CHEST Physician

Transplantation of hearts donated after circulatory death (DCD) is associated with short-term clinical outcomes similar to those of hearts donated after brain death (DBD), except for transient posttransplant right heart dysfunction, a single-center analysis suggests.

The right-heart dysfunction resolved by 3 weeks post transplant, and recipient mortality was similar for those receiving DCD and DBD, which is considered standard of care (SOC).

Furthermore, the median waiting list time was significantly shorter for DCD recipients than for SOC recipients (17 vs. 70 days).

The authors suggest that use of DCD hearts could expand the donor pool by as much as 30%.

“Now that we and others have demonstrated the safety of this technique, I believe it is our obligation as a transplant community to use these organs and not allow them to be wasted,” David A. D’Alessandro, MD, of Massachusetts General Hospital, Boston, told this news organization.

“I will caution that DCD heart transplantation is labor intensive, and there is a learning curve which can potentially put patients at risk,” he added. “It is vitally important, therefore, that we learn from each other’s experiences to flatten this curve.”

The study was published online in the Journal of the American College of Cardiology.
 

Similar outcomes

Dr. D’Alessandro and colleagues compared the hemodynamic and clinical profiles of 47 DCD hearts with 166 SOC hearts implanted at Massachusetts General Hospital between 2016 and 2022. DCD hearts were maintained with use of a proprietary warm perfusion circuit organ care system (OCS, TransMedics).

Baseline characteristics were similar between the groups, except the DCD heart recipients were younger (mean age, 55 vs. 59); they were less likely to be an inpatient at the time of transplant (26% vs. 49%); and they had lower pulmonary vascular resistance (1.73 WU vs. 2.26 WU).

The median time from DCD consent to transplant was significantly shorter than for SOC hearts (17 vs. 70 days). However, there was a higher, though not statistically significant, incidence of severe primary graft dysfunction at 24 hours post transplant with DCD (10.6% vs. SOC 3.6%), leading five DCD recipients (10.6%) and nine SOC recipients (5.4%) to receive venoarterial extracorporeal membrane oxygenation.

Right heart function was significantly impaired in DCD vs. SOC recipients 1 week post transplant, with higher median right atrial pressure (10 mm Hg vs. 7 mm Hg); higher right atrial pressure to pulmonary capillary wedge pressure ratio (0.64 vs. 0.57); and lower pulmonary arterial pulsatility index (1.66 vs. 2.52).

However, by 3 weeks post transplant, right heart function was similar between the groups, as was mortality at 30 days (0 vs. 2%) and 1 year (3% vs. 8%).

Furthermore, hospital length of stay following transplant, intensive care unit length of stay, ICU readmissions, and 30-day readmissions were similar between the groups.

“We and others will continue to push the boundaries of this technique to understand if we can safely extend the warm ischemic time, which could make additional organs available,” Dr. D’Alessandro said. “We will also be exploring additional ways to monitor and assess organ health and viability ex situ and potential avenues of treatment which could repair and optimize organ function.

“A successful DCD heart transplant program requires institutional and team commitment,” he added, “and there are clinical nuances which should be appreciated to minimize patient risks associated with the obligate learning curve.”

Ulrich P. Jorde, MD, of Montefiore Medical Center in New York, author of a related editorial, concluded that heart donation after circulatory death “promises significant expansion of the donor pool and will lead to many lives saved” and that “the current investigation is a timely and important contribution to this effort”.

However, he noted, “it must be acknowledged that donation after cardiac death has evoked significant controversy regarding the ethics of this approach,” particularly when using a technique called normothermic regional perfusion (NRP), in which, after declaration of death and ligation of cerebral vessels, the heart is resuscitated in situ using extracorporeal membrane oxygenation, as opposed to the proprietary warm perfusion OCS used in this study.

“Central to this discussion is the definition of death and its irreversibility,” Dr. Jorde noted. “In contrast to DBD, where brain death protocols are well established and accepted by societies across the globe, DCD protocol rules, e.g., standoff times after complete cessation of circulation, continue to vary even within national jurisdictions. Such variability and incomplete standardization of practice is particularly important when the organ is resuscitated in situ using normothermic regional perfusion.

“The International Society of Heart and Lung Transplantation has recently provided a framework within which donation after cardiac death, with or without the use of NRP, can be conducted to comply with ethical and legal norms and regulations, acknowledging that such norms and regulations may differ between societies,” he wrote. “To advance the field, and to ensure ongoing trust in the transplantation system, it is of critical importance that such discussions are held publicly and transparently.”
 

More ‘dry runs’

“Donor heart allographs are safe for our patients with heart failure if procured and transplanted in an organized and protocolized manner,” Philip J. Spencer, MD, a cardiovascular and transplant surgeon at Mayo Clinic in Rochester, Minn., told this news organization. “As the techniques are adopted globally, our patients will benefit.”

Nevertheless, like Dr. D’Alessandro, he noted that procurement of DCD hearts is more labor intensive. “A program and its patients must be willing to accept a higher number of ‘dry runs,’ which occurs when the team is sent for an organ and the donor does not progress to circulatory death in a time and manner appropriate for safe organ recovery.

“There is no doubt that being open to these organs will increase the patient’s chances of receiving a donor heart in a shorter period of time,” he said. “However, the experience of a dry run, or multiple, can be emotionally and financially stressful for the patient and the program.”

No commercial funding or relevant conflicts of interest were disclosed.

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

Transplantation of hearts donated after circulatory death (DCD) is associated with short-term clinical outcomes similar to those of hearts donated after brain death (DBD), except for transient posttransplant right heart dysfunction, a single-center analysis suggests.

The right-heart dysfunction resolved by 3 weeks post transplant, and recipient mortality was similar for those receiving DCD and DBD, which is considered standard of care (SOC).

Furthermore, the median waiting list time was significantly shorter for DCD recipients than for SOC recipients (17 vs. 70 days).

The authors suggest that use of DCD hearts could expand the donor pool by as much as 30%.

“Now that we and others have demonstrated the safety of this technique, I believe it is our obligation as a transplant community to use these organs and not allow them to be wasted,” David A. D’Alessandro, MD, of Massachusetts General Hospital, Boston, told this news organization.

“I will caution that DCD heart transplantation is labor intensive, and there is a learning curve which can potentially put patients at risk,” he added. “It is vitally important, therefore, that we learn from each other’s experiences to flatten this curve.”

The study was published online in the Journal of the American College of Cardiology.
 

Similar outcomes

Dr. D’Alessandro and colleagues compared the hemodynamic and clinical profiles of 47 DCD hearts with 166 SOC hearts implanted at Massachusetts General Hospital between 2016 and 2022. DCD hearts were maintained with use of a proprietary warm perfusion circuit organ care system (OCS, TransMedics).

Baseline characteristics were similar between the groups, except the DCD heart recipients were younger (mean age, 55 vs. 59); they were less likely to be an inpatient at the time of transplant (26% vs. 49%); and they had lower pulmonary vascular resistance (1.73 WU vs. 2.26 WU).

The median time from DCD consent to transplant was significantly shorter than for SOC hearts (17 vs. 70 days). However, there was a higher, though not statistically significant, incidence of severe primary graft dysfunction at 24 hours post transplant with DCD (10.6% vs. SOC 3.6%), leading five DCD recipients (10.6%) and nine SOC recipients (5.4%) to receive venoarterial extracorporeal membrane oxygenation.

Right heart function was significantly impaired in DCD vs. SOC recipients 1 week post transplant, with higher median right atrial pressure (10 mm Hg vs. 7 mm Hg); higher right atrial pressure to pulmonary capillary wedge pressure ratio (0.64 vs. 0.57); and lower pulmonary arterial pulsatility index (1.66 vs. 2.52).

However, by 3 weeks post transplant, right heart function was similar between the groups, as was mortality at 30 days (0 vs. 2%) and 1 year (3% vs. 8%).

Furthermore, hospital length of stay following transplant, intensive care unit length of stay, ICU readmissions, and 30-day readmissions were similar between the groups.

“We and others will continue to push the boundaries of this technique to understand if we can safely extend the warm ischemic time, which could make additional organs available,” Dr. D’Alessandro said. “We will also be exploring additional ways to monitor and assess organ health and viability ex situ and potential avenues of treatment which could repair and optimize organ function.

“A successful DCD heart transplant program requires institutional and team commitment,” he added, “and there are clinical nuances which should be appreciated to minimize patient risks associated with the obligate learning curve.”

Ulrich P. Jorde, MD, of Montefiore Medical Center in New York, author of a related editorial, concluded that heart donation after circulatory death “promises significant expansion of the donor pool and will lead to many lives saved” and that “the current investigation is a timely and important contribution to this effort”.

However, he noted, “it must be acknowledged that donation after cardiac death has evoked significant controversy regarding the ethics of this approach,” particularly when using a technique called normothermic regional perfusion (NRP), in which, after declaration of death and ligation of cerebral vessels, the heart is resuscitated in situ using extracorporeal membrane oxygenation, as opposed to the proprietary warm perfusion OCS used in this study.

“Central to this discussion is the definition of death and its irreversibility,” Dr. Jorde noted. “In contrast to DBD, where brain death protocols are well established and accepted by societies across the globe, DCD protocol rules, e.g., standoff times after complete cessation of circulation, continue to vary even within national jurisdictions. Such variability and incomplete standardization of practice is particularly important when the organ is resuscitated in situ using normothermic regional perfusion.

“The International Society of Heart and Lung Transplantation has recently provided a framework within which donation after cardiac death, with or without the use of NRP, can be conducted to comply with ethical and legal norms and regulations, acknowledging that such norms and regulations may differ between societies,” he wrote. “To advance the field, and to ensure ongoing trust in the transplantation system, it is of critical importance that such discussions are held publicly and transparently.”
 

More ‘dry runs’

“Donor heart allographs are safe for our patients with heart failure if procured and transplanted in an organized and protocolized manner,” Philip J. Spencer, MD, a cardiovascular and transplant surgeon at Mayo Clinic in Rochester, Minn., told this news organization. “As the techniques are adopted globally, our patients will benefit.”

Nevertheless, like Dr. D’Alessandro, he noted that procurement of DCD hearts is more labor intensive. “A program and its patients must be willing to accept a higher number of ‘dry runs,’ which occurs when the team is sent for an organ and the donor does not progress to circulatory death in a time and manner appropriate for safe organ recovery.

“There is no doubt that being open to these organs will increase the patient’s chances of receiving a donor heart in a shorter period of time,” he said. “However, the experience of a dry run, or multiple, can be emotionally and financially stressful for the patient and the program.”

No commercial funding or relevant conflicts of interest were disclosed.

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

Transplantation of hearts donated after circulatory death (DCD) is associated with short-term clinical outcomes similar to those of hearts donated after brain death (DBD), except for transient posttransplant right heart dysfunction, a single-center analysis suggests.

The right-heart dysfunction resolved by 3 weeks post transplant, and recipient mortality was similar for those receiving DCD and DBD, which is considered standard of care (SOC).

Furthermore, the median waiting list time was significantly shorter for DCD recipients than for SOC recipients (17 vs. 70 days).

The authors suggest that use of DCD hearts could expand the donor pool by as much as 30%.

“Now that we and others have demonstrated the safety of this technique, I believe it is our obligation as a transplant community to use these organs and not allow them to be wasted,” David A. D’Alessandro, MD, of Massachusetts General Hospital, Boston, told this news organization.

“I will caution that DCD heart transplantation is labor intensive, and there is a learning curve which can potentially put patients at risk,” he added. “It is vitally important, therefore, that we learn from each other’s experiences to flatten this curve.”

The study was published online in the Journal of the American College of Cardiology.
 

Similar outcomes

Dr. D’Alessandro and colleagues compared the hemodynamic and clinical profiles of 47 DCD hearts with 166 SOC hearts implanted at Massachusetts General Hospital between 2016 and 2022. DCD hearts were maintained with use of a proprietary warm perfusion circuit organ care system (OCS, TransMedics).

Baseline characteristics were similar between the groups, except the DCD heart recipients were younger (mean age, 55 vs. 59); they were less likely to be an inpatient at the time of transplant (26% vs. 49%); and they had lower pulmonary vascular resistance (1.73 WU vs. 2.26 WU).

The median time from DCD consent to transplant was significantly shorter than for SOC hearts (17 vs. 70 days). However, there was a higher, though not statistically significant, incidence of severe primary graft dysfunction at 24 hours post transplant with DCD (10.6% vs. SOC 3.6%), leading five DCD recipients (10.6%) and nine SOC recipients (5.4%) to receive venoarterial extracorporeal membrane oxygenation.

Right heart function was significantly impaired in DCD vs. SOC recipients 1 week post transplant, with higher median right atrial pressure (10 mm Hg vs. 7 mm Hg); higher right atrial pressure to pulmonary capillary wedge pressure ratio (0.64 vs. 0.57); and lower pulmonary arterial pulsatility index (1.66 vs. 2.52).

However, by 3 weeks post transplant, right heart function was similar between the groups, as was mortality at 30 days (0 vs. 2%) and 1 year (3% vs. 8%).

Furthermore, hospital length of stay following transplant, intensive care unit length of stay, ICU readmissions, and 30-day readmissions were similar between the groups.

“We and others will continue to push the boundaries of this technique to understand if we can safely extend the warm ischemic time, which could make additional organs available,” Dr. D’Alessandro said. “We will also be exploring additional ways to monitor and assess organ health and viability ex situ and potential avenues of treatment which could repair and optimize organ function.

“A successful DCD heart transplant program requires institutional and team commitment,” he added, “and there are clinical nuances which should be appreciated to minimize patient risks associated with the obligate learning curve.”

Ulrich P. Jorde, MD, of Montefiore Medical Center in New York, author of a related editorial, concluded that heart donation after circulatory death “promises significant expansion of the donor pool and will lead to many lives saved” and that “the current investigation is a timely and important contribution to this effort”.

However, he noted, “it must be acknowledged that donation after cardiac death has evoked significant controversy regarding the ethics of this approach,” particularly when using a technique called normothermic regional perfusion (NRP), in which, after declaration of death and ligation of cerebral vessels, the heart is resuscitated in situ using extracorporeal membrane oxygenation, as opposed to the proprietary warm perfusion OCS used in this study.

“Central to this discussion is the definition of death and its irreversibility,” Dr. Jorde noted. “In contrast to DBD, where brain death protocols are well established and accepted by societies across the globe, DCD protocol rules, e.g., standoff times after complete cessation of circulation, continue to vary even within national jurisdictions. Such variability and incomplete standardization of practice is particularly important when the organ is resuscitated in situ using normothermic regional perfusion.

“The International Society of Heart and Lung Transplantation has recently provided a framework within which donation after cardiac death, with or without the use of NRP, can be conducted to comply with ethical and legal norms and regulations, acknowledging that such norms and regulations may differ between societies,” he wrote. “To advance the field, and to ensure ongoing trust in the transplantation system, it is of critical importance that such discussions are held publicly and transparently.”
 

More ‘dry runs’

“Donor heart allographs are safe for our patients with heart failure if procured and transplanted in an organized and protocolized manner,” Philip J. Spencer, MD, a cardiovascular and transplant surgeon at Mayo Clinic in Rochester, Minn., told this news organization. “As the techniques are adopted globally, our patients will benefit.”

Nevertheless, like Dr. D’Alessandro, he noted that procurement of DCD hearts is more labor intensive. “A program and its patients must be willing to accept a higher number of ‘dry runs,’ which occurs when the team is sent for an organ and the donor does not progress to circulatory death in a time and manner appropriate for safe organ recovery.

“There is no doubt that being open to these organs will increase the patient’s chances of receiving a donor heart in a shorter period of time,” he said. “However, the experience of a dry run, or multiple, can be emotionally and financially stressful for the patient and the program.”

No commercial funding or relevant conflicts of interest were disclosed.

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

French children with peanut allergy tend to have reactions to other legumes, including soy, lentil, pea, bean, lupin, and fenugreek, and those other allergies often lead to anaphylactic reactions, a retrospective study from France reports.

“Among children allergic to peanut, at least two-thirds were sensitized to one other legume, and legume allergy was diagnosed in one-quarter of the sensitized patients,” wrote senior study author Amandine Divaret-Chauveau, MD, of Centre Hospitalier Universitaire de Nancy, Vandoeuvre-les-Nancy, and colleagues. The report is in Pediatric Allergy and Immunology.

People worldwide are eating more legumes these days, the authors noted. High in protein, low in unsaturated fats, with low production costs, legumes are important components of increasingly vegetarian, healthy, sustainable diets.

Food allergens are the most common childhood triggers of allergic reactions. Among children in France, legumes cause 14.6% of food-related anaphylactic reactions, with peanut as the main allergen, they added.

Dr. Divaret-Chauveau and colleagues assessed the prevalence and relevance of sensitization to legumes among all children and adolescents aged 1-17 years who had peanut allergy and had been admitted to one academic pediatric allergy department over roughly 3 years, beginning in early 2017. For the 195 study participants, peanut allergy had been confirmed, and they had been documented to have consumed or to have sensitization to at least one non-peanut legume; 69.7% were boys.

The researchers analyzed data on consumption history, skin prick tests, specific immunoglobulin E status, prior allergic reactions, and oral food challenges for each legume. They found the following:

• Among the 195 children with peanut allergy, 98.4% had at least one other atopic disease.
• Of the 195 children with peanut allergy, 122 (63.9%) were sensitized to at least one other legume. Of these 122 children, 66.3% were sensitized to fenugreek, 42.2% to lentil, 39.9% to soy, and 34.2% to lupin.
• Allergy to one or more legumes was confirmed for 27.9% of the 122 sensitized children, including 4.9% who had multiple legume allergies. Lentil, lupin, and pea were the main allergens.
• Of the 118 children also having a non-legume food allergy, the main food allergens were egg (57.6%), cow’s milk (33.0%), cashew (39.0%), pistachio (23.7%), and hazelnut (30.5%).
• Fifty percent of allergic reactions to non-peanut legumes were severe, often showing as asthma. Atopic comorbidities, including asthma, in most participants may have contributed to the severity of allergic reactions, the authors noted.

Allergy awareness needs to grow with plant-based diets

“The high prevalence of legume sensitization reported in our study highlights the need to explore legume consumption in children with PA [peanut allergy], and the need to investigate sensitization in the absence of consumption,” they added.

Jodi A. Shroba, MSN, APRN, CPNP, coordinator for the Food Allergy Program at Children’s Mercy Kansas City, in Missouri, told this news organization that few data are available in the literature regarding allergies to legumes other than peanut.

“It was interesting that these authors found such a high legume sensitization in their peanut-allergic patients,” Ms. Shroba, who was not involved in the study, said by email. “As more people are starting to eat plant-based diets, it is important that we better understand their allergenicity and cross-reactivity so we can better help guide patient management and education.”

Deborah Albright, MD, assistant professor of pediatrics at the University of Pittsburgh, agreed.

“As plant-based protein consumption broadens worldwide, awareness of the potential for cross-reactivity and co-allergy amongst legumes will become increasingly important,” she said by email.

“However, positive allergy tests do not reliably correlate with true food allergy; therefore, the diagnosis of legume co-allergy should be confirmed by the individual patient’s history, a formal food challenge, or both,” advised Dr. Albright. She was not involved in the study.

“Cross-sensitization to other legumes in patients with a single legume allergy is common; however, true clinical reactivity is often not present,” she added. “Also, legume allergy test sensitization rates and objective reactivity on food challenge can vary by region, depending on diet and pollen aeroallergen exposure.

“Systematic exploration of tolerance versus co-allergy to other legumes should be considered in patients allergic to peanut or other legumes,” Dr. Albright said.

The authors recommend further research and registry data collection of legume anaphylaxis.

Details regarding funding for the study were not provided. The authors, Ms. Shroba, and Dr. Albright report no relevant financial relationships.

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

French children with peanut allergy tend to have reactions to other legumes, including soy, lentil, pea, bean, lupin, and fenugreek, and those other allergies often lead to anaphylactic reactions, a retrospective study from France reports.

“Among children allergic to peanut, at least two-thirds were sensitized to one other legume, and legume allergy was diagnosed in one-quarter of the sensitized patients,” wrote senior study author Amandine Divaret-Chauveau, MD, of Centre Hospitalier Universitaire de Nancy, Vandoeuvre-les-Nancy, and colleagues. The report is in Pediatric Allergy and Immunology.

People worldwide are eating more legumes these days, the authors noted. High in protein, low in unsaturated fats, with low production costs, legumes are important components of increasingly vegetarian, healthy, sustainable diets.

Food allergens are the most common childhood triggers of allergic reactions. Among children in France, legumes cause 14.6% of food-related anaphylactic reactions, with peanut as the main allergen, they added.

Dr. Divaret-Chauveau and colleagues assessed the prevalence and relevance of sensitization to legumes among all children and adolescents aged 1-17 years who had peanut allergy and had been admitted to one academic pediatric allergy department over roughly 3 years, beginning in early 2017. For the 195 study participants, peanut allergy had been confirmed, and they had been documented to have consumed or to have sensitization to at least one non-peanut legume; 69.7% were boys.

The researchers analyzed data on consumption history, skin prick tests, specific immunoglobulin E status, prior allergic reactions, and oral food challenges for each legume. They found the following:

• Among the 195 children with peanut allergy, 98.4% had at least one other atopic disease.
• Of the 195 children with peanut allergy, 122 (63.9%) were sensitized to at least one other legume. Of these 122 children, 66.3% were sensitized to fenugreek, 42.2% to lentil, 39.9% to soy, and 34.2% to lupin.
• Allergy to one or more legumes was confirmed for 27.9% of the 122 sensitized children, including 4.9% who had multiple legume allergies. Lentil, lupin, and pea were the main allergens.
• Of the 118 children also having a non-legume food allergy, the main food allergens were egg (57.6%), cow’s milk (33.0%), cashew (39.0%), pistachio (23.7%), and hazelnut (30.5%).
• Fifty percent of allergic reactions to non-peanut legumes were severe, often showing as asthma. Atopic comorbidities, including asthma, in most participants may have contributed to the severity of allergic reactions, the authors noted.

Allergy awareness needs to grow with plant-based diets

“The high prevalence of legume sensitization reported in our study highlights the need to explore legume consumption in children with PA [peanut allergy], and the need to investigate sensitization in the absence of consumption,” they added.

Jodi A. Shroba, MSN, APRN, CPNP, coordinator for the Food Allergy Program at Children’s Mercy Kansas City, in Missouri, told this news organization that few data are available in the literature regarding allergies to legumes other than peanut.

“It was interesting that these authors found such a high legume sensitization in their peanut-allergic patients,” Ms. Shroba, who was not involved in the study, said by email. “As more people are starting to eat plant-based diets, it is important that we better understand their allergenicity and cross-reactivity so we can better help guide patient management and education.”

Deborah Albright, MD, assistant professor of pediatrics at the University of Pittsburgh, agreed.

“As plant-based protein consumption broadens worldwide, awareness of the potential for cross-reactivity and co-allergy amongst legumes will become increasingly important,” she said by email.

“However, positive allergy tests do not reliably correlate with true food allergy; therefore, the diagnosis of legume co-allergy should be confirmed by the individual patient’s history, a formal food challenge, or both,” advised Dr. Albright. She was not involved in the study.

“Cross-sensitization to other legumes in patients with a single legume allergy is common; however, true clinical reactivity is often not present,” she added. “Also, legume allergy test sensitization rates and objective reactivity on food challenge can vary by region, depending on diet and pollen aeroallergen exposure.

“Systematic exploration of tolerance versus co-allergy to other legumes should be considered in patients allergic to peanut or other legumes,” Dr. Albright said.

The authors recommend further research and registry data collection of legume anaphylaxis.

Details regarding funding for the study were not provided. The authors, Ms. Shroba, and Dr. Albright report no relevant financial relationships.

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

French children with peanut allergy tend to have reactions to other legumes, including soy, lentil, pea, bean, lupin, and fenugreek, and those other allergies often lead to anaphylactic reactions, a retrospective study from France reports.

“Among children allergic to peanut, at least two-thirds were sensitized to one other legume, and legume allergy was diagnosed in one-quarter of the sensitized patients,” wrote senior study author Amandine Divaret-Chauveau, MD, of Centre Hospitalier Universitaire de Nancy, Vandoeuvre-les-Nancy, and colleagues. The report is in Pediatric Allergy and Immunology.

People worldwide are eating more legumes these days, the authors noted. High in protein, low in unsaturated fats, with low production costs, legumes are important components of increasingly vegetarian, healthy, sustainable diets.

Food allergens are the most common childhood triggers of allergic reactions. Among children in France, legumes cause 14.6% of food-related anaphylactic reactions, with peanut as the main allergen, they added.

Dr. Divaret-Chauveau and colleagues assessed the prevalence and relevance of sensitization to legumes among all children and adolescents aged 1-17 years who had peanut allergy and had been admitted to one academic pediatric allergy department over roughly 3 years, beginning in early 2017. For the 195 study participants, peanut allergy had been confirmed, and they had been documented to have consumed or to have sensitization to at least one non-peanut legume; 69.7% were boys.

The researchers analyzed data on consumption history, skin prick tests, specific immunoglobulin E status, prior allergic reactions, and oral food challenges for each legume. They found the following:

• Among the 195 children with peanut allergy, 98.4% had at least one other atopic disease.
• Of the 195 children with peanut allergy, 122 (63.9%) were sensitized to at least one other legume. Of these 122 children, 66.3% were sensitized to fenugreek, 42.2% to lentil, 39.9% to soy, and 34.2% to lupin.
• Allergy to one or more legumes was confirmed for 27.9% of the 122 sensitized children, including 4.9% who had multiple legume allergies. Lentil, lupin, and pea were the main allergens.
• Of the 118 children also having a non-legume food allergy, the main food allergens were egg (57.6%), cow’s milk (33.0%), cashew (39.0%), pistachio (23.7%), and hazelnut (30.5%).
• Fifty percent of allergic reactions to non-peanut legumes were severe, often showing as asthma. Atopic comorbidities, including asthma, in most participants may have contributed to the severity of allergic reactions, the authors noted.

Allergy awareness needs to grow with plant-based diets

“The high prevalence of legume sensitization reported in our study highlights the need to explore legume consumption in children with PA [peanut allergy], and the need to investigate sensitization in the absence of consumption,” they added.

Jodi A. Shroba, MSN, APRN, CPNP, coordinator for the Food Allergy Program at Children’s Mercy Kansas City, in Missouri, told this news organization that few data are available in the literature regarding allergies to legumes other than peanut.

“It was interesting that these authors found such a high legume sensitization in their peanut-allergic patients,” Ms. Shroba, who was not involved in the study, said by email. “As more people are starting to eat plant-based diets, it is important that we better understand their allergenicity and cross-reactivity so we can better help guide patient management and education.”

Deborah Albright, MD, assistant professor of pediatrics at the University of Pittsburgh, agreed.

“As plant-based protein consumption broadens worldwide, awareness of the potential for cross-reactivity and co-allergy amongst legumes will become increasingly important,” she said by email.

“However, positive allergy tests do not reliably correlate with true food allergy; therefore, the diagnosis of legume co-allergy should be confirmed by the individual patient’s history, a formal food challenge, or both,” advised Dr. Albright. She was not involved in the study.

“Cross-sensitization to other legumes in patients with a single legume allergy is common; however, true clinical reactivity is often not present,” she added. “Also, legume allergy test sensitization rates and objective reactivity on food challenge can vary by region, depending on diet and pollen aeroallergen exposure.

“Systematic exploration of tolerance versus co-allergy to other legumes should be considered in patients allergic to peanut or other legumes,” Dr. Albright said.

The authors recommend further research and registry data collection of legume anaphylaxis.

Details regarding funding for the study were not provided. The authors, Ms. Shroba, and Dr. Albright report no relevant financial relationships.

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

COVID-19 causes DNA damage to the heart, affecting the body in a completely different way than the flu does, according to a study published in Immunology. 

The study looked at the hearts of patients who died from COVID-19, the flu, and other causes. The findings could provide clues about why coronavirus has led to complications such as ongoing heart issues.

“We found a lot of DNA damage that was unique to the COVID-19 patients, which wasn’t present in the flu patients,” Arutha Kulasinghe, one of the lead study authors and a research fellow at the University of Queensland, Brisbane, Australia, told the Brisbane Times.

“So in this study, COVID-19 and flu look very different in the way they affect the heart,” he said.

Dr. Kulasinghe and colleagues analyzed the hearts of seven COVID-19 patients, two flu patients, and six patients who died from other causes. They used transcriptomic profiling, which looks at the DNA landscape of an organ, to investigate heart tissue from the patients.

Because of previous studies about heart problems associated with COVID-19, he and colleagues expected to find extreme inflammation in the heart. Instead, they found that inflammation signals had been suppressed in the heart, and markers for DNA damage and repair were much higher. They’re still unsure of the underlying cause.

“The indications here are that there’s DNA damage here, it’s not inflammation,” Dr. Kulasinghe said. “There’s something else going on that we need to figure out.”

The damage was similar to the way chronic diseases such as diabetes and cancer appear in the heart, he said, with heart tissue showing DNA damage signals. 

Dr. Kulasinghe said he hopes other studies can build on the findings to develop risk models to understand which patients may face a higher risk of serious COVID-19 complications. In turn, this could help doctors provide early treatment. For instance, all seven COVID-19 patients had other chronic diseases, such as diabetes, hypertension, and heart disease. 

“Ideally in the future, if you have cardiovascular disease, if you’re obese or have other complications, and you’ve got a signature in your blood that indicates you are at risk of severe disease, then we can risk-stratify patients when they are diagnosed,” he said. 

The research is a preliminary step, Dr. Kulasinghe said, because of the small sample size. This type of study is often difficult to conduct because researchers have to wait for the availability of organs, as well as request permission from families for postmortem autopsies and biopsies, to be able to look at the effects on dead tissues.

“Our challenge now is to draw a clinical finding from this, which we can’t at this stage,” he added. “But it’s a really fundamental biological difference we’re observing [between COVID-19 and flu], which we need to validate with larger studies.”

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

COVID-19 causes DNA damage to the heart, affecting the body in a completely different way than the flu does, according to a study published in Immunology. 

The study looked at the hearts of patients who died from COVID-19, the flu, and other causes. The findings could provide clues about why coronavirus has led to complications such as ongoing heart issues.

“We found a lot of DNA damage that was unique to the COVID-19 patients, which wasn’t present in the flu patients,” Arutha Kulasinghe, one of the lead study authors and a research fellow at the University of Queensland, Brisbane, Australia, told the Brisbane Times.

“So in this study, COVID-19 and flu look very different in the way they affect the heart,” he said.

Dr. Kulasinghe and colleagues analyzed the hearts of seven COVID-19 patients, two flu patients, and six patients who died from other causes. They used transcriptomic profiling, which looks at the DNA landscape of an organ, to investigate heart tissue from the patients.

Because of previous studies about heart problems associated with COVID-19, he and colleagues expected to find extreme inflammation in the heart. Instead, they found that inflammation signals had been suppressed in the heart, and markers for DNA damage and repair were much higher. They’re still unsure of the underlying cause.

“The indications here are that there’s DNA damage here, it’s not inflammation,” Dr. Kulasinghe said. “There’s something else going on that we need to figure out.”

The damage was similar to the way chronic diseases such as diabetes and cancer appear in the heart, he said, with heart tissue showing DNA damage signals. 

Dr. Kulasinghe said he hopes other studies can build on the findings to develop risk models to understand which patients may face a higher risk of serious COVID-19 complications. In turn, this could help doctors provide early treatment. For instance, all seven COVID-19 patients had other chronic diseases, such as diabetes, hypertension, and heart disease. 

“Ideally in the future, if you have cardiovascular disease, if you’re obese or have other complications, and you’ve got a signature in your blood that indicates you are at risk of severe disease, then we can risk-stratify patients when they are diagnosed,” he said. 

The research is a preliminary step, Dr. Kulasinghe said, because of the small sample size. This type of study is often difficult to conduct because researchers have to wait for the availability of organs, as well as request permission from families for postmortem autopsies and biopsies, to be able to look at the effects on dead tissues.

“Our challenge now is to draw a clinical finding from this, which we can’t at this stage,” he added. “But it’s a really fundamental biological difference we’re observing [between COVID-19 and flu], which we need to validate with larger studies.”

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

COVID-19 causes DNA damage to the heart, affecting the body in a completely different way than the flu does, according to a study published in Immunology. 

The study looked at the hearts of patients who died from COVID-19, the flu, and other causes. The findings could provide clues about why coronavirus has led to complications such as ongoing heart issues.

“We found a lot of DNA damage that was unique to the COVID-19 patients, which wasn’t present in the flu patients,” Arutha Kulasinghe, one of the lead study authors and a research fellow at the University of Queensland, Brisbane, Australia, told the Brisbane Times.

“So in this study, COVID-19 and flu look very different in the way they affect the heart,” he said.

Dr. Kulasinghe and colleagues analyzed the hearts of seven COVID-19 patients, two flu patients, and six patients who died from other causes. They used transcriptomic profiling, which looks at the DNA landscape of an organ, to investigate heart tissue from the patients.

Because of previous studies about heart problems associated with COVID-19, he and colleagues expected to find extreme inflammation in the heart. Instead, they found that inflammation signals had been suppressed in the heart, and markers for DNA damage and repair were much higher. They’re still unsure of the underlying cause.

“The indications here are that there’s DNA damage here, it’s not inflammation,” Dr. Kulasinghe said. “There’s something else going on that we need to figure out.”

The damage was similar to the way chronic diseases such as diabetes and cancer appear in the heart, he said, with heart tissue showing DNA damage signals. 

Dr. Kulasinghe said he hopes other studies can build on the findings to develop risk models to understand which patients may face a higher risk of serious COVID-19 complications. In turn, this could help doctors provide early treatment. For instance, all seven COVID-19 patients had other chronic diseases, such as diabetes, hypertension, and heart disease. 

“Ideally in the future, if you have cardiovascular disease, if you’re obese or have other complications, and you’ve got a signature in your blood that indicates you are at risk of severe disease, then we can risk-stratify patients when they are diagnosed,” he said. 

The research is a preliminary step, Dr. Kulasinghe said, because of the small sample size. This type of study is often difficult to conduct because researchers have to wait for the availability of organs, as well as request permission from families for postmortem autopsies and biopsies, to be able to look at the effects on dead tissues.

“Our challenge now is to draw a clinical finding from this, which we can’t at this stage,” he added. “But it’s a really fundamental biological difference we’re observing [between COVID-19 and flu], which we need to validate with larger studies.”

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

For Tara Lagu, MD, the realization that the health care system was broken for patients with disabilities came when a woman she had been treating seemed to keep ignoring Dr. Lagu’s request to see a urologist.

When Dr. Lagu asked the patient’s two attentive daughters about the delay, their response surprised her. The women said they couldn’t find a urologist who was willing to see a patient in a wheelchair.

Ingram/thinkstock

Surprised and a bit doubtful, Dr. Lagu checked around. She found that, indeed, the only way to get her patient in to see the type of physician required was to send her by ambulance.

“It opened my eyes to how hard it is for patients with disabilities to navigate the health care system,” Dr. Lagu said.

Dr. Lagu, director of the Center for Health Services and Outcomes Research at Northwestern University in Chicago, decided to take a closer look at how her colleagues in medicine care for – or not, as the case proved – the roughly one in four American adults, and millions of children, with disabilities.

In a series of three focus groups, Dr. Lagu and colleagues identified a range of obstacles – including some physician attitudes – that prevent people with disabilities from getting adequate care.

Lack of experience, logistics often cited

Some physicians admitted that limited resources and training left them without the space and necessary knowledge to properly care for patients with disabilities. They felt they lacked the expertise or exposure to care for individuals with disabilities, nor did they have enough time and space to properly accommodate these patients, according to the researchers. Some said they struggled to coordinate care for individuals with disabilities and did not know which types of accessible equipment, such as adjustable tables and chair scales, were needed or how to use them.

Several physicians also noted that they are inadequately reimbursed for the special accommodations – including additional staff, equipment, and time – required to care for these patients. One primary care physician said he hired a sign-language interpreter for a patient but the bill for the services exceeded the amount insurance reimbursed. As a result, he said, he spent $30 of his own money per visit to see the patient.

Because of these limitations, some physicians in the focus groups said they try to turn away patients with disabilities. Both specialists and general practitioners said they had told patients with disabilities that they didn’t feel they could provide the care needed, and suggested they look elsewhere. A few were surprisingly – even upsettingly – honest, Dr. Lagu said, making statements such as: “I am not the doctor for you.”
 

‘We really need a rewrite’

Previous work has shown that people with disabilities have worse health outcomes, such as undetected cancer, obesity, and cardiovascular disease.

But “the disability itself isn’t what leads to worse outcomes,” said Allison Kessler, MD, section chief of the Renée Crown Center for Spinal Cord Innovation and associate director of the Shirley Ryan AbilityLab in Chicago*. This study does a good job at highlighting “the need for change on multiple levels,” said Dr. Kessler, who was not a member of the study team.

“People with disabilities have all these disparities in access and outcomes. We’ve never understood why. I think the why is complicated,” Dr. Lagu added. “I think this study suggests some of the negative outcomes are due to explicit bias.”

“It’s also clear that the current framework of health care in the United States does not lend to allowing physicians and medical providers the time needed to adequately address patient issues – those with disabilities or just multiple complex problems,” Colin O’Reilly, DO, vice president and chief medical officer at Children’s Specialized Hospital, an acute rehabilitation facility affiliated with RWJBarnabas Health, in New Brunswick, N.J. “We really need a rewrite.”

However, Dr. O’Reilly said, such a small study population with no control group and no mention of physician resources makes it difficult to come to a strong conclusion about physician bias and discriminatory attitudes against individuals with disabilities.

Dr. Lagu agreed, saying this research “is not conclusive in any way.” The excuses doctors use to discharge patients with disabilities, such as “we don’t accept your insurance,” “we aren’t taking new patients,” and “we can’t provide you with the appropriate care,” could be legitimate, the study authors wrote. But the “disparities in care for people with disabilities suggest that there is a pattern of more frequently denying care to them than people without a disability,” they added.

Dr. Kessler said many of her patients have told her they experience barriers to care. Some say finding an office with the necessary equipment is a challenge or that they often don’t feel welcome.

The Americans With Disabilities Act (ADA) is a federal civil rights law that prohibits discrimination against individuals with disabilities in all public and private places that are open to the general public, including medical offices.

“It is difficult to enforce the ADA in medical settings,” the researchers noted. “Explanations physicians gave in this study could, for any single case of denying care, be legitimate.” Knowing whether a particular instance of denial of care represents discrimination related to disability is “nearly impossible,” they wrote.

All the experts agreed that the study adds valuable insight into an ongoing health disparity. And while system and policy changes are required, Dr. Kessler said, individual physicians can take steps to improve the situation.

A physician in an academic setting can look at the curriculum and the medical school and see about increasing exposure to patients with disabilities earlier in training. In a practice, physicians can retrain staff to ask every patient if an accommodation is needed. “Each one of those changes can only help us move our system in the right direction,” Dr. Kessler said.

The study was supported by a grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

*Correction, 10/5/22: This article includes a corrected title for Dr. Allison Kessler.

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

For Tara Lagu, MD, the realization that the health care system was broken for patients with disabilities came when a woman she had been treating seemed to keep ignoring Dr. Lagu’s request to see a urologist.

When Dr. Lagu asked the patient’s two attentive daughters about the delay, their response surprised her. The women said they couldn’t find a urologist who was willing to see a patient in a wheelchair.

Ingram/thinkstock

Surprised and a bit doubtful, Dr. Lagu checked around. She found that, indeed, the only way to get her patient in to see the type of physician required was to send her by ambulance.

“It opened my eyes to how hard it is for patients with disabilities to navigate the health care system,” Dr. Lagu said.

Dr. Lagu, director of the Center for Health Services and Outcomes Research at Northwestern University in Chicago, decided to take a closer look at how her colleagues in medicine care for – or not, as the case proved – the roughly one in four American adults, and millions of children, with disabilities.

In a series of three focus groups, Dr. Lagu and colleagues identified a range of obstacles – including some physician attitudes – that prevent people with disabilities from getting adequate care.

Lack of experience, logistics often cited

Some physicians admitted that limited resources and training left them without the space and necessary knowledge to properly care for patients with disabilities. They felt they lacked the expertise or exposure to care for individuals with disabilities, nor did they have enough time and space to properly accommodate these patients, according to the researchers. Some said they struggled to coordinate care for individuals with disabilities and did not know which types of accessible equipment, such as adjustable tables and chair scales, were needed or how to use them.

Several physicians also noted that they are inadequately reimbursed for the special accommodations – including additional staff, equipment, and time – required to care for these patients. One primary care physician said he hired a sign-language interpreter for a patient but the bill for the services exceeded the amount insurance reimbursed. As a result, he said, he spent $30 of his own money per visit to see the patient.

Because of these limitations, some physicians in the focus groups said they try to turn away patients with disabilities. Both specialists and general practitioners said they had told patients with disabilities that they didn’t feel they could provide the care needed, and suggested they look elsewhere. A few were surprisingly – even upsettingly – honest, Dr. Lagu said, making statements such as: “I am not the doctor for you.”
 

‘We really need a rewrite’

Previous work has shown that people with disabilities have worse health outcomes, such as undetected cancer, obesity, and cardiovascular disease.

But “the disability itself isn’t what leads to worse outcomes,” said Allison Kessler, MD, section chief of the Renée Crown Center for Spinal Cord Innovation and associate director of the Shirley Ryan AbilityLab in Chicago*. This study does a good job at highlighting “the need for change on multiple levels,” said Dr. Kessler, who was not a member of the study team.

“People with disabilities have all these disparities in access and outcomes. We’ve never understood why. I think the why is complicated,” Dr. Lagu added. “I think this study suggests some of the negative outcomes are due to explicit bias.”

“It’s also clear that the current framework of health care in the United States does not lend to allowing physicians and medical providers the time needed to adequately address patient issues – those with disabilities or just multiple complex problems,” Colin O’Reilly, DO, vice president and chief medical officer at Children’s Specialized Hospital, an acute rehabilitation facility affiliated with RWJBarnabas Health, in New Brunswick, N.J. “We really need a rewrite.”

However, Dr. O’Reilly said, such a small study population with no control group and no mention of physician resources makes it difficult to come to a strong conclusion about physician bias and discriminatory attitudes against individuals with disabilities.

Dr. Lagu agreed, saying this research “is not conclusive in any way.” The excuses doctors use to discharge patients with disabilities, such as “we don’t accept your insurance,” “we aren’t taking new patients,” and “we can’t provide you with the appropriate care,” could be legitimate, the study authors wrote. But the “disparities in care for people with disabilities suggest that there is a pattern of more frequently denying care to them than people without a disability,” they added.

Dr. Kessler said many of her patients have told her they experience barriers to care. Some say finding an office with the necessary equipment is a challenge or that they often don’t feel welcome.

The Americans With Disabilities Act (ADA) is a federal civil rights law that prohibits discrimination against individuals with disabilities in all public and private places that are open to the general public, including medical offices.

“It is difficult to enforce the ADA in medical settings,” the researchers noted. “Explanations physicians gave in this study could, for any single case of denying care, be legitimate.” Knowing whether a particular instance of denial of care represents discrimination related to disability is “nearly impossible,” they wrote.

All the experts agreed that the study adds valuable insight into an ongoing health disparity. And while system and policy changes are required, Dr. Kessler said, individual physicians can take steps to improve the situation.

A physician in an academic setting can look at the curriculum and the medical school and see about increasing exposure to patients with disabilities earlier in training. In a practice, physicians can retrain staff to ask every patient if an accommodation is needed. “Each one of those changes can only help us move our system in the right direction,” Dr. Kessler said.

The study was supported by a grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

*Correction, 10/5/22: This article includes a corrected title for Dr. Allison Kessler.

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

For Tara Lagu, MD, the realization that the health care system was broken for patients with disabilities came when a woman she had been treating seemed to keep ignoring Dr. Lagu’s request to see a urologist.

When Dr. Lagu asked the patient’s two attentive daughters about the delay, their response surprised her. The women said they couldn’t find a urologist who was willing to see a patient in a wheelchair.

Ingram/thinkstock

Surprised and a bit doubtful, Dr. Lagu checked around. She found that, indeed, the only way to get her patient in to see the type of physician required was to send her by ambulance.

“It opened my eyes to how hard it is for patients with disabilities to navigate the health care system,” Dr. Lagu said.

Dr. Lagu, director of the Center for Health Services and Outcomes Research at Northwestern University in Chicago, decided to take a closer look at how her colleagues in medicine care for – or not, as the case proved – the roughly one in four American adults, and millions of children, with disabilities.

In a series of three focus groups, Dr. Lagu and colleagues identified a range of obstacles – including some physician attitudes – that prevent people with disabilities from getting adequate care.

Lack of experience, logistics often cited

Some physicians admitted that limited resources and training left them without the space and necessary knowledge to properly care for patients with disabilities. They felt they lacked the expertise or exposure to care for individuals with disabilities, nor did they have enough time and space to properly accommodate these patients, according to the researchers. Some said they struggled to coordinate care for individuals with disabilities and did not know which types of accessible equipment, such as adjustable tables and chair scales, were needed or how to use them.

Several physicians also noted that they are inadequately reimbursed for the special accommodations – including additional staff, equipment, and time – required to care for these patients. One primary care physician said he hired a sign-language interpreter for a patient but the bill for the services exceeded the amount insurance reimbursed. As a result, he said, he spent $30 of his own money per visit to see the patient.

Because of these limitations, some physicians in the focus groups said they try to turn away patients with disabilities. Both specialists and general practitioners said they had told patients with disabilities that they didn’t feel they could provide the care needed, and suggested they look elsewhere. A few were surprisingly – even upsettingly – honest, Dr. Lagu said, making statements such as: “I am not the doctor for you.”
 

‘We really need a rewrite’

Previous work has shown that people with disabilities have worse health outcomes, such as undetected cancer, obesity, and cardiovascular disease.

But “the disability itself isn’t what leads to worse outcomes,” said Allison Kessler, MD, section chief of the Renée Crown Center for Spinal Cord Innovation and associate director of the Shirley Ryan AbilityLab in Chicago*. This study does a good job at highlighting “the need for change on multiple levels,” said Dr. Kessler, who was not a member of the study team.

“People with disabilities have all these disparities in access and outcomes. We’ve never understood why. I think the why is complicated,” Dr. Lagu added. “I think this study suggests some of the negative outcomes are due to explicit bias.”

“It’s also clear that the current framework of health care in the United States does not lend to allowing physicians and medical providers the time needed to adequately address patient issues – those with disabilities or just multiple complex problems,” Colin O’Reilly, DO, vice president and chief medical officer at Children’s Specialized Hospital, an acute rehabilitation facility affiliated with RWJBarnabas Health, in New Brunswick, N.J. “We really need a rewrite.”

However, Dr. O’Reilly said, such a small study population with no control group and no mention of physician resources makes it difficult to come to a strong conclusion about physician bias and discriminatory attitudes against individuals with disabilities.

Dr. Lagu agreed, saying this research “is not conclusive in any way.” The excuses doctors use to discharge patients with disabilities, such as “we don’t accept your insurance,” “we aren’t taking new patients,” and “we can’t provide you with the appropriate care,” could be legitimate, the study authors wrote. But the “disparities in care for people with disabilities suggest that there is a pattern of more frequently denying care to them than people without a disability,” they added.

Dr. Kessler said many of her patients have told her they experience barriers to care. Some say finding an office with the necessary equipment is a challenge or that they often don’t feel welcome.

The Americans With Disabilities Act (ADA) is a federal civil rights law that prohibits discrimination against individuals with disabilities in all public and private places that are open to the general public, including medical offices.

“It is difficult to enforce the ADA in medical settings,” the researchers noted. “Explanations physicians gave in this study could, for any single case of denying care, be legitimate.” Knowing whether a particular instance of denial of care represents discrimination related to disability is “nearly impossible,” they wrote.

All the experts agreed that the study adds valuable insight into an ongoing health disparity. And while system and policy changes are required, Dr. Kessler said, individual physicians can take steps to improve the situation.

A physician in an academic setting can look at the curriculum and the medical school and see about increasing exposure to patients with disabilities earlier in training. In a practice, physicians can retrain staff to ask every patient if an accommodation is needed. “Each one of those changes can only help us move our system in the right direction,” Dr. Kessler said.

The study was supported by a grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

*Correction, 10/5/22: This article includes a corrected title for Dr. Allison Kessler.

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

The antifibrotic pirfenidone (Esbriet) did not change the decline in forced vital capacity percentage (FVC%) from baseline of 10% or more or the risk of death compared with placebo in patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD). However, the drug appeared to slow the rate of decline in lung function, a phase 2 study indicated.

“This is the first randomized double-blind, placebo-controlled trial focused only on patients with RA-ILD,” observed Joshua Solomon, MD, National Jewish Health, Denver, and fellow TRAIL1 Network investigators.

“Although we did not meet our composite primary endpoint, key secondary endpoints showed a safe and beneficial effect of pirfenidone in patients with rheumatoid arthritis and evidence of fibrotic interstitial lung disease and the totality of the evidence suggests that pirfenidone is effective in the treatment of RA-ILD,” they suggest.

The study was published online in the Lancet Respiratory Medicine.


 

TRAIL1

The treatment for Rheumatoid Arthritis and Interstitial Lung Disease 1 (TRAIL1) was carried out in 34 academic centers specializing in ILD. Patients had RA and the presence of ILD on high-resolution CT scan and, where possible, lung biopsy. A total of 231 patients were randomly assigned to the pirfenidone group and the remainder to placebo. The mean age of patients was 66 (interquartile range (IQR, 61.0-74.0) in the pirfenidone group and 69.56 (IQR, 63.-74.5) among placebo controls.

Patients received pirfenidone at a dose of 2,403 mg per day, given in divided doses of three 267-mg tablets, three times a day, titrated to full dose over the course of 2 weeks. High-resolution CT scans were done at the beginning and the end of the study interval. Several disease-modifying antirheumatic drugs (DMARDS) were used for the treatment of RA but no differences were observed between treatment groups accounting for the DMARD classes.

“The primary endpoint was the incidence of the composite endpoint of a decline from baseline in [FVC%] of 10% or more or death during the 52-week treatment period,” Dr. Solomon and colleagues observed. The primary outcome was measured in the intent-to-treat (ITT) population.

Some 11% of patients in the active treatment group vs. 15% of patients in the placebo group met the composite primary endpoint, as investigators reported. For the secondary endpoint of the change in FVC over 52 weeks, patients treated with pirfenidone had a slow rate of decline in lung function compared with placebo patients as measured by estimated annual change in absolute FVC (–66 ml vs. –146 mL; P = .0082).

Moreover, in a post hoc analysis by CT pattern, the effect of the antifibrotic therapy on decline in FVC was more pronounced in those with usual interstitial pneumonia pattern on imaging compared with those with any pattern of ILD, the investigators observed. Indeed, approximately half of patients with the usual interstitial pneumonia in the pirfenidone group had a significantly smaller reduction in annual change in FVC at 52 weeks compared with over three-quarters of patients with usual interstitial pneumonia treated with placebo.

In contrast, the two groups were similar with regard to the decline in FVC% by 10% more or the frequency of progression. All-cause mortality rates were similar between the two groups. Adverse events thought to be related to treatment were more frequently reported in the pirfenidone group at 44% vs. 30% of placebo patients, the most frequent of which were nausea, fatigue, and diarrhea.

“These adverse events were generally grade 1 and were not clinically significant,” as the authors emphasized, although 24% of patients receiving pirfenidone discontinued treatment because of AEs vs. only 10% of placebo patients.

Limitations of the trial included early termination because of slow recruitment and the COVID-19 pandemic. This led to underpowering of the study.

Wrong endpoint?

In an accompanying editorial, Marco Sebastiani and Andreina Manfredi, MD, said that the choice of the primary outcome of an FVC decline from a baseline of 10% or more could have negatively influenced results because an FVC decline of 10% or more was probably too challenging to show a difference between the two groups. Indeed, the updated 2022 guidelines proposed a decline of 5% or more in FVC as a “significant threshold” for disease progression in patients with progressive pulmonary fibrosis, as the editorialists pointed out.

Nevertheless, the editorialists felt that the effect of pirfenidone on the decline in FVC seems to be significant, particularly when patients with usual interstitial pneumonia are considered. ”The magnitude of the effect of pirfenidone in patients with usual interstitial pneumonia-rheumatoid arthritis-interstitial lung disease and idiopathic pulmonary fibrosis [enrolled in a different study] was very similar,” they noted, “suggesting that a careful identification of usual interstitial pneumonia pattern at HRCT [high resolution CT] could be relevant in patients with RA-ILD. Moreover, given that pirfenidone did not modify its safety in these patients, the fact that pirfenidone can be safely used with DMARD therapy is important in clinical practice.

Dr. Solomon had no conflicts of interest to declare. Dr. Sebastiani disclosed ties with Bristol Myers Squibb, Pfizer, Boehringer-Ingelheim, Lilly, Amgen, Janssen, and Celltrion. Dr. Manfredi disclosed ties with Bristol Myers Squibb, Lilly, and Boehringer-Ingelheim. The study was funded by Genentech.

The antifibrotic pirfenidone (Esbriet) did not change the decline in forced vital capacity percentage (FVC%) from baseline of 10% or more or the risk of death compared with placebo in patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD). However, the drug appeared to slow the rate of decline in lung function, a phase 2 study indicated.

“This is the first randomized double-blind, placebo-controlled trial focused only on patients with RA-ILD,” observed Joshua Solomon, MD, National Jewish Health, Denver, and fellow TRAIL1 Network investigators.

“Although we did not meet our composite primary endpoint, key secondary endpoints showed a safe and beneficial effect of pirfenidone in patients with rheumatoid arthritis and evidence of fibrotic interstitial lung disease and the totality of the evidence suggests that pirfenidone is effective in the treatment of RA-ILD,” they suggest.

The study was published online in the Lancet Respiratory Medicine.


 

TRAIL1

The treatment for Rheumatoid Arthritis and Interstitial Lung Disease 1 (TRAIL1) was carried out in 34 academic centers specializing in ILD. Patients had RA and the presence of ILD on high-resolution CT scan and, where possible, lung biopsy. A total of 231 patients were randomly assigned to the pirfenidone group and the remainder to placebo. The mean age of patients was 66 (interquartile range (IQR, 61.0-74.0) in the pirfenidone group and 69.56 (IQR, 63.-74.5) among placebo controls.

Patients received pirfenidone at a dose of 2,403 mg per day, given in divided doses of three 267-mg tablets, three times a day, titrated to full dose over the course of 2 weeks. High-resolution CT scans were done at the beginning and the end of the study interval. Several disease-modifying antirheumatic drugs (DMARDS) were used for the treatment of RA but no differences were observed between treatment groups accounting for the DMARD classes.

“The primary endpoint was the incidence of the composite endpoint of a decline from baseline in [FVC%] of 10% or more or death during the 52-week treatment period,” Dr. Solomon and colleagues observed. The primary outcome was measured in the intent-to-treat (ITT) population.

Some 11% of patients in the active treatment group vs. 15% of patients in the placebo group met the composite primary endpoint, as investigators reported. For the secondary endpoint of the change in FVC over 52 weeks, patients treated with pirfenidone had a slow rate of decline in lung function compared with placebo patients as measured by estimated annual change in absolute FVC (–66 ml vs. –146 mL; P = .0082).

Moreover, in a post hoc analysis by CT pattern, the effect of the antifibrotic therapy on decline in FVC was more pronounced in those with usual interstitial pneumonia pattern on imaging compared with those with any pattern of ILD, the investigators observed. Indeed, approximately half of patients with the usual interstitial pneumonia in the pirfenidone group had a significantly smaller reduction in annual change in FVC at 52 weeks compared with over three-quarters of patients with usual interstitial pneumonia treated with placebo.

In contrast, the two groups were similar with regard to the decline in FVC% by 10% more or the frequency of progression. All-cause mortality rates were similar between the two groups. Adverse events thought to be related to treatment were more frequently reported in the pirfenidone group at 44% vs. 30% of placebo patients, the most frequent of which were nausea, fatigue, and diarrhea.

“These adverse events were generally grade 1 and were not clinically significant,” as the authors emphasized, although 24% of patients receiving pirfenidone discontinued treatment because of AEs vs. only 10% of placebo patients.

Limitations of the trial included early termination because of slow recruitment and the COVID-19 pandemic. This led to underpowering of the study.

Wrong endpoint?

In an accompanying editorial, Marco Sebastiani and Andreina Manfredi, MD, said that the choice of the primary outcome of an FVC decline from a baseline of 10% or more could have negatively influenced results because an FVC decline of 10% or more was probably too challenging to show a difference between the two groups. Indeed, the updated 2022 guidelines proposed a decline of 5% or more in FVC as a “significant threshold” for disease progression in patients with progressive pulmonary fibrosis, as the editorialists pointed out.

Nevertheless, the editorialists felt that the effect of pirfenidone on the decline in FVC seems to be significant, particularly when patients with usual interstitial pneumonia are considered. ”The magnitude of the effect of pirfenidone in patients with usual interstitial pneumonia-rheumatoid arthritis-interstitial lung disease and idiopathic pulmonary fibrosis [enrolled in a different study] was very similar,” they noted, “suggesting that a careful identification of usual interstitial pneumonia pattern at HRCT [high resolution CT] could be relevant in patients with RA-ILD. Moreover, given that pirfenidone did not modify its safety in these patients, the fact that pirfenidone can be safely used with DMARD therapy is important in clinical practice.

Dr. Solomon had no conflicts of interest to declare. Dr. Sebastiani disclosed ties with Bristol Myers Squibb, Pfizer, Boehringer-Ingelheim, Lilly, Amgen, Janssen, and Celltrion. Dr. Manfredi disclosed ties with Bristol Myers Squibb, Lilly, and Boehringer-Ingelheim. The study was funded by Genentech.

The antifibrotic pirfenidone (Esbriet) did not change the decline in forced vital capacity percentage (FVC%) from baseline of 10% or more or the risk of death compared with placebo in patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD). However, the drug appeared to slow the rate of decline in lung function, a phase 2 study indicated.

“This is the first randomized double-blind, placebo-controlled trial focused only on patients with RA-ILD,” observed Joshua Solomon, MD, National Jewish Health, Denver, and fellow TRAIL1 Network investigators.

“Although we did not meet our composite primary endpoint, key secondary endpoints showed a safe and beneficial effect of pirfenidone in patients with rheumatoid arthritis and evidence of fibrotic interstitial lung disease and the totality of the evidence suggests that pirfenidone is effective in the treatment of RA-ILD,” they suggest.

The study was published online in the Lancet Respiratory Medicine.


 

TRAIL1

The treatment for Rheumatoid Arthritis and Interstitial Lung Disease 1 (TRAIL1) was carried out in 34 academic centers specializing in ILD. Patients had RA and the presence of ILD on high-resolution CT scan and, where possible, lung biopsy. A total of 231 patients were randomly assigned to the pirfenidone group and the remainder to placebo. The mean age of patients was 66 (interquartile range (IQR, 61.0-74.0) in the pirfenidone group and 69.56 (IQR, 63.-74.5) among placebo controls.

Patients received pirfenidone at a dose of 2,403 mg per day, given in divided doses of three 267-mg tablets, three times a day, titrated to full dose over the course of 2 weeks. High-resolution CT scans were done at the beginning and the end of the study interval. Several disease-modifying antirheumatic drugs (DMARDS) were used for the treatment of RA but no differences were observed between treatment groups accounting for the DMARD classes.

“The primary endpoint was the incidence of the composite endpoint of a decline from baseline in [FVC%] of 10% or more or death during the 52-week treatment period,” Dr. Solomon and colleagues observed. The primary outcome was measured in the intent-to-treat (ITT) population.

Some 11% of patients in the active treatment group vs. 15% of patients in the placebo group met the composite primary endpoint, as investigators reported. For the secondary endpoint of the change in FVC over 52 weeks, patients treated with pirfenidone had a slow rate of decline in lung function compared with placebo patients as measured by estimated annual change in absolute FVC (–66 ml vs. –146 mL; P = .0082).

Moreover, in a post hoc analysis by CT pattern, the effect of the antifibrotic therapy on decline in FVC was more pronounced in those with usual interstitial pneumonia pattern on imaging compared with those with any pattern of ILD, the investigators observed. Indeed, approximately half of patients with the usual interstitial pneumonia in the pirfenidone group had a significantly smaller reduction in annual change in FVC at 52 weeks compared with over three-quarters of patients with usual interstitial pneumonia treated with placebo.

In contrast, the two groups were similar with regard to the decline in FVC% by 10% more or the frequency of progression. All-cause mortality rates were similar between the two groups. Adverse events thought to be related to treatment were more frequently reported in the pirfenidone group at 44% vs. 30% of placebo patients, the most frequent of which were nausea, fatigue, and diarrhea.

“These adverse events were generally grade 1 and were not clinically significant,” as the authors emphasized, although 24% of patients receiving pirfenidone discontinued treatment because of AEs vs. only 10% of placebo patients.

Limitations of the trial included early termination because of slow recruitment and the COVID-19 pandemic. This led to underpowering of the study.

Wrong endpoint?

In an accompanying editorial, Marco Sebastiani and Andreina Manfredi, MD, said that the choice of the primary outcome of an FVC decline from a baseline of 10% or more could have negatively influenced results because an FVC decline of 10% or more was probably too challenging to show a difference between the two groups. Indeed, the updated 2022 guidelines proposed a decline of 5% or more in FVC as a “significant threshold” for disease progression in patients with progressive pulmonary fibrosis, as the editorialists pointed out.

Nevertheless, the editorialists felt that the effect of pirfenidone on the decline in FVC seems to be significant, particularly when patients with usual interstitial pneumonia are considered. ”The magnitude of the effect of pirfenidone in patients with usual interstitial pneumonia-rheumatoid arthritis-interstitial lung disease and idiopathic pulmonary fibrosis [enrolled in a different study] was very similar,” they noted, “suggesting that a careful identification of usual interstitial pneumonia pattern at HRCT [high resolution CT] could be relevant in patients with RA-ILD. Moreover, given that pirfenidone did not modify its safety in these patients, the fact that pirfenidone can be safely used with DMARD therapy is important in clinical practice.

Dr. Solomon had no conflicts of interest to declare. Dr. Sebastiani disclosed ties with Bristol Myers Squibb, Pfizer, Boehringer-Ingelheim, Lilly, Amgen, Janssen, and Celltrion. Dr. Manfredi disclosed ties with Bristol Myers Squibb, Lilly, and Boehringer-Ingelheim. The study was funded by Genentech.

STOCKHOLM – It remains inconclusive whether SARS-CoV-2 infection predisposes children and adolescents to a higher risk of type 1 diabetes. Data from two new studies and a recently published research letter add to the growing body of knowledge on the subject, but still can’t draw any definitive conclusions.

The latest results from a Norwegian and a Scottish study both examine incidence of type 1 diabetes in young people with a history of SARS-CoV-2 infection and were reported at the annual meeting of the European Association for the Study of Diabetes.

A 60% increased risk for type 1 diabetes at least 31 days after SARS-CoV-2 infection (adjusted hazard ratio, 1.63) was found in the Norwegian study, while in contrast, the Scottish study only found an increased risk in the first few months of the pandemic, in 2020, but importantly, no association over a much longer time period (March 2020–November 2021).

In a comment on Twitter on the two studies presented at EASD, session moderator Kamlesh Khunti, MD, professor of primary care diabetes and vascular medicine at the University of Leicester, (England), said: “In summary, two studies showing no or weak association of type 1 diabetes with COVID.”

But new data in the research letter published in JAMA Network Open, based on U.S. figures, also found an almost doubling of type 1 diabetes in children in the first few months after COVID-19 infection relative to infection with other respiratory viruses.

Lead author of the Scottish study, Helen Colhoun, PhD, honorary public health consultant at Public Health Scotland, commented: “Data in children are variable year on year, which emphasizes the need to be cautious over taking a tiny snapshot.”

Nevertheless, this is “a hugely important question and we must not drop the ball. [We must] keep looking at it and maintain scientific equipoise. ... [This] reinforces the need to carry on this analysis into the future to obtain an unequivocal picture,” she emphasized.
 

Norwegian study: If there is an association, the risk is small

German Tapia, PhD, from the Norwegian Institute of Public Health, Oslo, presented the results of a study of SARS-CoV-2 infection and subsequent risk of type 1 diabetes in 1.2 million children in Norway.

Of these, 424,354 children had been infected with SARS-CoV-2, and there were 990 incident cases of type 1 diabetes.

“What we do know about COVID-19 in children is that the symptoms are mild and only a small proportion are hospitalized with more serious symptoms. But we do not know the long-term effects of COVID-19 infection because this requires a longer follow-up period,” remarked Dr. Tapia, adding that other viral infections are thought to be linked to the development of type 1 diabetes, in particular, respiratory infections.

The data were sourced from the Norwegian Emergency Preparedness Register for COVID-19, which gathers daily data updates including infections (positive and negative results for free-of-charge testing), diagnoses (primary and secondary care), vaccinations (also free of charge), prescribed medications, and basic demographics.

“We link these data using the personal identification number that every Norwegian citizen has,” explained Dr. Tapia.

He presented results from two cohorts: firstly, results in children only, including those tested for SARS-CoV-2 infection, and secondly, a full national Norwegian population cohort.

Regarding the first cohort, those under 18 years who tested positive for SARS-CoV-2 infection, from March 2020 to March 2022, had a significantly increased risk of type 1 diabetes at least 31 days after infection, with an adjusted hazard ratio of 1.63 (95% confidence interval, 1.08-2.47; P = .02). Adjustments were made for age, sex, non-Nordic country of origin, geographic area, and socioeconomic factors.

For children who developed type 1 diabetes within 30 days of a SARS-CoV-2 infection, the HR was 1.26 (95% CI, 0.72-2.19; P = .42), which did not reach statistical significance.

“The fact that fewer people developed type 1 diabetes within 30 days is not surprising because we know that type 1 diabetes develops over a long period of time,” Dr. Tapia said.

“For this reason, we would not expect to find new cases of those people who develop type 1 diabetes within 30 days of COVID-19 infection,” he explained. In these cases, “it is most likely that they already had [type 1 diabetes], and the infection probably triggered clinical symptoms, so their type 1 diabetes was discovered.”

Turning to the full population cohort and diagnoses of type 1 diabetes over 30 days after SARS-CoV-2 infection, the Norwegian researchers found an association, with an HR of 1.57 (95% CI, 1.06-2.33; P = .03), while diagnosis of type 1 diabetes at 30 days or less generated a hazard ratio of 1.22 (95% CI, 0.72-2.19; P = .42).

“So very similar results were found, and after adjustment for confounders, results were still similar,” reported Dr. Tapia.

He also conducted a similar analysis with vaccination as an exposure but found no association between vaccination against SARS-CoV-2 and diagnosis of type 1 diabetes.

“From these results, we conclude that this suggests an increase in diagnosis of type 1 diabetes after SARS-CoV-2 infection, but it must be noted that the absolute risk of developing type 1 diabetes after infection in children is low, with most children not developing the disease,” he emphasized. “There are nearly half a million children who have been infected with SARS-CoV-2 in Norway, but only a very small proportion develop type 1 diabetes.”
 

Scottish study: No association found over longer term

Dr. Colhoun and colleagues looked at the relationship between incident type 1 diabetes and SARS-CoV-2 infection in children in Scotland using e-health record linkage.

The study involved 1.8 million people under 35 years of age and found very weak, if any, evidence of an association between incident type 1 diabetes and SARS-CoV-2.

Examining data between March 2020 and November 2021, Dr. Colhoun and colleagues identified 365,080 individuals up to age 35 with at least one detected SARS-CoV-2 infection during follow-up and 1,074 who developed type 1 diabetes.

“In children under 16 years, suspected cases of type 1 diabetes are admitted to hospital, and 97% of diagnosis dates are recorded in the Scottish Care Information – Diabetes Collaboration register [SCI-Diabetes] prior to or within 2 days of the first hospital admission for type 1 diabetes,” Dr. Colhoun said, stressing the timeliness of the data.

“We found the incidence of type 1 diabetes diagnosis increased 1.2-fold in those aged 0-14 years, but we did not find any association at an individual level of COVID-19 infection over 30 days prior to a type 1 diabetes diagnosis, in this particular dataset,” she reported. In young people aged 15-34, there was a linear increase in incident type 1 diabetes from 2015 to 2021 with no pandemic increase.

Referring to the 1.2-fold increase soon after the pandemic started, she explained that, in 0- to 14-year-olds, the increase followed a drop in the preceding months prepandemic in 2019. They also found that the seasonal pattern of type 1 diabetes diagnoses remained roughly the same across the pandemic months, with typical peaks in February and September.

In the cohort of under 35s, researchers also found a rate ratio of 2.62 (95% CI, 1.81-3.78) within a 30-day window of SARS-CoV-2 infection, but beyond 30 days, no evidence was seen of an association, with a RR of 0.86 (95% CI, 0.62-1.21; P = .40), she reported.

She explained her reasons for not considering diagnoses within 30 days of COVID-19 as causative. Echoing Dr. Tapia, Dr. Colhoun said the median time from symptom onset to diagnosis of type 1 diabetes is 25 days. “This suggests that 50% have had symptoms for over 25 days at diagnosis.”

She also stressed that when they compared the timing of SARS-CoV-2 testing with diagnosis, they found a much higher rate of COVID-19 testing around diagnosis. “This was not least because everyone admitted to hospital had to have a COVID-19 test.”
 

Latest U.S. data point to a link

Meanwhile, for the new data reported in JAMA Network Open, medical student Ellen K. Kendall of Case Western Reserve University, Cleveland, matched 571,256 pediatric patients: 285,628 with COVID-19 and 285,628 with non–COVID-19 respiratory infections.

By 6 months after COVID-19, 123 patients (0.043%) had received a new diagnosis of type 1 diabetes, but only 72 (0.025%) were diagnosed with type 1 diabetes within 6 months after non–COVID-19 respiratory infection.

At 1, 3, and 6 months after infection, risk of diagnosis of type 1 diabetes was greater among those infected with SARS-CoV-2, compared with those with non–COVID-19 respiratory infection (1 month: HR, 1.96; 3 months: HR, 2.10; and 6 months: HR, 1.83), and in subgroups of patients aged 0-9 years, a group unlikely to develop type 2 diabetes.

“In this study, new type 1 diabetes diagnoses were more likely to occur among pediatric patients with prior COVID-19 than among those with other respiratory infections (or with other encounters with health systems),” noted Ms. Kendall and coauthors. “Respiratory infections have previously been associated with onset of type 1 diabetes, but this risk was even higher among those with COVID-19 in our study, raising concern for long-term, post–COVID-19 autoimmune complications among youths.”

“The increased risk of new-onset type 1 diabetes after COVID-19 adds an important consideration for risk–benefit discussions for prevention and treatment of SARS-CoV-2 infection in pediatric populations,” they concluded.

A study from the Centers for Disease Control and Prevention published in January 2022, also concluded there was a link between COVID-19 and diabetes in children, but not with other acute respiratory infections. Children were 2.5 times more likely to be diagnosed with diabetes following a SARS-CoV-2 infection, it found.

However, the study has been criticized because it pooled all types of diabetes together and did not account for other health conditions, medications that can increase blood glucose levels, race, obesity, and other social determinants of health that might influence a child’s risk of acquiring COVID-19 or diabetes.

“I’ve no doubt that the CDC data were incorrect because the incidence rate for ... diabetes, even in those never exposed to COVID-19 infection, was 10 times the rate ever reported in the U.S.,” Dr. Colhoun said. “There’s no way these data are correct. I believe there was a confusion between incidence and prevalence of diabetes.”

“This paper caused a great deal of panic, especially among those who have a child with type 1diabetes, so we need to be very careful not to cause undue alarm until we have more definitive evidence in this arena,” she stressed.

However, she also acknowledged that the new Norwegian study was well conducted, and she has no methodological concerns about it, so “I think we just have to wait and see.”

Given the inconclusiveness on the issue, there is an ongoing CoviDiab registry collecting data on this very subject.

Dr. Tapia presented on behalf of lead author Dr. Gulseth, who has reported no relevant financial relationships. Dr. Colhoun also reported no relevant financial relationships.

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

STOCKHOLM – It remains inconclusive whether SARS-CoV-2 infection predisposes children and adolescents to a higher risk of type 1 diabetes. Data from two new studies and a recently published research letter add to the growing body of knowledge on the subject, but still can’t draw any definitive conclusions.

The latest results from a Norwegian and a Scottish study both examine incidence of type 1 diabetes in young people with a history of SARS-CoV-2 infection and were reported at the annual meeting of the European Association for the Study of Diabetes.

A 60% increased risk for type 1 diabetes at least 31 days after SARS-CoV-2 infection (adjusted hazard ratio, 1.63) was found in the Norwegian study, while in contrast, the Scottish study only found an increased risk in the first few months of the pandemic, in 2020, but importantly, no association over a much longer time period (March 2020–November 2021).

In a comment on Twitter on the two studies presented at EASD, session moderator Kamlesh Khunti, MD, professor of primary care diabetes and vascular medicine at the University of Leicester, (England), said: “In summary, two studies showing no or weak association of type 1 diabetes with COVID.”

But new data in the research letter published in JAMA Network Open, based on U.S. figures, also found an almost doubling of type 1 diabetes in children in the first few months after COVID-19 infection relative to infection with other respiratory viruses.

Lead author of the Scottish study, Helen Colhoun, PhD, honorary public health consultant at Public Health Scotland, commented: “Data in children are variable year on year, which emphasizes the need to be cautious over taking a tiny snapshot.”

Nevertheless, this is “a hugely important question and we must not drop the ball. [We must] keep looking at it and maintain scientific equipoise. ... [This] reinforces the need to carry on this analysis into the future to obtain an unequivocal picture,” she emphasized.
 

Norwegian study: If there is an association, the risk is small

German Tapia, PhD, from the Norwegian Institute of Public Health, Oslo, presented the results of a study of SARS-CoV-2 infection and subsequent risk of type 1 diabetes in 1.2 million children in Norway.

Of these, 424,354 children had been infected with SARS-CoV-2, and there were 990 incident cases of type 1 diabetes.

“What we do know about COVID-19 in children is that the symptoms are mild and only a small proportion are hospitalized with more serious symptoms. But we do not know the long-term effects of COVID-19 infection because this requires a longer follow-up period,” remarked Dr. Tapia, adding that other viral infections are thought to be linked to the development of type 1 diabetes, in particular, respiratory infections.

The data were sourced from the Norwegian Emergency Preparedness Register for COVID-19, which gathers daily data updates including infections (positive and negative results for free-of-charge testing), diagnoses (primary and secondary care), vaccinations (also free of charge), prescribed medications, and basic demographics.

“We link these data using the personal identification number that every Norwegian citizen has,” explained Dr. Tapia.

He presented results from two cohorts: firstly, results in children only, including those tested for SARS-CoV-2 infection, and secondly, a full national Norwegian population cohort.

Regarding the first cohort, those under 18 years who tested positive for SARS-CoV-2 infection, from March 2020 to March 2022, had a significantly increased risk of type 1 diabetes at least 31 days after infection, with an adjusted hazard ratio of 1.63 (95% confidence interval, 1.08-2.47; P = .02). Adjustments were made for age, sex, non-Nordic country of origin, geographic area, and socioeconomic factors.

For children who developed type 1 diabetes within 30 days of a SARS-CoV-2 infection, the HR was 1.26 (95% CI, 0.72-2.19; P = .42), which did not reach statistical significance.

“The fact that fewer people developed type 1 diabetes within 30 days is not surprising because we know that type 1 diabetes develops over a long period of time,” Dr. Tapia said.

“For this reason, we would not expect to find new cases of those people who develop type 1 diabetes within 30 days of COVID-19 infection,” he explained. In these cases, “it is most likely that they already had [type 1 diabetes], and the infection probably triggered clinical symptoms, so their type 1 diabetes was discovered.”

Turning to the full population cohort and diagnoses of type 1 diabetes over 30 days after SARS-CoV-2 infection, the Norwegian researchers found an association, with an HR of 1.57 (95% CI, 1.06-2.33; P = .03), while diagnosis of type 1 diabetes at 30 days or less generated a hazard ratio of 1.22 (95% CI, 0.72-2.19; P = .42).

“So very similar results were found, and after adjustment for confounders, results were still similar,” reported Dr. Tapia.

He also conducted a similar analysis with vaccination as an exposure but found no association between vaccination against SARS-CoV-2 and diagnosis of type 1 diabetes.

“From these results, we conclude that this suggests an increase in diagnosis of type 1 diabetes after SARS-CoV-2 infection, but it must be noted that the absolute risk of developing type 1 diabetes after infection in children is low, with most children not developing the disease,” he emphasized. “There are nearly half a million children who have been infected with SARS-CoV-2 in Norway, but only a very small proportion develop type 1 diabetes.”
 

Scottish study: No association found over longer term

Dr. Colhoun and colleagues looked at the relationship between incident type 1 diabetes and SARS-CoV-2 infection in children in Scotland using e-health record linkage.

The study involved 1.8 million people under 35 years of age and found very weak, if any, evidence of an association between incident type 1 diabetes and SARS-CoV-2.

Examining data between March 2020 and November 2021, Dr. Colhoun and colleagues identified 365,080 individuals up to age 35 with at least one detected SARS-CoV-2 infection during follow-up and 1,074 who developed type 1 diabetes.

“In children under 16 years, suspected cases of type 1 diabetes are admitted to hospital, and 97% of diagnosis dates are recorded in the Scottish Care Information – Diabetes Collaboration register [SCI-Diabetes] prior to or within 2 days of the first hospital admission for type 1 diabetes,” Dr. Colhoun said, stressing the timeliness of the data.

“We found the incidence of type 1 diabetes diagnosis increased 1.2-fold in those aged 0-14 years, but we did not find any association at an individual level of COVID-19 infection over 30 days prior to a type 1 diabetes diagnosis, in this particular dataset,” she reported. In young people aged 15-34, there was a linear increase in incident type 1 diabetes from 2015 to 2021 with no pandemic increase.

Referring to the 1.2-fold increase soon after the pandemic started, she explained that, in 0- to 14-year-olds, the increase followed a drop in the preceding months prepandemic in 2019. They also found that the seasonal pattern of type 1 diabetes diagnoses remained roughly the same across the pandemic months, with typical peaks in February and September.

In the cohort of under 35s, researchers also found a rate ratio of 2.62 (95% CI, 1.81-3.78) within a 30-day window of SARS-CoV-2 infection, but beyond 30 days, no evidence was seen of an association, with a RR of 0.86 (95% CI, 0.62-1.21; P = .40), she reported.

She explained her reasons for not considering diagnoses within 30 days of COVID-19 as causative. Echoing Dr. Tapia, Dr. Colhoun said the median time from symptom onset to diagnosis of type 1 diabetes is 25 days. “This suggests that 50% have had symptoms for over 25 days at diagnosis.”

She also stressed that when they compared the timing of SARS-CoV-2 testing with diagnosis, they found a much higher rate of COVID-19 testing around diagnosis. “This was not least because everyone admitted to hospital had to have a COVID-19 test.”
 

Latest U.S. data point to a link

Meanwhile, for the new data reported in JAMA Network Open, medical student Ellen K. Kendall of Case Western Reserve University, Cleveland, matched 571,256 pediatric patients: 285,628 with COVID-19 and 285,628 with non–COVID-19 respiratory infections.

By 6 months after COVID-19, 123 patients (0.043%) had received a new diagnosis of type 1 diabetes, but only 72 (0.025%) were diagnosed with type 1 diabetes within 6 months after non–COVID-19 respiratory infection.

At 1, 3, and 6 months after infection, risk of diagnosis of type 1 diabetes was greater among those infected with SARS-CoV-2, compared with those with non–COVID-19 respiratory infection (1 month: HR, 1.96; 3 months: HR, 2.10; and 6 months: HR, 1.83), and in subgroups of patients aged 0-9 years, a group unlikely to develop type 2 diabetes.

“In this study, new type 1 diabetes diagnoses were more likely to occur among pediatric patients with prior COVID-19 than among those with other respiratory infections (or with other encounters with health systems),” noted Ms. Kendall and coauthors. “Respiratory infections have previously been associated with onset of type 1 diabetes, but this risk was even higher among those with COVID-19 in our study, raising concern for long-term, post–COVID-19 autoimmune complications among youths.”

“The increased risk of new-onset type 1 diabetes after COVID-19 adds an important consideration for risk–benefit discussions for prevention and treatment of SARS-CoV-2 infection in pediatric populations,” they concluded.

A study from the Centers for Disease Control and Prevention published in January 2022, also concluded there was a link between COVID-19 and diabetes in children, but not with other acute respiratory infections. Children were 2.5 times more likely to be diagnosed with diabetes following a SARS-CoV-2 infection, it found.

However, the study has been criticized because it pooled all types of diabetes together and did not account for other health conditions, medications that can increase blood glucose levels, race, obesity, and other social determinants of health that might influence a child’s risk of acquiring COVID-19 or diabetes.

“I’ve no doubt that the CDC data were incorrect because the incidence rate for ... diabetes, even in those never exposed to COVID-19 infection, was 10 times the rate ever reported in the U.S.,” Dr. Colhoun said. “There’s no way these data are correct. I believe there was a confusion between incidence and prevalence of diabetes.”

“This paper caused a great deal of panic, especially among those who have a child with type 1diabetes, so we need to be very careful not to cause undue alarm until we have more definitive evidence in this arena,” she stressed.

However, she also acknowledged that the new Norwegian study was well conducted, and she has no methodological concerns about it, so “I think we just have to wait and see.”

Given the inconclusiveness on the issue, there is an ongoing CoviDiab registry collecting data on this very subject.

Dr. Tapia presented on behalf of lead author Dr. Gulseth, who has reported no relevant financial relationships. Dr. Colhoun also reported no relevant financial relationships.

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

STOCKHOLM – It remains inconclusive whether SARS-CoV-2 infection predisposes children and adolescents to a higher risk of type 1 diabetes. Data from two new studies and a recently published research letter add to the growing body of knowledge on the subject, but still can’t draw any definitive conclusions.

The latest results from a Norwegian and a Scottish study both examine incidence of type 1 diabetes in young people with a history of SARS-CoV-2 infection and were reported at the annual meeting of the European Association for the Study of Diabetes.

A 60% increased risk for type 1 diabetes at least 31 days after SARS-CoV-2 infection (adjusted hazard ratio, 1.63) was found in the Norwegian study, while in contrast, the Scottish study only found an increased risk in the first few months of the pandemic, in 2020, but importantly, no association over a much longer time period (March 2020–November 2021).

In a comment on Twitter on the two studies presented at EASD, session moderator Kamlesh Khunti, MD, professor of primary care diabetes and vascular medicine at the University of Leicester, (England), said: “In summary, two studies showing no or weak association of type 1 diabetes with COVID.”

But new data in the research letter published in JAMA Network Open, based on U.S. figures, also found an almost doubling of type 1 diabetes in children in the first few months after COVID-19 infection relative to infection with other respiratory viruses.

Lead author of the Scottish study, Helen Colhoun, PhD, honorary public health consultant at Public Health Scotland, commented: “Data in children are variable year on year, which emphasizes the need to be cautious over taking a tiny snapshot.”

Nevertheless, this is “a hugely important question and we must not drop the ball. [We must] keep looking at it and maintain scientific equipoise. ... [This] reinforces the need to carry on this analysis into the future to obtain an unequivocal picture,” she emphasized.
 

Norwegian study: If there is an association, the risk is small

German Tapia, PhD, from the Norwegian Institute of Public Health, Oslo, presented the results of a study of SARS-CoV-2 infection and subsequent risk of type 1 diabetes in 1.2 million children in Norway.

Of these, 424,354 children had been infected with SARS-CoV-2, and there were 990 incident cases of type 1 diabetes.

“What we do know about COVID-19 in children is that the symptoms are mild and only a small proportion are hospitalized with more serious symptoms. But we do not know the long-term effects of COVID-19 infection because this requires a longer follow-up period,” remarked Dr. Tapia, adding that other viral infections are thought to be linked to the development of type 1 diabetes, in particular, respiratory infections.

The data were sourced from the Norwegian Emergency Preparedness Register for COVID-19, which gathers daily data updates including infections (positive and negative results for free-of-charge testing), diagnoses (primary and secondary care), vaccinations (also free of charge), prescribed medications, and basic demographics.

“We link these data using the personal identification number that every Norwegian citizen has,” explained Dr. Tapia.

He presented results from two cohorts: firstly, results in children only, including those tested for SARS-CoV-2 infection, and secondly, a full national Norwegian population cohort.

Regarding the first cohort, those under 18 years who tested positive for SARS-CoV-2 infection, from March 2020 to March 2022, had a significantly increased risk of type 1 diabetes at least 31 days after infection, with an adjusted hazard ratio of 1.63 (95% confidence interval, 1.08-2.47; P = .02). Adjustments were made for age, sex, non-Nordic country of origin, geographic area, and socioeconomic factors.

For children who developed type 1 diabetes within 30 days of a SARS-CoV-2 infection, the HR was 1.26 (95% CI, 0.72-2.19; P = .42), which did not reach statistical significance.

“The fact that fewer people developed type 1 diabetes within 30 days is not surprising because we know that type 1 diabetes develops over a long period of time,” Dr. Tapia said.

“For this reason, we would not expect to find new cases of those people who develop type 1 diabetes within 30 days of COVID-19 infection,” he explained. In these cases, “it is most likely that they already had [type 1 diabetes], and the infection probably triggered clinical symptoms, so their type 1 diabetes was discovered.”

Turning to the full population cohort and diagnoses of type 1 diabetes over 30 days after SARS-CoV-2 infection, the Norwegian researchers found an association, with an HR of 1.57 (95% CI, 1.06-2.33; P = .03), while diagnosis of type 1 diabetes at 30 days or less generated a hazard ratio of 1.22 (95% CI, 0.72-2.19; P = .42).

“So very similar results were found, and after adjustment for confounders, results were still similar,” reported Dr. Tapia.

He also conducted a similar analysis with vaccination as an exposure but found no association between vaccination against SARS-CoV-2 and diagnosis of type 1 diabetes.

“From these results, we conclude that this suggests an increase in diagnosis of type 1 diabetes after SARS-CoV-2 infection, but it must be noted that the absolute risk of developing type 1 diabetes after infection in children is low, with most children not developing the disease,” he emphasized. “There are nearly half a million children who have been infected with SARS-CoV-2 in Norway, but only a very small proportion develop type 1 diabetes.”
 

Scottish study: No association found over longer term

Dr. Colhoun and colleagues looked at the relationship between incident type 1 diabetes and SARS-CoV-2 infection in children in Scotland using e-health record linkage.

The study involved 1.8 million people under 35 years of age and found very weak, if any, evidence of an association between incident type 1 diabetes and SARS-CoV-2.

Examining data between March 2020 and November 2021, Dr. Colhoun and colleagues identified 365,080 individuals up to age 35 with at least one detected SARS-CoV-2 infection during follow-up and 1,074 who developed type 1 diabetes.

“In children under 16 years, suspected cases of type 1 diabetes are admitted to hospital, and 97% of diagnosis dates are recorded in the Scottish Care Information – Diabetes Collaboration register [SCI-Diabetes] prior to or within 2 days of the first hospital admission for type 1 diabetes,” Dr. Colhoun said, stressing the timeliness of the data.

“We found the incidence of type 1 diabetes diagnosis increased 1.2-fold in those aged 0-14 years, but we did not find any association at an individual level of COVID-19 infection over 30 days prior to a type 1 diabetes diagnosis, in this particular dataset,” she reported. In young people aged 15-34, there was a linear increase in incident type 1 diabetes from 2015 to 2021 with no pandemic increase.

Referring to the 1.2-fold increase soon after the pandemic started, she explained that, in 0- to 14-year-olds, the increase followed a drop in the preceding months prepandemic in 2019. They also found that the seasonal pattern of type 1 diabetes diagnoses remained roughly the same across the pandemic months, with typical peaks in February and September.

In the cohort of under 35s, researchers also found a rate ratio of 2.62 (95% CI, 1.81-3.78) within a 30-day window of SARS-CoV-2 infection, but beyond 30 days, no evidence was seen of an association, with a RR of 0.86 (95% CI, 0.62-1.21; P = .40), she reported.

She explained her reasons for not considering diagnoses within 30 days of COVID-19 as causative. Echoing Dr. Tapia, Dr. Colhoun said the median time from symptom onset to diagnosis of type 1 diabetes is 25 days. “This suggests that 50% have had symptoms for over 25 days at diagnosis.”

She also stressed that when they compared the timing of SARS-CoV-2 testing with diagnosis, they found a much higher rate of COVID-19 testing around diagnosis. “This was not least because everyone admitted to hospital had to have a COVID-19 test.”
 

Latest U.S. data point to a link

Meanwhile, for the new data reported in JAMA Network Open, medical student Ellen K. Kendall of Case Western Reserve University, Cleveland, matched 571,256 pediatric patients: 285,628 with COVID-19 and 285,628 with non–COVID-19 respiratory infections.

By 6 months after COVID-19, 123 patients (0.043%) had received a new diagnosis of type 1 diabetes, but only 72 (0.025%) were diagnosed with type 1 diabetes within 6 months after non–COVID-19 respiratory infection.

At 1, 3, and 6 months after infection, risk of diagnosis of type 1 diabetes was greater among those infected with SARS-CoV-2, compared with those with non–COVID-19 respiratory infection (1 month: HR, 1.96; 3 months: HR, 2.10; and 6 months: HR, 1.83), and in subgroups of patients aged 0-9 years, a group unlikely to develop type 2 diabetes.

“In this study, new type 1 diabetes diagnoses were more likely to occur among pediatric patients with prior COVID-19 than among those with other respiratory infections (or with other encounters with health systems),” noted Ms. Kendall and coauthors. “Respiratory infections have previously been associated with onset of type 1 diabetes, but this risk was even higher among those with COVID-19 in our study, raising concern for long-term, post–COVID-19 autoimmune complications among youths.”

“The increased risk of new-onset type 1 diabetes after COVID-19 adds an important consideration for risk–benefit discussions for prevention and treatment of SARS-CoV-2 infection in pediatric populations,” they concluded.

A study from the Centers for Disease Control and Prevention published in January 2022, also concluded there was a link between COVID-19 and diabetes in children, but not with other acute respiratory infections. Children were 2.5 times more likely to be diagnosed with diabetes following a SARS-CoV-2 infection, it found.

However, the study has been criticized because it pooled all types of diabetes together and did not account for other health conditions, medications that can increase blood glucose levels, race, obesity, and other social determinants of health that might influence a child’s risk of acquiring COVID-19 or diabetes.

“I’ve no doubt that the CDC data were incorrect because the incidence rate for ... diabetes, even in those never exposed to COVID-19 infection, was 10 times the rate ever reported in the U.S.,” Dr. Colhoun said. “There’s no way these data are correct. I believe there was a confusion between incidence and prevalence of diabetes.”

“This paper caused a great deal of panic, especially among those who have a child with type 1diabetes, so we need to be very careful not to cause undue alarm until we have more definitive evidence in this arena,” she stressed.

However, she also acknowledged that the new Norwegian study was well conducted, and she has no methodological concerns about it, so “I think we just have to wait and see.”

Given the inconclusiveness on the issue, there is an ongoing CoviDiab registry collecting data on this very subject.

Dr. Tapia presented on behalf of lead author Dr. Gulseth, who has reported no relevant financial relationships. Dr. Colhoun also reported no relevant financial relationships.

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

CHEST Physician presents the 2022 edition of Pulmonology Data Trends (click to view the digital edition). This special issue provides updates on hot topics in pulmonology through original infographics and visual storytelling. 

Inside this issue:

• Comorbidities, Racial Disparities, and Geographic Differences in Asthma
  Navitha Ramesh, MD, FCCP
• Post-COVID-19 Effects
  Viren Kaul, MD, FCCP, FACP
• New Pathogens, COVID-19, and Antibiotic Resistance in the Field of Pneumonia
  Marcos I. Restrepo, MD, MSc, PhD, FCCP
• COPD Characteristics and Health Disparities
  Muhammad Adrish, MD, MBA, FCCP
• Reducing Tuberculosis Globally and the Impact of COVID-19
  Patricio Escalante, MD, MSc, FCCP and Paige K. Marty, MD
• New Treatment Pathways for Cystic Fibrosis
  David Finklea, MD
• Risk Assessment in Pulmonary Arterial Hypertension
  Sandeep Sahay, MD, MSc, FCCP, ATSF
• Rising Incidence of Bronchiectasis and Associated Burdens
  Anne E. O'Donnell, MD, FCCP
• ILD: Diagnostic Considerations and Socioeconomic Barriers
  Daniel Dilling, MD, FCCP, FACP, FAST
• Advances in Lung Cancer Diagnostics and Treatment
  Eric S. Edell, MD, FCCP

CHEST Physician presents the 2022 edition of Pulmonology Data Trends (click to view the digital edition). This special issue provides updates on hot topics in pulmonology through original infographics and visual storytelling. 

Inside this issue:

• Comorbidities, Racial Disparities, and Geographic Differences in Asthma
  Navitha Ramesh, MD, FCCP
• Post-COVID-19 Effects
  Viren Kaul, MD, FCCP, FACP
• New Pathogens, COVID-19, and Antibiotic Resistance in the Field of Pneumonia
  Marcos I. Restrepo, MD, MSc, PhD, FCCP
• COPD Characteristics and Health Disparities
  Muhammad Adrish, MD, MBA, FCCP
• Reducing Tuberculosis Globally and the Impact of COVID-19
  Patricio Escalante, MD, MSc, FCCP and Paige K. Marty, MD
• New Treatment Pathways for Cystic Fibrosis
  David Finklea, MD
• Risk Assessment in Pulmonary Arterial Hypertension
  Sandeep Sahay, MD, MSc, FCCP, ATSF
• Rising Incidence of Bronchiectasis and Associated Burdens
  Anne E. O'Donnell, MD, FCCP
• ILD: Diagnostic Considerations and Socioeconomic Barriers
  Daniel Dilling, MD, FCCP, FACP, FAST
• Advances in Lung Cancer Diagnostics and Treatment
  Eric S. Edell, MD, FCCP

CHEST Physician presents the 2022 edition of Pulmonology Data Trends (click to view the digital edition). This special issue provides updates on hot topics in pulmonology through original infographics and visual storytelling. 

Inside this issue:

• Comorbidities, Racial Disparities, and Geographic Differences in Asthma
  Navitha Ramesh, MD, FCCP
• Post-COVID-19 Effects
  Viren Kaul, MD, FCCP, FACP
• New Pathogens, COVID-19, and Antibiotic Resistance in the Field of Pneumonia
  Marcos I. Restrepo, MD, MSc, PhD, FCCP
• COPD Characteristics and Health Disparities
  Muhammad Adrish, MD, MBA, FCCP
• Reducing Tuberculosis Globally and the Impact of COVID-19
  Patricio Escalante, MD, MSc, FCCP and Paige K. Marty, MD
• New Treatment Pathways for Cystic Fibrosis
  David Finklea, MD
• Risk Assessment in Pulmonary Arterial Hypertension
  Sandeep Sahay, MD, MSc, FCCP, ATSF
• Rising Incidence of Bronchiectasis and Associated Burdens
  Anne E. O'Donnell, MD, FCCP
• ILD: Diagnostic Considerations and Socioeconomic Barriers
  Daniel Dilling, MD, FCCP, FACP, FAST
• Advances in Lung Cancer Diagnostics and Treatment
  Eric S. Edell, MD, FCCP

Long COVID is likely to cost the U.S. economy trillions of dollars and will almost certainly affect multiple industries, from restaurants struggling to replace low-wage workers, to airlines scrambling to replace crew, to overwhelmed hospitals, experts are predicting.

“There’s a lot we need to do to understand what it takes to enable disabled people to participate more in the economy,” said Katie Bach, a senior fellow with Brookings Institution and the author of a study looking into long COVID’s impact on the labor market.

Data from June 2022 from the Centers for Disease Control and Prevention shows that, of the 40% of American adults who contracted COVID-19, nearly one in five still have long COVID symptoms. That works out to 1 in 13, or 7.5%, of the overall U.S. adult population.

Drawing from the CDC data, Ms. Bach estimates in her August 2022 report that as many as 4 million working-age Americans are too sick with long COVID to perform their jobs. That works out to as much as $230 billion in lost wages, or almost 1% of the U.S. GDP.

“This is a big deal,” she said. “We’re talking potentially hundreds of billions of dollars a year and that this is big enough to have a measurable impact on the labor market.”

Other sources have suggested lower figures, but the conclusions are the same: Long COVID is an urgent issue that will cost tens of billions of dollars a year in lost wages alone, Ms. Bach said. But it’s not just lost income for workers. There is a cost for businesses and the public.

Throughout the pandemic, COVID-19’s crippling force could be felt across multiple industries. While business has picked up again, staffing shortages remain a challenge. At some airports this summer, air passengers spent hours in security lines; were stranded for days as flights were canceled, rebooked, and canceled again on short notice; and waited weeks for lost luggage. Restaurants have had to cut back their hours. Those seeking medical care had longer than usual wait times in EDs and urgent care clinics. Some EDs temporarily closed.

These challenges have been attributed in part to the “great resignation” and in part because so many infected workers were out, especially during the Omicron waves. But increasingly, economists and health care professionals alike worry about long COVID’s impact on employers and the broader economy.

David Cutler, PhD, a professor of economics at Harvard University, Cambridge, Mass., believes the total economic loss could be as high as $3.7 trillion, when factoring in the lost quality of life, the cost in lost earnings, and the cost of higher spending on medical care. His estimate is more than a trillion dollars higher than a previous projection he and fellow economist Lawrence Summers, PhD, made in 2020. The reason? Long COVID.

“The higher estimate is largely a result of the greater prevalence of long COVID than we had guessed at the time,” Dr. Cutler wrote in a paper released in July.

“There are about 10 times the number of people with long COVID as have died of COVID. Because long COVID is so new, there is uncertainty about all of the numbers involved in the calculations. Still, the costs here are conservative, based on only cases to date.”

In Ms. Bach’s Brookings report, she projected that, if recovery from long COVID does not pick up and the population of Americans with long COVID were to grow by 10% a year, the annual cost of lost wages alone could reach half a trillion dollars in a decade.

Meanwhile, a working paper by the National Bureau of Economic Research found that workers who missed an entire week of work because of probable COVID-19 illnesses were roughly 7 percentage points less likely to be working a year later, compared with those who did not miss work for health reasons.

“It’s not just individuals with long COVID who are suffering from this. It impacts their families, their livelihoods, and the economy on a global scale. So, we have to raise awareness about those ripple effects,” said Linda Geng, MD, a clinical assistant professor of medicine with Stanford (Calif.) University’s Primary Care and Population Health. 

“I think it’s hard for the public to grasp ... and understand the scale of this public health crisis.”
 

Debilitating fatigue

Long COVID is roughly defined; the CDC defines it as symptoms that linger 3 or more months after a patient first catches the virus.

The symptoms vary and include profound fatigue and brain issues.

“It’s a new degree of extreme and debilitating fatigue and exhaustion, to the point where you can’t do your daily tasks,” said Dr. Geng, who is also the codirector of Stanford’s Post-Acute COVID-19 Syndrome Clinic.

“People can be so debilitated, they can’t even do basic things, like the activities of daily living, let alone do their job, particularly if it’s physically or mentally demanding.”

Patients can also have postexertional malaise, where they feel especially bad and symptoms worsen when they exert themselves physically or mentally, Dr. Geng said. Compounding the issue for many long COVID patients is their trouble getting restful sleep. Those with brain fog have issues with memory, processing information, focused concentration, confusion, making mistakes, and multitasking. Pain is another debilitating symptom that can disrupt daily life and ability to work.

Even people with relatively mild infections can end up with long COVID, Dr. Geng said, noting that many of the patients at the Stanford clinic were never hospitalized with their initial infections. While existing research and Dr. Geng’s clinical experience show that long COVID can hit any age, she most commonly sees patients from ages 20 to their 60s, with an average age in the 40s – people in their prime working ages.

Jason Furman, PhD, a former White House economic adviser who is now a professor at Harvard University, noted in August that the labor force participation rate was far below what could be explained by standard demographic changes like an aging population, with the decline evident across all age groups. Dr. Furman does not speculate about why, but others have.

“We are pessimistic: Both the aging of the population and the impact of long COVID imply that the participation rate will be slow to return to its prepandemic level,” Anna Wong, Yelena Shulyatyeva, Andrew Husby, and Eliza Winger, economists with Bloomberg Economics, wrote in a research note. 
 

Supportive policies 

There is some evidence that vaccination reduces the risk of long COVID, but not completely, and it is too early to know if repeat infections increase long COVID risks. There is also no definitive data on how fast or how many people are recovering. Economists often assume that those with long COVID will recover at some point, Ms. Bach noted, but she is careful not to make assumptions.

“If people aren’t recovering, then this group keeps getting bigger,” she said. “We’re still adding, and if people aren’t coming out of that group, this becomes a bigger and bigger problem.”

For now, the number of new people being diagnosed with long COVID appears to have slowed, Ms. Bach said, but it remains to be seen whether the trend can be sustained.

“If people are impaired longer than we think and if the impairment turns out to be severe, then we can have a lot of people who need services like disability insurance,” Dr. Cutler said.

“That could put a really big strain on public sector programs and our ability to meet those needs.”

Policies that support the research and clinical work necessary to prevent and treat long COVID are essential, experts say.

“To me, that is the biggest economic imperative, to say nothing of human suffering,” said Ms. Bach. 

Employers also have a role, and experts say there are a number of accommodations businesses should consider. What happens when an employee has long COVID? Can accommodations be made that allow them to continue working productively? If they spend a great deal of time commuting, can they work from home? What can employers do so that family members do not have to drop out of the workforce to take care of loved ones with long COVID? 
 

Disability insurance

To be sure, there is one piece of the puzzle that does not quite fit, according to Dr. Cutler and Ms. Bach. There is no sign yet of a large increase in federal disability insurance applications, and no one quite knows why. Publicly available government data shows that online applications actually dipped by about 4% each year between 2019 and 2021. Applications in 2022 appear on track to remain slightly below prepandemic levels. 

To qualify for Social Security Disability Insurance (SSDI), people need to have a disability that lasts at least a year. 

“If you’re disabled with long COVID, who knows, right? You don’t know,” said Ms. Bach. “Two of the most dominant symptoms of long COVID are fatigue and brain fog. So, I’ve heard from people that the process of going through an SSDI application is really hard.”

Some long COVID patients told Ms. Bach they simply assumed they would not get SSDI and did not even bother applying. She stressed that working Americans with debilitating long COVID should be aware that their condition is protected by the Americans with Disabilities Act. But the challenge, based on guidance issued by the government, is that not all cases of long COVID qualify as a disability and that individual assessments are necessary.

While more long COVID data are needed, Ms. Bach believes there is enough information for decisionmakers to go after the issue more aggressively. She pointed to the $1.15 billion in funding that Congress earmarked for the National Institutes of Health over the course of 4 years in support of research into the long-term health effects of COVID-19.

“Now, $250 million a year sounds like a lot of money until you start talking about the cost of lost wages – just lost wages,” Ms. Bach said. “That’s not lost productivity. That’s not the cost of people whose family members are sick. Who have to reduce their own labor force participation. That’s not medical costs. Suddenly, $250 million doesn’t really sound like that much.”

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

Long COVID is likely to cost the U.S. economy trillions of dollars and will almost certainly affect multiple industries, from restaurants struggling to replace low-wage workers, to airlines scrambling to replace crew, to overwhelmed hospitals, experts are predicting.

“There’s a lot we need to do to understand what it takes to enable disabled people to participate more in the economy,” said Katie Bach, a senior fellow with Brookings Institution and the author of a study looking into long COVID’s impact on the labor market.

Data from June 2022 from the Centers for Disease Control and Prevention shows that, of the 40% of American adults who contracted COVID-19, nearly one in five still have long COVID symptoms. That works out to 1 in 13, or 7.5%, of the overall U.S. adult population.

Drawing from the CDC data, Ms. Bach estimates in her August 2022 report that as many as 4 million working-age Americans are too sick with long COVID to perform their jobs. That works out to as much as $230 billion in lost wages, or almost 1% of the U.S. GDP.

“This is a big deal,” she said. “We’re talking potentially hundreds of billions of dollars a year and that this is big enough to have a measurable impact on the labor market.”

Other sources have suggested lower figures, but the conclusions are the same: Long COVID is an urgent issue that will cost tens of billions of dollars a year in lost wages alone, Ms. Bach said. But it’s not just lost income for workers. There is a cost for businesses and the public.

Throughout the pandemic, COVID-19’s crippling force could be felt across multiple industries. While business has picked up again, staffing shortages remain a challenge. At some airports this summer, air passengers spent hours in security lines; were stranded for days as flights were canceled, rebooked, and canceled again on short notice; and waited weeks for lost luggage. Restaurants have had to cut back their hours. Those seeking medical care had longer than usual wait times in EDs and urgent care clinics. Some EDs temporarily closed.

These challenges have been attributed in part to the “great resignation” and in part because so many infected workers were out, especially during the Omicron waves. But increasingly, economists and health care professionals alike worry about long COVID’s impact on employers and the broader economy.

David Cutler, PhD, a professor of economics at Harvard University, Cambridge, Mass., believes the total economic loss could be as high as $3.7 trillion, when factoring in the lost quality of life, the cost in lost earnings, and the cost of higher spending on medical care. His estimate is more than a trillion dollars higher than a previous projection he and fellow economist Lawrence Summers, PhD, made in 2020. The reason? Long COVID.

“The higher estimate is largely a result of the greater prevalence of long COVID than we had guessed at the time,” Dr. Cutler wrote in a paper released in July.

“There are about 10 times the number of people with long COVID as have died of COVID. Because long COVID is so new, there is uncertainty about all of the numbers involved in the calculations. Still, the costs here are conservative, based on only cases to date.”

In Ms. Bach’s Brookings report, she projected that, if recovery from long COVID does not pick up and the population of Americans with long COVID were to grow by 10% a year, the annual cost of lost wages alone could reach half a trillion dollars in a decade.

Meanwhile, a working paper by the National Bureau of Economic Research found that workers who missed an entire week of work because of probable COVID-19 illnesses were roughly 7 percentage points less likely to be working a year later, compared with those who did not miss work for health reasons.

“It’s not just individuals with long COVID who are suffering from this. It impacts their families, their livelihoods, and the economy on a global scale. So, we have to raise awareness about those ripple effects,” said Linda Geng, MD, a clinical assistant professor of medicine with Stanford (Calif.) University’s Primary Care and Population Health. 

“I think it’s hard for the public to grasp ... and understand the scale of this public health crisis.”
 

Debilitating fatigue

Long COVID is roughly defined; the CDC defines it as symptoms that linger 3 or more months after a patient first catches the virus.

The symptoms vary and include profound fatigue and brain issues.

“It’s a new degree of extreme and debilitating fatigue and exhaustion, to the point where you can’t do your daily tasks,” said Dr. Geng, who is also the codirector of Stanford’s Post-Acute COVID-19 Syndrome Clinic.

“People can be so debilitated, they can’t even do basic things, like the activities of daily living, let alone do their job, particularly if it’s physically or mentally demanding.”

Patients can also have postexertional malaise, where they feel especially bad and symptoms worsen when they exert themselves physically or mentally, Dr. Geng said. Compounding the issue for many long COVID patients is their trouble getting restful sleep. Those with brain fog have issues with memory, processing information, focused concentration, confusion, making mistakes, and multitasking. Pain is another debilitating symptom that can disrupt daily life and ability to work.

Even people with relatively mild infections can end up with long COVID, Dr. Geng said, noting that many of the patients at the Stanford clinic were never hospitalized with their initial infections. While existing research and Dr. Geng’s clinical experience show that long COVID can hit any age, she most commonly sees patients from ages 20 to their 60s, with an average age in the 40s – people in their prime working ages.

Jason Furman, PhD, a former White House economic adviser who is now a professor at Harvard University, noted in August that the labor force participation rate was far below what could be explained by standard demographic changes like an aging population, with the decline evident across all age groups. Dr. Furman does not speculate about why, but others have.

“We are pessimistic: Both the aging of the population and the impact of long COVID imply that the participation rate will be slow to return to its prepandemic level,” Anna Wong, Yelena Shulyatyeva, Andrew Husby, and Eliza Winger, economists with Bloomberg Economics, wrote in a research note. 
 

Supportive policies 

There is some evidence that vaccination reduces the risk of long COVID, but not completely, and it is too early to know if repeat infections increase long COVID risks. There is also no definitive data on how fast or how many people are recovering. Economists often assume that those with long COVID will recover at some point, Ms. Bach noted, but she is careful not to make assumptions.

“If people aren’t recovering, then this group keeps getting bigger,” she said. “We’re still adding, and if people aren’t coming out of that group, this becomes a bigger and bigger problem.”

For now, the number of new people being diagnosed with long COVID appears to have slowed, Ms. Bach said, but it remains to be seen whether the trend can be sustained.

“If people are impaired longer than we think and if the impairment turns out to be severe, then we can have a lot of people who need services like disability insurance,” Dr. Cutler said.

“That could put a really big strain on public sector programs and our ability to meet those needs.”

Policies that support the research and clinical work necessary to prevent and treat long COVID are essential, experts say.

“To me, that is the biggest economic imperative, to say nothing of human suffering,” said Ms. Bach. 

Employers also have a role, and experts say there are a number of accommodations businesses should consider. What happens when an employee has long COVID? Can accommodations be made that allow them to continue working productively? If they spend a great deal of time commuting, can they work from home? What can employers do so that family members do not have to drop out of the workforce to take care of loved ones with long COVID? 
 

Disability insurance

To be sure, there is one piece of the puzzle that does not quite fit, according to Dr. Cutler and Ms. Bach. There is no sign yet of a large increase in federal disability insurance applications, and no one quite knows why. Publicly available government data shows that online applications actually dipped by about 4% each year between 2019 and 2021. Applications in 2022 appear on track to remain slightly below prepandemic levels. 

To qualify for Social Security Disability Insurance (SSDI), people need to have a disability that lasts at least a year. 

“If you’re disabled with long COVID, who knows, right? You don’t know,” said Ms. Bach. “Two of the most dominant symptoms of long COVID are fatigue and brain fog. So, I’ve heard from people that the process of going through an SSDI application is really hard.”

Some long COVID patients told Ms. Bach they simply assumed they would not get SSDI and did not even bother applying. She stressed that working Americans with debilitating long COVID should be aware that their condition is protected by the Americans with Disabilities Act. But the challenge, based on guidance issued by the government, is that not all cases of long COVID qualify as a disability and that individual assessments are necessary.

While more long COVID data are needed, Ms. Bach believes there is enough information for decisionmakers to go after the issue more aggressively. She pointed to the $1.15 billion in funding that Congress earmarked for the National Institutes of Health over the course of 4 years in support of research into the long-term health effects of COVID-19.

“Now, $250 million a year sounds like a lot of money until you start talking about the cost of lost wages – just lost wages,” Ms. Bach said. “That’s not lost productivity. That’s not the cost of people whose family members are sick. Who have to reduce their own labor force participation. That’s not medical costs. Suddenly, $250 million doesn’t really sound like that much.”

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

Long COVID is likely to cost the U.S. economy trillions of dollars and will almost certainly affect multiple industries, from restaurants struggling to replace low-wage workers, to airlines scrambling to replace crew, to overwhelmed hospitals, experts are predicting.

“There’s a lot we need to do to understand what it takes to enable disabled people to participate more in the economy,” said Katie Bach, a senior fellow with Brookings Institution and the author of a study looking into long COVID’s impact on the labor market.

Data from June 2022 from the Centers for Disease Control and Prevention shows that, of the 40% of American adults who contracted COVID-19, nearly one in five still have long COVID symptoms. That works out to 1 in 13, or 7.5%, of the overall U.S. adult population.

Drawing from the CDC data, Ms. Bach estimates in her August 2022 report that as many as 4 million working-age Americans are too sick with long COVID to perform their jobs. That works out to as much as $230 billion in lost wages, or almost 1% of the U.S. GDP.

“This is a big deal,” she said. “We’re talking potentially hundreds of billions of dollars a year and that this is big enough to have a measurable impact on the labor market.”

Other sources have suggested lower figures, but the conclusions are the same: Long COVID is an urgent issue that will cost tens of billions of dollars a year in lost wages alone, Ms. Bach said. But it’s not just lost income for workers. There is a cost for businesses and the public.

Throughout the pandemic, COVID-19’s crippling force could be felt across multiple industries. While business has picked up again, staffing shortages remain a challenge. At some airports this summer, air passengers spent hours in security lines; were stranded for days as flights were canceled, rebooked, and canceled again on short notice; and waited weeks for lost luggage. Restaurants have had to cut back their hours. Those seeking medical care had longer than usual wait times in EDs and urgent care clinics. Some EDs temporarily closed.

These challenges have been attributed in part to the “great resignation” and in part because so many infected workers were out, especially during the Omicron waves. But increasingly, economists and health care professionals alike worry about long COVID’s impact on employers and the broader economy.

David Cutler, PhD, a professor of economics at Harvard University, Cambridge, Mass., believes the total economic loss could be as high as $3.7 trillion, when factoring in the lost quality of life, the cost in lost earnings, and the cost of higher spending on medical care. His estimate is more than a trillion dollars higher than a previous projection he and fellow economist Lawrence Summers, PhD, made in 2020. The reason? Long COVID.

“The higher estimate is largely a result of the greater prevalence of long COVID than we had guessed at the time,” Dr. Cutler wrote in a paper released in July.

“There are about 10 times the number of people with long COVID as have died of COVID. Because long COVID is so new, there is uncertainty about all of the numbers involved in the calculations. Still, the costs here are conservative, based on only cases to date.”

In Ms. Bach’s Brookings report, she projected that, if recovery from long COVID does not pick up and the population of Americans with long COVID were to grow by 10% a year, the annual cost of lost wages alone could reach half a trillion dollars in a decade.

Meanwhile, a working paper by the National Bureau of Economic Research found that workers who missed an entire week of work because of probable COVID-19 illnesses were roughly 7 percentage points less likely to be working a year later, compared with those who did not miss work for health reasons.

“It’s not just individuals with long COVID who are suffering from this. It impacts their families, their livelihoods, and the economy on a global scale. So, we have to raise awareness about those ripple effects,” said Linda Geng, MD, a clinical assistant professor of medicine with Stanford (Calif.) University’s Primary Care and Population Health. 

“I think it’s hard for the public to grasp ... and understand the scale of this public health crisis.”
 

Debilitating fatigue

Long COVID is roughly defined; the CDC defines it as symptoms that linger 3 or more months after a patient first catches the virus.

The symptoms vary and include profound fatigue and brain issues.

“It’s a new degree of extreme and debilitating fatigue and exhaustion, to the point where you can’t do your daily tasks,” said Dr. Geng, who is also the codirector of Stanford’s Post-Acute COVID-19 Syndrome Clinic.

“People can be so debilitated, they can’t even do basic things, like the activities of daily living, let alone do their job, particularly if it’s physically or mentally demanding.”

Patients can also have postexertional malaise, where they feel especially bad and symptoms worsen when they exert themselves physically or mentally, Dr. Geng said. Compounding the issue for many long COVID patients is their trouble getting restful sleep. Those with brain fog have issues with memory, processing information, focused concentration, confusion, making mistakes, and multitasking. Pain is another debilitating symptom that can disrupt daily life and ability to work.

Even people with relatively mild infections can end up with long COVID, Dr. Geng said, noting that many of the patients at the Stanford clinic were never hospitalized with their initial infections. While existing research and Dr. Geng’s clinical experience show that long COVID can hit any age, she most commonly sees patients from ages 20 to their 60s, with an average age in the 40s – people in their prime working ages.

Jason Furman, PhD, a former White House economic adviser who is now a professor at Harvard University, noted in August that the labor force participation rate was far below what could be explained by standard demographic changes like an aging population, with the decline evident across all age groups. Dr. Furman does not speculate about why, but others have.

“We are pessimistic: Both the aging of the population and the impact of long COVID imply that the participation rate will be slow to return to its prepandemic level,” Anna Wong, Yelena Shulyatyeva, Andrew Husby, and Eliza Winger, economists with Bloomberg Economics, wrote in a research note. 
 

Supportive policies 

There is some evidence that vaccination reduces the risk of long COVID, but not completely, and it is too early to know if repeat infections increase long COVID risks. There is also no definitive data on how fast or how many people are recovering. Economists often assume that those with long COVID will recover at some point, Ms. Bach noted, but she is careful not to make assumptions.

“If people aren’t recovering, then this group keeps getting bigger,” she said. “We’re still adding, and if people aren’t coming out of that group, this becomes a bigger and bigger problem.”

For now, the number of new people being diagnosed with long COVID appears to have slowed, Ms. Bach said, but it remains to be seen whether the trend can be sustained.

“If people are impaired longer than we think and if the impairment turns out to be severe, then we can have a lot of people who need services like disability insurance,” Dr. Cutler said.

“That could put a really big strain on public sector programs and our ability to meet those needs.”

Policies that support the research and clinical work necessary to prevent and treat long COVID are essential, experts say.

“To me, that is the biggest economic imperative, to say nothing of human suffering,” said Ms. Bach. 

Employers also have a role, and experts say there are a number of accommodations businesses should consider. What happens when an employee has long COVID? Can accommodations be made that allow them to continue working productively? If they spend a great deal of time commuting, can they work from home? What can employers do so that family members do not have to drop out of the workforce to take care of loved ones with long COVID? 
 

Disability insurance

To be sure, there is one piece of the puzzle that does not quite fit, according to Dr. Cutler and Ms. Bach. There is no sign yet of a large increase in federal disability insurance applications, and no one quite knows why. Publicly available government data shows that online applications actually dipped by about 4% each year between 2019 and 2021. Applications in 2022 appear on track to remain slightly below prepandemic levels. 

To qualify for Social Security Disability Insurance (SSDI), people need to have a disability that lasts at least a year. 

“If you’re disabled with long COVID, who knows, right? You don’t know,” said Ms. Bach. “Two of the most dominant symptoms of long COVID are fatigue and brain fog. So, I’ve heard from people that the process of going through an SSDI application is really hard.”

Some long COVID patients told Ms. Bach they simply assumed they would not get SSDI and did not even bother applying. She stressed that working Americans with debilitating long COVID should be aware that their condition is protected by the Americans with Disabilities Act. But the challenge, based on guidance issued by the government, is that not all cases of long COVID qualify as a disability and that individual assessments are necessary.

While more long COVID data are needed, Ms. Bach believes there is enough information for decisionmakers to go after the issue more aggressively. She pointed to the $1.15 billion in funding that Congress earmarked for the National Institutes of Health over the course of 4 years in support of research into the long-term health effects of COVID-19.

“Now, $250 million a year sounds like a lot of money until you start talking about the cost of lost wages – just lost wages,” Ms. Bach said. “That’s not lost productivity. That’s not the cost of people whose family members are sick. Who have to reduce their own labor force participation. That’s not medical costs. Suddenly, $250 million doesn’t really sound like that much.”

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

Herpes to the rescue

Let’s face it: When people hear the word “herpes,” their first thoughts are not positive. But what if herpes could be a hero?

Scientists have found a way to make a strain of herpes that kills cancer because, hey, it’s 2022, and anything is possible. Trials have been going well and this seems like a safe and effective way to fight cancer.

Aunt_Spray/Thinkstock

Viruses may be one of our oldest enemies, but it’s also been said that the enemy of my enemy is my friend. So why not make herpes the enemy of cancer, thereby turning it into our friend? The genetically modified herpes virus is injected directly into tumors, where it destroys cancer cells from within. But wait, there’s more! The patient’s immune system also senses the virus and springs into action against it and the cancer in which it is residing.

During the phase 1 trial, three of the nine patients saw tumor reduction and the therapy proved safe as well. Future trials will be able to more specifically target various cancer types and make the treatment better. For once, we are rooting for you, herpes.
 

A breath of not-so-fresh air

There’s nothing quite like that first real warm day of spring. You can finally open the windows and clear out the old stuffy air that’s been hanging around all winter long. It’s a ritual that’s now backed up with some science in the form of a new study. Turns out that there’s actually a fair amount of smog in the average home. That’s right, smog’s not just for the big city anymore.

PxHere

As part of the HOMEChem project, a whole host of scientists gathered together under one roof in a typical suburban house and immediately started doing chores. Cooking, cleaning, the works. No, it wasn’t because they had trashed the place the night before. They had set up instrumentation all around the house to measure the chemical makeup of the air inside. A scientist’s idea of a wild party.

The results are perhaps not all that surprising, but interesting nonetheless. Your homemade smog certainly won’t kill you, but there’s both an increased amount and higher concentration of airborne toxins in indoor air, compared with outdoors. Benzene and formaldehyde were common, as were acrolein (a pulmonary toxicant emitted by lumber and burning fats) and isocyanic acid (which can react with proteins in the human body). The researchers noted that most of these chemicals can be removed with proper ventilation.

Although cleaning is certainly responsible for a fair share of the chemicals, cooking generally produced more toxic compounds, similar to what’s found in wildfire smoke. One of the researchers said this makes sense, since a wildfire can be considered an “extreme form of cooking.” Scientists may not know how to party, but their idea of a barbecue sounds … interesting. We’re looking forward to an upcoming study out of California: Can a 1-million acre wildfire adequately cook a ribeye steak?
 

We’re dying to try composting ... with humans, that is

We here at LOTME are not really fans of politicians, except as objects of ridicule. That is kind of fun. Whether we’re watching Fox News, listening to NPR, or reading Vladimir Putin’s fashion blog, one thing remains clear: If you want actual information, don’t ask a politician.

Recompose

There are, of course, always exceptions, and we just found one: California state representative Cristina Garcia. Rep. Garcia sponsored a bill just signed into law by Gov. Gavin Newsom that legalizes the practice of human composting, the reduction of remains by “placing bodies in individual vessels and fostering gentle transformation into a nutrient-dense soil.”

Since we’ve written about this sort of thing before – Washington was the first state to legalize the process back in 2019 – we’re more interested now in what Rep. Garcia told NBC News while describing her motivation: “I’ve always wanted to be a tree. The idea of having my family sitting under my shade one day – that brings a lot of joy.” How great is that? Tree-hugging is just not enough. Be the tree.

California is the fifth state to provide its residents with the human composting option, the other three being Colorado, Oregon, and Vermont. The process “typically involves putting a body into a steel vessel, then covering it with organic materials like straw, wood chips and alfalfa. Microbes break down the corpse and the plant matter, transforming the various components into nutrient-rich soil in roughly 30 days,” Smithsonian Magazine explained.

We just happen to have some good news for Rep. Garcia about that wanting-to-be-a-tree business. She’s already pretty close. For more on that, we go to our correspondent from beyond the grave, Carl Sagan, who shares a thought about trees. And no, we couldn’t just write out his quote here. You have to hear it in Dr. Sagan’s own voice.
 

That’ll be one pandemic with extra distress. Hold the goals

When the COVID-19 pandemic first hit it put a lot of stuff on hold for everyone. Couldn’t eat inside at your favorite restaurant, attend that long-awaited concert, or travel out of the country. Those were all pretty bad, but it was the disruption of pursuing long-term goals that seemed to have the most effect on people’s mental health.

xijian/Getty Images

Investigators from the University of Waterloo (Ont.) looked at how putting such goals on hold affected people’s mental well-being. The study’s 226 participants were asked about their “COVID-frozen” goals and the degree to which they were able to actively pursue each goal and how committed they were to achieving it.

What they found was that the participants’ COVID-frozen goals were associated with feelings of psychological distress, such as anxiety, depressive symptoms, stress, and lowered life satisfaction. It was only when participants were able to disengage from goal rumination that well-being was impacted positively.

“Goal rumination is compulsive and can aggravate worries and frustrations while also taking away mental resources from other goals,” Candice Hubley, lead author and a PhD candidate in psychology, said in a written statement. So in short, you’re only stressing yourself out more about something that is far off in the distance when you could be focusing more on short-term, tangible goals instead.

Now, no one is saying to give up on your goals. Just take them one at a time. You’ll have better life satisfaction and your COVID-frozen goals will thaw out before you know it.

Herpes to the rescue

Let’s face it: When people hear the word “herpes,” their first thoughts are not positive. But what if herpes could be a hero?

Scientists have found a way to make a strain of herpes that kills cancer because, hey, it’s 2022, and anything is possible. Trials have been going well and this seems like a safe and effective way to fight cancer.

Aunt_Spray/Thinkstock

Viruses may be one of our oldest enemies, but it’s also been said that the enemy of my enemy is my friend. So why not make herpes the enemy of cancer, thereby turning it into our friend? The genetically modified herpes virus is injected directly into tumors, where it destroys cancer cells from within. But wait, there’s more! The patient’s immune system also senses the virus and springs into action against it and the cancer in which it is residing.

During the phase 1 trial, three of the nine patients saw tumor reduction and the therapy proved safe as well. Future trials will be able to more specifically target various cancer types and make the treatment better. For once, we are rooting for you, herpes.
 

A breath of not-so-fresh air

There’s nothing quite like that first real warm day of spring. You can finally open the windows and clear out the old stuffy air that’s been hanging around all winter long. It’s a ritual that’s now backed up with some science in the form of a new study. Turns out that there’s actually a fair amount of smog in the average home. That’s right, smog’s not just for the big city anymore.

PxHere

As part of the HOMEChem project, a whole host of scientists gathered together under one roof in a typical suburban house and immediately started doing chores. Cooking, cleaning, the works. No, it wasn’t because they had trashed the place the night before. They had set up instrumentation all around the house to measure the chemical makeup of the air inside. A scientist’s idea of a wild party.

The results are perhaps not all that surprising, but interesting nonetheless. Your homemade smog certainly won’t kill you, but there’s both an increased amount and higher concentration of airborne toxins in indoor air, compared with outdoors. Benzene and formaldehyde were common, as were acrolein (a pulmonary toxicant emitted by lumber and burning fats) and isocyanic acid (which can react with proteins in the human body). The researchers noted that most of these chemicals can be removed with proper ventilation.

Although cleaning is certainly responsible for a fair share of the chemicals, cooking generally produced more toxic compounds, similar to what’s found in wildfire smoke. One of the researchers said this makes sense, since a wildfire can be considered an “extreme form of cooking.” Scientists may not know how to party, but their idea of a barbecue sounds … interesting. We’re looking forward to an upcoming study out of California: Can a 1-million acre wildfire adequately cook a ribeye steak?
 

We’re dying to try composting ... with humans, that is

We here at LOTME are not really fans of politicians, except as objects of ridicule. That is kind of fun. Whether we’re watching Fox News, listening to NPR, or reading Vladimir Putin’s fashion blog, one thing remains clear: If you want actual information, don’t ask a politician.

Recompose

There are, of course, always exceptions, and we just found one: California state representative Cristina Garcia. Rep. Garcia sponsored a bill just signed into law by Gov. Gavin Newsom that legalizes the practice of human composting, the reduction of remains by “placing bodies in individual vessels and fostering gentle transformation into a nutrient-dense soil.”

Since we’ve written about this sort of thing before – Washington was the first state to legalize the process back in 2019 – we’re more interested now in what Rep. Garcia told NBC News while describing her motivation: “I’ve always wanted to be a tree. The idea of having my family sitting under my shade one day – that brings a lot of joy.” How great is that? Tree-hugging is just not enough. Be the tree.

California is the fifth state to provide its residents with the human composting option, the other three being Colorado, Oregon, and Vermont. The process “typically involves putting a body into a steel vessel, then covering it with organic materials like straw, wood chips and alfalfa. Microbes break down the corpse and the plant matter, transforming the various components into nutrient-rich soil in roughly 30 days,” Smithsonian Magazine explained.

We just happen to have some good news for Rep. Garcia about that wanting-to-be-a-tree business. She’s already pretty close. For more on that, we go to our correspondent from beyond the grave, Carl Sagan, who shares a thought about trees. And no, we couldn’t just write out his quote here. You have to hear it in Dr. Sagan’s own voice.
 

That’ll be one pandemic with extra distress. Hold the goals

When the COVID-19 pandemic first hit it put a lot of stuff on hold for everyone. Couldn’t eat inside at your favorite restaurant, attend that long-awaited concert, or travel out of the country. Those were all pretty bad, but it was the disruption of pursuing long-term goals that seemed to have the most effect on people’s mental health.

xijian/Getty Images

Investigators from the University of Waterloo (Ont.) looked at how putting such goals on hold affected people’s mental well-being. The study’s 226 participants were asked about their “COVID-frozen” goals and the degree to which they were able to actively pursue each goal and how committed they were to achieving it.

What they found was that the participants’ COVID-frozen goals were associated with feelings of psychological distress, such as anxiety, depressive symptoms, stress, and lowered life satisfaction. It was only when participants were able to disengage from goal rumination that well-being was impacted positively.

“Goal rumination is compulsive and can aggravate worries and frustrations while also taking away mental resources from other goals,” Candice Hubley, lead author and a PhD candidate in psychology, said in a written statement. So in short, you’re only stressing yourself out more about something that is far off in the distance when you could be focusing more on short-term, tangible goals instead.

Now, no one is saying to give up on your goals. Just take them one at a time. You’ll have better life satisfaction and your COVID-frozen goals will thaw out before you know it.

Herpes to the rescue

Let’s face it: When people hear the word “herpes,” their first thoughts are not positive. But what if herpes could be a hero?

Scientists have found a way to make a strain of herpes that kills cancer because, hey, it’s 2022, and anything is possible. Trials have been going well and this seems like a safe and effective way to fight cancer.

Aunt_Spray/Thinkstock

Viruses may be one of our oldest enemies, but it’s also been said that the enemy of my enemy is my friend. So why not make herpes the enemy of cancer, thereby turning it into our friend? The genetically modified herpes virus is injected directly into tumors, where it destroys cancer cells from within. But wait, there’s more! The patient’s immune system also senses the virus and springs into action against it and the cancer in which it is residing.

During the phase 1 trial, three of the nine patients saw tumor reduction and the therapy proved safe as well. Future trials will be able to more specifically target various cancer types and make the treatment better. For once, we are rooting for you, herpes.
 

A breath of not-so-fresh air

There’s nothing quite like that first real warm day of spring. You can finally open the windows and clear out the old stuffy air that’s been hanging around all winter long. It’s a ritual that’s now backed up with some science in the form of a new study. Turns out that there’s actually a fair amount of smog in the average home. That’s right, smog’s not just for the big city anymore.

PxHere

As part of the HOMEChem project, a whole host of scientists gathered together under one roof in a typical suburban house and immediately started doing chores. Cooking, cleaning, the works. No, it wasn’t because they had trashed the place the night before. They had set up instrumentation all around the house to measure the chemical makeup of the air inside. A scientist’s idea of a wild party.

The results are perhaps not all that surprising, but interesting nonetheless. Your homemade smog certainly won’t kill you, but there’s both an increased amount and higher concentration of airborne toxins in indoor air, compared with outdoors. Benzene and formaldehyde were common, as were acrolein (a pulmonary toxicant emitted by lumber and burning fats) and isocyanic acid (which can react with proteins in the human body). The researchers noted that most of these chemicals can be removed with proper ventilation.

Although cleaning is certainly responsible for a fair share of the chemicals, cooking generally produced more toxic compounds, similar to what’s found in wildfire smoke. One of the researchers said this makes sense, since a wildfire can be considered an “extreme form of cooking.” Scientists may not know how to party, but their idea of a barbecue sounds … interesting. We’re looking forward to an upcoming study out of California: Can a 1-million acre wildfire adequately cook a ribeye steak?
 

We’re dying to try composting ... with humans, that is

We here at LOTME are not really fans of politicians, except as objects of ridicule. That is kind of fun. Whether we’re watching Fox News, listening to NPR, or reading Vladimir Putin’s fashion blog, one thing remains clear: If you want actual information, don’t ask a politician.

Recompose

There are, of course, always exceptions, and we just found one: California state representative Cristina Garcia. Rep. Garcia sponsored a bill just signed into law by Gov. Gavin Newsom that legalizes the practice of human composting, the reduction of remains by “placing bodies in individual vessels and fostering gentle transformation into a nutrient-dense soil.”

Since we’ve written about this sort of thing before – Washington was the first state to legalize the process back in 2019 – we’re more interested now in what Rep. Garcia told NBC News while describing her motivation: “I’ve always wanted to be a tree. The idea of having my family sitting under my shade one day – that brings a lot of joy.” How great is that? Tree-hugging is just not enough. Be the tree.

California is the fifth state to provide its residents with the human composting option, the other three being Colorado, Oregon, and Vermont. The process “typically involves putting a body into a steel vessel, then covering it with organic materials like straw, wood chips and alfalfa. Microbes break down the corpse and the plant matter, transforming the various components into nutrient-rich soil in roughly 30 days,” Smithsonian Magazine explained.

We just happen to have some good news for Rep. Garcia about that wanting-to-be-a-tree business. She’s already pretty close. For more on that, we go to our correspondent from beyond the grave, Carl Sagan, who shares a thought about trees. And no, we couldn’t just write out his quote here. You have to hear it in Dr. Sagan’s own voice.
 

That’ll be one pandemic with extra distress. Hold the goals

When the COVID-19 pandemic first hit it put a lot of stuff on hold for everyone. Couldn’t eat inside at your favorite restaurant, attend that long-awaited concert, or travel out of the country. Those were all pretty bad, but it was the disruption of pursuing long-term goals that seemed to have the most effect on people’s mental health.

xijian/Getty Images

Investigators from the University of Waterloo (Ont.) looked at how putting such goals on hold affected people’s mental well-being. The study’s 226 participants were asked about their “COVID-frozen” goals and the degree to which they were able to actively pursue each goal and how committed they were to achieving it.

What they found was that the participants’ COVID-frozen goals were associated with feelings of psychological distress, such as anxiety, depressive symptoms, stress, and lowered life satisfaction. It was only when participants were able to disengage from goal rumination that well-being was impacted positively.

“Goal rumination is compulsive and can aggravate worries and frustrations while also taking away mental resources from other goals,” Candice Hubley, lead author and a PhD candidate in psychology, said in a written statement. So in short, you’re only stressing yourself out more about something that is far off in the distance when you could be focusing more on short-term, tangible goals instead.

Now, no one is saying to give up on your goals. Just take them one at a time. You’ll have better life satisfaction and your COVID-frozen goals will thaw out before you know it.

Patients with gastrointestinal esophageal reflux disease (GERD) have more than three times the risk of developing nontuberculous mycobacterial pulmonary disease (NTM-PD), compared with those without GERD, according to a population-based retrospective cohort study.

“GERD is a common comorbidity of nontuberculous mycobacterial pulmonary disease [but] whether GERD is associated with an increased risk of developing NTM-PD is unknown,” Hayoung Choi, MD, PhD, Hallym University, Seoul, Republic of Korea, and colleagues reported.

“Our study showed the relation between GERD and NTM infections, but preventing NTM is not simple,” Dr. Choi added in an email. “What needs to be understood is that GERD increases health care utilization in patients with NTM pulmonary disease; hence, clinicians who treat patients with NTM pulmonary disease need to be aware of the burden of GERD and treat the gastrointestinal illness simultaneously,” he added.

The study was published online in the journal CHEST.
 

Sample cohort

Data from the Korean National Health Insurance Service-National Sample Cohort between 2002 and 2015 were used to assess the impact of GERD on NTM-PD. The incidence and risk of NTM-PD were compared between 17,424 patients with GERD and 69,000 patients without GERD in a matched cohort. GERD was defined as patients having received more than 3 months of proton pump inhibitors (PPIs).

During a median follow-up of 5.1 years, the age- and sex-adjusted incidence of NTM-PD was significantly higher in the GERD cohort, at a rate of 34.8/100,000 person-years, than in the matched cohort, at a rate of only 10.5/100,000 person-years (P < .001), the authors reported.

As for risk factors for NTM-PD, being 60 years of age and older was associated with a 3.5-times higher risk of NTM-PD at an adjusted hazard ratio of 3.57 (95% confidence interval, 1.58-8.07), while bronchiectasis was associated with over an 18-times higher risk of NTM-PD in the GERD cohort at an adjusted HR of 18.69 (95% CI, 6.68-552.28). Those with GERD who developed NTM-PD had higher all-cause and respiratory disease–related emergency department visits or hospitalizations compared with patients with GERD who did not develop NTM-PD (P = .011), the investigators noted.

As the authors pointed out, the incidence of NTM-PD in the Korean population ranged from 6 to 19 cases/100,000 between 2008 and 2016; thus, the burden of incident NTM-PD associated with GERD appears to be considerable. As Dr. Choi explained, a combination of three factors influenced the development of NTM infections. The first is environmental, from water source, climate, or region; the second is patient influences, including such factors as immunodeficiency and comorbidities (including bronchiectasis); and the third is microbiological factors, including various NTM species.

Bile aspirating into the lung during GERD may be another possible pathway, as the authors suggested. Even if acid secretion is suppressed by PPI treatment in patients with GERD, NTM-PD may be induced or aggravated through mechanisms such as bile reflux. The fact that patients over the age of 60 were more prone to develop NTM-PD suggests that a decrease in gastric emptying and increased micro-aspiration or reflux associated with impaired swallowing (which are more common in elderly patients) may also be at play.

“Bronchiectasis is also a very well known risk factor for NTM pulmonary disease,” Dr. Choi emphasized. Thus, he recommends clinicians carefully observe clinical, radiological, and microbiological changes to detect NTM pulmonary disease when managing patients with bronchiectasis.

“The results of the present study have several potential clinical implications,” Dr. Choi and colleagues observed. First, NTM-PD should be suspected when new-onset worsening of respiratory symptoms develops during regular follow-up in patients with GERD. Second, because results indicate that older age and bronchiectasis significantly increase the risk of NTM-PD, “more active strategies (e.g., screening of symptoms and regular chest x-rays)” might be helpful in patients with GERD and these risk factors, the authors suggested. Because patients with GERD who developed NTM-PD had more respiratory disease–related ED visits and hospitalizations than those who did not develop NTM-PD, when GERD and NTM-PD are combined, clinicians should focus on the variations of respiratory symptoms, they suggested.

The authors cautioned, however, that because the study was one in a Korean population, studies in other countries and different ethnicities are needed before findings can be generalized.

More common than TB

Asked to comment on the findings, NTM-PD expert Theodore Marras, MD, clinician investigator, Krembil Research Institute, Toronto, noted that non-TB M-PD is about 10 times more common than TB and that could be an underestimate as there have been very large increases in the incidence of NTM-PD in recent years. “It’s an environmental germ – it’s in our water – and certain people are particularly susceptible to it, typically older age women who have underlying bronchiectasis,” Dr. Marras told this news organization. “And while there are ethnic differences in incidence rates between East Asian people and Black African people, immigration is not the main driver for the increase as far as we can tell,” he said.

He personally treats a lot of NTM-PD and he also believes that GERD is an important risk factor for all types of lung infections including NTM lung disease. “So without a doubt, I believe that GERD should be treated in patients with NTM-PD,” Dr. Marras emphasized. The big question is how to treat GERD, as there may be concerns with acid-suppressive agents such as proton pump inhibitors that “the reflux that comes back up may harbor more germs in it and if that reflux comes up high enough, we are at risk of aspirating some of that fluid into our lungs, especially when we’re asleep,” he said.

Some experts therefore argue in favor of using motility agents instead of PPIs. However, if Dr. Marras has a patient with heartburn, “you have to treat it,” he stressed. Similarly, if a patient has evidence of esophageal erosions, physicians need to treat those as well. However, if neither feature is present, “I tend to like the motility agents preferentially or use them in combination with a PPI,” Dr. Marras said.

Dr. Marras also thinks the study is encouraging physicians involved in treating these patients to think about controlling GERD both when they are treating patients and after they are treated to try to reduce recurrence.

The authors had no financial disclosures to make. Dr. Marras has given several talks on NTM lung disease, one sponsored by AstraZeneca and the other by Novartis.

Patients with gastrointestinal esophageal reflux disease (GERD) have more than three times the risk of developing nontuberculous mycobacterial pulmonary disease (NTM-PD), compared with those without GERD, according to a population-based retrospective cohort study.

“GERD is a common comorbidity of nontuberculous mycobacterial pulmonary disease [but] whether GERD is associated with an increased risk of developing NTM-PD is unknown,” Hayoung Choi, MD, PhD, Hallym University, Seoul, Republic of Korea, and colleagues reported.

“Our study showed the relation between GERD and NTM infections, but preventing NTM is not simple,” Dr. Choi added in an email. “What needs to be understood is that GERD increases health care utilization in patients with NTM pulmonary disease; hence, clinicians who treat patients with NTM pulmonary disease need to be aware of the burden of GERD and treat the gastrointestinal illness simultaneously,” he added.

The study was published online in the journal CHEST.
 

Sample cohort

Data from the Korean National Health Insurance Service-National Sample Cohort between 2002 and 2015 were used to assess the impact of GERD on NTM-PD. The incidence and risk of NTM-PD were compared between 17,424 patients with GERD and 69,000 patients without GERD in a matched cohort. GERD was defined as patients having received more than 3 months of proton pump inhibitors (PPIs).

During a median follow-up of 5.1 years, the age- and sex-adjusted incidence of NTM-PD was significantly higher in the GERD cohort, at a rate of 34.8/100,000 person-years, than in the matched cohort, at a rate of only 10.5/100,000 person-years (P < .001), the authors reported.

As for risk factors for NTM-PD, being 60 years of age and older was associated with a 3.5-times higher risk of NTM-PD at an adjusted hazard ratio of 3.57 (95% confidence interval, 1.58-8.07), while bronchiectasis was associated with over an 18-times higher risk of NTM-PD in the GERD cohort at an adjusted HR of 18.69 (95% CI, 6.68-552.28). Those with GERD who developed NTM-PD had higher all-cause and respiratory disease–related emergency department visits or hospitalizations compared with patients with GERD who did not develop NTM-PD (P = .011), the investigators noted.

As the authors pointed out, the incidence of NTM-PD in the Korean population ranged from 6 to 19 cases/100,000 between 2008 and 2016; thus, the burden of incident NTM-PD associated with GERD appears to be considerable. As Dr. Choi explained, a combination of three factors influenced the development of NTM infections. The first is environmental, from water source, climate, or region; the second is patient influences, including such factors as immunodeficiency and comorbidities (including bronchiectasis); and the third is microbiological factors, including various NTM species.

Bile aspirating into the lung during GERD may be another possible pathway, as the authors suggested. Even if acid secretion is suppressed by PPI treatment in patients with GERD, NTM-PD may be induced or aggravated through mechanisms such as bile reflux. The fact that patients over the age of 60 were more prone to develop NTM-PD suggests that a decrease in gastric emptying and increased micro-aspiration or reflux associated with impaired swallowing (which are more common in elderly patients) may also be at play.

“Bronchiectasis is also a very well known risk factor for NTM pulmonary disease,” Dr. Choi emphasized. Thus, he recommends clinicians carefully observe clinical, radiological, and microbiological changes to detect NTM pulmonary disease when managing patients with bronchiectasis.

“The results of the present study have several potential clinical implications,” Dr. Choi and colleagues observed. First, NTM-PD should be suspected when new-onset worsening of respiratory symptoms develops during regular follow-up in patients with GERD. Second, because results indicate that older age and bronchiectasis significantly increase the risk of NTM-PD, “more active strategies (e.g., screening of symptoms and regular chest x-rays)” might be helpful in patients with GERD and these risk factors, the authors suggested. Because patients with GERD who developed NTM-PD had more respiratory disease–related ED visits and hospitalizations than those who did not develop NTM-PD, when GERD and NTM-PD are combined, clinicians should focus on the variations of respiratory symptoms, they suggested.

The authors cautioned, however, that because the study was one in a Korean population, studies in other countries and different ethnicities are needed before findings can be generalized.

More common than TB

Asked to comment on the findings, NTM-PD expert Theodore Marras, MD, clinician investigator, Krembil Research Institute, Toronto, noted that non-TB M-PD is about 10 times more common than TB and that could be an underestimate as there have been very large increases in the incidence of NTM-PD in recent years. “It’s an environmental germ – it’s in our water – and certain people are particularly susceptible to it, typically older age women who have underlying bronchiectasis,” Dr. Marras told this news organization. “And while there are ethnic differences in incidence rates between East Asian people and Black African people, immigration is not the main driver for the increase as far as we can tell,” he said.

He personally treats a lot of NTM-PD and he also believes that GERD is an important risk factor for all types of lung infections including NTM lung disease. “So without a doubt, I believe that GERD should be treated in patients with NTM-PD,” Dr. Marras emphasized. The big question is how to treat GERD, as there may be concerns with acid-suppressive agents such as proton pump inhibitors that “the reflux that comes back up may harbor more germs in it and if that reflux comes up high enough, we are at risk of aspirating some of that fluid into our lungs, especially when we’re asleep,” he said.

Some experts therefore argue in favor of using motility agents instead of PPIs. However, if Dr. Marras has a patient with heartburn, “you have to treat it,” he stressed. Similarly, if a patient has evidence of esophageal erosions, physicians need to treat those as well. However, if neither feature is present, “I tend to like the motility agents preferentially or use them in combination with a PPI,” Dr. Marras said.

Dr. Marras also thinks the study is encouraging physicians involved in treating these patients to think about controlling GERD both when they are treating patients and after they are treated to try to reduce recurrence.

The authors had no financial disclosures to make. Dr. Marras has given several talks on NTM lung disease, one sponsored by AstraZeneca and the other by Novartis.

Patients with gastrointestinal esophageal reflux disease (GERD) have more than three times the risk of developing nontuberculous mycobacterial pulmonary disease (NTM-PD), compared with those without GERD, according to a population-based retrospective cohort study.

“GERD is a common comorbidity of nontuberculous mycobacterial pulmonary disease [but] whether GERD is associated with an increased risk of developing NTM-PD is unknown,” Hayoung Choi, MD, PhD, Hallym University, Seoul, Republic of Korea, and colleagues reported.

“Our study showed the relation between GERD and NTM infections, but preventing NTM is not simple,” Dr. Choi added in an email. “What needs to be understood is that GERD increases health care utilization in patients with NTM pulmonary disease; hence, clinicians who treat patients with NTM pulmonary disease need to be aware of the burden of GERD and treat the gastrointestinal illness simultaneously,” he added.

The study was published online in the journal CHEST.
 

Sample cohort

Data from the Korean National Health Insurance Service-National Sample Cohort between 2002 and 2015 were used to assess the impact of GERD on NTM-PD. The incidence and risk of NTM-PD were compared between 17,424 patients with GERD and 69,000 patients without GERD in a matched cohort. GERD was defined as patients having received more than 3 months of proton pump inhibitors (PPIs).

During a median follow-up of 5.1 years, the age- and sex-adjusted incidence of NTM-PD was significantly higher in the GERD cohort, at a rate of 34.8/100,000 person-years, than in the matched cohort, at a rate of only 10.5/100,000 person-years (P < .001), the authors reported.

As for risk factors for NTM-PD, being 60 years of age and older was associated with a 3.5-times higher risk of NTM-PD at an adjusted hazard ratio of 3.57 (95% confidence interval, 1.58-8.07), while bronchiectasis was associated with over an 18-times higher risk of NTM-PD in the GERD cohort at an adjusted HR of 18.69 (95% CI, 6.68-552.28). Those with GERD who developed NTM-PD had higher all-cause and respiratory disease–related emergency department visits or hospitalizations compared with patients with GERD who did not develop NTM-PD (P = .011), the investigators noted.

As the authors pointed out, the incidence of NTM-PD in the Korean population ranged from 6 to 19 cases/100,000 between 2008 and 2016; thus, the burden of incident NTM-PD associated with GERD appears to be considerable. As Dr. Choi explained, a combination of three factors influenced the development of NTM infections. The first is environmental, from water source, climate, or region; the second is patient influences, including such factors as immunodeficiency and comorbidities (including bronchiectasis); and the third is microbiological factors, including various NTM species.

Bile aspirating into the lung during GERD may be another possible pathway, as the authors suggested. Even if acid secretion is suppressed by PPI treatment in patients with GERD, NTM-PD may be induced or aggravated through mechanisms such as bile reflux. The fact that patients over the age of 60 were more prone to develop NTM-PD suggests that a decrease in gastric emptying and increased micro-aspiration or reflux associated with impaired swallowing (which are more common in elderly patients) may also be at play.

“Bronchiectasis is also a very well known risk factor for NTM pulmonary disease,” Dr. Choi emphasized. Thus, he recommends clinicians carefully observe clinical, radiological, and microbiological changes to detect NTM pulmonary disease when managing patients with bronchiectasis.

“The results of the present study have several potential clinical implications,” Dr. Choi and colleagues observed. First, NTM-PD should be suspected when new-onset worsening of respiratory symptoms develops during regular follow-up in patients with GERD. Second, because results indicate that older age and bronchiectasis significantly increase the risk of NTM-PD, “more active strategies (e.g., screening of symptoms and regular chest x-rays)” might be helpful in patients with GERD and these risk factors, the authors suggested. Because patients with GERD who developed NTM-PD had more respiratory disease–related ED visits and hospitalizations than those who did not develop NTM-PD, when GERD and NTM-PD are combined, clinicians should focus on the variations of respiratory symptoms, they suggested.

The authors cautioned, however, that because the study was one in a Korean population, studies in other countries and different ethnicities are needed before findings can be generalized.

More common than TB

Asked to comment on the findings, NTM-PD expert Theodore Marras, MD, clinician investigator, Krembil Research Institute, Toronto, noted that non-TB M-PD is about 10 times more common than TB and that could be an underestimate as there have been very large increases in the incidence of NTM-PD in recent years. “It’s an environmental germ – it’s in our water – and certain people are particularly susceptible to it, typically older age women who have underlying bronchiectasis,” Dr. Marras told this news organization. “And while there are ethnic differences in incidence rates between East Asian people and Black African people, immigration is not the main driver for the increase as far as we can tell,” he said.

He personally treats a lot of NTM-PD and he also believes that GERD is an important risk factor for all types of lung infections including NTM lung disease. “So without a doubt, I believe that GERD should be treated in patients with NTM-PD,” Dr. Marras emphasized. The big question is how to treat GERD, as there may be concerns with acid-suppressive agents such as proton pump inhibitors that “the reflux that comes back up may harbor more germs in it and if that reflux comes up high enough, we are at risk of aspirating some of that fluid into our lungs, especially when we’re asleep,” he said.

Some experts therefore argue in favor of using motility agents instead of PPIs. However, if Dr. Marras has a patient with heartburn, “you have to treat it,” he stressed. Similarly, if a patient has evidence of esophageal erosions, physicians need to treat those as well. However, if neither feature is present, “I tend to like the motility agents preferentially or use them in combination with a PPI,” Dr. Marras said.

Dr. Marras also thinks the study is encouraging physicians involved in treating these patients to think about controlling GERD both when they are treating patients and after they are treated to try to reduce recurrence.

The authors had no financial disclosures to make. Dr. Marras has given several talks on NTM lung disease, one sponsored by AstraZeneca and the other by Novartis.