Jim Kling

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

A “digital twin” model successfully predicted adverse outcomes in intensive care unit (ICU) patients treated for sepsis. The research used an adaptive approach, updating time-sensitive values such as blood pressure and vitals every 15 minutes. The approach also took into account treatment decisions and has potential as a decision-making and educational tool.

The digital twin could reduce the risk for some interventions, according to Amos Lal, MD, who presented the study at the CHEST Annual Meeting. That’s because the model can predict the outcome. “You don’t actually have to make an intervention to the patient, which might be risky. By doing that, you can actually prevent a lot of harm,” said Dr. Lal, assistant professor of medicine at Mayo Clinic in Rochester, Minnesota.

The researchers used a one-dimensional convolutional neural network (CNN), similar to two-dimensional CNNs that are used to classify images, substituting the color channels used in imaging with 38 time-dependent variables. They applied it to predicting outcomes in the ICU, focusing on data generated within the first 24 hours of admission. The team made the model dynamic by adding time-sensitive data like vitals, laboratory values, and interventions every 15 minutes. That contrasts with existing models that are usually static, relying on values at admission or at 24 hours, for example. It also takes into account time-insensitive data like age, gender, and comorbidities. “Combining these two and coming up with the prediction model in real time can give you a more informed decision about how these patients are going to perform over a period of 2 weeks or 4 weeks of their stay within the ICU. And of course, as we get more and more data within the first 24 hours, the performance of the model improves as well,” said Dr. Lal.

The researchers tested the model by creating a virtual model of the patient and then performing an intervention on the patient and a simulated intervention on the virtual patient. “Then we advance the clock and the patient either improved or deteriorated, and we compared how the digital twin performed, whether the changes were concordant or discordant [between the virtual and real-world patients],” said Dr. Lal.

The model was designed to predict which patients with sepsis would be at greater risk for death or ICU stays longer than 14 days. It was created using data from 28,617 patients with critical care sepsis at a single hospital who were treated between 2011 and 2018, with 70% used as a training set, 20% as a test set, and 10% as a validation set. The researchers conducted an external validation using MIMIC-IV data on 30,903 patients from the Beth Israel Deaconess Medical Center in Boston. The model included 31 time-independent variables and 38 time-dependent variables that were collected every 15 minutes at the Mayo Clinic and every 60 minutes at Beth Israel Deaconess. Surgical patients represented 24% of the Mayo dataset and 58% of the MIMIC-IV dataset, but otherwise the two groups were demographically similar.

At 24 hours, the area under the receiver operating characteristic curve for predicting 14-day mortality was −0.82 in the Mayo validation cohort and −0.78 in the MIMIC validation cohort. The model improved in accuracy over time as more data were accumulated.

The session’s co-moderators, Sandeep Jain, MD, and Casey Cable, MD, praised the work. Dr. Cable, associate professor of pulmonary care medicine at VCU Health, Richmond, Virginia, noted that the model used both surgical patients and medical patients with sepsis, and the two groups can present quite differently. Another variable was the COVID pandemic, where some patients presented at the hospital when they were quite sick. “I’m curious how different starting points would play into it,” she said.

She called for institutions to develop such models on their own rather than relying on companies that might develop software solutions. “I think that this needs to be clinician-led, from the ground up,” said Dr. Cable.

Dr. Jain, an associate professor of pulmonary care medicine at Broward Health, suggested that such models might need to be individualized for each institution, but “my fear is it could become too expensive, so I think a group like CHEST could come together and [create] an open source system to have their researchers jumpstart the research on this,” he said.

Dr. Lal, Dr. Jain, and Dr. Cable reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

A “digital twin” model successfully predicted adverse outcomes in intensive care unit (ICU) patients treated for sepsis. The research used an adaptive approach, updating time-sensitive values such as blood pressure and vitals every 15 minutes. The approach also took into account treatment decisions and has potential as a decision-making and educational tool.

The digital twin could reduce the risk for some interventions, according to Amos Lal, MD, who presented the study at the CHEST Annual Meeting. That’s because the model can predict the outcome. “You don’t actually have to make an intervention to the patient, which might be risky. By doing that, you can actually prevent a lot of harm,” said Dr. Lal, assistant professor of medicine at Mayo Clinic in Rochester, Minnesota.

The researchers used a one-dimensional convolutional neural network (CNN), similar to two-dimensional CNNs that are used to classify images, substituting the color channels used in imaging with 38 time-dependent variables. They applied it to predicting outcomes in the ICU, focusing on data generated within the first 24 hours of admission. The team made the model dynamic by adding time-sensitive data like vitals, laboratory values, and interventions every 15 minutes. That contrasts with existing models that are usually static, relying on values at admission or at 24 hours, for example. It also takes into account time-insensitive data like age, gender, and comorbidities. “Combining these two and coming up with the prediction model in real time can give you a more informed decision about how these patients are going to perform over a period of 2 weeks or 4 weeks of their stay within the ICU. And of course, as we get more and more data within the first 24 hours, the performance of the model improves as well,” said Dr. Lal.

The researchers tested the model by creating a virtual model of the patient and then performing an intervention on the patient and a simulated intervention on the virtual patient. “Then we advance the clock and the patient either improved or deteriorated, and we compared how the digital twin performed, whether the changes were concordant or discordant [between the virtual and real-world patients],” said Dr. Lal.

The model was designed to predict which patients with sepsis would be at greater risk for death or ICU stays longer than 14 days. It was created using data from 28,617 patients with critical care sepsis at a single hospital who were treated between 2011 and 2018, with 70% used as a training set, 20% as a test set, and 10% as a validation set. The researchers conducted an external validation using MIMIC-IV data on 30,903 patients from the Beth Israel Deaconess Medical Center in Boston. The model included 31 time-independent variables and 38 time-dependent variables that were collected every 15 minutes at the Mayo Clinic and every 60 minutes at Beth Israel Deaconess. Surgical patients represented 24% of the Mayo dataset and 58% of the MIMIC-IV dataset, but otherwise the two groups were demographically similar.

At 24 hours, the area under the receiver operating characteristic curve for predicting 14-day mortality was −0.82 in the Mayo validation cohort and −0.78 in the MIMIC validation cohort. The model improved in accuracy over time as more data were accumulated.

The session’s co-moderators, Sandeep Jain, MD, and Casey Cable, MD, praised the work. Dr. Cable, associate professor of pulmonary care medicine at VCU Health, Richmond, Virginia, noted that the model used both surgical patients and medical patients with sepsis, and the two groups can present quite differently. Another variable was the COVID pandemic, where some patients presented at the hospital when they were quite sick. “I’m curious how different starting points would play into it,” she said.

She called for institutions to develop such models on their own rather than relying on companies that might develop software solutions. “I think that this needs to be clinician-led, from the ground up,” said Dr. Cable.

Dr. Jain, an associate professor of pulmonary care medicine at Broward Health, suggested that such models might need to be individualized for each institution, but “my fear is it could become too expensive, so I think a group like CHEST could come together and [create] an open source system to have their researchers jumpstart the research on this,” he said.

Dr. Lal, Dr. Jain, and Dr. Cable reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

A “digital twin” model successfully predicted adverse outcomes in intensive care unit (ICU) patients treated for sepsis. The research used an adaptive approach, updating time-sensitive values such as blood pressure and vitals every 15 minutes. The approach also took into account treatment decisions and has potential as a decision-making and educational tool.

The digital twin could reduce the risk for some interventions, according to Amos Lal, MD, who presented the study at the CHEST Annual Meeting. That’s because the model can predict the outcome. “You don’t actually have to make an intervention to the patient, which might be risky. By doing that, you can actually prevent a lot of harm,” said Dr. Lal, assistant professor of medicine at Mayo Clinic in Rochester, Minnesota.

The researchers used a one-dimensional convolutional neural network (CNN), similar to two-dimensional CNNs that are used to classify images, substituting the color channels used in imaging with 38 time-dependent variables. They applied it to predicting outcomes in the ICU, focusing on data generated within the first 24 hours of admission. The team made the model dynamic by adding time-sensitive data like vitals, laboratory values, and interventions every 15 minutes. That contrasts with existing models that are usually static, relying on values at admission or at 24 hours, for example. It also takes into account time-insensitive data like age, gender, and comorbidities. “Combining these two and coming up with the prediction model in real time can give you a more informed decision about how these patients are going to perform over a period of 2 weeks or 4 weeks of their stay within the ICU. And of course, as we get more and more data within the first 24 hours, the performance of the model improves as well,” said Dr. Lal.

The researchers tested the model by creating a virtual model of the patient and then performing an intervention on the patient and a simulated intervention on the virtual patient. “Then we advance the clock and the patient either improved or deteriorated, and we compared how the digital twin performed, whether the changes were concordant or discordant [between the virtual and real-world patients],” said Dr. Lal.

The model was designed to predict which patients with sepsis would be at greater risk for death or ICU stays longer than 14 days. It was created using data from 28,617 patients with critical care sepsis at a single hospital who were treated between 2011 and 2018, with 70% used as a training set, 20% as a test set, and 10% as a validation set. The researchers conducted an external validation using MIMIC-IV data on 30,903 patients from the Beth Israel Deaconess Medical Center in Boston. The model included 31 time-independent variables and 38 time-dependent variables that were collected every 15 minutes at the Mayo Clinic and every 60 minutes at Beth Israel Deaconess. Surgical patients represented 24% of the Mayo dataset and 58% of the MIMIC-IV dataset, but otherwise the two groups were demographically similar.

At 24 hours, the area under the receiver operating characteristic curve for predicting 14-day mortality was −0.82 in the Mayo validation cohort and −0.78 in the MIMIC validation cohort. The model improved in accuracy over time as more data were accumulated.

The session’s co-moderators, Sandeep Jain, MD, and Casey Cable, MD, praised the work. Dr. Cable, associate professor of pulmonary care medicine at VCU Health, Richmond, Virginia, noted that the model used both surgical patients and medical patients with sepsis, and the two groups can present quite differently. Another variable was the COVID pandemic, where some patients presented at the hospital when they were quite sick. “I’m curious how different starting points would play into it,” she said.

She called for institutions to develop such models on their own rather than relying on companies that might develop software solutions. “I think that this needs to be clinician-led, from the ground up,” said Dr. Cable.

Dr. Jain, an associate professor of pulmonary care medicine at Broward Health, suggested that such models might need to be individualized for each institution, but “my fear is it could become too expensive, so I think a group like CHEST could come together and [create] an open source system to have their researchers jumpstart the research on this,” he said.

Dr. Lal, Dr. Jain, and Dr. Cable reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

BOSTON — Patients with pulmonary embolism (PE) who also present with interstitial lung disease (ILD) have worse outcomes with respect to in-hospital mortality, length of hospital stay, hospital cost, and all-cause readmission, according to results from a new retrospective analysis.

“There’s a lot of evidence now that demonstrates that ILD, in general, leads to worse mortality, morbidity in hospital complications, and overall [outcomes]. It’s not hard to extrapolate this to pulmonary embolism outcomes, too. Unfortunately, there’s not a whole lot of evidence out there to really demonstrate it,” Leah Yuan, MD, said during a presentation of the results at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The question is complicated by the nebulous nature of ILD, which includes a diverse set of diseases and etiologies, and different levels of inflammation and fibrosis. It has been employed in the Pulmonary Embolism Severity Index but counts for only 10 points out of 210. “If you look at ILD and PE outcomes, there’s nothing really out there [in the literature],” Yuan said in an interview. She is a resident physician at Cook County Health and Hospitals System.

The new study suggested that ILD could have an important influence and perhaps should have greater weight in risk stratification of patients with PE, she said. “We looked at all-cause readmissions and we looked at in-hospital mortality, [both] of which are significant for increased odds ratio. One thing that I’m very curious to see is whether there is increased PE readmissions [associated with ILD], which is something that we couldn’t find to be significant in our study,” said Yuan.

The researchers used data from hospitalizations for PE drawn from the Nationwide Readmissions Database in 2019, using International Classification of Diseases, Tenth Revision, codes to identify admissions. Among a total of 105,133 patients admitted for PE, 158 patients also had ILD. The mean age was 63.6 years for those without ILD (SD, 0.1) and 66.5 years for those with ILD (SD, 1.3).

Admission with ILD was associated with all-cause readmission (odds ratio [OR], 4.12; P < .01), in-hospital mortality (OR, 2.17; P = .01), a longer length of stay (+2.07 days; P < .01), and higher hospitalization charges (+$22,627; P < .01).

In the Q&A period after the presentation, Parth Rali, MD, professor of thoracic medicine and surgery at Temple University, Philadelphia, suggested phenotyping patients to better understand the location of the PE in relation to the ILD. “It may not fall into your classic PE classification. It may just depend on where the clot is in relationship to the interstitial lung disease. I think that’s where the field is going to evolve,” he later said in an interview.

“What is interesting is that patients with interstitial lung disease have a lot of fibrotic disease, and they do not need to have a large clot burden to make them sick. An example [is someone] who has undergone a lung transplant evaluation, and if their right lung is completely diseased from interstitial lung disease and if they get a big blood clot on the right side, it doesn’t affect them because the lung is already fibrotic, so the clot doesn’t matter. If they get a small clot [in the left lung], even though if you look at the standard PE classification they may qualify as a low-risk PE or even as an intermediate-low-risk PE, they are much sicker because that’s the functioning part of the lung,” said Rali.

He advised physicians to pay close attention to the location of PEs in relation to fibrotic tissue in patients with ILD. A PE in healthy lung tissue could have an outsized effect on hemodynamics, whereas a PE in fibrotic tissue may be clinically insignificant and not require treatment. “So it goes both ways: You don’t overtreat and you don’t undertreat,” Rali said.

Yuan and Rali disclosed no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — Patients with pulmonary embolism (PE) who also present with interstitial lung disease (ILD) have worse outcomes with respect to in-hospital mortality, length of hospital stay, hospital cost, and all-cause readmission, according to results from a new retrospective analysis.

“There’s a lot of evidence now that demonstrates that ILD, in general, leads to worse mortality, morbidity in hospital complications, and overall [outcomes]. It’s not hard to extrapolate this to pulmonary embolism outcomes, too. Unfortunately, there’s not a whole lot of evidence out there to really demonstrate it,” Leah Yuan, MD, said during a presentation of the results at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The question is complicated by the nebulous nature of ILD, which includes a diverse set of diseases and etiologies, and different levels of inflammation and fibrosis. It has been employed in the Pulmonary Embolism Severity Index but counts for only 10 points out of 210. “If you look at ILD and PE outcomes, there’s nothing really out there [in the literature],” Yuan said in an interview. She is a resident physician at Cook County Health and Hospitals System.

The new study suggested that ILD could have an important influence and perhaps should have greater weight in risk stratification of patients with PE, she said. “We looked at all-cause readmissions and we looked at in-hospital mortality, [both] of which are significant for increased odds ratio. One thing that I’m very curious to see is whether there is increased PE readmissions [associated with ILD], which is something that we couldn’t find to be significant in our study,” said Yuan.

The researchers used data from hospitalizations for PE drawn from the Nationwide Readmissions Database in 2019, using International Classification of Diseases, Tenth Revision, codes to identify admissions. Among a total of 105,133 patients admitted for PE, 158 patients also had ILD. The mean age was 63.6 years for those without ILD (SD, 0.1) and 66.5 years for those with ILD (SD, 1.3).

Admission with ILD was associated with all-cause readmission (odds ratio [OR], 4.12; P < .01), in-hospital mortality (OR, 2.17; P = .01), a longer length of stay (+2.07 days; P < .01), and higher hospitalization charges (+$22,627; P < .01).

In the Q&A period after the presentation, Parth Rali, MD, professor of thoracic medicine and surgery at Temple University, Philadelphia, suggested phenotyping patients to better understand the location of the PE in relation to the ILD. “It may not fall into your classic PE classification. It may just depend on where the clot is in relationship to the interstitial lung disease. I think that’s where the field is going to evolve,” he later said in an interview.

“What is interesting is that patients with interstitial lung disease have a lot of fibrotic disease, and they do not need to have a large clot burden to make them sick. An example [is someone] who has undergone a lung transplant evaluation, and if their right lung is completely diseased from interstitial lung disease and if they get a big blood clot on the right side, it doesn’t affect them because the lung is already fibrotic, so the clot doesn’t matter. If they get a small clot [in the left lung], even though if you look at the standard PE classification they may qualify as a low-risk PE or even as an intermediate-low-risk PE, they are much sicker because that’s the functioning part of the lung,” said Rali.

He advised physicians to pay close attention to the location of PEs in relation to fibrotic tissue in patients with ILD. A PE in healthy lung tissue could have an outsized effect on hemodynamics, whereas a PE in fibrotic tissue may be clinically insignificant and not require treatment. “So it goes both ways: You don’t overtreat and you don’t undertreat,” Rali said.

Yuan and Rali disclosed no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — Patients with pulmonary embolism (PE) who also present with interstitial lung disease (ILD) have worse outcomes with respect to in-hospital mortality, length of hospital stay, hospital cost, and all-cause readmission, according to results from a new retrospective analysis.

“There’s a lot of evidence now that demonstrates that ILD, in general, leads to worse mortality, morbidity in hospital complications, and overall [outcomes]. It’s not hard to extrapolate this to pulmonary embolism outcomes, too. Unfortunately, there’s not a whole lot of evidence out there to really demonstrate it,” Leah Yuan, MD, said during a presentation of the results at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The question is complicated by the nebulous nature of ILD, which includes a diverse set of diseases and etiologies, and different levels of inflammation and fibrosis. It has been employed in the Pulmonary Embolism Severity Index but counts for only 10 points out of 210. “If you look at ILD and PE outcomes, there’s nothing really out there [in the literature],” Yuan said in an interview. She is a resident physician at Cook County Health and Hospitals System.

The new study suggested that ILD could have an important influence and perhaps should have greater weight in risk stratification of patients with PE, she said. “We looked at all-cause readmissions and we looked at in-hospital mortality, [both] of which are significant for increased odds ratio. One thing that I’m very curious to see is whether there is increased PE readmissions [associated with ILD], which is something that we couldn’t find to be significant in our study,” said Yuan.

The researchers used data from hospitalizations for PE drawn from the Nationwide Readmissions Database in 2019, using International Classification of Diseases, Tenth Revision, codes to identify admissions. Among a total of 105,133 patients admitted for PE, 158 patients also had ILD. The mean age was 63.6 years for those without ILD (SD, 0.1) and 66.5 years for those with ILD (SD, 1.3).

Admission with ILD was associated with all-cause readmission (odds ratio [OR], 4.12; P < .01), in-hospital mortality (OR, 2.17; P = .01), a longer length of stay (+2.07 days; P < .01), and higher hospitalization charges (+$22,627; P < .01).

In the Q&A period after the presentation, Parth Rali, MD, professor of thoracic medicine and surgery at Temple University, Philadelphia, suggested phenotyping patients to better understand the location of the PE in relation to the ILD. “It may not fall into your classic PE classification. It may just depend on where the clot is in relationship to the interstitial lung disease. I think that’s where the field is going to evolve,” he later said in an interview.

“What is interesting is that patients with interstitial lung disease have a lot of fibrotic disease, and they do not need to have a large clot burden to make them sick. An example [is someone] who has undergone a lung transplant evaluation, and if their right lung is completely diseased from interstitial lung disease and if they get a big blood clot on the right side, it doesn’t affect them because the lung is already fibrotic, so the clot doesn’t matter. If they get a small clot [in the left lung], even though if you look at the standard PE classification they may qualify as a low-risk PE or even as an intermediate-low-risk PE, they are much sicker because that’s the functioning part of the lung,” said Rali.

He advised physicians to pay close attention to the location of PEs in relation to fibrotic tissue in patients with ILD. A PE in healthy lung tissue could have an outsized effect on hemodynamics, whereas a PE in fibrotic tissue may be clinically insignificant and not require treatment. “So it goes both ways: You don’t overtreat and you don’t undertreat,” Rali said.

Yuan and Rali disclosed no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — The use of sodium-glucose cotransporter-2 (SGLT2) inhibitors is associated with reduced short- and long-term mortality among patients with pulmonary arterial hypertension (PAH), according to results from a new propensity score–matched analysis.

“There are a lot of new studies that show benefits [of SGLT2 inhibitors] in heart failure, in [chronic kidney disease], and of course, in diabetes. Group one pulmonary hypertension includes not only the inflammatory cascades but also fibrotic and neurovascularization, and all these different parts of the pathophysiology are linked to each other. There are studies that show that SGLT2 inhibitors can have an impact on inflammatory cascades, fibrosis, and vascular remodeling in general. Together, all this data triggered this idea for me, and that’s when I decided to conduct further studies,” said Irakli Lemonjava, MD, who presented the study at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The researchers drew data on 125,634 adult patients from the TriNetX database who were diagnosed with PAH after January 1, 2013. They used propensity score matching to account for demographic characteristics and 10 organ system disorders to compare patients with exposure to SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin; n = 6238) with those without such exposure (n = 6243).

At 1 year, 8.1% of patients taking SGLT2 inhibitors had died, compared with 15.5% of patients not taking SGLT2 inhibitors (risk reduction [RR], 0.52; P < .0001). The values were 13% and 22.5% (RR, 0.579; P < .0001) at 3 years and 14.6% and 25% at 5 years (RR, 0.583; P < .0001).

The study generated discussion during the Q&A period following the talk. One audience member asked if the group was able to access patients both inside and outside the United States. “Because I wonder if access to GLP2 inhibitors is actually a surrogate marker for access to other medications,” the questioner said.

Although the finding is intriguing, it shouldn’t change clinical practice, according to Lemonjava. “I don’t think we can make any changes based on what I shared today. Our purpose was to trigger the question. I think the numbers are so impressive that it will trigger more studies. I think if in the future it’s demonstrated by clinical trials that [SGLT2 inhibitors are beneficial], it will not be a problem to prescribe for someone with pulmonary arterial hypertension because they do not have many side effects,” he said. Lemonjava is a resident physician at Jefferson Einstein Philadelphia Hospital, Philadelphia.

Session co-moderator said Syed Rehan Quadery, MD, praised the study but emphasized the remaining uncertainty. “It’s an excellent proof of concept study. More trials need to [be done] on it, and we don’t understand the mechanism of action in which it improves survival in patients with pulmonary artery hypertension. The majority of the patients with pulmonary hypertension are much older and they have comorbidities, including cardiovascular risk factors, and maybe that is one of the ways in which this drug helps. Plus, there are multiple mechanisms in which it may be working, including anti-inflammatory as well as antiproliferative mechanisms through inhibiting the Notch-3 signaling pathway,” said Quadery, who is a consultant respiratory physician at National Pulmonary Hypertension Unit, Dublin, Ireland.

Quadery and his co-moderator Zeenat Safdar, MD, both noted that SGLT2 inhibitors have already been demonstrated to improve outcomes in heart failure. “[SGLT2 inhibition] improves survival, it decreases hospitalization, it improves morbidity and mortality. There are a lot of things that can be shown in different [animal or in vitro] models. In humans, we actually don’t know exactly how it works, but we know that it does. If it works in left heart failure, it also [could] work in right heart failure,” said Safdar, who is the director of the Houston Methodist Lung Center, Houston Methodist Hospital, Houston.

The study was independently supported. Lemonjava, Quadery, and Safdar reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — The use of sodium-glucose cotransporter-2 (SGLT2) inhibitors is associated with reduced short- and long-term mortality among patients with pulmonary arterial hypertension (PAH), according to results from a new propensity score–matched analysis.

“There are a lot of new studies that show benefits [of SGLT2 inhibitors] in heart failure, in [chronic kidney disease], and of course, in diabetes. Group one pulmonary hypertension includes not only the inflammatory cascades but also fibrotic and neurovascularization, and all these different parts of the pathophysiology are linked to each other. There are studies that show that SGLT2 inhibitors can have an impact on inflammatory cascades, fibrosis, and vascular remodeling in general. Together, all this data triggered this idea for me, and that’s when I decided to conduct further studies,” said Irakli Lemonjava, MD, who presented the study at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The researchers drew data on 125,634 adult patients from the TriNetX database who were diagnosed with PAH after January 1, 2013. They used propensity score matching to account for demographic characteristics and 10 organ system disorders to compare patients with exposure to SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin; n = 6238) with those without such exposure (n = 6243).

At 1 year, 8.1% of patients taking SGLT2 inhibitors had died, compared with 15.5% of patients not taking SGLT2 inhibitors (risk reduction [RR], 0.52; P < .0001). The values were 13% and 22.5% (RR, 0.579; P < .0001) at 3 years and 14.6% and 25% at 5 years (RR, 0.583; P < .0001).

The study generated discussion during the Q&A period following the talk. One audience member asked if the group was able to access patients both inside and outside the United States. “Because I wonder if access to GLP2 inhibitors is actually a surrogate marker for access to other medications,” the questioner said.

Although the finding is intriguing, it shouldn’t change clinical practice, according to Lemonjava. “I don’t think we can make any changes based on what I shared today. Our purpose was to trigger the question. I think the numbers are so impressive that it will trigger more studies. I think if in the future it’s demonstrated by clinical trials that [SGLT2 inhibitors are beneficial], it will not be a problem to prescribe for someone with pulmonary arterial hypertension because they do not have many side effects,” he said. Lemonjava is a resident physician at Jefferson Einstein Philadelphia Hospital, Philadelphia.

Session co-moderator said Syed Rehan Quadery, MD, praised the study but emphasized the remaining uncertainty. “It’s an excellent proof of concept study. More trials need to [be done] on it, and we don’t understand the mechanism of action in which it improves survival in patients with pulmonary artery hypertension. The majority of the patients with pulmonary hypertension are much older and they have comorbidities, including cardiovascular risk factors, and maybe that is one of the ways in which this drug helps. Plus, there are multiple mechanisms in which it may be working, including anti-inflammatory as well as antiproliferative mechanisms through inhibiting the Notch-3 signaling pathway,” said Quadery, who is a consultant respiratory physician at National Pulmonary Hypertension Unit, Dublin, Ireland.

Quadery and his co-moderator Zeenat Safdar, MD, both noted that SGLT2 inhibitors have already been demonstrated to improve outcomes in heart failure. “[SGLT2 inhibition] improves survival, it decreases hospitalization, it improves morbidity and mortality. There are a lot of things that can be shown in different [animal or in vitro] models. In humans, we actually don’t know exactly how it works, but we know that it does. If it works in left heart failure, it also [could] work in right heart failure,” said Safdar, who is the director of the Houston Methodist Lung Center, Houston Methodist Hospital, Houston.

The study was independently supported. Lemonjava, Quadery, and Safdar reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — The use of sodium-glucose cotransporter-2 (SGLT2) inhibitors is associated with reduced short- and long-term mortality among patients with pulmonary arterial hypertension (PAH), according to results from a new propensity score–matched analysis.

“There are a lot of new studies that show benefits [of SGLT2 inhibitors] in heart failure, in [chronic kidney disease], and of course, in diabetes. Group one pulmonary hypertension includes not only the inflammatory cascades but also fibrotic and neurovascularization, and all these different parts of the pathophysiology are linked to each other. There are studies that show that SGLT2 inhibitors can have an impact on inflammatory cascades, fibrosis, and vascular remodeling in general. Together, all this data triggered this idea for me, and that’s when I decided to conduct further studies,” said Irakli Lemonjava, MD, who presented the study at the American College of Chest Physicians (CHEST) 2024 Annual Meeting.

The researchers drew data on 125,634 adult patients from the TriNetX database who were diagnosed with PAH after January 1, 2013. They used propensity score matching to account for demographic characteristics and 10 organ system disorders to compare patients with exposure to SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin; n = 6238) with those without such exposure (n = 6243).

At 1 year, 8.1% of patients taking SGLT2 inhibitors had died, compared with 15.5% of patients not taking SGLT2 inhibitors (risk reduction [RR], 0.52; P < .0001). The values were 13% and 22.5% (RR, 0.579; P < .0001) at 3 years and 14.6% and 25% at 5 years (RR, 0.583; P < .0001).

The study generated discussion during the Q&A period following the talk. One audience member asked if the group was able to access patients both inside and outside the United States. “Because I wonder if access to GLP2 inhibitors is actually a surrogate marker for access to other medications,” the questioner said.

Although the finding is intriguing, it shouldn’t change clinical practice, according to Lemonjava. “I don’t think we can make any changes based on what I shared today. Our purpose was to trigger the question. I think the numbers are so impressive that it will trigger more studies. I think if in the future it’s demonstrated by clinical trials that [SGLT2 inhibitors are beneficial], it will not be a problem to prescribe for someone with pulmonary arterial hypertension because they do not have many side effects,” he said. Lemonjava is a resident physician at Jefferson Einstein Philadelphia Hospital, Philadelphia.

Session co-moderator said Syed Rehan Quadery, MD, praised the study but emphasized the remaining uncertainty. “It’s an excellent proof of concept study. More trials need to [be done] on it, and we don’t understand the mechanism of action in which it improves survival in patients with pulmonary artery hypertension. The majority of the patients with pulmonary hypertension are much older and they have comorbidities, including cardiovascular risk factors, and maybe that is one of the ways in which this drug helps. Plus, there are multiple mechanisms in which it may be working, including anti-inflammatory as well as antiproliferative mechanisms through inhibiting the Notch-3 signaling pathway,” said Quadery, who is a consultant respiratory physician at National Pulmonary Hypertension Unit, Dublin, Ireland.

Quadery and his co-moderator Zeenat Safdar, MD, both noted that SGLT2 inhibitors have already been demonstrated to improve outcomes in heart failure. “[SGLT2 inhibition] improves survival, it decreases hospitalization, it improves morbidity and mortality. There are a lot of things that can be shown in different [animal or in vitro] models. In humans, we actually don’t know exactly how it works, but we know that it does. If it works in left heart failure, it also [could] work in right heart failure,” said Safdar, who is the director of the Houston Methodist Lung Center, Houston Methodist Hospital, Houston.

The study was independently supported. Lemonjava, Quadery, and Safdar reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

BOSTON — Gastroesophageal reflux disease (GERD) is associated with better in-hospital outcomes for patients hospitalized with chronic obstructive pulmonary disease (COPD). The finding is a surprise, considering that GERD has been associated with more COPD exacerbations. GERD is also more common among patients with COPD than in the general population.

“It was a very surprising result. We double-checked the analysis once we got it the first time because the whole expectation was that the outcomes will be worse. But because it’s a retrospective study and it’s based on a national database, there are some limitations,” said ABM Nasibul Alam, MD, who presented the study at the annual meeting of the American College of Chest Physicians (CHEST) . Alam is an internal medicine resident at Northwestern Medicine McHenry Hospital, McHenry, Illinois.

One possible conclusion is that acid reflux therapies received in hospital may be benefitting COPD. The retrospective nature of the study precludes establishing a causal relationship, but there are possible mechanisms that could account for a benefit, according to Alam.

“They might prevent micro-aspirations or silent aspirations in COPD patients. Sometimes you may not have a clinical diagnosis of GERD, but the patient might have silent micro-aspirations, so it might contribute to decreasing that,” said Alam.

The study was conducted to fill a gap in the literature. “Some studies have shown that the lung function in COPD patients gets moderately decreased if they have coexisting GERD, but there aren’t any studies that have looked into how it impacts COPD patients when they’re hospitalized, and especially acute complications,” said Alam.

The researchers retrospectively analyzed data from the Nationwide Readmissions Database from 2017 to 2020, utilizing ICD-10 codes to identify 3,798,952 hospitalized adults with a primary diagnosis of COPD, of which 26.97% also had GERD. Individuals without GERD were more likely to be male (47.72% vs 39.88%).

After multivariate adjustment, the presence of GERD was associated with a lower mortality rate (adjusted odds ratio [aOR], 0.717; P < .001) and reduced risks for acute respiratory failure (aOR, 0.915; P < .001), need for noninvasive mechanical ventilation (aOR, 0.907; P < .001), need for invasive ventilation for 24 hours or more (aOR, 0.727; P < .001), acute kidney injury (aOR, 0.877; P < .001), septic shock (aOR, 0.731; ^P < .001), and acute heart failure (aOR, 0.762; P < .001).

Despite these improved in-hospital outcomes, the researchers found that patients with GERD were at a higher risk for 30-day readmission (aOR, 1.08; P < .001). They also had slightly longer lengths of stay (+0.09 day; P < .001) and lower total charges (−$2824.5996; P < .001).

There have also been studies suggesting that GERD can directly lead to worse lung function among patients with COPD. “So it will be interesting to see if these medications have some kind of impact on the lung function as well. We need more robust studies [to determine that],” said Alam.

It is also important to keep in mind the long-term risk of proton pump inhibitors, especially in older patients. “We have to have good data before we start recommending this,” said Alam.

He suggested that physicians should begin to think more holistically about COPD management and consider the comorbidities. Alam has studied vitamin B12 deficiency in patients with COPD and found an association with cardiovascular comorbidities. “There are so many comorbidities with COPD. COPD itself puts patients at risk of cardiovascular comorbidity, for example. So when we have patients with COPD, we have to think about all those comorbidities and have to manage the patients comprehensively rather than just focusing on the specific targeted interventions,” said Alam.

The study should encourage further research, according to Kunal Deokar, MD, who moderated the session where the study was presented. “It does give us a signal that probably we should have more studies to look into whether patients hospitalized for COPD with GERD really have lower mortality rates, and what will be the effect of treatment on these patients,” said Deokar, who is an assistant professor of pulmonary medicine at the All India Institute of Medical Sciences, Delhi, India.

Alam and Deokar disclosed no relevant financial relationships.

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

BOSTON — Gastroesophageal reflux disease (GERD) is associated with better in-hospital outcomes for patients hospitalized with chronic obstructive pulmonary disease (COPD). The finding is a surprise, considering that GERD has been associated with more COPD exacerbations. GERD is also more common among patients with COPD than in the general population.

“It was a very surprising result. We double-checked the analysis once we got it the first time because the whole expectation was that the outcomes will be worse. But because it’s a retrospective study and it’s based on a national database, there are some limitations,” said ABM Nasibul Alam, MD, who presented the study at the annual meeting of the American College of Chest Physicians (CHEST) . Alam is an internal medicine resident at Northwestern Medicine McHenry Hospital, McHenry, Illinois.

One possible conclusion is that acid reflux therapies received in hospital may be benefitting COPD. The retrospective nature of the study precludes establishing a causal relationship, but there are possible mechanisms that could account for a benefit, according to Alam.

“They might prevent micro-aspirations or silent aspirations in COPD patients. Sometimes you may not have a clinical diagnosis of GERD, but the patient might have silent micro-aspirations, so it might contribute to decreasing that,” said Alam.

The study was conducted to fill a gap in the literature. “Some studies have shown that the lung function in COPD patients gets moderately decreased if they have coexisting GERD, but there aren’t any studies that have looked into how it impacts COPD patients when they’re hospitalized, and especially acute complications,” said Alam.

The researchers retrospectively analyzed data from the Nationwide Readmissions Database from 2017 to 2020, utilizing ICD-10 codes to identify 3,798,952 hospitalized adults with a primary diagnosis of COPD, of which 26.97% also had GERD. Individuals without GERD were more likely to be male (47.72% vs 39.88%).

After multivariate adjustment, the presence of GERD was associated with a lower mortality rate (adjusted odds ratio [aOR], 0.717; P < .001) and reduced risks for acute respiratory failure (aOR, 0.915; P < .001), need for noninvasive mechanical ventilation (aOR, 0.907; P < .001), need for invasive ventilation for 24 hours or more (aOR, 0.727; P < .001), acute kidney injury (aOR, 0.877; P < .001), septic shock (aOR, 0.731; ^P < .001), and acute heart failure (aOR, 0.762; P < .001).

Despite these improved in-hospital outcomes, the researchers found that patients with GERD were at a higher risk for 30-day readmission (aOR, 1.08; P < .001). They also had slightly longer lengths of stay (+0.09 day; P < .001) and lower total charges (−$2824.5996; P < .001).

There have also been studies suggesting that GERD can directly lead to worse lung function among patients with COPD. “So it will be interesting to see if these medications have some kind of impact on the lung function as well. We need more robust studies [to determine that],” said Alam.

It is also important to keep in mind the long-term risk of proton pump inhibitors, especially in older patients. “We have to have good data before we start recommending this,” said Alam.

He suggested that physicians should begin to think more holistically about COPD management and consider the comorbidities. Alam has studied vitamin B12 deficiency in patients with COPD and found an association with cardiovascular comorbidities. “There are so many comorbidities with COPD. COPD itself puts patients at risk of cardiovascular comorbidity, for example. So when we have patients with COPD, we have to think about all those comorbidities and have to manage the patients comprehensively rather than just focusing on the specific targeted interventions,” said Alam.

The study should encourage further research, according to Kunal Deokar, MD, who moderated the session where the study was presented. “It does give us a signal that probably we should have more studies to look into whether patients hospitalized for COPD with GERD really have lower mortality rates, and what will be the effect of treatment on these patients,” said Deokar, who is an assistant professor of pulmonary medicine at the All India Institute of Medical Sciences, Delhi, India.

Alam and Deokar disclosed no relevant financial relationships.

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

BOSTON — Gastroesophageal reflux disease (GERD) is associated with better in-hospital outcomes for patients hospitalized with chronic obstructive pulmonary disease (COPD). The finding is a surprise, considering that GERD has been associated with more COPD exacerbations. GERD is also more common among patients with COPD than in the general population.

“It was a very surprising result. We double-checked the analysis once we got it the first time because the whole expectation was that the outcomes will be worse. But because it’s a retrospective study and it’s based on a national database, there are some limitations,” said ABM Nasibul Alam, MD, who presented the study at the annual meeting of the American College of Chest Physicians (CHEST) . Alam is an internal medicine resident at Northwestern Medicine McHenry Hospital, McHenry, Illinois.

One possible conclusion is that acid reflux therapies received in hospital may be benefitting COPD. The retrospective nature of the study precludes establishing a causal relationship, but there are possible mechanisms that could account for a benefit, according to Alam.

“They might prevent micro-aspirations or silent aspirations in COPD patients. Sometimes you may not have a clinical diagnosis of GERD, but the patient might have silent micro-aspirations, so it might contribute to decreasing that,” said Alam.

The study was conducted to fill a gap in the literature. “Some studies have shown that the lung function in COPD patients gets moderately decreased if they have coexisting GERD, but there aren’t any studies that have looked into how it impacts COPD patients when they’re hospitalized, and especially acute complications,” said Alam.

The researchers retrospectively analyzed data from the Nationwide Readmissions Database from 2017 to 2020, utilizing ICD-10 codes to identify 3,798,952 hospitalized adults with a primary diagnosis of COPD, of which 26.97% also had GERD. Individuals without GERD were more likely to be male (47.72% vs 39.88%).

After multivariate adjustment, the presence of GERD was associated with a lower mortality rate (adjusted odds ratio [aOR], 0.717; P < .001) and reduced risks for acute respiratory failure (aOR, 0.915; P < .001), need for noninvasive mechanical ventilation (aOR, 0.907; P < .001), need for invasive ventilation for 24 hours or more (aOR, 0.727; P < .001), acute kidney injury (aOR, 0.877; P < .001), septic shock (aOR, 0.731; ^P < .001), and acute heart failure (aOR, 0.762; P < .001).

Despite these improved in-hospital outcomes, the researchers found that patients with GERD were at a higher risk for 30-day readmission (aOR, 1.08; P < .001). They also had slightly longer lengths of stay (+0.09 day; P < .001) and lower total charges (−$2824.5996; P < .001).

There have also been studies suggesting that GERD can directly lead to worse lung function among patients with COPD. “So it will be interesting to see if these medications have some kind of impact on the lung function as well. We need more robust studies [to determine that],” said Alam.

It is also important to keep in mind the long-term risk of proton pump inhibitors, especially in older patients. “We have to have good data before we start recommending this,” said Alam.

He suggested that physicians should begin to think more holistically about COPD management and consider the comorbidities. Alam has studied vitamin B12 deficiency in patients with COPD and found an association with cardiovascular comorbidities. “There are so many comorbidities with COPD. COPD itself puts patients at risk of cardiovascular comorbidity, for example. So when we have patients with COPD, we have to think about all those comorbidities and have to manage the patients comprehensively rather than just focusing on the specific targeted interventions,” said Alam.

The study should encourage further research, according to Kunal Deokar, MD, who moderated the session where the study was presented. “It does give us a signal that probably we should have more studies to look into whether patients hospitalized for COPD with GERD really have lower mortality rates, and what will be the effect of treatment on these patients,” said Deokar, who is an assistant professor of pulmonary medicine at the All India Institute of Medical Sciences, Delhi, India.

Alam and Deokar disclosed no relevant financial relationships.

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

Among patients with Crohn’s disease, a multicenter prospective cohort study found that anti-TNF therapy failed to achieve remission at 3 years in about two-thirds of cases, and that high drug concentrations early in treatment are linked to greater probability of sustained remission.

“The relationship between drug concentrations, immunogenicity and clinical response is likely to be multidirectional; as an observational study, we cannot definitively show the low drug levels are causative. However, our data are consistent with those from elsewhere and confirm the importance of achieving good drug levels to maximize the chances of success with anti-TNF therapy,” said Nicholas Kennedy, MBBS, PhD, a consultant gastroenterologist at Royal Devon University Healthcare NHS Foundation Trust, Exeter, United Kingdom, and coauthor of the study published in The Lancet Gastroenterology & Hepatology .

“We also showed that adequate dosing of thiopurines was needed to prevent immunogenicity, along the lines typically used to treat Crohn’s disease rather than the lower doses sometimes proposed,” he added.

The findings come from the Personalized Anti-TNF Therapy in Crohn’s Disease (PANTS) study conducted in the UK, which included 955 patients treated with infliximab and 655 treated with adalimumab between March 2014 and September 2017. The participants were 6 years or older, the median age was 32.5 years, and 51% were female. 

The latest findings come from a 2-year extension of the original 1-year PANTS study, published in 2019, which found that low drug concentrations predicted anti-TNF treatment failure — a result likely attributable in part to immunogenicity, since low-drug concentrations predicted the presence of anti-drug antibodies, and anti-drug antibodies in turn predicted low drug concentrations, according to Miguel Regueiro, MD, AGAF, chief of the Digestive Diseases Institute and a professor of medicine at the Cleveland Clinic, Ohio.

“This is one of the more important studies looking at the longitudinal care of patients with Crohn’s disease on infliximab and adalimumab,” said Dr. Regueiro, who was not involved with the study.

The extension study found that anti-drug antibodies and undetectable drug levels were associated with both treatment without an accompanying immunomodulator and carriage of the HLA-DQA1*05 genetic risk factor, though the latter was true only for treatment with infliximab.

Cleveland Clinic

A version of this article appeared on Medscape.com.

Among patients with Crohn’s disease, a multicenter prospective cohort study found that anti-TNF therapy failed to achieve remission at 3 years in about two-thirds of cases, and that high drug concentrations early in treatment are linked to greater probability of sustained remission.

“The relationship between drug concentrations, immunogenicity and clinical response is likely to be multidirectional; as an observational study, we cannot definitively show the low drug levels are causative. However, our data are consistent with those from elsewhere and confirm the importance of achieving good drug levels to maximize the chances of success with anti-TNF therapy,” said Nicholas Kennedy, MBBS, PhD, a consultant gastroenterologist at Royal Devon University Healthcare NHS Foundation Trust, Exeter, United Kingdom, and coauthor of the study published in The Lancet Gastroenterology & Hepatology .

“We also showed that adequate dosing of thiopurines was needed to prevent immunogenicity, along the lines typically used to treat Crohn’s disease rather than the lower doses sometimes proposed,” he added.

The findings come from the Personalized Anti-TNF Therapy in Crohn’s Disease (PANTS) study conducted in the UK, which included 955 patients treated with infliximab and 655 treated with adalimumab between March 2014 and September 2017. The participants were 6 years or older, the median age was 32.5 years, and 51% were female. 

The latest findings come from a 2-year extension of the original 1-year PANTS study, published in 2019, which found that low drug concentrations predicted anti-TNF treatment failure — a result likely attributable in part to immunogenicity, since low-drug concentrations predicted the presence of anti-drug antibodies, and anti-drug antibodies in turn predicted low drug concentrations, according to Miguel Regueiro, MD, AGAF, chief of the Digestive Diseases Institute and a professor of medicine at the Cleveland Clinic, Ohio.

“This is one of the more important studies looking at the longitudinal care of patients with Crohn’s disease on infliximab and adalimumab,” said Dr. Regueiro, who was not involved with the study.

The extension study found that anti-drug antibodies and undetectable drug levels were associated with both treatment without an accompanying immunomodulator and carriage of the HLA-DQA1*05 genetic risk factor, though the latter was true only for treatment with infliximab.

Cleveland Clinic

A version of this article appeared on Medscape.com.

Among patients with Crohn’s disease, a multicenter prospective cohort study found that anti-TNF therapy failed to achieve remission at 3 years in about two-thirds of cases, and that high drug concentrations early in treatment are linked to greater probability of sustained remission.

“The relationship between drug concentrations, immunogenicity and clinical response is likely to be multidirectional; as an observational study, we cannot definitively show the low drug levels are causative. However, our data are consistent with those from elsewhere and confirm the importance of achieving good drug levels to maximize the chances of success with anti-TNF therapy,” said Nicholas Kennedy, MBBS, PhD, a consultant gastroenterologist at Royal Devon University Healthcare NHS Foundation Trust, Exeter, United Kingdom, and coauthor of the study published in The Lancet Gastroenterology & Hepatology .

“We also showed that adequate dosing of thiopurines was needed to prevent immunogenicity, along the lines typically used to treat Crohn’s disease rather than the lower doses sometimes proposed,” he added.

The findings come from the Personalized Anti-TNF Therapy in Crohn’s Disease (PANTS) study conducted in the UK, which included 955 patients treated with infliximab and 655 treated with adalimumab between March 2014 and September 2017. The participants were 6 years or older, the median age was 32.5 years, and 51% were female. 

The latest findings come from a 2-year extension of the original 1-year PANTS study, published in 2019, which found that low drug concentrations predicted anti-TNF treatment failure — a result likely attributable in part to immunogenicity, since low-drug concentrations predicted the presence of anti-drug antibodies, and anti-drug antibodies in turn predicted low drug concentrations, according to Miguel Regueiro, MD, AGAF, chief of the Digestive Diseases Institute and a professor of medicine at the Cleveland Clinic, Ohio.

“This is one of the more important studies looking at the longitudinal care of patients with Crohn’s disease on infliximab and adalimumab,” said Dr. Regueiro, who was not involved with the study.

The extension study found that anti-drug antibodies and undetectable drug levels were associated with both treatment without an accompanying immunomodulator and carriage of the HLA-DQA1*05 genetic risk factor, though the latter was true only for treatment with infliximab.

Cleveland Clinic

A version of this article appeared on Medscape.com.

Nasal Staphylococcus aureus (SA) carriage is associated with SA surgical site and bloodstream infections following a surgical procedure, according to findings from a new prospective, multicenter clinical study published in the August issue of Open Forum Infectious Diseases.

“This was a pan-European study with many hospitals, many different clinical settings, and as far as I’m aware, it hasn’t been done before. [The new study] covers a lot of European countries and a lot of surgical specialties,” said lead author Jan Kluytmans, MD. The study also captures the current state of preventive strategies in surgery, such as changes in air flow, dress, and skin preparation, he added.

The study included 5004 patients from 33 hospitals in ten European countries, of whom 67.3% were found to be SA carriers. The median age was 65 years, and 49.8% of patients were male. Open cardiac, and knee and hip prosthesis surgeries made up the largest fraction, but there were 12 types of surgery included in the study.

There were 100 SA surgical site or blood infections. The researchers found an association between surgical site or blood infection and SA carriage at any site (adjusted hazard ratio [aHR], 4.6; 95% CI, 2.1-10.0) and nasal SA carriage (aHR, 4.2; 95% CI, 2.0-8.6). Extranasal SA carriage was not associated with an increased infection risk.

Each 1-unit increase in nasal bacteria was associated with an increase in infection risk (aHR, 1.23; 95% CI, 1.05-1.43).

A strength of the study is that it is the largest prospective study yet conducted on SA carriage in surgical patients, but the researchers were unable to do a subgroup of methicillin-resistant SA (MRSA) due to small numbers of infections.

The study confirms the value of the decolonization strategy, which the World Health Organization has endorsed with the highest level of scientific evidence that is available in preventive strategies in surgery. WHO strongly recommends decolonization for cardiothoracic and orthopedic surgery using intranasal applications of mupirocin 2% ointment with or without a combination of chlorhexidine gluconate body wash. It has a conditional recommendation for a similar procedure before other types of surgery.

However, “It is not widely practiced, and although that was not a surprise to me, I think it’s really disappointing to see that proven effective strategies are not being practiced,” said Dr. Kluytmans, professor of medical microbiology at University Medical Center Utrecht, Utrecht University, the Netherlands. “If I would come into surgery being a carrier, and not be decolonized, I would really be quite angry because it puts you at risk, which is preventable. I think that’s something we owe to our patients,” he said.

He said that some may have concerns about the potential for decolonization to contribute to antibiotic resistance, but the short-term prophylaxis — typically a few days — should not foster resistance, according to Dr. Kluytmans. “If you use it short term, just before surgery, it has been shown in many studies that resistance isn’t a big problem and it can be monitored.”

The link specifically to SA nasal carriage is a mystery, according to Dr. Kluytmans. “It puzzles me still how it gets from the nares to the wound during surgery. So that’s my million-dollar question that I would like to resolve. We would like to study it, but we haven’t quite a bright idea how to do that,” he said.

The results are compelling, according to Heather Evans, MD, who was asked for comment. “On the face of it, this looks like a no-brainer. We should be decolonizing all patients that go to the operating room, and it’s not a terribly unpleasant thing for a patient to undergo to have decolonization done. Particularly for patients who are at higher risk for having a severe complication, like someone that has an operation that’s involving an implant, for example, I think it really makes a lot of sense to do this low-cost intervention for those patients,” said Dr. Evans, professor of medicine at The Medical University of South Carolina as well as the president of the Surgical Infection Society.

She noted that many facilities test for methicillin-resistant SA, but usual not SA more broadly. “This is a very interesting and compelling study that makes us rethink that, and maybe it isn’t even worth testing to see if you have staph aureus, maybe we should just be putting Betadine in everyone’s nostrils when they come to the operating room. It just seems like it would be a pretty low-cost intervention and something that could potentially have a big impact,” said Dr. Evans.

Although she was impressed by the study, Dr. Evans noted that the researchers tested for carriage at sites unrelated to the surgical site. “It really made me wonder if it would have added even more credibility to the study if there had been a sample taken after surgical prep was done to demonstrate that there is actually no staph aureus present on the skin at the time that the wound was made,” she said.

The question ties into the recent “Trojan horse” hypothesis, which suggests that endemic carriage of bacteria is responsible for most surgical site infections, rather than the long-held belief that operating room contamination is to blame. “That would sort of fly with this study, that the patient is walking around with Staph aureus and not necessarily on their skin or at their surgical site, but it’s endemic in their body,” said Dr. Evans.

Dr. Kluytmans and Dr. Evans have no relevant financial disclosures.

Nasal Staphylococcus aureus (SA) carriage is associated with SA surgical site and bloodstream infections following a surgical procedure, according to findings from a new prospective, multicenter clinical study published in the August issue of Open Forum Infectious Diseases.

“This was a pan-European study with many hospitals, many different clinical settings, and as far as I’m aware, it hasn’t been done before. [The new study] covers a lot of European countries and a lot of surgical specialties,” said lead author Jan Kluytmans, MD. The study also captures the current state of preventive strategies in surgery, such as changes in air flow, dress, and skin preparation, he added.

The study included 5004 patients from 33 hospitals in ten European countries, of whom 67.3% were found to be SA carriers. The median age was 65 years, and 49.8% of patients were male. Open cardiac, and knee and hip prosthesis surgeries made up the largest fraction, but there were 12 types of surgery included in the study.

There were 100 SA surgical site or blood infections. The researchers found an association between surgical site or blood infection and SA carriage at any site (adjusted hazard ratio [aHR], 4.6; 95% CI, 2.1-10.0) and nasal SA carriage (aHR, 4.2; 95% CI, 2.0-8.6). Extranasal SA carriage was not associated with an increased infection risk.

Each 1-unit increase in nasal bacteria was associated with an increase in infection risk (aHR, 1.23; 95% CI, 1.05-1.43).

A strength of the study is that it is the largest prospective study yet conducted on SA carriage in surgical patients, but the researchers were unable to do a subgroup of methicillin-resistant SA (MRSA) due to small numbers of infections.

The study confirms the value of the decolonization strategy, which the World Health Organization has endorsed with the highest level of scientific evidence that is available in preventive strategies in surgery. WHO strongly recommends decolonization for cardiothoracic and orthopedic surgery using intranasal applications of mupirocin 2% ointment with or without a combination of chlorhexidine gluconate body wash. It has a conditional recommendation for a similar procedure before other types of surgery.

However, “It is not widely practiced, and although that was not a surprise to me, I think it’s really disappointing to see that proven effective strategies are not being practiced,” said Dr. Kluytmans, professor of medical microbiology at University Medical Center Utrecht, Utrecht University, the Netherlands. “If I would come into surgery being a carrier, and not be decolonized, I would really be quite angry because it puts you at risk, which is preventable. I think that’s something we owe to our patients,” he said.

He said that some may have concerns about the potential for decolonization to contribute to antibiotic resistance, but the short-term prophylaxis — typically a few days — should not foster resistance, according to Dr. Kluytmans. “If you use it short term, just before surgery, it has been shown in many studies that resistance isn’t a big problem and it can be monitored.”

The link specifically to SA nasal carriage is a mystery, according to Dr. Kluytmans. “It puzzles me still how it gets from the nares to the wound during surgery. So that’s my million-dollar question that I would like to resolve. We would like to study it, but we haven’t quite a bright idea how to do that,” he said.

The results are compelling, according to Heather Evans, MD, who was asked for comment. “On the face of it, this looks like a no-brainer. We should be decolonizing all patients that go to the operating room, and it’s not a terribly unpleasant thing for a patient to undergo to have decolonization done. Particularly for patients who are at higher risk for having a severe complication, like someone that has an operation that’s involving an implant, for example, I think it really makes a lot of sense to do this low-cost intervention for those patients,” said Dr. Evans, professor of medicine at The Medical University of South Carolina as well as the president of the Surgical Infection Society.

She noted that many facilities test for methicillin-resistant SA, but usual not SA more broadly. “This is a very interesting and compelling study that makes us rethink that, and maybe it isn’t even worth testing to see if you have staph aureus, maybe we should just be putting Betadine in everyone’s nostrils when they come to the operating room. It just seems like it would be a pretty low-cost intervention and something that could potentially have a big impact,” said Dr. Evans.

Although she was impressed by the study, Dr. Evans noted that the researchers tested for carriage at sites unrelated to the surgical site. “It really made me wonder if it would have added even more credibility to the study if there had been a sample taken after surgical prep was done to demonstrate that there is actually no staph aureus present on the skin at the time that the wound was made,” she said.

The question ties into the recent “Trojan horse” hypothesis, which suggests that endemic carriage of bacteria is responsible for most surgical site infections, rather than the long-held belief that operating room contamination is to blame. “That would sort of fly with this study, that the patient is walking around with Staph aureus and not necessarily on their skin or at their surgical site, but it’s endemic in their body,” said Dr. Evans.

Dr. Kluytmans and Dr. Evans have no relevant financial disclosures.

Nasal Staphylococcus aureus (SA) carriage is associated with SA surgical site and bloodstream infections following a surgical procedure, according to findings from a new prospective, multicenter clinical study published in the August issue of Open Forum Infectious Diseases.

“This was a pan-European study with many hospitals, many different clinical settings, and as far as I’m aware, it hasn’t been done before. [The new study] covers a lot of European countries and a lot of surgical specialties,” said lead author Jan Kluytmans, MD. The study also captures the current state of preventive strategies in surgery, such as changes in air flow, dress, and skin preparation, he added.

The study included 5004 patients from 33 hospitals in ten European countries, of whom 67.3% were found to be SA carriers. The median age was 65 years, and 49.8% of patients were male. Open cardiac, and knee and hip prosthesis surgeries made up the largest fraction, but there were 12 types of surgery included in the study.

There were 100 SA surgical site or blood infections. The researchers found an association between surgical site or blood infection and SA carriage at any site (adjusted hazard ratio [aHR], 4.6; 95% CI, 2.1-10.0) and nasal SA carriage (aHR, 4.2; 95% CI, 2.0-8.6). Extranasal SA carriage was not associated with an increased infection risk.

Each 1-unit increase in nasal bacteria was associated with an increase in infection risk (aHR, 1.23; 95% CI, 1.05-1.43).

A strength of the study is that it is the largest prospective study yet conducted on SA carriage in surgical patients, but the researchers were unable to do a subgroup of methicillin-resistant SA (MRSA) due to small numbers of infections.

The study confirms the value of the decolonization strategy, which the World Health Organization has endorsed with the highest level of scientific evidence that is available in preventive strategies in surgery. WHO strongly recommends decolonization for cardiothoracic and orthopedic surgery using intranasal applications of mupirocin 2% ointment with or without a combination of chlorhexidine gluconate body wash. It has a conditional recommendation for a similar procedure before other types of surgery.

However, “It is not widely practiced, and although that was not a surprise to me, I think it’s really disappointing to see that proven effective strategies are not being practiced,” said Dr. Kluytmans, professor of medical microbiology at University Medical Center Utrecht, Utrecht University, the Netherlands. “If I would come into surgery being a carrier, and not be decolonized, I would really be quite angry because it puts you at risk, which is preventable. I think that’s something we owe to our patients,” he said.

He said that some may have concerns about the potential for decolonization to contribute to antibiotic resistance, but the short-term prophylaxis — typically a few days — should not foster resistance, according to Dr. Kluytmans. “If you use it short term, just before surgery, it has been shown in many studies that resistance isn’t a big problem and it can be monitored.”

The link specifically to SA nasal carriage is a mystery, according to Dr. Kluytmans. “It puzzles me still how it gets from the nares to the wound during surgery. So that’s my million-dollar question that I would like to resolve. We would like to study it, but we haven’t quite a bright idea how to do that,” he said.

The results are compelling, according to Heather Evans, MD, who was asked for comment. “On the face of it, this looks like a no-brainer. We should be decolonizing all patients that go to the operating room, and it’s not a terribly unpleasant thing for a patient to undergo to have decolonization done. Particularly for patients who are at higher risk for having a severe complication, like someone that has an operation that’s involving an implant, for example, I think it really makes a lot of sense to do this low-cost intervention for those patients,” said Dr. Evans, professor of medicine at The Medical University of South Carolina as well as the president of the Surgical Infection Society.

She noted that many facilities test for methicillin-resistant SA, but usual not SA more broadly. “This is a very interesting and compelling study that makes us rethink that, and maybe it isn’t even worth testing to see if you have staph aureus, maybe we should just be putting Betadine in everyone’s nostrils when they come to the operating room. It just seems like it would be a pretty low-cost intervention and something that could potentially have a big impact,” said Dr. Evans.

Although she was impressed by the study, Dr. Evans noted that the researchers tested for carriage at sites unrelated to the surgical site. “It really made me wonder if it would have added even more credibility to the study if there had been a sample taken after surgical prep was done to demonstrate that there is actually no staph aureus present on the skin at the time that the wound was made,” she said.

The question ties into the recent “Trojan horse” hypothesis, which suggests that endemic carriage of bacteria is responsible for most surgical site infections, rather than the long-held belief that operating room contamination is to blame. “That would sort of fly with this study, that the patient is walking around with Staph aureus and not necessarily on their skin or at their surgical site, but it’s endemic in their body,” said Dr. Evans.

Dr. Kluytmans and Dr. Evans have no relevant financial disclosures.

TOPLINE:

More gastrointestinal and nervous symptom adverse events (AEs) are linked to apremilast than deucravacitinib, which is associated with more cutaneous AEs, according to a retrospective comparison using US Food and Drug Administration (FDA) data.

METHODOLOGY:

• To evaluate the adverse events associated with apremilast, an oral phosphodiesterase-4 (PDE4) inhibitor, and deucravacitinib, an oral tyrosine kinase 2 (TYK2) inhibitor, data were drawn from the FDA’s Adverse Event Reporting System database.
• The Medex_UIMA_1.8.3 system was used to standardize drug names, and MedDRA terminology was used to encode, categorize, and localize signals.
• AE event signals were grouped by skin and subcutaneous tissue disorders, gastrointestinal disorders, infections and infestations, and nervous system disorders.

TAKEAWAY:

• There were 95,734 AE reports for apremilast and 760 AE reports for deucravacitinib, and AEs were found to be significant over time.
• The more common cutaneous AEs were psoriasis recurrence and acne (associated with apremilast) and skin burning and erythema (associated with deucravacitinib).
• The more common gastrointestinal AEs were diarrhea and nausea (apremilast) and mouth ulceration (deucravacitinib).
• Deucravacitinib-related pruritus and rash, as well as apremilast-related tension headache, were more common in women than men; deucravacitinib-related skin burning was more common in men.

IN PRACTICE:

The results “can help the doctors to choose the right treatment options based on the baseline characteristics of different patients,” said Yuanyuan Xu, a graduate student in the Department of Dermatology, Sichuan University, Chengdu, China.

SOURCE:

Mr. Xu presented the study as a poster at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2024 annual meeting.

LIMITATIONS:

The study was retrospective and cannot prove causality, and there were far fewer AE reports related to deucravacitinib, likely because the drug was introduced more recently.

DISCLOSURES:

The study received no funding, and the authors had no relevant financial disclosures.

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

TOPLINE:

More gastrointestinal and nervous symptom adverse events (AEs) are linked to apremilast than deucravacitinib, which is associated with more cutaneous AEs, according to a retrospective comparison using US Food and Drug Administration (FDA) data.

METHODOLOGY:

• To evaluate the adverse events associated with apremilast, an oral phosphodiesterase-4 (PDE4) inhibitor, and deucravacitinib, an oral tyrosine kinase 2 (TYK2) inhibitor, data were drawn from the FDA’s Adverse Event Reporting System database.
• The Medex_UIMA_1.8.3 system was used to standardize drug names, and MedDRA terminology was used to encode, categorize, and localize signals.
• AE event signals were grouped by skin and subcutaneous tissue disorders, gastrointestinal disorders, infections and infestations, and nervous system disorders.

TAKEAWAY:

• There were 95,734 AE reports for apremilast and 760 AE reports for deucravacitinib, and AEs were found to be significant over time.
• The more common cutaneous AEs were psoriasis recurrence and acne (associated with apremilast) and skin burning and erythema (associated with deucravacitinib).
• The more common gastrointestinal AEs were diarrhea and nausea (apremilast) and mouth ulceration (deucravacitinib).
• Deucravacitinib-related pruritus and rash, as well as apremilast-related tension headache, were more common in women than men; deucravacitinib-related skin burning was more common in men.

IN PRACTICE:

The results “can help the doctors to choose the right treatment options based on the baseline characteristics of different patients,” said Yuanyuan Xu, a graduate student in the Department of Dermatology, Sichuan University, Chengdu, China.

SOURCE:

Mr. Xu presented the study as a poster at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2024 annual meeting.

LIMITATIONS:

The study was retrospective and cannot prove causality, and there were far fewer AE reports related to deucravacitinib, likely because the drug was introduced more recently.

DISCLOSURES:

The study received no funding, and the authors had no relevant financial disclosures.

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

TOPLINE:

More gastrointestinal and nervous symptom adverse events (AEs) are linked to apremilast than deucravacitinib, which is associated with more cutaneous AEs, according to a retrospective comparison using US Food and Drug Administration (FDA) data.

METHODOLOGY:

• To evaluate the adverse events associated with apremilast, an oral phosphodiesterase-4 (PDE4) inhibitor, and deucravacitinib, an oral tyrosine kinase 2 (TYK2) inhibitor, data were drawn from the FDA’s Adverse Event Reporting System database.
• The Medex_UIMA_1.8.3 system was used to standardize drug names, and MedDRA terminology was used to encode, categorize, and localize signals.
• AE event signals were grouped by skin and subcutaneous tissue disorders, gastrointestinal disorders, infections and infestations, and nervous system disorders.

TAKEAWAY:

• There were 95,734 AE reports for apremilast and 760 AE reports for deucravacitinib, and AEs were found to be significant over time.
• The more common cutaneous AEs were psoriasis recurrence and acne (associated with apremilast) and skin burning and erythema (associated with deucravacitinib).
• The more common gastrointestinal AEs were diarrhea and nausea (apremilast) and mouth ulceration (deucravacitinib).
• Deucravacitinib-related pruritus and rash, as well as apremilast-related tension headache, were more common in women than men; deucravacitinib-related skin burning was more common in men.

IN PRACTICE:

The results “can help the doctors to choose the right treatment options based on the baseline characteristics of different patients,” said Yuanyuan Xu, a graduate student in the Department of Dermatology, Sichuan University, Chengdu, China.

SOURCE:

Mr. Xu presented the study as a poster at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2024 annual meeting.

LIMITATIONS:

The study was retrospective and cannot prove causality, and there were far fewer AE reports related to deucravacitinib, likely because the drug was introduced more recently.

DISCLOSURES:

The study received no funding, and the authors had no relevant financial disclosures.

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

TOPLINE:

Rates of major adverse cardiovascular events (MACE) do not differ significantly among individual biologics used for psoriasis or psoriatic arthritis (PsA), a database analysis finds. 

METHODOLOGY:

• Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
• The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
• Subset analyses compared MACE in patients with and without existing cardiovascular disease.

TAKEAWAY:

• Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
• There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.

IN PRACTICE:

Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.

SOURCE:

Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. 

LIMITATIONS:

The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.

DISCLOSURES:

Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.

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

TOPLINE:

Rates of major adverse cardiovascular events (MACE) do not differ significantly among individual biologics used for psoriasis or psoriatic arthritis (PsA), a database analysis finds. 

METHODOLOGY:

• Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
• The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
• Subset analyses compared MACE in patients with and without existing cardiovascular disease.

TAKEAWAY:

• Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
• There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.

IN PRACTICE:

Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.

SOURCE:

Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. 

LIMITATIONS:

The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.

DISCLOSURES:

Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.

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

TOPLINE:

Rates of major adverse cardiovascular events (MACE) do not differ significantly among individual biologics used for psoriasis or psoriatic arthritis (PsA), a database analysis finds. 

METHODOLOGY:

• Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
• The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
• Subset analyses compared MACE in patients with and without existing cardiovascular disease.

TAKEAWAY:

• Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
• There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.

IN PRACTICE:

Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.

SOURCE:

Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. 

LIMITATIONS:

The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.

DISCLOSURES:

Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.

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

SEATTLE — Tissue resident memory (TRM) T cells are a hot topic lately in the treatment of psoriasis. These cells reside in the skin and other tissues and promote the inflammatory response, likely contributing to psoriasis symptoms. In fact, flare-ups often recur at the same site, a phenomenon that might be driven by these resident memory cells, according to Liv Eidsmo, MD, PhD.

This has led to their use as biomarkers in clinical trials for new therapies, but TRM T cells have a complex biology that is far from fully understood, Dr. Eidsmo said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. “With time, we’re understanding that the regulation of the functionality is more complicated than we thought, so following these cells as a positive outcome of a clinical trial is a little bit premature,” said Dr. Eidsmo, who is a consultant dermatologist at the University of Copenhagen, Copenhagen, Denmark.

Treatment strategies focus on inhibition of interleukin (IL)-23, which is an activator of TRM T cells and probably keeps them alive, according to Dr. Eidsmo. “The hope is that these cells can be silenced by IL-23 inhibition, which is a great idea, and it probably works. It’s just a matter of what is the readout of long-term remission, because the big challenge in the clinical world is when do we stop these expensive biological treatments? When can we feel secure that patients are in deep remission?” she asked.

TRM cells are also far from the only immune cells involved in psoriasis. Others include keratinocytes, Langerhans cells, and fibroblasts. Dr. Eidsmo referenced a recent spatial analysis that used single-cell and spatial RNA sequencing to identify the localization of specific cell populations and inflammatory pathways within psoriasis lesions and epidermal compartments as well as also suggested crosstalk links between cell types. Epigenetic changes in stem cells may also maintain a lower threshold for tissue inflammation.

Dr. Eidsmo advised caution in eliminating TRM T cells, which play a key role in protecting against melanoma and other cancers, especially later in life. “We don’t want to get rid of them. We want to have the right balance.”

She noted a study in her own lab that mapped TRM T cells in healthy epidermis and found that they could be renewed from both circulating precursors and cells within the epidermis. “So getting rid of the mature TRM T cells will most likely just lead to a new generation of the same subset.”

Other data show that there are a wide range of subsets of TRM T cells, and she recommended focusing on the functionality of TRM T cells rather than sheer numbers. “This is something we’re working on now: Can we change the functionality [of TRM T cells], rather than eradicate them and hope for the best in the next generation? Can we change the functionality of the T cells we already have in the skin?”

There is also epigenetic data in TRM T cells, keratinocytes, stem cells, and other cells thus suggesting complexity and plasticity in the system that remains poorly understood. 

Taken together, the research is at too early of a stage to be clinically useful, said Dr. Eidsmo. “We need to go back to the drawing board and just realize what we need to measure, and with the new techniques coming out, maybe spatial [measurement] at a high resolution, we can find biomarkers that better dictate the future of this. Be a little bit wary when you read the outcomes from the clinical trials that are ongoing, because right now, it’s a bit of a race between different biologics. These cells are used as a readout of efficacy of the treatments, and we’re not quite there yet.”

During the Q&A session after the presentation, one audience member asked about the heterogeneity of cells found within the skin of patients with psoriasis and pointed out that many proinflammatory cells likely play a role in tumor control. Dr. Eidsmo responded that her group’s analysis of a large database of patients with metastatic melanoma found that a factor that is important to the development of TRM T cells was strongly correlated to survival in patients with metastatic melanoma receiving immune checkpoint blockade. “So we really don’t want to eradicate them,” she said.

Also during the Q&A, Iain McInnes, MD, PhD, commented about the need to understand the previous events that drove the creation of memory T cells. “For me, the question is about the hierarchy, the primacy of what really drives the memory. In the infectious world, we’re trained to think [that memory responses] are T cell driven memory, but I wonder whether you have an idea of whether the T cell is responding to other memories, particularly in the stroma. Because certainly in the arthropathies, we have really good evidence now of epigenetic change in the synovial stroma and subsets,” said Dr. McInnes, who is director of the Institute of Infection, Immunity, and Inflammation at the University of Glasgow, Glasgow, Scotland.

Dr. Eidsmo responded that she believes responses are different among different individuals. “We know too little about how these two systems interact with one another. I think the TRM T cells are very good at amplifying the stroma to recruit cells in. I think we need to think of two-step therapies. You need to normalize this [stromal] environment. How you can do that, I don’t know.”

Dr. McInnes agreed. “As a myeloid doctor, I strongly believe that perpetuators are innate and the adaptive is following on. But how do we test that? That’s really hard,” he said. 

Dr. Eidsmo did not list any disclosures. Dr. McInnes has financial relationships with AbbVie, AstraZeneca, Bristol-Myers Squibb, Boehringer, Compugen, Cabaletta, Causeway, Dextera, Eli Lilly, Celgene, MoonLake, Pfizer, Novartis, Janssen, Roche, Versus Arthritis, MRC, and UCB. 

SEATTLE — Tissue resident memory (TRM) T cells are a hot topic lately in the treatment of psoriasis. These cells reside in the skin and other tissues and promote the inflammatory response, likely contributing to psoriasis symptoms. In fact, flare-ups often recur at the same site, a phenomenon that might be driven by these resident memory cells, according to Liv Eidsmo, MD, PhD.

This has led to their use as biomarkers in clinical trials for new therapies, but TRM T cells have a complex biology that is far from fully understood, Dr. Eidsmo said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. “With time, we’re understanding that the regulation of the functionality is more complicated than we thought, so following these cells as a positive outcome of a clinical trial is a little bit premature,” said Dr. Eidsmo, who is a consultant dermatologist at the University of Copenhagen, Copenhagen, Denmark.

Treatment strategies focus on inhibition of interleukin (IL)-23, which is an activator of TRM T cells and probably keeps them alive, according to Dr. Eidsmo. “The hope is that these cells can be silenced by IL-23 inhibition, which is a great idea, and it probably works. It’s just a matter of what is the readout of long-term remission, because the big challenge in the clinical world is when do we stop these expensive biological treatments? When can we feel secure that patients are in deep remission?” she asked.

TRM cells are also far from the only immune cells involved in psoriasis. Others include keratinocytes, Langerhans cells, and fibroblasts. Dr. Eidsmo referenced a recent spatial analysis that used single-cell and spatial RNA sequencing to identify the localization of specific cell populations and inflammatory pathways within psoriasis lesions and epidermal compartments as well as also suggested crosstalk links between cell types. Epigenetic changes in stem cells may also maintain a lower threshold for tissue inflammation.

Dr. Eidsmo advised caution in eliminating TRM T cells, which play a key role in protecting against melanoma and other cancers, especially later in life. “We don’t want to get rid of them. We want to have the right balance.”

She noted a study in her own lab that mapped TRM T cells in healthy epidermis and found that they could be renewed from both circulating precursors and cells within the epidermis. “So getting rid of the mature TRM T cells will most likely just lead to a new generation of the same subset.”

Other data show that there are a wide range of subsets of TRM T cells, and she recommended focusing on the functionality of TRM T cells rather than sheer numbers. “This is something we’re working on now: Can we change the functionality [of TRM T cells], rather than eradicate them and hope for the best in the next generation? Can we change the functionality of the T cells we already have in the skin?”

There is also epigenetic data in TRM T cells, keratinocytes, stem cells, and other cells thus suggesting complexity and plasticity in the system that remains poorly understood. 

Taken together, the research is at too early of a stage to be clinically useful, said Dr. Eidsmo. “We need to go back to the drawing board and just realize what we need to measure, and with the new techniques coming out, maybe spatial [measurement] at a high resolution, we can find biomarkers that better dictate the future of this. Be a little bit wary when you read the outcomes from the clinical trials that are ongoing, because right now, it’s a bit of a race between different biologics. These cells are used as a readout of efficacy of the treatments, and we’re not quite there yet.”

During the Q&A session after the presentation, one audience member asked about the heterogeneity of cells found within the skin of patients with psoriasis and pointed out that many proinflammatory cells likely play a role in tumor control. Dr. Eidsmo responded that her group’s analysis of a large database of patients with metastatic melanoma found that a factor that is important to the development of TRM T cells was strongly correlated to survival in patients with metastatic melanoma receiving immune checkpoint blockade. “So we really don’t want to eradicate them,” she said.

Also during the Q&A, Iain McInnes, MD, PhD, commented about the need to understand the previous events that drove the creation of memory T cells. “For me, the question is about the hierarchy, the primacy of what really drives the memory. In the infectious world, we’re trained to think [that memory responses] are T cell driven memory, but I wonder whether you have an idea of whether the T cell is responding to other memories, particularly in the stroma. Because certainly in the arthropathies, we have really good evidence now of epigenetic change in the synovial stroma and subsets,” said Dr. McInnes, who is director of the Institute of Infection, Immunity, and Inflammation at the University of Glasgow, Glasgow, Scotland.

Dr. Eidsmo responded that she believes responses are different among different individuals. “We know too little about how these two systems interact with one another. I think the TRM T cells are very good at amplifying the stroma to recruit cells in. I think we need to think of two-step therapies. You need to normalize this [stromal] environment. How you can do that, I don’t know.”

Dr. McInnes agreed. “As a myeloid doctor, I strongly believe that perpetuators are innate and the adaptive is following on. But how do we test that? That’s really hard,” he said. 

Dr. Eidsmo did not list any disclosures. Dr. McInnes has financial relationships with AbbVie, AstraZeneca, Bristol-Myers Squibb, Boehringer, Compugen, Cabaletta, Causeway, Dextera, Eli Lilly, Celgene, MoonLake, Pfizer, Novartis, Janssen, Roche, Versus Arthritis, MRC, and UCB. 

SEATTLE — Tissue resident memory (TRM) T cells are a hot topic lately in the treatment of psoriasis. These cells reside in the skin and other tissues and promote the inflammatory response, likely contributing to psoriasis symptoms. In fact, flare-ups often recur at the same site, a phenomenon that might be driven by these resident memory cells, according to Liv Eidsmo, MD, PhD.

This has led to their use as biomarkers in clinical trials for new therapies, but TRM T cells have a complex biology that is far from fully understood, Dr. Eidsmo said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. “With time, we’re understanding that the regulation of the functionality is more complicated than we thought, so following these cells as a positive outcome of a clinical trial is a little bit premature,” said Dr. Eidsmo, who is a consultant dermatologist at the University of Copenhagen, Copenhagen, Denmark.

Treatment strategies focus on inhibition of interleukin (IL)-23, which is an activator of TRM T cells and probably keeps them alive, according to Dr. Eidsmo. “The hope is that these cells can be silenced by IL-23 inhibition, which is a great idea, and it probably works. It’s just a matter of what is the readout of long-term remission, because the big challenge in the clinical world is when do we stop these expensive biological treatments? When can we feel secure that patients are in deep remission?” she asked.

TRM cells are also far from the only immune cells involved in psoriasis. Others include keratinocytes, Langerhans cells, and fibroblasts. Dr. Eidsmo referenced a recent spatial analysis that used single-cell and spatial RNA sequencing to identify the localization of specific cell populations and inflammatory pathways within psoriasis lesions and epidermal compartments as well as also suggested crosstalk links between cell types. Epigenetic changes in stem cells may also maintain a lower threshold for tissue inflammation.

Dr. Eidsmo advised caution in eliminating TRM T cells, which play a key role in protecting against melanoma and other cancers, especially later in life. “We don’t want to get rid of them. We want to have the right balance.”

She noted a study in her own lab that mapped TRM T cells in healthy epidermis and found that they could be renewed from both circulating precursors and cells within the epidermis. “So getting rid of the mature TRM T cells will most likely just lead to a new generation of the same subset.”

Other data show that there are a wide range of subsets of TRM T cells, and she recommended focusing on the functionality of TRM T cells rather than sheer numbers. “This is something we’re working on now: Can we change the functionality [of TRM T cells], rather than eradicate them and hope for the best in the next generation? Can we change the functionality of the T cells we already have in the skin?”

There is also epigenetic data in TRM T cells, keratinocytes, stem cells, and other cells thus suggesting complexity and plasticity in the system that remains poorly understood. 

Taken together, the research is at too early of a stage to be clinically useful, said Dr. Eidsmo. “We need to go back to the drawing board and just realize what we need to measure, and with the new techniques coming out, maybe spatial [measurement] at a high resolution, we can find biomarkers that better dictate the future of this. Be a little bit wary when you read the outcomes from the clinical trials that are ongoing, because right now, it’s a bit of a race between different biologics. These cells are used as a readout of efficacy of the treatments, and we’re not quite there yet.”

During the Q&A session after the presentation, one audience member asked about the heterogeneity of cells found within the skin of patients with psoriasis and pointed out that many proinflammatory cells likely play a role in tumor control. Dr. Eidsmo responded that her group’s analysis of a large database of patients with metastatic melanoma found that a factor that is important to the development of TRM T cells was strongly correlated to survival in patients with metastatic melanoma receiving immune checkpoint blockade. “So we really don’t want to eradicate them,” she said.

Also during the Q&A, Iain McInnes, MD, PhD, commented about the need to understand the previous events that drove the creation of memory T cells. “For me, the question is about the hierarchy, the primacy of what really drives the memory. In the infectious world, we’re trained to think [that memory responses] are T cell driven memory, but I wonder whether you have an idea of whether the T cell is responding to other memories, particularly in the stroma. Because certainly in the arthropathies, we have really good evidence now of epigenetic change in the synovial stroma and subsets,” said Dr. McInnes, who is director of the Institute of Infection, Immunity, and Inflammation at the University of Glasgow, Glasgow, Scotland.

Dr. Eidsmo responded that she believes responses are different among different individuals. “We know too little about how these two systems interact with one another. I think the TRM T cells are very good at amplifying the stroma to recruit cells in. I think we need to think of two-step therapies. You need to normalize this [stromal] environment. How you can do that, I don’t know.”

Dr. McInnes agreed. “As a myeloid doctor, I strongly believe that perpetuators are innate and the adaptive is following on. But how do we test that? That’s really hard,” he said. 

Dr. Eidsmo did not list any disclosures. Dr. McInnes has financial relationships with AbbVie, AstraZeneca, Bristol-Myers Squibb, Boehringer, Compugen, Cabaletta, Causeway, Dextera, Eli Lilly, Celgene, MoonLake, Pfizer, Novartis, Janssen, Roche, Versus Arthritis, MRC, and UCB.