatigue, for example, which can have an overlap with a lot of other conditions. The published median average delay in diagnosis after first presenting symptoms is about 2.2 years. But it’s often longer.”
 

Determining Type of Lung Fibrosis

Conventional diagnosis based on lab tests for inflammatory biomarkers and extensive clinical history is “fairly straightforward,” Dr. Reicher continued, for determining that a patient has some form of lung fibrosis. “The critical element is to find out what type of lung fibrosis and then begin appropriate therapy. The literature lists about 200 different subtypes, but the top 5 make up the majority of cases. The focus with Fibresolve is on improving noninvasive sensitivity, especially for the cases that are less straightforward, but rather indeterminate and therefore particularly challenging,” Dr. Reicher stated.

Will adjunctive diagnostic use of Fibresolve obviate the need for invasive confirmatory tests? Dr. Reicher was cautious. “We like to be thoughtful about our positioning of artificial intelligence and prefer to say that it puts complementary information in the hands of the physician. It’s really up to the clinicians to decide if they have sufficient information to avoid that biopsy.” The uniqueness of Fibresolve, Dr. Reicher pointed out, is that it is widely accessible and does not require hyper-specialized providers. “You can use it at any center that has standard CT scans.”
 

Reducing Burden on Physicians

An essential feature of Fibresolve use is that its software analysis is conducted centrally. “Part of our goal is to reduce the burden on the clinicians as much as possible, and we try to offload as much of the technical work from them as we can.”

The clinicians send images to IMVARIA Inc. (typically electronically) where they are processed rapidly, and a report is generated with outputs identifying the specific classification, perhaps with one indicating that the findings are suggestive of IPF. Dr. Reicher observed that the Fibresolve’s deep learning algorithm was trained on thousands of cases. “We’re very confident in the results that it puts out,” he said.

“We’re very excited. This is the first FDA-authorized diagnostic tool of any type in lung fibrosis. We really think this supports doctors and patients in areas where there’s a high unmet need,” Dr. Reicher said.

IMVARIA is next developing, in collaboration with the Mayo Clinic, a Fibresolve application for use in lung cancer, he said.

When clinicians suspect lung fibrosis and particularly its most devastating form, idiopathic pulmonary fibrosis (IPF), a noninvasive artificial intelligence (AI)-driven digital diagnostic tool may identify subtype classifications facilitating proper treatment at earlier disease stages. On January 16, 2024, the tool, Fibresolve, developed and produced by the digital biomarker company IMVARIA Inc., received the first-ever US Food and Drug Administration (FDA) marketing authorization of a Breakthrough Designated AI diagnostic tool. Simultaneously, the American Medical Association adopted relevant CPT [Current Procedural Terminology] billing codes, according to an IMVARIA Inc. press release.

Diagnosis and treatment of the lung inflammation and fibrosis that drive IPF lung function decline are often long delayed, Joshua Reicher, MD, CEO of IMVARIA Inc. and an adjunct clinical professor at Stanford (California) University said in an interview for CHEST Physician.

“There are multiple challenges with this somewhat uncommon condition. Part of the frequent delays in diagnosis is the lack of access to local experts. Another part is vague presenting symptoms like general fatigue, for example, which can have an overlap with a lot of other conditions. The published median average delay in diagnosis after first presenting symptoms is about 2.2 years. But it’s often longer.”
 

Determining Type of Lung Fibrosis

Conventional diagnosis based on lab tests for inflammatory biomarkers and extensive clinical history is “fairly straightforward,” Dr. Reicher continued, for determining that a patient has some form of lung fibrosis. “The critical element is to find out what type of lung fibrosis and then begin appropriate therapy. The literature lists about 200 different subtypes, but the top 5 make up the majority of cases. The focus with Fibresolve is on improving noninvasive sensitivity, especially for the cases that are less straightforward, but rather indeterminate and therefore particularly challenging,” Dr. Reicher stated.

Will adjunctive diagnostic use of Fibresolve obviate the need for invasive confirmatory tests? Dr. Reicher was cautious. “We like to be thoughtful about our positioning of artificial intelligence and prefer to say that it puts complementary information in the hands of the physician. It’s really up to the clinicians to decide if they have sufficient information to avoid that biopsy.” The uniqueness of Fibresolve, Dr. Reicher pointed out, is that it is widely accessible and does not require hyper-specialized providers. “You can use it at any center that has standard CT scans.”
 

Reducing Burden on Physicians

An essential feature of Fibresolve use is that its software analysis is conducted centrally. “Part of our goal is to reduce the burden on the clinicians as much as possible, and we try to offload as much of the technical work from them as we can.”

The clinicians send images to IMVARIA Inc. (typically electronically) where they are processed rapidly, and a report is generated with outputs identifying the specific classification, perhaps with one indicating that the findings are suggestive of IPF. Dr. Reicher observed that the Fibresolve’s deep learning algorithm was trained on thousands of cases. “We’re very confident in the results that it puts out,” he said.

“We’re very excited. This is the first FDA-authorized diagnostic tool of any type in lung fibrosis. We really think this supports doctors and patients in areas where there’s a high unmet need,” Dr. Reicher said.

IMVARIA is next developing, in collaboration with the Mayo Clinic, a Fibresolve application for use in lung cancer, he said.

When clinicians suspect lung fibrosis and particularly its most devastating form, idiopathic pulmonary fibrosis (IPF), a noninvasive artificial intelligence (AI)-driven digital diagnostic tool may identify subtype classifications facilitating proper treatment at earlier disease stages. On January 16, 2024, the tool, Fibresolve, developed and produced by the digital biomarker company IMVARIA Inc., received the first-ever US Food and Drug Administration (FDA) marketing authorization of a Breakthrough Designated AI diagnostic tool. Simultaneously, the American Medical Association adopted relevant CPT [Current Procedural Terminology] billing codes, according to an IMVARIA Inc. press release.

Diagnosis and treatment of the lung inflammation and fibrosis that drive IPF lung function decline are often long delayed, Joshua Reicher, MD, CEO of IMVARIA Inc. and an adjunct clinical professor at Stanford (California) University said in an interview for CHEST Physician.

“There are multiple challenges with this somewhat uncommon condition. Part of the frequent delays in diagnosis is the lack of access to local experts. Another part is vague presenting symptoms like general fatigue, for example, which can have an overlap with a lot of other conditions. The published median average delay in diagnosis after first presenting symptoms is about 2.2 years. But it’s often longer.”
 

Determining Type of Lung Fibrosis

Conventional diagnosis based on lab tests for inflammatory biomarkers and extensive clinical history is “fairly straightforward,” Dr. Reicher continued, for determining that a patient has some form of lung fibrosis. “The critical element is to find out what type of lung fibrosis and then begin appropriate therapy. The literature lists about 200 different subtypes, but the top 5 make up the majority of cases. The focus with Fibresolve is on improving noninvasive sensitivity, especially for the cases that are less straightforward, but rather indeterminate and therefore particularly challenging,” Dr. Reicher stated.

Will adjunctive diagnostic use of Fibresolve obviate the need for invasive confirmatory tests? Dr. Reicher was cautious. “We like to be thoughtful about our positioning of artificial intelligence and prefer to say that it puts complementary information in the hands of the physician. It’s really up to the clinicians to decide if they have sufficient information to avoid that biopsy.” The uniqueness of Fibresolve, Dr. Reicher pointed out, is that it is widely accessible and does not require hyper-specialized providers. “You can use it at any center that has standard CT scans.”
 

Reducing Burden on Physicians

An essential feature of Fibresolve use is that its software analysis is conducted centrally. “Part of our goal is to reduce the burden on the clinicians as much as possible, and we try to offload as much of the technical work from them as we can.”

The clinicians send images to IMVARIA Inc. (typically electronically) where they are processed rapidly, and a report is generated with outputs identifying the specific classification, perhaps with one indicating that the findings are suggestive of IPF. Dr. Reicher observed that the Fibresolve’s deep learning algorithm was trained on thousands of cases. “We’re very confident in the results that it puts out,” he said.

“We’re very excited. This is the first FDA-authorized diagnostic tool of any type in lung fibrosis. We really think this supports doctors and patients in areas where there’s a high unmet need,” Dr. Reicher said.

IMVARIA is next developing, in collaboration with the Mayo Clinic, a Fibresolve application for use in lung cancer, he said.

TOPLINE:

Individuals with either high or low body mass index (BMI) showed an increased risk for respiratory symptoms and diseases than those with BMI in the normal range.

METHODOLOGY:

• The researchers reviewed data from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2012; the study population included 12,719 adults older than 40 years with data on respiratory symptoms; 51% were female, and 53.3% were non-Hispanic White individuals.
• The study population was divided into quartiles based on BMI as follows: 3180 individuals with BMI of 13.2-24.9 kg/m², 3175 with BMI of 24.9-28.4 kg/m², 3180 with BMI of 28.4-32.5 kg/m², and 3184 with BMI of 32.5-82.0 kg/m².
• The study sought to assess the correlation between BMI and respiratory symptoms (cough, wheezing, and dyspnea), chronic obstructive pulmonary disease (COPD), and asthma in unadjusted and adjusted models based on sex, race, marital status, poverty-income ratio (PIR), education level, and smoking status.

TAKEAWAY:

• In a logistic regression and curve fitting analysis, BMI showed a U-shaped relationship with respiratory symptoms, asthma, and COPD, with increased risk in individuals with high or low BMI than those with BMIs in the middle quartiles.
• In a stratified analysis by race, the risk for cough was significantly higher among non-Hispanic Black individuals than other races (P < .0001), and a higher BMI was associated with an increased risk for COPD in non-Hispanic Black individuals (odds ratio, 1.053; P < .0001).
• The researchers found no significant impact of biological sex on the relationship between BMI and respiratory symptoms, COPD, or asthma.
• The results support previous studies showing that a BMI that is too low can be detrimental to health.

IN PRACTICE:

“These results suggest that the risk of small airway obstruction in underweight individuals deserves more attention and that excessive wasting may also affect the prognosis of patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Yuefeng Sun of Shandong University of Traditional Chinese Medicine, Jinan, China. The study was published online on January 10, 2024, in Scientific Reports. 

LIMITATIONS:

The cross-sectional NHANES database prevented conclusions of causality, and potential confounding factors that were not accounted for could have affected the results.

DISCLOSURES:

The study was supported by the Shandong Province Taishan Scholar Project. The researchers had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.

TOPLINE:

Individuals with either high or low body mass index (BMI) showed an increased risk for respiratory symptoms and diseases than those with BMI in the normal range.

METHODOLOGY:

• The researchers reviewed data from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2012; the study population included 12,719 adults older than 40 years with data on respiratory symptoms; 51% were female, and 53.3% were non-Hispanic White individuals.
• The study population was divided into quartiles based on BMI as follows: 3180 individuals with BMI of 13.2-24.9 kg/m², 3175 with BMI of 24.9-28.4 kg/m², 3180 with BMI of 28.4-32.5 kg/m², and 3184 with BMI of 32.5-82.0 kg/m².
• The study sought to assess the correlation between BMI and respiratory symptoms (cough, wheezing, and dyspnea), chronic obstructive pulmonary disease (COPD), and asthma in unadjusted and adjusted models based on sex, race, marital status, poverty-income ratio (PIR), education level, and smoking status.

TAKEAWAY:

• In a logistic regression and curve fitting analysis, BMI showed a U-shaped relationship with respiratory symptoms, asthma, and COPD, with increased risk in individuals with high or low BMI than those with BMIs in the middle quartiles.
• In a stratified analysis by race, the risk for cough was significantly higher among non-Hispanic Black individuals than other races (P < .0001), and a higher BMI was associated with an increased risk for COPD in non-Hispanic Black individuals (odds ratio, 1.053; P < .0001).
• The researchers found no significant impact of biological sex on the relationship between BMI and respiratory symptoms, COPD, or asthma.
• The results support previous studies showing that a BMI that is too low can be detrimental to health.

IN PRACTICE:

“These results suggest that the risk of small airway obstruction in underweight individuals deserves more attention and that excessive wasting may also affect the prognosis of patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Yuefeng Sun of Shandong University of Traditional Chinese Medicine, Jinan, China. The study was published online on January 10, 2024, in Scientific Reports. 

LIMITATIONS:

The cross-sectional NHANES database prevented conclusions of causality, and potential confounding factors that were not accounted for could have affected the results.

DISCLOSURES:

The study was supported by the Shandong Province Taishan Scholar Project. The researchers had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.

TOPLINE:

Individuals with either high or low body mass index (BMI) showed an increased risk for respiratory symptoms and diseases than those with BMI in the normal range.

METHODOLOGY:

• The researchers reviewed data from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2012; the study population included 12,719 adults older than 40 years with data on respiratory symptoms; 51% were female, and 53.3% were non-Hispanic White individuals.
• The study population was divided into quartiles based on BMI as follows: 3180 individuals with BMI of 13.2-24.9 kg/m², 3175 with BMI of 24.9-28.4 kg/m², 3180 with BMI of 28.4-32.5 kg/m², and 3184 with BMI of 32.5-82.0 kg/m².
• The study sought to assess the correlation between BMI and respiratory symptoms (cough, wheezing, and dyspnea), chronic obstructive pulmonary disease (COPD), and asthma in unadjusted and adjusted models based on sex, race, marital status, poverty-income ratio (PIR), education level, and smoking status.

TAKEAWAY:

• In a logistic regression and curve fitting analysis, BMI showed a U-shaped relationship with respiratory symptoms, asthma, and COPD, with increased risk in individuals with high or low BMI than those with BMIs in the middle quartiles.
• In a stratified analysis by race, the risk for cough was significantly higher among non-Hispanic Black individuals than other races (P < .0001), and a higher BMI was associated with an increased risk for COPD in non-Hispanic Black individuals (odds ratio, 1.053; P < .0001).
• The researchers found no significant impact of biological sex on the relationship between BMI and respiratory symptoms, COPD, or asthma.
• The results support previous studies showing that a BMI that is too low can be detrimental to health.

IN PRACTICE:

“These results suggest that the risk of small airway obstruction in underweight individuals deserves more attention and that excessive wasting may also affect the prognosis of patients with COPD,” the researchers wrote. 

SOURCE:

The lead author on the study was Yuefeng Sun of Shandong University of Traditional Chinese Medicine, Jinan, China. The study was published online on January 10, 2024, in Scientific Reports. 

LIMITATIONS:

The cross-sectional NHANES database prevented conclusions of causality, and potential confounding factors that were not accounted for could have affected the results.

DISCLOSURES:

The study was supported by the Shandong Province Taishan Scholar Project. The researchers had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.