Pulmonology

The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.

Key takeaways

• Right ventricular (RV) dilation or dysfunction in patients hospitalized with acute COVID-19 is associated with an elevated risk for in-hospital death.
• The impact of RV dilation or dysfunction on in-hospital mortality is similar for patients with acute COVID-19 and those with influenza, pneumonia, or acute respiratory distress syndrome (ARDS), but COVID-19 patients have greater absolute in-hospital mortality.
• RV dilatation or dysfunction in patients with acute COVID-19 is associated with a diagnosis of venous thromboembolism and subsequent intubation and mechanical ventilation.

Why this matters

• Right ventricular dysfunction increases mortality risk in acute COVID-19, and this study shows that RV dilation and dysfunction among such hospitalized patients has a similar impact on risk for in-hospital death in acute COVID-19 and in other respiratory illnesses.
• The findings suggest that abnormal RV findings should be considered a mortality risk marker in patients with acute respiratory illness, especially COVID-19.

Study design

• The retrospective study involved 225 consecutive patients admitted for acute COVID-19 from March 2020 to February 2021 at four major hospitals in the same metropolitan region and a control group of 6,150 adults admitted to the hospital for influenza, pneumonia, or ARDS; mean age in the study cohort was 63 years.
• All participants underwent echocardiography during their hospitalization, including evaluation of any RV dilation or dysfunction.
• Associations between RV measurements and in-hospital mortality, the primary outcome, were adjusted for potential confounders.

Key results

• Patients in the COVID-19 group were more likely than were those in the control group to be male (66% vs. 54%; P < .001), to identify as Hispanic (38% vs. 15%; P < .001), and to have a higher mean body mass index (29.4 vs. 27.9 kg/m²; P = .008).
• Compared with the control group, patients in the COVID-19 group more often required admission to the intensive care unit (75% vs. 54%; P < .001), mechanical ventilation (P < .001), and initiation of renal replacement therapy (P = .002), and more often were diagnosed with deep-vein thrombosis or pulmonary embolism (25% vs. 14%; P < .001). The median length of hospital stay was 20 days in the COVID-19 group, compared with 10 days in the control group (P < .001).
• In-hospital mortality was 21.3% in the COVID-19 group and 11.8% in the control group (P = .001). Those hospitalized with COVID-19 had an adjusted relative risk (RR) of 1.54 (95% confidence interval [CI], 1.06-2.24; P = .02) for in-hospital mortality, compared with those hospitalized for other respiratory illnesses.
• Mild RV dilation was associated with an adjusted RR of 1.4 (95% CI, 1.17-1.69; P = .0003) for in-hospital death, and moderate to severe RV dilation was associated with an adjusted RR of 2.0 (95% CI, 1.62-2.47; P < .0001).
• The corresponding adjusted risks for mild RV dysfunction and greater-than-mild RV dysfunction were, respectively, 1.39 (95% CI, 1.10-1.77; P = .007) and 1.68 (95% CI, 1.17-2.42; P = .005).
• The RR for in-hospital mortality associated with RV dilation and dysfunction was similar in those with COVID-19 and those with other respiratory illness, but the former had a higher baseline risk that yielded a greater absolute risk in the COVID-19 group.

Limitations

• The study was based primarily on a retrospective review of electronic health records, which poses a risk for misclassification. 
• Echocardiography was performed without blinding operators to patient clinical status, and echocardiograms were interpreted in a single university hospital system, so were not externally validated.
• Because echocardiograms obtained during hospitalization could not be compared with previous echocardiograms, it could not be determined whether any of the patients had preexisting RV dilation or dysfunction.
• Strain imaging was not feasible in many cases.

Disclosures

• The study received no commercial funding.
• The authors disclosed no financial relationships.

This is a summary of a preprint research study, Association of Right Ventricular Dilation and Dysfunction on Echocardiogram With In-Hospital Mortality Among Patients Hospitalized with COVID-19 Compared With Other Acute Respiratory Illness, written by researchers at the University of California, San Francisco, department of medicine, and Zuckerberg San Francisco General Hospital, division of cardiology. A version of this article first appeared on Medscape.com.

The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.

Key takeaways

• Right ventricular (RV) dilation or dysfunction in patients hospitalized with acute COVID-19 is associated with an elevated risk for in-hospital death.
• The impact of RV dilation or dysfunction on in-hospital mortality is similar for patients with acute COVID-19 and those with influenza, pneumonia, or acute respiratory distress syndrome (ARDS), but COVID-19 patients have greater absolute in-hospital mortality.
• RV dilatation or dysfunction in patients with acute COVID-19 is associated with a diagnosis of venous thromboembolism and subsequent intubation and mechanical ventilation.

Why this matters

• Right ventricular dysfunction increases mortality risk in acute COVID-19, and this study shows that RV dilation and dysfunction among such hospitalized patients has a similar impact on risk for in-hospital death in acute COVID-19 and in other respiratory illnesses.
• The findings suggest that abnormal RV findings should be considered a mortality risk marker in patients with acute respiratory illness, especially COVID-19.

Study design

• The retrospective study involved 225 consecutive patients admitted for acute COVID-19 from March 2020 to February 2021 at four major hospitals in the same metropolitan region and a control group of 6,150 adults admitted to the hospital for influenza, pneumonia, or ARDS; mean age in the study cohort was 63 years.
• All participants underwent echocardiography during their hospitalization, including evaluation of any RV dilation or dysfunction.
• Associations between RV measurements and in-hospital mortality, the primary outcome, were adjusted for potential confounders.

Key results

• Patients in the COVID-19 group were more likely than were those in the control group to be male (66% vs. 54%; P < .001), to identify as Hispanic (38% vs. 15%; P < .001), and to have a higher mean body mass index (29.4 vs. 27.9 kg/m²; P = .008).
• Compared with the control group, patients in the COVID-19 group more often required admission to the intensive care unit (75% vs. 54%; P < .001), mechanical ventilation (P < .001), and initiation of renal replacement therapy (P = .002), and more often were diagnosed with deep-vein thrombosis or pulmonary embolism (25% vs. 14%; P < .001). The median length of hospital stay was 20 days in the COVID-19 group, compared with 10 days in the control group (P < .001).
• In-hospital mortality was 21.3% in the COVID-19 group and 11.8% in the control group (P = .001). Those hospitalized with COVID-19 had an adjusted relative risk (RR) of 1.54 (95% confidence interval [CI], 1.06-2.24; P = .02) for in-hospital mortality, compared with those hospitalized for other respiratory illnesses.
• Mild RV dilation was associated with an adjusted RR of 1.4 (95% CI, 1.17-1.69; P = .0003) for in-hospital death, and moderate to severe RV dilation was associated with an adjusted RR of 2.0 (95% CI, 1.62-2.47; P < .0001).
• The corresponding adjusted risks for mild RV dysfunction and greater-than-mild RV dysfunction were, respectively, 1.39 (95% CI, 1.10-1.77; P = .007) and 1.68 (95% CI, 1.17-2.42; P = .005).
• The RR for in-hospital mortality associated with RV dilation and dysfunction was similar in those with COVID-19 and those with other respiratory illness, but the former had a higher baseline risk that yielded a greater absolute risk in the COVID-19 group.

Limitations

• The study was based primarily on a retrospective review of electronic health records, which poses a risk for misclassification. 
• Echocardiography was performed without blinding operators to patient clinical status, and echocardiograms were interpreted in a single university hospital system, so were not externally validated.
• Because echocardiograms obtained during hospitalization could not be compared with previous echocardiograms, it could not be determined whether any of the patients had preexisting RV dilation or dysfunction.
• Strain imaging was not feasible in many cases.

Disclosures

• The study received no commercial funding.
• The authors disclosed no financial relationships.

This is a summary of a preprint research study, Association of Right Ventricular Dilation and Dysfunction on Echocardiogram With In-Hospital Mortality Among Patients Hospitalized with COVID-19 Compared With Other Acute Respiratory Illness, written by researchers at the University of California, San Francisco, department of medicine, and Zuckerberg San Francisco General Hospital, division of cardiology. A version of this article first appeared on Medscape.com.

The study covered in this summary was published in medRxiv.org as a preprint and has not yet been peer reviewed.

Key takeaways

• Right ventricular (RV) dilation or dysfunction in patients hospitalized with acute COVID-19 is associated with an elevated risk for in-hospital death.
• The impact of RV dilation or dysfunction on in-hospital mortality is similar for patients with acute COVID-19 and those with influenza, pneumonia, or acute respiratory distress syndrome (ARDS), but COVID-19 patients have greater absolute in-hospital mortality.
• RV dilatation or dysfunction in patients with acute COVID-19 is associated with a diagnosis of venous thromboembolism and subsequent intubation and mechanical ventilation.

Why this matters

• Right ventricular dysfunction increases mortality risk in acute COVID-19, and this study shows that RV dilation and dysfunction among such hospitalized patients has a similar impact on risk for in-hospital death in acute COVID-19 and in other respiratory illnesses.
• The findings suggest that abnormal RV findings should be considered a mortality risk marker in patients with acute respiratory illness, especially COVID-19.

Study design

• The retrospective study involved 225 consecutive patients admitted for acute COVID-19 from March 2020 to February 2021 at four major hospitals in the same metropolitan region and a control group of 6,150 adults admitted to the hospital for influenza, pneumonia, or ARDS; mean age in the study cohort was 63 years.
• All participants underwent echocardiography during their hospitalization, including evaluation of any RV dilation or dysfunction.
• Associations between RV measurements and in-hospital mortality, the primary outcome, were adjusted for potential confounders.

Key results

• Patients in the COVID-19 group were more likely than were those in the control group to be male (66% vs. 54%; P < .001), to identify as Hispanic (38% vs. 15%; P < .001), and to have a higher mean body mass index (29.4 vs. 27.9 kg/m²; P = .008).
• Compared with the control group, patients in the COVID-19 group more often required admission to the intensive care unit (75% vs. 54%; P < .001), mechanical ventilation (P < .001), and initiation of renal replacement therapy (P = .002), and more often were diagnosed with deep-vein thrombosis or pulmonary embolism (25% vs. 14%; P < .001). The median length of hospital stay was 20 days in the COVID-19 group, compared with 10 days in the control group (P < .001).
• In-hospital mortality was 21.3% in the COVID-19 group and 11.8% in the control group (P = .001). Those hospitalized with COVID-19 had an adjusted relative risk (RR) of 1.54 (95% confidence interval [CI], 1.06-2.24; P = .02) for in-hospital mortality, compared with those hospitalized for other respiratory illnesses.
• Mild RV dilation was associated with an adjusted RR of 1.4 (95% CI, 1.17-1.69; P = .0003) for in-hospital death, and moderate to severe RV dilation was associated with an adjusted RR of 2.0 (95% CI, 1.62-2.47; P < .0001).
• The corresponding adjusted risks for mild RV dysfunction and greater-than-mild RV dysfunction were, respectively, 1.39 (95% CI, 1.10-1.77; P = .007) and 1.68 (95% CI, 1.17-2.42; P = .005).
• The RR for in-hospital mortality associated with RV dilation and dysfunction was similar in those with COVID-19 and those with other respiratory illness, but the former had a higher baseline risk that yielded a greater absolute risk in the COVID-19 group.

Limitations

• The study was based primarily on a retrospective review of electronic health records, which poses a risk for misclassification. 
• Echocardiography was performed without blinding operators to patient clinical status, and echocardiograms were interpreted in a single university hospital system, so were not externally validated.
• Because echocardiograms obtained during hospitalization could not be compared with previous echocardiograms, it could not be determined whether any of the patients had preexisting RV dilation or dysfunction.
• Strain imaging was not feasible in many cases.

Disclosures

• The study received no commercial funding.
• The authors disclosed no financial relationships.

This is a summary of a preprint research study, Association of Right Ventricular Dilation and Dysfunction on Echocardiogram With In-Hospital Mortality Among Patients Hospitalized with COVID-19 Compared With Other Acute Respiratory Illness, written by researchers at the University of California, San Francisco, department of medicine, and Zuckerberg San Francisco General Hospital, division of cardiology. A version of this article first appeared on Medscape.com.

Differences in the safety and efficacy between the biologics approved for the treatment of severe eosinophilic asthma are so minimal as to not meet clinically important thresholds, a network meta-analysis shows.

“We know relatively little of the comparative effectiveness or safety of biologics approved for the treatment of asthma [but since] the number of these biologics continue to rise and their indications are increasing, the opportunities to use these biologics will only continue to increase, and we need to know more about their comparative effectiveness to optimize their use,” Ayobami Akenroye, MD, MPH, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said in an interview.

“But the decision to use one biologic or not is complex and goes beyond comparative effectiveness, and factors such as insurance coverage, convenience of self-administration, and comorbidities all play a role in the choice of biologics,” she said, adding that all the outcomes assessed in the study contribute to or reflect a patient’s underlying asthma control.

The study was published online in the Journal of Allergy and Clinical Immunology.
 

Interleukin pathways

Drugs that target various interleukin signaling pathways involved in the pathogenesis of asthma include mepolizumab (Nucala), benralizumab (Fasenra), and dupilumab (Dupixent), all of which have been shown to decrease exacerbation rates, improve lung function, and enhance quality of life for patients with severe eosinophilic asthma. In a Bayesian network meta-analysis that allows for simultaneous comparisons of these three treatments, investigators analyzed eight randomized, placebo-controlled trials that compared each of the drugs with placebo. In total, the trials involved 6,461 patients; the duration of follow-up was between 24 and 56 weeks.

“In the subgroup of patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics were significantly better than placebo in reducing exacerbations,” Dr. Akenroye and colleagues reported. For example, dupilumab reduced the exacerbation risk by 68% at a risk ratio of 0.32 (95% confidence interval, 0.23-0.45), while mepolizumab reduced it by almost as much at 63% (RR, 0.37; 95% CI, 0.30-0.45).

Benralizumab was slightly less effective than the other two biologics, reducing exacerbation risk by 51% (RR, 0.49; 95% CI, 0.43-0.55). “In patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics had a probability of 1 in improving the exacerbation rate by 20% or more ... in comparison to placebo,” the authors wrote.

Regarding each drug’s effect in improving forced expiratory volume in 1 second (FEV₁), the mean difference in milliliters with dupilumab before and after treatment was 230 (95% CI, 160-300), while for benralizumab, the MD was 150 (95% CI, 100-220) before and after treatment. With mepolizumab, the MD in FEV₁ before and after treatment was also 150. In the same subgroup of patients with eosinophil counts of at least300 cells/mcL, all three biologics again had a probability of 1 in improving FEV₁ by 50 mL or more above the placebo effect. A third endpoint that was analyzed was the potential reduction in asthma control questionnaire (ACQ) scores. With mepolizumab, the MD before and after treatment was –0.65 (95% CI, –0.81 to –0.45); with dupilumab, it was –0.48 (95% CI, –0.83 to –0.14); and with dupilumab, it was –0.32 (95% CI, –0.43 to –0.21).

“Dupilumab was significantly better than benralizumab in improving exacerbations,” the authors noted (RR, 0.66; 95% CI, 0.47-0.94), while mepolizumab was also better than benralizumab (RR, 0.75; 95% CI, 0.60-0.95). On the other hand, both dupilumab and benralizumab led to greater improvements in FEV₁ than mepolizumab, although the effects of dupilumab and benralizumab on ACQ scores were not significantly different for patients whose lower eosinophil counts were between 150 and 299 cells/mcL.

As for safety outcomes, both mepolizumab and benralizumab were associated with a lower risk of serious adverse events, but dupilumab was not different from placebo in terms of overall safety, according to the authors. “The ultimate choice of biologic for each patient would ... depend on multiple factors including cost considerations and timing of administration.

“[However], these results may be helpful to clinicians as they optimize patient care,” they concluded. Limitations to the analysis include the fact that indirect comparisons cannot replace randomized trials that compare the three drugs directly.

It’s estimated that 5%-10% of the 26 million individuals with asthma in the United States have severe disease.

Dr. Akenroye disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Differences in the safety and efficacy between the biologics approved for the treatment of severe eosinophilic asthma are so minimal as to not meet clinically important thresholds, a network meta-analysis shows.

“We know relatively little of the comparative effectiveness or safety of biologics approved for the treatment of asthma [but since] the number of these biologics continue to rise and their indications are increasing, the opportunities to use these biologics will only continue to increase, and we need to know more about their comparative effectiveness to optimize their use,” Ayobami Akenroye, MD, MPH, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said in an interview.

“But the decision to use one biologic or not is complex and goes beyond comparative effectiveness, and factors such as insurance coverage, convenience of self-administration, and comorbidities all play a role in the choice of biologics,” she said, adding that all the outcomes assessed in the study contribute to or reflect a patient’s underlying asthma control.

The study was published online in the Journal of Allergy and Clinical Immunology.
 

Interleukin pathways

Drugs that target various interleukin signaling pathways involved in the pathogenesis of asthma include mepolizumab (Nucala), benralizumab (Fasenra), and dupilumab (Dupixent), all of which have been shown to decrease exacerbation rates, improve lung function, and enhance quality of life for patients with severe eosinophilic asthma. In a Bayesian network meta-analysis that allows for simultaneous comparisons of these three treatments, investigators analyzed eight randomized, placebo-controlled trials that compared each of the drugs with placebo. In total, the trials involved 6,461 patients; the duration of follow-up was between 24 and 56 weeks.

“In the subgroup of patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics were significantly better than placebo in reducing exacerbations,” Dr. Akenroye and colleagues reported. For example, dupilumab reduced the exacerbation risk by 68% at a risk ratio of 0.32 (95% confidence interval, 0.23-0.45), while mepolizumab reduced it by almost as much at 63% (RR, 0.37; 95% CI, 0.30-0.45).

Benralizumab was slightly less effective than the other two biologics, reducing exacerbation risk by 51% (RR, 0.49; 95% CI, 0.43-0.55). “In patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics had a probability of 1 in improving the exacerbation rate by 20% or more ... in comparison to placebo,” the authors wrote.

Regarding each drug’s effect in improving forced expiratory volume in 1 second (FEV₁), the mean difference in milliliters with dupilumab before and after treatment was 230 (95% CI, 160-300), while for benralizumab, the MD was 150 (95% CI, 100-220) before and after treatment. With mepolizumab, the MD in FEV₁ before and after treatment was also 150. In the same subgroup of patients with eosinophil counts of at least300 cells/mcL, all three biologics again had a probability of 1 in improving FEV₁ by 50 mL or more above the placebo effect. A third endpoint that was analyzed was the potential reduction in asthma control questionnaire (ACQ) scores. With mepolizumab, the MD before and after treatment was –0.65 (95% CI, –0.81 to –0.45); with dupilumab, it was –0.48 (95% CI, –0.83 to –0.14); and with dupilumab, it was –0.32 (95% CI, –0.43 to –0.21).

“Dupilumab was significantly better than benralizumab in improving exacerbations,” the authors noted (RR, 0.66; 95% CI, 0.47-0.94), while mepolizumab was also better than benralizumab (RR, 0.75; 95% CI, 0.60-0.95). On the other hand, both dupilumab and benralizumab led to greater improvements in FEV₁ than mepolizumab, although the effects of dupilumab and benralizumab on ACQ scores were not significantly different for patients whose lower eosinophil counts were between 150 and 299 cells/mcL.

As for safety outcomes, both mepolizumab and benralizumab were associated with a lower risk of serious adverse events, but dupilumab was not different from placebo in terms of overall safety, according to the authors. “The ultimate choice of biologic for each patient would ... depend on multiple factors including cost considerations and timing of administration.

“[However], these results may be helpful to clinicians as they optimize patient care,” they concluded. Limitations to the analysis include the fact that indirect comparisons cannot replace randomized trials that compare the three drugs directly.

It’s estimated that 5%-10% of the 26 million individuals with asthma in the United States have severe disease.

Dr. Akenroye disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Differences in the safety and efficacy between the biologics approved for the treatment of severe eosinophilic asthma are so minimal as to not meet clinically important thresholds, a network meta-analysis shows.

“We know relatively little of the comparative effectiveness or safety of biologics approved for the treatment of asthma [but since] the number of these biologics continue to rise and their indications are increasing, the opportunities to use these biologics will only continue to increase, and we need to know more about their comparative effectiveness to optimize their use,” Ayobami Akenroye, MD, MPH, of Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said in an interview.

“But the decision to use one biologic or not is complex and goes beyond comparative effectiveness, and factors such as insurance coverage, convenience of self-administration, and comorbidities all play a role in the choice of biologics,” she said, adding that all the outcomes assessed in the study contribute to or reflect a patient’s underlying asthma control.

The study was published online in the Journal of Allergy and Clinical Immunology.
 

Interleukin pathways

Drugs that target various interleukin signaling pathways involved in the pathogenesis of asthma include mepolizumab (Nucala), benralizumab (Fasenra), and dupilumab (Dupixent), all of which have been shown to decrease exacerbation rates, improve lung function, and enhance quality of life for patients with severe eosinophilic asthma. In a Bayesian network meta-analysis that allows for simultaneous comparisons of these three treatments, investigators analyzed eight randomized, placebo-controlled trials that compared each of the drugs with placebo. In total, the trials involved 6,461 patients; the duration of follow-up was between 24 and 56 weeks.

“In the subgroup of patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics were significantly better than placebo in reducing exacerbations,” Dr. Akenroye and colleagues reported. For example, dupilumab reduced the exacerbation risk by 68% at a risk ratio of 0.32 (95% confidence interval, 0.23-0.45), while mepolizumab reduced it by almost as much at 63% (RR, 0.37; 95% CI, 0.30-0.45).

Benralizumab was slightly less effective than the other two biologics, reducing exacerbation risk by 51% (RR, 0.49; 95% CI, 0.43-0.55). “In patients with eosinophil counts of ≥ 300 cells/mcL, all three biologics had a probability of 1 in improving the exacerbation rate by 20% or more ... in comparison to placebo,” the authors wrote.

Regarding each drug’s effect in improving forced expiratory volume in 1 second (FEV₁), the mean difference in milliliters with dupilumab before and after treatment was 230 (95% CI, 160-300), while for benralizumab, the MD was 150 (95% CI, 100-220) before and after treatment. With mepolizumab, the MD in FEV₁ before and after treatment was also 150. In the same subgroup of patients with eosinophil counts of at least300 cells/mcL, all three biologics again had a probability of 1 in improving FEV₁ by 50 mL or more above the placebo effect. A third endpoint that was analyzed was the potential reduction in asthma control questionnaire (ACQ) scores. With mepolizumab, the MD before and after treatment was –0.65 (95% CI, –0.81 to –0.45); with dupilumab, it was –0.48 (95% CI, –0.83 to –0.14); and with dupilumab, it was –0.32 (95% CI, –0.43 to –0.21).

“Dupilumab was significantly better than benralizumab in improving exacerbations,” the authors noted (RR, 0.66; 95% CI, 0.47-0.94), while mepolizumab was also better than benralizumab (RR, 0.75; 95% CI, 0.60-0.95). On the other hand, both dupilumab and benralizumab led to greater improvements in FEV₁ than mepolizumab, although the effects of dupilumab and benralizumab on ACQ scores were not significantly different for patients whose lower eosinophil counts were between 150 and 299 cells/mcL.

As for safety outcomes, both mepolizumab and benralizumab were associated with a lower risk of serious adverse events, but dupilumab was not different from placebo in terms of overall safety, according to the authors. “The ultimate choice of biologic for each patient would ... depend on multiple factors including cost considerations and timing of administration.

“[However], these results may be helpful to clinicians as they optimize patient care,” they concluded. Limitations to the analysis include the fact that indirect comparisons cannot replace randomized trials that compare the three drugs directly.

It’s estimated that 5%-10% of the 26 million individuals with asthma in the United States have severe disease.

Dr. Akenroye disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Falsely elevated pulse oximeter readings are leading to less oxygen supplementation for people of color, a recent study finds.

The new research suggests that skin color–related differences in pulse oximeter readings are in fact impacting clinical decision-making, lead author Eric R. Gottlieb, MD, of Brigham and Women’s Hospital and Massachusetts Institute of Technology, both in Boston, and colleagues wrote. This suggests that technology needs to updated to improve health equity, they continued, in their paper published in JAMA Internal Medicine.

“It has been known for decades that these readings are affected by various surface pigmentations, including nail polish and skin melanin, which may affect light absorption and scattering,” the investigators wrote. “This increases the risk of hidden hypoxemia [among patients with darker skin], in which patients have falsely elevated SpO₂ readings, usually defined as 92% or greater, with a blood hemoglobin oxygen saturation less than 88%.”

Although published reports on this phenomenon date back to the 1980s, clinical significance has been largely discounted, they said, citing a 2008 paper on the topic, which stated that “oximetry need not have exact accuracy” to determine if a patient needs oxygen supplementation.
 

‘We’re not providing equal care’

Questioning the validity of this statement, Dr. Gottlieb and colleagues conducted a retrospective cohort study involving 3,069 patients admitted to intensive care at the Beth Israel Deaconess Medical Center in Boston between 2008 and 2019, thereby excluding patients treated during the COVID-19 pandemic. The population consisted of four races/ethnicities: White (87%), Black (7%), Hispanic (4%), and Asian (3%).

Aligning with previous studies, multivariable linear regression analyses showed that Asian, Black, and Hispanic patients had significantly higher SpO₂ readings than White patients in relation to hemoglobin oxygen saturation values, suggesting falsely elevated readings.

Further modeling showed that these same patient groups also received lower oxygen delivery rates, which were not explained directly by race/ethnicity, but instead were mediated by the discrepancy between SpO₂ and hemoglobin oxygen saturation values. In other words, physicians were responding consistently to pulse oximetry readings, rather than exhibiting a direct racial/ethnic bias in their clinical decision-making.

“We’re not providing equal care,” Dr. Gottlieb said in an interview. “It’s not that the patients are sicker, or have other socioeconomic explanations for why this happens to them. It’s us. It’s our technology. And that’s something that really has to be fixed.”

The investigators offered a cautionary view of corrective algorithms, as these “have exacerbated disparities and are subject to ethical concerns;” for example, with glomerular filtration rate estimations in Black patients.

Dr. Gottlieb also cautioned against action by individual physicians, who may now be inclined to change how they interpret pulse oximeter readings based on a patient’s race or ethnicity.

“I don’t think that we can expect physicians, every time they see a patient, to be second guessing whether the number basically reflects the truth,” he said.

Instead, Dr. Gottlieb suggested that the burden of change rests upon the shoulders of institutions, including hospitals and device manufacturers, both of which “really need to take the responsibility” for making sure that pulse oximeters are “equitable and have similar performance across races.”

While Dr. Gottlieb said that skin color likely plays the greatest role in measurement discrepancies, he encouraged stakeholders “to think broadly about this, and not just assume that it’s entirely skin color,” noting a small amount of evidence indicating that blood chemistry may also play a role. Still, he predicted that colorimetry – the direct measurement of skin color – will probably be incorporated into pulse oximeters of the future.
 

Black patients 3X more likely to have hidden hypoxia than White patients

Michael Sjoding, MD, of the University of Michigan, Ann Arbor, was one of the first to raise awareness of skin color–related issues with pulse oximeters during the throes of the COVID-19 pandemic. His study, which involved more than 10,000 patients, showed that Black patients were threefold more likely to have hidden hypoxia than White patients.

The present study shows that such discrepancies are indeed clinically significant, Dr. Sjoding said in an interview. And these data are needed, he added, to bring about change.

“What is being asked is potentially a big deal,” Dr. Sjoding said. “Pulse oximeters are everywhere, and it would be a big undertaking to redesign pulse oximeters and purchase new pulse oximeters. You need a compelling body of evidence to do that. I think it’s there now, clearly. So I’m hopeful that we’re going to finally move forward, towards having devices that we are confident work accurately in everyone.”

Why it has taken so long to gather this evidence, however, is a thornier topic, considering race-related discrepancies in pulse oximeter readings were first documented more than 3 decades ago.

“We sort of rediscovered something that had been known and had been described in the past,” Dr. Sjoding said. He explained how he and many of his colleagues had completed pulmonary fellowships, yet none of them knew of these potential issues with pulse oximeters until they began to observe differences in their own patients during the pandemic.

“I’ll give previous generations of researchers the benefit of the doubt,” Dr. Sjoding said, pointing out that techniques in data gathering and analysis have advanced considerably over the years. “The types of studies that were done before were very different than what we did.”

Yet Dr. Sjoding entertained the possibility that other factors may have been at play.

“I think definitely there’s a social commentary on prioritization of research,” he said.

The study was supported by grants from the National Institutes of Health. The investigators and Dr. Sjoding reported no conflicts of interest.

Falsely elevated pulse oximeter readings are leading to less oxygen supplementation for people of color, a recent study finds.

The new research suggests that skin color–related differences in pulse oximeter readings are in fact impacting clinical decision-making, lead author Eric R. Gottlieb, MD, of Brigham and Women’s Hospital and Massachusetts Institute of Technology, both in Boston, and colleagues wrote. This suggests that technology needs to updated to improve health equity, they continued, in their paper published in JAMA Internal Medicine.

“It has been known for decades that these readings are affected by various surface pigmentations, including nail polish and skin melanin, which may affect light absorption and scattering,” the investigators wrote. “This increases the risk of hidden hypoxemia [among patients with darker skin], in which patients have falsely elevated SpO₂ readings, usually defined as 92% or greater, with a blood hemoglobin oxygen saturation less than 88%.”

Although published reports on this phenomenon date back to the 1980s, clinical significance has been largely discounted, they said, citing a 2008 paper on the topic, which stated that “oximetry need not have exact accuracy” to determine if a patient needs oxygen supplementation.
 

‘We’re not providing equal care’

Questioning the validity of this statement, Dr. Gottlieb and colleagues conducted a retrospective cohort study involving 3,069 patients admitted to intensive care at the Beth Israel Deaconess Medical Center in Boston between 2008 and 2019, thereby excluding patients treated during the COVID-19 pandemic. The population consisted of four races/ethnicities: White (87%), Black (7%), Hispanic (4%), and Asian (3%).

Aligning with previous studies, multivariable linear regression analyses showed that Asian, Black, and Hispanic patients had significantly higher SpO₂ readings than White patients in relation to hemoglobin oxygen saturation values, suggesting falsely elevated readings.

Further modeling showed that these same patient groups also received lower oxygen delivery rates, which were not explained directly by race/ethnicity, but instead were mediated by the discrepancy between SpO₂ and hemoglobin oxygen saturation values. In other words, physicians were responding consistently to pulse oximetry readings, rather than exhibiting a direct racial/ethnic bias in their clinical decision-making.

“We’re not providing equal care,” Dr. Gottlieb said in an interview. “It’s not that the patients are sicker, or have other socioeconomic explanations for why this happens to them. It’s us. It’s our technology. And that’s something that really has to be fixed.”

The investigators offered a cautionary view of corrective algorithms, as these “have exacerbated disparities and are subject to ethical concerns;” for example, with glomerular filtration rate estimations in Black patients.

Dr. Gottlieb also cautioned against action by individual physicians, who may now be inclined to change how they interpret pulse oximeter readings based on a patient’s race or ethnicity.

“I don’t think that we can expect physicians, every time they see a patient, to be second guessing whether the number basically reflects the truth,” he said.

Instead, Dr. Gottlieb suggested that the burden of change rests upon the shoulders of institutions, including hospitals and device manufacturers, both of which “really need to take the responsibility” for making sure that pulse oximeters are “equitable and have similar performance across races.”

While Dr. Gottlieb said that skin color likely plays the greatest role in measurement discrepancies, he encouraged stakeholders “to think broadly about this, and not just assume that it’s entirely skin color,” noting a small amount of evidence indicating that blood chemistry may also play a role. Still, he predicted that colorimetry – the direct measurement of skin color – will probably be incorporated into pulse oximeters of the future.
 

Black patients 3X more likely to have hidden hypoxia than White patients

Michael Sjoding, MD, of the University of Michigan, Ann Arbor, was one of the first to raise awareness of skin color–related issues with pulse oximeters during the throes of the COVID-19 pandemic. His study, which involved more than 10,000 patients, showed that Black patients were threefold more likely to have hidden hypoxia than White patients.

The present study shows that such discrepancies are indeed clinically significant, Dr. Sjoding said in an interview. And these data are needed, he added, to bring about change.

“What is being asked is potentially a big deal,” Dr. Sjoding said. “Pulse oximeters are everywhere, and it would be a big undertaking to redesign pulse oximeters and purchase new pulse oximeters. You need a compelling body of evidence to do that. I think it’s there now, clearly. So I’m hopeful that we’re going to finally move forward, towards having devices that we are confident work accurately in everyone.”

Why it has taken so long to gather this evidence, however, is a thornier topic, considering race-related discrepancies in pulse oximeter readings were first documented more than 3 decades ago.

“We sort of rediscovered something that had been known and had been described in the past,” Dr. Sjoding said. He explained how he and many of his colleagues had completed pulmonary fellowships, yet none of them knew of these potential issues with pulse oximeters until they began to observe differences in their own patients during the pandemic.

“I’ll give previous generations of researchers the benefit of the doubt,” Dr. Sjoding said, pointing out that techniques in data gathering and analysis have advanced considerably over the years. “The types of studies that were done before were very different than what we did.”

Yet Dr. Sjoding entertained the possibility that other factors may have been at play.

“I think definitely there’s a social commentary on prioritization of research,” he said.

The study was supported by grants from the National Institutes of Health. The investigators and Dr. Sjoding reported no conflicts of interest.

Falsely elevated pulse oximeter readings are leading to less oxygen supplementation for people of color, a recent study finds.

The new research suggests that skin color–related differences in pulse oximeter readings are in fact impacting clinical decision-making, lead author Eric R. Gottlieb, MD, of Brigham and Women’s Hospital and Massachusetts Institute of Technology, both in Boston, and colleagues wrote. This suggests that technology needs to updated to improve health equity, they continued, in their paper published in JAMA Internal Medicine.

“It has been known for decades that these readings are affected by various surface pigmentations, including nail polish and skin melanin, which may affect light absorption and scattering,” the investigators wrote. “This increases the risk of hidden hypoxemia [among patients with darker skin], in which patients have falsely elevated SpO₂ readings, usually defined as 92% or greater, with a blood hemoglobin oxygen saturation less than 88%.”

Although published reports on this phenomenon date back to the 1980s, clinical significance has been largely discounted, they said, citing a 2008 paper on the topic, which stated that “oximetry need not have exact accuracy” to determine if a patient needs oxygen supplementation.
 

‘We’re not providing equal care’

Questioning the validity of this statement, Dr. Gottlieb and colleagues conducted a retrospective cohort study involving 3,069 patients admitted to intensive care at the Beth Israel Deaconess Medical Center in Boston between 2008 and 2019, thereby excluding patients treated during the COVID-19 pandemic. The population consisted of four races/ethnicities: White (87%), Black (7%), Hispanic (4%), and Asian (3%).

Aligning with previous studies, multivariable linear regression analyses showed that Asian, Black, and Hispanic patients had significantly higher SpO₂ readings than White patients in relation to hemoglobin oxygen saturation values, suggesting falsely elevated readings.

Further modeling showed that these same patient groups also received lower oxygen delivery rates, which were not explained directly by race/ethnicity, but instead were mediated by the discrepancy between SpO₂ and hemoglobin oxygen saturation values. In other words, physicians were responding consistently to pulse oximetry readings, rather than exhibiting a direct racial/ethnic bias in their clinical decision-making.

“We’re not providing equal care,” Dr. Gottlieb said in an interview. “It’s not that the patients are sicker, or have other socioeconomic explanations for why this happens to them. It’s us. It’s our technology. And that’s something that really has to be fixed.”

The investigators offered a cautionary view of corrective algorithms, as these “have exacerbated disparities and are subject to ethical concerns;” for example, with glomerular filtration rate estimations in Black patients.

Dr. Gottlieb also cautioned against action by individual physicians, who may now be inclined to change how they interpret pulse oximeter readings based on a patient’s race or ethnicity.

“I don’t think that we can expect physicians, every time they see a patient, to be second guessing whether the number basically reflects the truth,” he said.

Instead, Dr. Gottlieb suggested that the burden of change rests upon the shoulders of institutions, including hospitals and device manufacturers, both of which “really need to take the responsibility” for making sure that pulse oximeters are “equitable and have similar performance across races.”

While Dr. Gottlieb said that skin color likely plays the greatest role in measurement discrepancies, he encouraged stakeholders “to think broadly about this, and not just assume that it’s entirely skin color,” noting a small amount of evidence indicating that blood chemistry may also play a role. Still, he predicted that colorimetry – the direct measurement of skin color – will probably be incorporated into pulse oximeters of the future.
 

Black patients 3X more likely to have hidden hypoxia than White patients

Michael Sjoding, MD, of the University of Michigan, Ann Arbor, was one of the first to raise awareness of skin color–related issues with pulse oximeters during the throes of the COVID-19 pandemic. His study, which involved more than 10,000 patients, showed that Black patients were threefold more likely to have hidden hypoxia than White patients.

The present study shows that such discrepancies are indeed clinically significant, Dr. Sjoding said in an interview. And these data are needed, he added, to bring about change.

“What is being asked is potentially a big deal,” Dr. Sjoding said. “Pulse oximeters are everywhere, and it would be a big undertaking to redesign pulse oximeters and purchase new pulse oximeters. You need a compelling body of evidence to do that. I think it’s there now, clearly. So I’m hopeful that we’re going to finally move forward, towards having devices that we are confident work accurately in everyone.”

Why it has taken so long to gather this evidence, however, is a thornier topic, considering race-related discrepancies in pulse oximeter readings were first documented more than 3 decades ago.

“We sort of rediscovered something that had been known and had been described in the past,” Dr. Sjoding said. He explained how he and many of his colleagues had completed pulmonary fellowships, yet none of them knew of these potential issues with pulse oximeters until they began to observe differences in their own patients during the pandemic.

“I’ll give previous generations of researchers the benefit of the doubt,” Dr. Sjoding said, pointing out that techniques in data gathering and analysis have advanced considerably over the years. “The types of studies that were done before were very different than what we did.”

Yet Dr. Sjoding entertained the possibility that other factors may have been at play.

“I think definitely there’s a social commentary on prioritization of research,” he said.

The study was supported by grants from the National Institutes of Health. The investigators and Dr. Sjoding reported no conflicts of interest.

Adults with severe asthma (SA) experienced significantly fewer exacerbations on biologic therapies, compared with those who did not use biologics, based on data from more than 2,000 individuals.

The development of biologics to target specific inflammatory pathways “has transformed the management of uncontrolled SA,” but data on the real-world use of biologics in severe asthma patients treated by subspecialists are limited, wrote Reynold A. Panettieri, Jr., MD, of Rutgers, State University of New Jersey, New Brunswick, and colleagues.

In a study published in the Annals of Allergy, Asthma & Immunology, the researchers reviewed data from CHRONICLE, an ongoing, prospective, real-world noninterventional study of adults aged 18 years and older with severe asthma in the United States.

The study population included 2,847 patients enrolled in the CHRONICLE study between February 2018 and February 2021; 68.8% were women, 74.6% were White. The patients ranged in age from 18 to 89 years, with a mean age of 54.2 years.

Biologic use was defined as patients who started or had ongoing use of biologics between 12 months before enrollment and the patient’s most recent data collection. Switches were defined as stopping one biologic and starting another within 6 months; stops were defined as discontinuing a biologic without switching to another within 6 months. A total of 66% of the patients were using biologics at the time of study enrollment. The most common biologic was omalizumab (47%), followed by benralizumab (27%), mepolizumab (26%), and dupilumab (18%).

Overall, 89% of the patients had ongoing biologic use, 16% had biologic switches, and 13% had stops.

Patients who started biologics or switched biologics had significant reductions in asthma exacerbations at 6 months, compared with nonbiologic users of 58% (1.80 vs. 0.76 per patient-year) and 49% (1.47 vs. 0.75 per patient-year), respectively (P < .001 for both). Asthma exacerbations declined by 70% among biologics users for whom data were available for 12 months before and 12 months after starting biologics.

Exacerbations decreased at 6 months after biologic initiation across all subgroups of patients, notably patients with pre-biologic FEV₁ < 80% and patients with FEV₁ ≥ 80% (66% and 53%, respectively); never smokers and current/former smokers (63% and 50%, respectively); and patients with COPD and without COPD (58% and 52%, respectively).

The researchers also found a greater reduction in exacerbations among patients who switched from anti-IgE therapy to anti–IL-5/IL-5R/IL-4R therapy, compared with those who switched among anti–IL-5/IL-5R/IL-4R therapies (58% vs. 46%).

Patients who stopped or switched biologics appeared to have more severe or treatment-refractory disease than those with ongoing biologic use, the researchers noted. The most common reason for stopping or switching was worsening symptoms.

The study findings were limited by several factors, including the focus only on adults in the United States with subspecialist-treated SA, which may limit generalizability to children or other populations, the researchers noted. Other limitations included the variation in clinical decisions and insurance coverage and the inability to conduct longitudinal assessments, they said.

The results demonstrate that starting or switching biologics was consistently associated with fewer exacerbations in severe asthma. However, more research is needed to determine why some patients were not receiving biologics because they were not considered clinically eligible by their subspecialist health care providers, the researchers concluded.

The current study and the CHRONICLE study were supported by AstraZeneca. Lead author Dr. Panettieri disclosed serving on the advisory boards for and receiving grant support from AstraZeneca, Sanofi, Genentech, Regeneron, and Novartis.

Adults with severe asthma (SA) experienced significantly fewer exacerbations on biologic therapies, compared with those who did not use biologics, based on data from more than 2,000 individuals.

The development of biologics to target specific inflammatory pathways “has transformed the management of uncontrolled SA,” but data on the real-world use of biologics in severe asthma patients treated by subspecialists are limited, wrote Reynold A. Panettieri, Jr., MD, of Rutgers, State University of New Jersey, New Brunswick, and colleagues.

In a study published in the Annals of Allergy, Asthma & Immunology, the researchers reviewed data from CHRONICLE, an ongoing, prospective, real-world noninterventional study of adults aged 18 years and older with severe asthma in the United States.

The study population included 2,847 patients enrolled in the CHRONICLE study between February 2018 and February 2021; 68.8% were women, 74.6% were White. The patients ranged in age from 18 to 89 years, with a mean age of 54.2 years.

Biologic use was defined as patients who started or had ongoing use of biologics between 12 months before enrollment and the patient’s most recent data collection. Switches were defined as stopping one biologic and starting another within 6 months; stops were defined as discontinuing a biologic without switching to another within 6 months. A total of 66% of the patients were using biologics at the time of study enrollment. The most common biologic was omalizumab (47%), followed by benralizumab (27%), mepolizumab (26%), and dupilumab (18%).

Overall, 89% of the patients had ongoing biologic use, 16% had biologic switches, and 13% had stops.

Patients who started biologics or switched biologics had significant reductions in asthma exacerbations at 6 months, compared with nonbiologic users of 58% (1.80 vs. 0.76 per patient-year) and 49% (1.47 vs. 0.75 per patient-year), respectively (P < .001 for both). Asthma exacerbations declined by 70% among biologics users for whom data were available for 12 months before and 12 months after starting biologics.

Exacerbations decreased at 6 months after biologic initiation across all subgroups of patients, notably patients with pre-biologic FEV₁ < 80% and patients with FEV₁ ≥ 80% (66% and 53%, respectively); never smokers and current/former smokers (63% and 50%, respectively); and patients with COPD and without COPD (58% and 52%, respectively).

The researchers also found a greater reduction in exacerbations among patients who switched from anti-IgE therapy to anti–IL-5/IL-5R/IL-4R therapy, compared with those who switched among anti–IL-5/IL-5R/IL-4R therapies (58% vs. 46%).

Patients who stopped or switched biologics appeared to have more severe or treatment-refractory disease than those with ongoing biologic use, the researchers noted. The most common reason for stopping or switching was worsening symptoms.

The study findings were limited by several factors, including the focus only on adults in the United States with subspecialist-treated SA, which may limit generalizability to children or other populations, the researchers noted. Other limitations included the variation in clinical decisions and insurance coverage and the inability to conduct longitudinal assessments, they said.

The results demonstrate that starting or switching biologics was consistently associated with fewer exacerbations in severe asthma. However, more research is needed to determine why some patients were not receiving biologics because they were not considered clinically eligible by their subspecialist health care providers, the researchers concluded.

The current study and the CHRONICLE study were supported by AstraZeneca. Lead author Dr. Panettieri disclosed serving on the advisory boards for and receiving grant support from AstraZeneca, Sanofi, Genentech, Regeneron, and Novartis.

Adults with severe asthma (SA) experienced significantly fewer exacerbations on biologic therapies, compared with those who did not use biologics, based on data from more than 2,000 individuals.

The development of biologics to target specific inflammatory pathways “has transformed the management of uncontrolled SA,” but data on the real-world use of biologics in severe asthma patients treated by subspecialists are limited, wrote Reynold A. Panettieri, Jr., MD, of Rutgers, State University of New Jersey, New Brunswick, and colleagues.

In a study published in the Annals of Allergy, Asthma & Immunology, the researchers reviewed data from CHRONICLE, an ongoing, prospective, real-world noninterventional study of adults aged 18 years and older with severe asthma in the United States.

The study population included 2,847 patients enrolled in the CHRONICLE study between February 2018 and February 2021; 68.8% were women, 74.6% were White. The patients ranged in age from 18 to 89 years, with a mean age of 54.2 years.

Biologic use was defined as patients who started or had ongoing use of biologics between 12 months before enrollment and the patient’s most recent data collection. Switches were defined as stopping one biologic and starting another within 6 months; stops were defined as discontinuing a biologic without switching to another within 6 months. A total of 66% of the patients were using biologics at the time of study enrollment. The most common biologic was omalizumab (47%), followed by benralizumab (27%), mepolizumab (26%), and dupilumab (18%).

Overall, 89% of the patients had ongoing biologic use, 16% had biologic switches, and 13% had stops.

Patients who started biologics or switched biologics had significant reductions in asthma exacerbations at 6 months, compared with nonbiologic users of 58% (1.80 vs. 0.76 per patient-year) and 49% (1.47 vs. 0.75 per patient-year), respectively (P < .001 for both). Asthma exacerbations declined by 70% among biologics users for whom data were available for 12 months before and 12 months after starting biologics.

Exacerbations decreased at 6 months after biologic initiation across all subgroups of patients, notably patients with pre-biologic FEV₁ < 80% and patients with FEV₁ ≥ 80% (66% and 53%, respectively); never smokers and current/former smokers (63% and 50%, respectively); and patients with COPD and without COPD (58% and 52%, respectively).

The researchers also found a greater reduction in exacerbations among patients who switched from anti-IgE therapy to anti–IL-5/IL-5R/IL-4R therapy, compared with those who switched among anti–IL-5/IL-5R/IL-4R therapies (58% vs. 46%).

Patients who stopped or switched biologics appeared to have more severe or treatment-refractory disease than those with ongoing biologic use, the researchers noted. The most common reason for stopping or switching was worsening symptoms.

The study findings were limited by several factors, including the focus only on adults in the United States with subspecialist-treated SA, which may limit generalizability to children or other populations, the researchers noted. Other limitations included the variation in clinical decisions and insurance coverage and the inability to conduct longitudinal assessments, they said.

The results demonstrate that starting or switching biologics was consistently associated with fewer exacerbations in severe asthma. However, more research is needed to determine why some patients were not receiving biologics because they were not considered clinically eligible by their subspecialist health care providers, the researchers concluded.

The current study and the CHRONICLE study were supported by AstraZeneca. Lead author Dr. Panettieri disclosed serving on the advisory boards for and receiving grant support from AstraZeneca, Sanofi, Genentech, Regeneron, and Novartis.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Young children with allergies may be more likely to develop attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) by the time they’re 18, according to a large retrospective study.

“Our study provides strong evidence for the association between allergic disorders in early childhood and the development of ADHD,” Shay Nemet, MD, of the Kaplan Medical Center, Rehovot, Israel, and colleagues write in Pediatric Allergy and Immunology. “The risk of those children to develop ASD was less significant.”

The researchers analyzed data from 117,022 consecutive children diagnosed with at least one allergic disorder – asthma, conjunctivitis, rhinitis, and drug, food, or skin allergy – and 116,968 children without allergies in the Clalit Health Services pediatric database. The children had been treated from 2000 to 2018; the mean follow-up period was 11 years.

The children who were diagnosed with one or more allergies (mean age, 4.5 years) were significantly more likely to develop ADHD (odds ratio, 2.45; 95% confidence interval, 2.39-2.51), ASD (OR, 1.17; 95% CI, 1.08-1.27), or both ADHD and ASD (OR, 1.56; 95% CI, 1.35-1.79) than were the control children who did not have allergies.

Children diagnosed with rhinitis (OR, 3.96; 95% CI, 3.80-4.12) and conjunctivitis (OR, 3.63; 95% CI, 3.53-3.74) were the most likely to develop ADHD.
 

Allergy correlation with ADHD and ASD

Cy B. Nadler, PhD, a clinical psychologist and the director of Autism Services at Children’s Mercy Kansas City, Missouri, told this news organization that children and adults with neurodevelopmental differences are also more likely to have other health problems.

“Clinicians practicing in subspecialties such as allergy and immunology may have opportunities to help psychologists identify developmental and behavioral concerns early in childhood,” he added.

“Studies like this can’t be accomplished without large health care databases, but this approach has drawbacks, too,” Dr. Nadler said in an email. “Without more information about these patients’ co-occurring medical and behavioral conditions, we are almost certainly missing important contributors to the observed associations.”

Dr. Nadler, who was not involved in the study, noted that in the multivariable analysis that controlled for age at study entry, gender, and number of annual visits, the link between allergy and ASD diagnosis was not significant.

“It is important to remember not to interpret these study results as causal,” he added.

Desha M. Jordan, MD, FAAP, an assistant professor of pediatrics at UPMC Children’s Hospital of Pittsburgh, called the study “an interesting new area that has been speculated about for some time” and “one of the first I have seen with statistically significant correlations found between ADHD, ASD, and allergic conditions.”
 

More questions for future studies

Health care providers need to understand the potential sequelae of allergic conditions so that they can manage their patients appropriately, she advised.

Although symptoms and diagnoses were confirmed for all patients, the study’s retrospective design and the possibility of recall bias were limitations, said Dr. Jordan in an email. She also was not involved in the study.

“For example, the family of a child diagnosed with ADHD or ASD may have been more mindful of anything out of the norm in that child’s past, while the family of a child without these conditions may not have recalled allergic symptoms as important,” she explained.

Another question that arises is whether some patients were treated and managed well while others were not and whether this disparity in care affected the development or severity of ADHD or ASD, she added.

“Is a patient with a well-controlled allergic condition less likely to develop ADHD or ASD than a patient with an uncontrolled allergic condition? Does a well-controlled patient ever return to the same probability of getting ADHD or ASD as a nonallergic patient?”

“While this study expands our understanding of these conditions and their interrelationships, it also brings up many additional questions and opens a new segment of research,” Dr. Jordan said. “More studies in this area are necessary to confirm the findings of this paper.”

The study was partially funded by the Israel Ambulatory Pediatric Association. The authors, Dr. Nadler, and Dr. Jordan report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Young children with allergies may be more likely to develop attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) by the time they’re 18, according to a large retrospective study.

“Our study provides strong evidence for the association between allergic disorders in early childhood and the development of ADHD,” Shay Nemet, MD, of the Kaplan Medical Center, Rehovot, Israel, and colleagues write in Pediatric Allergy and Immunology. “The risk of those children to develop ASD was less significant.”

The researchers analyzed data from 117,022 consecutive children diagnosed with at least one allergic disorder – asthma, conjunctivitis, rhinitis, and drug, food, or skin allergy – and 116,968 children without allergies in the Clalit Health Services pediatric database. The children had been treated from 2000 to 2018; the mean follow-up period was 11 years.

The children who were diagnosed with one or more allergies (mean age, 4.5 years) were significantly more likely to develop ADHD (odds ratio, 2.45; 95% confidence interval, 2.39-2.51), ASD (OR, 1.17; 95% CI, 1.08-1.27), or both ADHD and ASD (OR, 1.56; 95% CI, 1.35-1.79) than were the control children who did not have allergies.

Children diagnosed with rhinitis (OR, 3.96; 95% CI, 3.80-4.12) and conjunctivitis (OR, 3.63; 95% CI, 3.53-3.74) were the most likely to develop ADHD.
 

Allergy correlation with ADHD and ASD

Cy B. Nadler, PhD, a clinical psychologist and the director of Autism Services at Children’s Mercy Kansas City, Missouri, told this news organization that children and adults with neurodevelopmental differences are also more likely to have other health problems.

“Clinicians practicing in subspecialties such as allergy and immunology may have opportunities to help psychologists identify developmental and behavioral concerns early in childhood,” he added.

“Studies like this can’t be accomplished without large health care databases, but this approach has drawbacks, too,” Dr. Nadler said in an email. “Without more information about these patients’ co-occurring medical and behavioral conditions, we are almost certainly missing important contributors to the observed associations.”

Dr. Nadler, who was not involved in the study, noted that in the multivariable analysis that controlled for age at study entry, gender, and number of annual visits, the link between allergy and ASD diagnosis was not significant.

“It is important to remember not to interpret these study results as causal,” he added.

Desha M. Jordan, MD, FAAP, an assistant professor of pediatrics at UPMC Children’s Hospital of Pittsburgh, called the study “an interesting new area that has been speculated about for some time” and “one of the first I have seen with statistically significant correlations found between ADHD, ASD, and allergic conditions.”
 

More questions for future studies

Health care providers need to understand the potential sequelae of allergic conditions so that they can manage their patients appropriately, she advised.

Although symptoms and diagnoses were confirmed for all patients, the study’s retrospective design and the possibility of recall bias were limitations, said Dr. Jordan in an email. She also was not involved in the study.

“For example, the family of a child diagnosed with ADHD or ASD may have been more mindful of anything out of the norm in that child’s past, while the family of a child without these conditions may not have recalled allergic symptoms as important,” she explained.

Another question that arises is whether some patients were treated and managed well while others were not and whether this disparity in care affected the development or severity of ADHD or ASD, she added.

“Is a patient with a well-controlled allergic condition less likely to develop ADHD or ASD than a patient with an uncontrolled allergic condition? Does a well-controlled patient ever return to the same probability of getting ADHD or ASD as a nonallergic patient?”

“While this study expands our understanding of these conditions and their interrelationships, it also brings up many additional questions and opens a new segment of research,” Dr. Jordan said. “More studies in this area are necessary to confirm the findings of this paper.”

The study was partially funded by the Israel Ambulatory Pediatric Association. The authors, Dr. Nadler, and Dr. Jordan report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Young children with allergies may be more likely to develop attention-deficit/hyperactivity disorder and autism spectrum disorder (ASD) by the time they’re 18, according to a large retrospective study.

“Our study provides strong evidence for the association between allergic disorders in early childhood and the development of ADHD,” Shay Nemet, MD, of the Kaplan Medical Center, Rehovot, Israel, and colleagues write in Pediatric Allergy and Immunology. “The risk of those children to develop ASD was less significant.”

The researchers analyzed data from 117,022 consecutive children diagnosed with at least one allergic disorder – asthma, conjunctivitis, rhinitis, and drug, food, or skin allergy – and 116,968 children without allergies in the Clalit Health Services pediatric database. The children had been treated from 2000 to 2018; the mean follow-up period was 11 years.

The children who were diagnosed with one or more allergies (mean age, 4.5 years) were significantly more likely to develop ADHD (odds ratio, 2.45; 95% confidence interval, 2.39-2.51), ASD (OR, 1.17; 95% CI, 1.08-1.27), or both ADHD and ASD (OR, 1.56; 95% CI, 1.35-1.79) than were the control children who did not have allergies.

Children diagnosed with rhinitis (OR, 3.96; 95% CI, 3.80-4.12) and conjunctivitis (OR, 3.63; 95% CI, 3.53-3.74) were the most likely to develop ADHD.
 

Allergy correlation with ADHD and ASD

Cy B. Nadler, PhD, a clinical psychologist and the director of Autism Services at Children’s Mercy Kansas City, Missouri, told this news organization that children and adults with neurodevelopmental differences are also more likely to have other health problems.

“Clinicians practicing in subspecialties such as allergy and immunology may have opportunities to help psychologists identify developmental and behavioral concerns early in childhood,” he added.

“Studies like this can’t be accomplished without large health care databases, but this approach has drawbacks, too,” Dr. Nadler said in an email. “Without more information about these patients’ co-occurring medical and behavioral conditions, we are almost certainly missing important contributors to the observed associations.”

Dr. Nadler, who was not involved in the study, noted that in the multivariable analysis that controlled for age at study entry, gender, and number of annual visits, the link between allergy and ASD diagnosis was not significant.

“It is important to remember not to interpret these study results as causal,” he added.

Desha M. Jordan, MD, FAAP, an assistant professor of pediatrics at UPMC Children’s Hospital of Pittsburgh, called the study “an interesting new area that has been speculated about for some time” and “one of the first I have seen with statistically significant correlations found between ADHD, ASD, and allergic conditions.”
 

More questions for future studies

Health care providers need to understand the potential sequelae of allergic conditions so that they can manage their patients appropriately, she advised.

Although symptoms and diagnoses were confirmed for all patients, the study’s retrospective design and the possibility of recall bias were limitations, said Dr. Jordan in an email. She also was not involved in the study.

“For example, the family of a child diagnosed with ADHD or ASD may have been more mindful of anything out of the norm in that child’s past, while the family of a child without these conditions may not have recalled allergic symptoms as important,” she explained.

Another question that arises is whether some patients were treated and managed well while others were not and whether this disparity in care affected the development or severity of ADHD or ASD, she added.

“Is a patient with a well-controlled allergic condition less likely to develop ADHD or ASD than a patient with an uncontrolled allergic condition? Does a well-controlled patient ever return to the same probability of getting ADHD or ASD as a nonallergic patient?”

“While this study expands our understanding of these conditions and their interrelationships, it also brings up many additional questions and opens a new segment of research,” Dr. Jordan said. “More studies in this area are necessary to confirm the findings of this paper.”

The study was partially funded by the Israel Ambulatory Pediatric Association. The authors, Dr. Nadler, and Dr. Jordan report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

In an online statement the U.S. Centers for Disease Control and Prevention announced its decision to recommend higher-dose and adjuvanted influenza vaccines for people aged 65 years or older. Fluzone High-Dose Quadrivalent, Flublok Quadrivalent, and Fluad Quadrivalent flu vaccines are among those specified in the release.

The organization says that these higher-dose vaccines may be more effective for the aging population, who often have difficulty mounting a strong enough immune response to protect themselves against the flu virus. People older than 65 years struggle the most during flu season and have the highest proportion of hospitalizations and deaths from flu, according to the release.

But the CDC believes that higher-dose vaccines have the potential to better protect against that danger. One study, from The New England Journal of Medicine, reported that high-dose/adjuvanted vaccines prevented flu in older patients 24% better than did lower-dose/nonadjuvanted vaccines.

These types of vaccines work by creating a larger immune response than a standard vaccine dose. In particular, adjuvanted vaccines contain an extra ingredient within them that helps the immune system produce a stronger reaction to the vaccine. These may be things like aluminum salts, which signal the body to respond faster. Higher-dose vaccines similarly promote a stronger immune response by having more particles of the target virus in their mixture. In theory, this means the body will create an enhanced response to the vaccine. For example, a higher-dose vaccine may quadruple the amount of antigens, compared with the standard dose.

The hope is that this recommendation may increase vaccine use across the board, says José Romero, MD, the director of the CDC’s National Center for Immunization and Respiratory Diseases. As quoted in the CDC announcement, Dr. Romero said that this may help reduce racial inequities in access to flu vaccines. A 2019 meta-analysis concluded that Black and Hispanic people are around 30%-40% less likely to get the flu vaccine. So increasing the access to this medication “could help reduce health disparities by making these vaccines more available to racial and ethnic minority groups,” said Dr. Romero.

The decision, spearheaded by CDC Director Rochelle Walensky, MD, follows recommendations from the Advisory Committee on Immunization Practices, which presented on this topic during a June 22 meeting. It is now part of official CDC policy and will continue to be developed as the 2022-2023 flu season approaches.

In addition, the organization says they’ll reveal more details for their plan later this summer, in their Morbidity and Mortality Weekly Report (MMWR). For now, seniors should know that they should try to get the recommended high-dose vaccines, but if they can’t, then a standard dose of whatever their provider has on hand will do.

At this point, there is still no specific vaccine recommendation for people aged under 65 years. The CDC historically avoids specifying one type of vaccine over another and says each should still be effective in younger patients.

A version of this article first appeared on Medscape.com.

In an online statement the U.S. Centers for Disease Control and Prevention announced its decision to recommend higher-dose and adjuvanted influenza vaccines for people aged 65 years or older. Fluzone High-Dose Quadrivalent, Flublok Quadrivalent, and Fluad Quadrivalent flu vaccines are among those specified in the release.

The organization says that these higher-dose vaccines may be more effective for the aging population, who often have difficulty mounting a strong enough immune response to protect themselves against the flu virus. People older than 65 years struggle the most during flu season and have the highest proportion of hospitalizations and deaths from flu, according to the release.

But the CDC believes that higher-dose vaccines have the potential to better protect against that danger. One study, from The New England Journal of Medicine, reported that high-dose/adjuvanted vaccines prevented flu in older patients 24% better than did lower-dose/nonadjuvanted vaccines.

These types of vaccines work by creating a larger immune response than a standard vaccine dose. In particular, adjuvanted vaccines contain an extra ingredient within them that helps the immune system produce a stronger reaction to the vaccine. These may be things like aluminum salts, which signal the body to respond faster. Higher-dose vaccines similarly promote a stronger immune response by having more particles of the target virus in their mixture. In theory, this means the body will create an enhanced response to the vaccine. For example, a higher-dose vaccine may quadruple the amount of antigens, compared with the standard dose.

The hope is that this recommendation may increase vaccine use across the board, says José Romero, MD, the director of the CDC’s National Center for Immunization and Respiratory Diseases. As quoted in the CDC announcement, Dr. Romero said that this may help reduce racial inequities in access to flu vaccines. A 2019 meta-analysis concluded that Black and Hispanic people are around 30%-40% less likely to get the flu vaccine. So increasing the access to this medication “could help reduce health disparities by making these vaccines more available to racial and ethnic minority groups,” said Dr. Romero.

The decision, spearheaded by CDC Director Rochelle Walensky, MD, follows recommendations from the Advisory Committee on Immunization Practices, which presented on this topic during a June 22 meeting. It is now part of official CDC policy and will continue to be developed as the 2022-2023 flu season approaches.

In addition, the organization says they’ll reveal more details for their plan later this summer, in their Morbidity and Mortality Weekly Report (MMWR). For now, seniors should know that they should try to get the recommended high-dose vaccines, but if they can’t, then a standard dose of whatever their provider has on hand will do.

At this point, there is still no specific vaccine recommendation for people aged under 65 years. The CDC historically avoids specifying one type of vaccine over another and says each should still be effective in younger patients.

A version of this article first appeared on Medscape.com.

In an online statement the U.S. Centers for Disease Control and Prevention announced its decision to recommend higher-dose and adjuvanted influenza vaccines for people aged 65 years or older. Fluzone High-Dose Quadrivalent, Flublok Quadrivalent, and Fluad Quadrivalent flu vaccines are among those specified in the release.

The organization says that these higher-dose vaccines may be more effective for the aging population, who often have difficulty mounting a strong enough immune response to protect themselves against the flu virus. People older than 65 years struggle the most during flu season and have the highest proportion of hospitalizations and deaths from flu, according to the release.

But the CDC believes that higher-dose vaccines have the potential to better protect against that danger. One study, from The New England Journal of Medicine, reported that high-dose/adjuvanted vaccines prevented flu in older patients 24% better than did lower-dose/nonadjuvanted vaccines.

These types of vaccines work by creating a larger immune response than a standard vaccine dose. In particular, adjuvanted vaccines contain an extra ingredient within them that helps the immune system produce a stronger reaction to the vaccine. These may be things like aluminum salts, which signal the body to respond faster. Higher-dose vaccines similarly promote a stronger immune response by having more particles of the target virus in their mixture. In theory, this means the body will create an enhanced response to the vaccine. For example, a higher-dose vaccine may quadruple the amount of antigens, compared with the standard dose.

The hope is that this recommendation may increase vaccine use across the board, says José Romero, MD, the director of the CDC’s National Center for Immunization and Respiratory Diseases. As quoted in the CDC announcement, Dr. Romero said that this may help reduce racial inequities in access to flu vaccines. A 2019 meta-analysis concluded that Black and Hispanic people are around 30%-40% less likely to get the flu vaccine. So increasing the access to this medication “could help reduce health disparities by making these vaccines more available to racial and ethnic minority groups,” said Dr. Romero.

The decision, spearheaded by CDC Director Rochelle Walensky, MD, follows recommendations from the Advisory Committee on Immunization Practices, which presented on this topic during a June 22 meeting. It is now part of official CDC policy and will continue to be developed as the 2022-2023 flu season approaches.

In addition, the organization says they’ll reveal more details for their plan later this summer, in their Morbidity and Mortality Weekly Report (MMWR). For now, seniors should know that they should try to get the recommended high-dose vaccines, but if they can’t, then a standard dose of whatever their provider has on hand will do.

At this point, there is still no specific vaccine recommendation for people aged under 65 years. The CDC historically avoids specifying one type of vaccine over another and says each should still be effective in younger patients.

A version of this article first appeared on Medscape.com.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

Air pollution levels mediated the impact of temperature on oxygen saturation in adults with chronic obstructive pulmonary disease (COPD) based on data from 117 individuals.

COPD is attributed to environmental factors including air pollution, and air pollution has been linked to increased risk of hospitalization and mortality because of acute COPD exacerbation, wrote Huan Minh Tran, PhD, of Taipei (Taiwan) Medical University and colleagues. However, the effects of air pollution on climate-associated health outcomes in COPD have not been explored, they said.

In a study published in Science of The Total Environment the researchers identified 117 adult COPD patients at a single center in Taiwan. They measured lung function, 6-minute walking distance, oxygen desaturation, white blood cell count, and percent emphysema (defined as low attenuation area [LAA]) and linked them to 0- to 1-year, 0- to 3-year, and 0- to 5-year lags in exposures to relative humidity (RH), temperature, and air pollution. The mean age of the participants was 72.9 years; 93% were men.

Pollution was defined in terms of fine particulate matter (PM2.5).

Overall, an increase in RH by 1% was associated with increases in forced expiratory volume in 1 second (FEV₁), eosinophils, and lymphocytes.

A 1% increase in RH also was associated with a decrease in the total-lobe LAA.

As for temperature, an increase of 1° C was associated with decreased oxygen desaturation and with decreases in right-, left-, and upper-lobe LAA values.

When the researchers examined the impact of pollution, they found that a 1 mcg/m³ increase in PM2.5 was associated with a decrease in the FEV₁ as well as with an increase in oxygen desaturation. A 1 mcg/m³ increase in PM10 and PM2.5 was associated with increases in the total-, right-, left, and upper-lobe LAA; increases in lower-lobe LAA were associated with an increase in PM2.5 only.

“This is reasonable because PM2.5 can travel and deposit in distal parts of the lung, while PM10 is preferably deposited in the larger airways of the upper lung regions,” the researchers wrote in their discussion.

A one part per billion increase in nitrogen dioxide (NO₂) was associated with decreased FEV₁ and increased upper-lobe LAA.

“We observed that NO₂ fully mediated the association between RH and FEV₁, while PM2.5 fully mediated associations of temperature with oxygen saturation and emphysema severity in COPD patients,” the researchers added.

The study findings were limited by several factors including the relatively small and homogeneous male, Taiwanese population, which may limit generalizability, the researchers noted. Other limitations included the lack of control for factors such as body mass index, occupational exposure, comorbidities, medication use, and indoor air pollution, they said.

However, the results suggest that air pollution could have an effect on the established associations between climate and adverse health outcomes in COPD, and more research is needed. Climate change–related air pollution is an important public health issue, especially with regards to respiratory disease,” they concluded.

The study was supported by the Ministry of Science and Technology of Taiwan. The researchers had no financial conflicts to disclose.

When asthma patients are having frequent clinical deteriorations, clinicians need to evaluate them for the presence and severity of bronchiectasis, according to the authors of a retrospective study in the Journal of Allergy and Clinical Immunology: In Practice. While bronchiectasis is known to worsen the clinical and functional outcomes in patients with asthma, data regarding the long-term effects of bronchiectasis on the clinical course of asthma have been limited, stated corresponding author Jung-Kyu Lee, MD, division of pulmonary and critical care medicine, Seoul (Republic of Korea) Metropolitan Government – Seoul National University.

Moderate to severe acute clinical deterioration risks were increased among the 251 patients (mean age 66.6 years, 77.2% men) with bronchiectasis out of 667 asthma patients included in the study. All studied patients underwent chest computed tomography and pulmonary function tests from 2013 to 2019 at two tertiary hospitals in Seoul. The primary outcome, annual incidence of moderate to severe acute exacerbations requiring additional treatment (systemic steroids, antibiotics, or both), was significantly higher in patients with bronchiectasis after a mean follow-up period of 3.96 years. Compared with patients who did not exhibit bronchiectasis, the annual rates of severe exacerbations (0.15 ± 0.43 vs. 0.08 ± 0.27; P = .010), moderate to severe (0.47 ± 0.79 vs. 0.34 ± 0.63; P = .018), and acute exacerbations during the follow-up period (49.8% vs. 39.4%; P = .009) were all significantly higher. There was no difference in the proportion of frequent exacerbators between the two groups, however. Severe acute exacerbations leading to hospitalizations, also, were more frequent in the group with bronchiectasis.
 

Risk factors explored

Significant factors conferring greater risk of severe and moderate to severe acute exacerbations in multivariable analysis included low body mass index, low baseline forced expiratory volume in 1 second (FEV₁), high use of inhaled corticosteroids, high medication possession, and high neutrophil/lymphocyte ratios. The existence of bronchiectasis remained an independent risk factor for severe and moderate to severe acute exacerbations despite adjustment for all other factors. While bronchiectasis score showed no association with annual rate of acute exacerbation, progression of bronchiectasis confirmed on follow-up CT was associated with increased risks of severe and moderate to severe acute exacerbation.

Included patients had a diagnosis of asthma confirmed by variable expiratory airflow limitation with pulmonary function tests (that is, positive bronchodilator response, positive bronchial provocation test, or excessive variation in lung function between visits). Past histories of tuberculosis and nontuberculous mycobacterial lung disease, lower absolute and predicted values of both baseline FEV₁ and forced vital capacity were more common among patients with bronchiectasis.

Dividing the study population into a group that had at least one moderate to severe acute exacerbation during the follow-up period and a group that did not, the researchers identified characteristics shared by exacerbators: a greater proportion were women, they had lower forced vital capacity and lung-diffusing capacity for carbon monoxide, higher blood FVC and blood neutrophil/lymphocyte ratio, and more medication use (inhaled corticosteroids, long-acting antimuscarinic agent, leukotriene-receptor antagonist, and methylxanthine), compared with the nonexacerbators. More bronchiectasis, more severe bronchiectasis (higher bronchiectasis score), and more progression of bronchiectasis were common among the exacerbators.

Higher acute exacerbation risks accompanied bronchiectasis, at 1.47-fold for moderate, 1.72-fold for severe, and 1.50-fold for moderate to severe exacerbations. Higher risk for severe and moderate to severe exacerbations was conferred by bronchiectasis progression, also.

The researchers pointed to contradictory effects of inhaled corticosteroid use, noting both corticosteroids’ essential role in controlling airway inflammation and hyperresponsiveness, exacerbations, and lung-function decline in asthma patients and that longer or greater inhaled corticosteroid use is associated with both clinical deterioration in asthma and bronchiectasis, and exacerbation history. For bronchiectasis, however, inhaled corticosteroid use offers no benefit while increasing susceptibility to infection and its risks through partial immunosuppression.

“Considering these contradictory effects of inhaled corticosteroid use, further research is needed regarding its risks and benefits in asthma patients with bronchiectasis, including differences in the benefit of inhaled corticosteroid use according to patient phenotype,” Dr. Kim and his colleagues concluded.
 

The role of corticosteroids

“One of the more important points discussed in this observational cohort study is the role of inhaled corticosteroid use in bronchiectasis,” said Mary Jo Farmer, MD, PhD, director of pulmonary hypertension services, Baystate Health, and assistant professor of medicine, University of Massachusetts – Baystate, both in Springfield, in an interview with this news organization. She cited a review finding no significant benefit versus placebo in spirometry, exacerbation rate, or sputum volume in the Cochrane Database of Systematic Reviews and another suggesting that quality of life was improved with inhaled corticosteroid use in individuals with blood eosinophils greater than 3%, compared with those not using inhaled corticosteroids or having lower eosinophil counts in the European Respiratory Journal. She cited also higher percentages (48% versus 23%) of adrenal insufficiency in bronchiectasis patients among those taking inhaled corticosteroids versus those not taking them.

Dr. Farmer added, “According to the 2018 Cochrane review of inhaled corticosteroid treatment for non–cystic fibrosis bronchiectasis, results from most randomized, placebo-controlled trials have been disappointing in terms of effects on most endpoints such as pulmonary function and exacerbation frequency. As such, the European Respiratory Society guidelines for the management of adult bronchiectasis advise against prescribing inhaled corticosteroids to patients with bronchiectasis, unless otherwise indicated by either an asthma or chronic obstructive pulmonary disease diagnosis. Also, inhaled corticosteroid treatment in asthma and COPD is associated with common side effects such as oral candidiasis, dysphonia and, in some cases, systemic corticosteroid effects. The rate of adverse events from inhaled corticosteroid treatment of bronchiectasis, however, is largely unknown.Dr. Lee and Dr. Farmer reported no relevant financial relationships. The study was independently supported.

When asthma patients are having frequent clinical deteriorations, clinicians need to evaluate them for the presence and severity of bronchiectasis, according to the authors of a retrospective study in the Journal of Allergy and Clinical Immunology: In Practice. While bronchiectasis is known to worsen the clinical and functional outcomes in patients with asthma, data regarding the long-term effects of bronchiectasis on the clinical course of asthma have been limited, stated corresponding author Jung-Kyu Lee, MD, division of pulmonary and critical care medicine, Seoul (Republic of Korea) Metropolitan Government – Seoul National University.

Moderate to severe acute clinical deterioration risks were increased among the 251 patients (mean age 66.6 years, 77.2% men) with bronchiectasis out of 667 asthma patients included in the study. All studied patients underwent chest computed tomography and pulmonary function tests from 2013 to 2019 at two tertiary hospitals in Seoul. The primary outcome, annual incidence of moderate to severe acute exacerbations requiring additional treatment (systemic steroids, antibiotics, or both), was significantly higher in patients with bronchiectasis after a mean follow-up period of 3.96 years. Compared with patients who did not exhibit bronchiectasis, the annual rates of severe exacerbations (0.15 ± 0.43 vs. 0.08 ± 0.27; P = .010), moderate to severe (0.47 ± 0.79 vs. 0.34 ± 0.63; P = .018), and acute exacerbations during the follow-up period (49.8% vs. 39.4%; P = .009) were all significantly higher. There was no difference in the proportion of frequent exacerbators between the two groups, however. Severe acute exacerbations leading to hospitalizations, also, were more frequent in the group with bronchiectasis.
 

Risk factors explored

Significant factors conferring greater risk of severe and moderate to severe acute exacerbations in multivariable analysis included low body mass index, low baseline forced expiratory volume in 1 second (FEV₁), high use of inhaled corticosteroids, high medication possession, and high neutrophil/lymphocyte ratios. The existence of bronchiectasis remained an independent risk factor for severe and moderate to severe acute exacerbations despite adjustment for all other factors. While bronchiectasis score showed no association with annual rate of acute exacerbation, progression of bronchiectasis confirmed on follow-up CT was associated with increased risks of severe and moderate to severe acute exacerbation.

Included patients had a diagnosis of asthma confirmed by variable expiratory airflow limitation with pulmonary function tests (that is, positive bronchodilator response, positive bronchial provocation test, or excessive variation in lung function between visits). Past histories of tuberculosis and nontuberculous mycobacterial lung disease, lower absolute and predicted values of both baseline FEV₁ and forced vital capacity were more common among patients with bronchiectasis.

Dividing the study population into a group that had at least one moderate to severe acute exacerbation during the follow-up period and a group that did not, the researchers identified characteristics shared by exacerbators: a greater proportion were women, they had lower forced vital capacity and lung-diffusing capacity for carbon monoxide, higher blood FVC and blood neutrophil/lymphocyte ratio, and more medication use (inhaled corticosteroids, long-acting antimuscarinic agent, leukotriene-receptor antagonist, and methylxanthine), compared with the nonexacerbators. More bronchiectasis, more severe bronchiectasis (higher bronchiectasis score), and more progression of bronchiectasis were common among the exacerbators.

Higher acute exacerbation risks accompanied bronchiectasis, at 1.47-fold for moderate, 1.72-fold for severe, and 1.50-fold for moderate to severe exacerbations. Higher risk for severe and moderate to severe exacerbations was conferred by bronchiectasis progression, also.

The researchers pointed to contradictory effects of inhaled corticosteroid use, noting both corticosteroids’ essential role in controlling airway inflammation and hyperresponsiveness, exacerbations, and lung-function decline in asthma patients and that longer or greater inhaled corticosteroid use is associated with both clinical deterioration in asthma and bronchiectasis, and exacerbation history. For bronchiectasis, however, inhaled corticosteroid use offers no benefit while increasing susceptibility to infection and its risks through partial immunosuppression.

“Considering these contradictory effects of inhaled corticosteroid use, further research is needed regarding its risks and benefits in asthma patients with bronchiectasis, including differences in the benefit of inhaled corticosteroid use according to patient phenotype,” Dr. Kim and his colleagues concluded.
 

The role of corticosteroids

“One of the more important points discussed in this observational cohort study is the role of inhaled corticosteroid use in bronchiectasis,” said Mary Jo Farmer, MD, PhD, director of pulmonary hypertension services, Baystate Health, and assistant professor of medicine, University of Massachusetts – Baystate, both in Springfield, in an interview with this news organization. She cited a review finding no significant benefit versus placebo in spirometry, exacerbation rate, or sputum volume in the Cochrane Database of Systematic Reviews and another suggesting that quality of life was improved with inhaled corticosteroid use in individuals with blood eosinophils greater than 3%, compared with those not using inhaled corticosteroids or having lower eosinophil counts in the European Respiratory Journal. She cited also higher percentages (48% versus 23%) of adrenal insufficiency in bronchiectasis patients among those taking inhaled corticosteroids versus those not taking them.

Dr. Farmer added, “According to the 2018 Cochrane review of inhaled corticosteroid treatment for non–cystic fibrosis bronchiectasis, results from most randomized, placebo-controlled trials have been disappointing in terms of effects on most endpoints such as pulmonary function and exacerbation frequency. As such, the European Respiratory Society guidelines for the management of adult bronchiectasis advise against prescribing inhaled corticosteroids to patients with bronchiectasis, unless otherwise indicated by either an asthma or chronic obstructive pulmonary disease diagnosis. Also, inhaled corticosteroid treatment in asthma and COPD is associated with common side effects such as oral candidiasis, dysphonia and, in some cases, systemic corticosteroid effects. The rate of adverse events from inhaled corticosteroid treatment of bronchiectasis, however, is largely unknown.Dr. Lee and Dr. Farmer reported no relevant financial relationships. The study was independently supported.

When asthma patients are having frequent clinical deteriorations, clinicians need to evaluate them for the presence and severity of bronchiectasis, according to the authors of a retrospective study in the Journal of Allergy and Clinical Immunology: In Practice. While bronchiectasis is known to worsen the clinical and functional outcomes in patients with asthma, data regarding the long-term effects of bronchiectasis on the clinical course of asthma have been limited, stated corresponding author Jung-Kyu Lee, MD, division of pulmonary and critical care medicine, Seoul (Republic of Korea) Metropolitan Government – Seoul National University.

Moderate to severe acute clinical deterioration risks were increased among the 251 patients (mean age 66.6 years, 77.2% men) with bronchiectasis out of 667 asthma patients included in the study. All studied patients underwent chest computed tomography and pulmonary function tests from 2013 to 2019 at two tertiary hospitals in Seoul. The primary outcome, annual incidence of moderate to severe acute exacerbations requiring additional treatment (systemic steroids, antibiotics, or both), was significantly higher in patients with bronchiectasis after a mean follow-up period of 3.96 years. Compared with patients who did not exhibit bronchiectasis, the annual rates of severe exacerbations (0.15 ± 0.43 vs. 0.08 ± 0.27; P = .010), moderate to severe (0.47 ± 0.79 vs. 0.34 ± 0.63; P = .018), and acute exacerbations during the follow-up period (49.8% vs. 39.4%; P = .009) were all significantly higher. There was no difference in the proportion of frequent exacerbators between the two groups, however. Severe acute exacerbations leading to hospitalizations, also, were more frequent in the group with bronchiectasis.
 

Risk factors explored

Significant factors conferring greater risk of severe and moderate to severe acute exacerbations in multivariable analysis included low body mass index, low baseline forced expiratory volume in 1 second (FEV₁), high use of inhaled corticosteroids, high medication possession, and high neutrophil/lymphocyte ratios. The existence of bronchiectasis remained an independent risk factor for severe and moderate to severe acute exacerbations despite adjustment for all other factors. While bronchiectasis score showed no association with annual rate of acute exacerbation, progression of bronchiectasis confirmed on follow-up CT was associated with increased risks of severe and moderate to severe acute exacerbation.

Included patients had a diagnosis of asthma confirmed by variable expiratory airflow limitation with pulmonary function tests (that is, positive bronchodilator response, positive bronchial provocation test, or excessive variation in lung function between visits). Past histories of tuberculosis and nontuberculous mycobacterial lung disease, lower absolute and predicted values of both baseline FEV₁ and forced vital capacity were more common among patients with bronchiectasis.

Dividing the study population into a group that had at least one moderate to severe acute exacerbation during the follow-up period and a group that did not, the researchers identified characteristics shared by exacerbators: a greater proportion were women, they had lower forced vital capacity and lung-diffusing capacity for carbon monoxide, higher blood FVC and blood neutrophil/lymphocyte ratio, and more medication use (inhaled corticosteroids, long-acting antimuscarinic agent, leukotriene-receptor antagonist, and methylxanthine), compared with the nonexacerbators. More bronchiectasis, more severe bronchiectasis (higher bronchiectasis score), and more progression of bronchiectasis were common among the exacerbators.

Higher acute exacerbation risks accompanied bronchiectasis, at 1.47-fold for moderate, 1.72-fold for severe, and 1.50-fold for moderate to severe exacerbations. Higher risk for severe and moderate to severe exacerbations was conferred by bronchiectasis progression, also.

The researchers pointed to contradictory effects of inhaled corticosteroid use, noting both corticosteroids’ essential role in controlling airway inflammation and hyperresponsiveness, exacerbations, and lung-function decline in asthma patients and that longer or greater inhaled corticosteroid use is associated with both clinical deterioration in asthma and bronchiectasis, and exacerbation history. For bronchiectasis, however, inhaled corticosteroid use offers no benefit while increasing susceptibility to infection and its risks through partial immunosuppression.

“Considering these contradictory effects of inhaled corticosteroid use, further research is needed regarding its risks and benefits in asthma patients with bronchiectasis, including differences in the benefit of inhaled corticosteroid use according to patient phenotype,” Dr. Kim and his colleagues concluded.
 

The role of corticosteroids

“One of the more important points discussed in this observational cohort study is the role of inhaled corticosteroid use in bronchiectasis,” said Mary Jo Farmer, MD, PhD, director of pulmonary hypertension services, Baystate Health, and assistant professor of medicine, University of Massachusetts – Baystate, both in Springfield, in an interview with this news organization. She cited a review finding no significant benefit versus placebo in spirometry, exacerbation rate, or sputum volume in the Cochrane Database of Systematic Reviews and another suggesting that quality of life was improved with inhaled corticosteroid use in individuals with blood eosinophils greater than 3%, compared with those not using inhaled corticosteroids or having lower eosinophil counts in the European Respiratory Journal. She cited also higher percentages (48% versus 23%) of adrenal insufficiency in bronchiectasis patients among those taking inhaled corticosteroids versus those not taking them.

Dr. Farmer added, “According to the 2018 Cochrane review of inhaled corticosteroid treatment for non–cystic fibrosis bronchiectasis, results from most randomized, placebo-controlled trials have been disappointing in terms of effects on most endpoints such as pulmonary function and exacerbation frequency. As such, the European Respiratory Society guidelines for the management of adult bronchiectasis advise against prescribing inhaled corticosteroids to patients with bronchiectasis, unless otherwise indicated by either an asthma or chronic obstructive pulmonary disease diagnosis. Also, inhaled corticosteroid treatment in asthma and COPD is associated with common side effects such as oral candidiasis, dysphonia and, in some cases, systemic corticosteroid effects. The rate of adverse events from inhaled corticosteroid treatment of bronchiectasis, however, is largely unknown.Dr. Lee and Dr. Farmer reported no relevant financial relationships. The study was independently supported.

Acute exacerbations (AEs) are both common in rheumatoid arthritis–associated interstitial lung disease (RA-ILD) and are a frequent cause of imminent mortality, a retrospective Japanese study suggests.

The same is also true for patients with idiopathic pulmonary fibrosis (IPF) for whom an AE is the most frequent cause of death as well, the same comparative study indicates.

“Several studies have reported that acute exacerbation, which occurs during the clinical course of idiopathic pulmonary fibrosis (IPF), also occurs in rheumatoid arthritis–associated interstitial lung disease (RA-ILD),” lead author Junji Otsuka, MD, PhD, of the National Hospital Organization Omuta National Hospital, Fukuoka, Japan, and colleagues observed.

“[We found that] AE was not uncommon in RA-ILD or IPF ... but the prognosis after AE of RA-ILD was significantly better than that of IPF [even though] the most frequent cause of death in RA-ILD and IPF was AE,” they stated.

The study was published online in Respiratory Medicine.

Patient features

The study involved 149 RA-ILD patients with a median age of 72 years at RA onset. The median time from ILD diagnosis to onset of AE was 48.5 months, while the median survival time after the onset of AE was 196 days (range 1-3,463 days), as the authors detailed. “All patients were treated with corticosteroids,” the authors noted, and almost all of them were treated with steroid pulse therapy.

Noninvasive positive pressure ventilation (NPPV) was used to maintain oxygenation in 18.5% of patients with severe respiratory failure, while invasive positive pressure ventilation (IPPV) was used in almost 26% of patients with the same degree of respiratory failure. Features of patients who developed an AE were then compared with those who did not.

Interestingly, no significant differences in clinical parameters were seen between those who developed an AE and those who did not. Nor were there any significant differences between the 2 groups in the length of time from the ILD diagnosis to the development of an AE. Some 18% of RA-ILD patients developed an AE, as did over 27% of patients with IPF, investigators report.

The median survival after RA-ILD patients developed an AE was 277 days, compared with only 60 days for those with IPF (P = .038). In a multivariable analysis, hypoalbuminemia at an odds ratio of .090 (95% confidence interval, 0.011-0.733; P = .012) as well as percent carbon monoxide diffusion capacity at an OR of .810 (95% CI, 0.814-0.964; P < .01) were both independent risk factors for the development of an AE, the investigators pointed out.

The best cut-off level for predicting the risk of an AE was 3.0 g/dL (95% CI, 0.011-0.733; P = .012) for serum albumin and 53% (95% CI, 0.814-0.964; P < .01) for carbon monoxide diffusion capacity. As Dr. Otsuka noted in an email to this news organization, low serum albumin likely correlates with a generally poor condition, while low carbon monoxide diffusion capacity is likely due to lung fibrosis.

“But if low albumin and low carbon monoxide diffusion capacity are due to the progression of ILD, both values may be difficult to improve,” he added.
 

Survivors versus nonsurvivors

Of those patients with RA-ILD who developed an AE, approximately half recovered. Among the IPF patients who developed an AE during the study period, approximately 39% recovered from the event, while 70% did not. Comparing RA-ILD patients who survived versus whose who did not, again, no significant demographic or clinical differences were seen between the 2 groups. On the other hand, the number of patients treated with immunosuppressants for their AE was significantly higher among patients who did not survive the AE, compared with those who did (P =.022), investigators note.

Similarly, the number of patients who required NPPV was also significantly higher among those who did not survive, compared with those who did. In fact, “none of the surviving patients used NPPV (P <0.01),” the authors stress. The number of patients who required IPPV was also significantly higher among nonsurvivors than among survivors (P =.017), and of the small number of patients who were treated with IPPV, all but one died without recovery.

As the authors suggested, these findings suggest that RA-ILD patients who recover from an AE with the help of corticosteroids alone have a relatively decent prognosis. In contrast, those who require immunosuppressive drugs in addition to steroids or mechanical ventilation for AE management can be expected to have a poor prognosis.

The same can also be said for IPF patients and even with the help of mechanical ventilation “with IPF patients, the survival rate is low anyway, so the indication for mechanical ventilation should be carefully judged,” Dr. Otsuka stressed.
 

Cause of death

The authors also compared the cause of death between patients with RA-ILD and those with IPF. “In RA-ILD patients, the most frequent cause of death was AE,” they report, at close to 35% of all patients with RA-ILD. This was also true for IPF patients among whom AE was the cause of death for over 44%. “These results indicate that, as in IPF, AE develops in the clinical course of RA-ILD with considerable frequency,” investigators note.

“During the clinical course of RA-ILD, as with IPD, it is necessary to pay attention to AE,” they stress. Dr. Otsuka added: “It may be difficult to change the prognosis of these patients.”

“However, knowing which patients are more likely to develop AE may help predict the prognosis, and it may be improved if antifibrotic agents are used for these patients,” he said. Elizabeth Volkmann, MD, director, UCLA scleroderma program, University of California, Los Angeles, felt that understanding the risk factors for AEs in this patient population may help physicians identify a subgroup of patients with RA-ILD who require closer monitoring and follow-up.

“These patients may also require more aggressive treatment for RA-ILD to prevent AEs,” she said in an email to this news organization. Given that the study was retrospective in nature, Dr. Volkmann cautioned that there were likely multiple confounding factors that could have affected survival in this patient population and not to take away from the study that survival was solely affected by immunosuppressant use, for example.

“It is possible that patients [treated with] immunosuppressants had other features of their disease that independently heightened their risk of mortality,” Dr. Volkmann said. Similarly, physicians should not assume that the high mortality rate seen in RA-ILD patients who were treated with mechanical ventilation had anything to do with mechanical ventilation itself, as patients requiring ventilation are likely to have worse outcomes, as she stressed.

As for hypoalbuminemia, Dr. Volkmann pointed out that hypoalbuminemia is often a sign of malnutrition in these patients. “Studies have demonstrated that malnutrition is an independent predictor of mortality in patients with ILD,” she emphasized.

“Optimizing patients’ nutritional status could potentially help lower the risk of AEs,” Dr. Volkmann suggested.

Limitations of the study include the fact that it was a single-center design study and included only a limited number of patients.

No specific funding source was noted. The authors have no conflicts of interest to declare.

Acute exacerbations (AEs) are both common in rheumatoid arthritis–associated interstitial lung disease (RA-ILD) and are a frequent cause of imminent mortality, a retrospective Japanese study suggests.

The same is also true for patients with idiopathic pulmonary fibrosis (IPF) for whom an AE is the most frequent cause of death as well, the same comparative study indicates.

“Several studies have reported that acute exacerbation, which occurs during the clinical course of idiopathic pulmonary fibrosis (IPF), also occurs in rheumatoid arthritis–associated interstitial lung disease (RA-ILD),” lead author Junji Otsuka, MD, PhD, of the National Hospital Organization Omuta National Hospital, Fukuoka, Japan, and colleagues observed.

“[We found that] AE was not uncommon in RA-ILD or IPF ... but the prognosis after AE of RA-ILD was significantly better than that of IPF [even though] the most frequent cause of death in RA-ILD and IPF was AE,” they stated.

The study was published online in Respiratory Medicine.

Patient features

The study involved 149 RA-ILD patients with a median age of 72 years at RA onset. The median time from ILD diagnosis to onset of AE was 48.5 months, while the median survival time after the onset of AE was 196 days (range 1-3,463 days), as the authors detailed. “All patients were treated with corticosteroids,” the authors noted, and almost all of them were treated with steroid pulse therapy.

Noninvasive positive pressure ventilation (NPPV) was used to maintain oxygenation in 18.5% of patients with severe respiratory failure, while invasive positive pressure ventilation (IPPV) was used in almost 26% of patients with the same degree of respiratory failure. Features of patients who developed an AE were then compared with those who did not.

Interestingly, no significant differences in clinical parameters were seen between those who developed an AE and those who did not. Nor were there any significant differences between the 2 groups in the length of time from the ILD diagnosis to the development of an AE. Some 18% of RA-ILD patients developed an AE, as did over 27% of patients with IPF, investigators report.

The median survival after RA-ILD patients developed an AE was 277 days, compared with only 60 days for those with IPF (P = .038). In a multivariable analysis, hypoalbuminemia at an odds ratio of .090 (95% confidence interval, 0.011-0.733; P = .012) as well as percent carbon monoxide diffusion capacity at an OR of .810 (95% CI, 0.814-0.964; P < .01) were both independent risk factors for the development of an AE, the investigators pointed out.

The best cut-off level for predicting the risk of an AE was 3.0 g/dL (95% CI, 0.011-0.733; P = .012) for serum albumin and 53% (95% CI, 0.814-0.964; P < .01) for carbon monoxide diffusion capacity. As Dr. Otsuka noted in an email to this news organization, low serum albumin likely correlates with a generally poor condition, while low carbon monoxide diffusion capacity is likely due to lung fibrosis.

“But if low albumin and low carbon monoxide diffusion capacity are due to the progression of ILD, both values may be difficult to improve,” he added.
 

Survivors versus nonsurvivors

Of those patients with RA-ILD who developed an AE, approximately half recovered. Among the IPF patients who developed an AE during the study period, approximately 39% recovered from the event, while 70% did not. Comparing RA-ILD patients who survived versus whose who did not, again, no significant demographic or clinical differences were seen between the 2 groups. On the other hand, the number of patients treated with immunosuppressants for their AE was significantly higher among patients who did not survive the AE, compared with those who did (P =.022), investigators note.

Similarly, the number of patients who required NPPV was also significantly higher among those who did not survive, compared with those who did. In fact, “none of the surviving patients used NPPV (P <0.01),” the authors stress. The number of patients who required IPPV was also significantly higher among nonsurvivors than among survivors (P =.017), and of the small number of patients who were treated with IPPV, all but one died without recovery.

As the authors suggested, these findings suggest that RA-ILD patients who recover from an AE with the help of corticosteroids alone have a relatively decent prognosis. In contrast, those who require immunosuppressive drugs in addition to steroids or mechanical ventilation for AE management can be expected to have a poor prognosis.

The same can also be said for IPF patients and even with the help of mechanical ventilation “with IPF patients, the survival rate is low anyway, so the indication for mechanical ventilation should be carefully judged,” Dr. Otsuka stressed.
 

Cause of death

The authors also compared the cause of death between patients with RA-ILD and those with IPF. “In RA-ILD patients, the most frequent cause of death was AE,” they report, at close to 35% of all patients with RA-ILD. This was also true for IPF patients among whom AE was the cause of death for over 44%. “These results indicate that, as in IPF, AE develops in the clinical course of RA-ILD with considerable frequency,” investigators note.

“During the clinical course of RA-ILD, as with IPD, it is necessary to pay attention to AE,” they stress. Dr. Otsuka added: “It may be difficult to change the prognosis of these patients.”

“However, knowing which patients are more likely to develop AE may help predict the prognosis, and it may be improved if antifibrotic agents are used for these patients,” he said. Elizabeth Volkmann, MD, director, UCLA scleroderma program, University of California, Los Angeles, felt that understanding the risk factors for AEs in this patient population may help physicians identify a subgroup of patients with RA-ILD who require closer monitoring and follow-up.

“These patients may also require more aggressive treatment for RA-ILD to prevent AEs,” she said in an email to this news organization. Given that the study was retrospective in nature, Dr. Volkmann cautioned that there were likely multiple confounding factors that could have affected survival in this patient population and not to take away from the study that survival was solely affected by immunosuppressant use, for example.

“It is possible that patients [treated with] immunosuppressants had other features of their disease that independently heightened their risk of mortality,” Dr. Volkmann said. Similarly, physicians should not assume that the high mortality rate seen in RA-ILD patients who were treated with mechanical ventilation had anything to do with mechanical ventilation itself, as patients requiring ventilation are likely to have worse outcomes, as she stressed.

As for hypoalbuminemia, Dr. Volkmann pointed out that hypoalbuminemia is often a sign of malnutrition in these patients. “Studies have demonstrated that malnutrition is an independent predictor of mortality in patients with ILD,” she emphasized.

“Optimizing patients’ nutritional status could potentially help lower the risk of AEs,” Dr. Volkmann suggested.

Limitations of the study include the fact that it was a single-center design study and included only a limited number of patients.

No specific funding source was noted. The authors have no conflicts of interest to declare.

Acute exacerbations (AEs) are both common in rheumatoid arthritis–associated interstitial lung disease (RA-ILD) and are a frequent cause of imminent mortality, a retrospective Japanese study suggests.

The same is also true for patients with idiopathic pulmonary fibrosis (IPF) for whom an AE is the most frequent cause of death as well, the same comparative study indicates.

“Several studies have reported that acute exacerbation, which occurs during the clinical course of idiopathic pulmonary fibrosis (IPF), also occurs in rheumatoid arthritis–associated interstitial lung disease (RA-ILD),” lead author Junji Otsuka, MD, PhD, of the National Hospital Organization Omuta National Hospital, Fukuoka, Japan, and colleagues observed.

“[We found that] AE was not uncommon in RA-ILD or IPF ... but the prognosis after AE of RA-ILD was significantly better than that of IPF [even though] the most frequent cause of death in RA-ILD and IPF was AE,” they stated.

The study was published online in Respiratory Medicine.

Patient features

The study involved 149 RA-ILD patients with a median age of 72 years at RA onset. The median time from ILD diagnosis to onset of AE was 48.5 months, while the median survival time after the onset of AE was 196 days (range 1-3,463 days), as the authors detailed. “All patients were treated with corticosteroids,” the authors noted, and almost all of them were treated with steroid pulse therapy.

Noninvasive positive pressure ventilation (NPPV) was used to maintain oxygenation in 18.5% of patients with severe respiratory failure, while invasive positive pressure ventilation (IPPV) was used in almost 26% of patients with the same degree of respiratory failure. Features of patients who developed an AE were then compared with those who did not.

Interestingly, no significant differences in clinical parameters were seen between those who developed an AE and those who did not. Nor were there any significant differences between the 2 groups in the length of time from the ILD diagnosis to the development of an AE. Some 18% of RA-ILD patients developed an AE, as did over 27% of patients with IPF, investigators report.

The median survival after RA-ILD patients developed an AE was 277 days, compared with only 60 days for those with IPF (P = .038). In a multivariable analysis, hypoalbuminemia at an odds ratio of .090 (95% confidence interval, 0.011-0.733; P = .012) as well as percent carbon monoxide diffusion capacity at an OR of .810 (95% CI, 0.814-0.964; P < .01) were both independent risk factors for the development of an AE, the investigators pointed out.

The best cut-off level for predicting the risk of an AE was 3.0 g/dL (95% CI, 0.011-0.733; P = .012) for serum albumin and 53% (95% CI, 0.814-0.964; P < .01) for carbon monoxide diffusion capacity. As Dr. Otsuka noted in an email to this news organization, low serum albumin likely correlates with a generally poor condition, while low carbon monoxide diffusion capacity is likely due to lung fibrosis.

“But if low albumin and low carbon monoxide diffusion capacity are due to the progression of ILD, both values may be difficult to improve,” he added.
 

Survivors versus nonsurvivors

Of those patients with RA-ILD who developed an AE, approximately half recovered. Among the IPF patients who developed an AE during the study period, approximately 39% recovered from the event, while 70% did not. Comparing RA-ILD patients who survived versus whose who did not, again, no significant demographic or clinical differences were seen between the 2 groups. On the other hand, the number of patients treated with immunosuppressants for their AE was significantly higher among patients who did not survive the AE, compared with those who did (P =.022), investigators note.

Similarly, the number of patients who required NPPV was also significantly higher among those who did not survive, compared with those who did. In fact, “none of the surviving patients used NPPV (P <0.01),” the authors stress. The number of patients who required IPPV was also significantly higher among nonsurvivors than among survivors (P =.017), and of the small number of patients who were treated with IPPV, all but one died without recovery.

As the authors suggested, these findings suggest that RA-ILD patients who recover from an AE with the help of corticosteroids alone have a relatively decent prognosis. In contrast, those who require immunosuppressive drugs in addition to steroids or mechanical ventilation for AE management can be expected to have a poor prognosis.

The same can also be said for IPF patients and even with the help of mechanical ventilation “with IPF patients, the survival rate is low anyway, so the indication for mechanical ventilation should be carefully judged,” Dr. Otsuka stressed.
 

Cause of death

The authors also compared the cause of death between patients with RA-ILD and those with IPF. “In RA-ILD patients, the most frequent cause of death was AE,” they report, at close to 35% of all patients with RA-ILD. This was also true for IPF patients among whom AE was the cause of death for over 44%. “These results indicate that, as in IPF, AE develops in the clinical course of RA-ILD with considerable frequency,” investigators note.

“During the clinical course of RA-ILD, as with IPD, it is necessary to pay attention to AE,” they stress. Dr. Otsuka added: “It may be difficult to change the prognosis of these patients.”

“However, knowing which patients are more likely to develop AE may help predict the prognosis, and it may be improved if antifibrotic agents are used for these patients,” he said. Elizabeth Volkmann, MD, director, UCLA scleroderma program, University of California, Los Angeles, felt that understanding the risk factors for AEs in this patient population may help physicians identify a subgroup of patients with RA-ILD who require closer monitoring and follow-up.

“These patients may also require more aggressive treatment for RA-ILD to prevent AEs,” she said in an email to this news organization. Given that the study was retrospective in nature, Dr. Volkmann cautioned that there were likely multiple confounding factors that could have affected survival in this patient population and not to take away from the study that survival was solely affected by immunosuppressant use, for example.

“It is possible that patients [treated with] immunosuppressants had other features of their disease that independently heightened their risk of mortality,” Dr. Volkmann said. Similarly, physicians should not assume that the high mortality rate seen in RA-ILD patients who were treated with mechanical ventilation had anything to do with mechanical ventilation itself, as patients requiring ventilation are likely to have worse outcomes, as she stressed.

As for hypoalbuminemia, Dr. Volkmann pointed out that hypoalbuminemia is often a sign of malnutrition in these patients. “Studies have demonstrated that malnutrition is an independent predictor of mortality in patients with ILD,” she emphasized.

“Optimizing patients’ nutritional status could potentially help lower the risk of AEs,” Dr. Volkmann suggested.

Limitations of the study include the fact that it was a single-center design study and included only a limited number of patients.

No specific funding source was noted. The authors have no conflicts of interest to declare.