Federal Practitioner

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

The Food and Drug Administration has expanded the indication of dapagliflozin (Farxiga, AstraZeneca) to include treatment of heart failure across the full spectrum of left ventricular ejection fraction (LVEF) – including HF with mildly reduced ejection fraction (HFmrEF) and with preserved ejection fraction (HFpEF).

The sodium-glucose cotransporter 2 (SGLT2) inhibitor was previously approved in the United States for adults with heart failure with reduced ejection fraction (HFrEF).

The expanded indication is based on data from the phase 3 DELIVER trial, which showed clear clinical benefits of the SGLT2 inhibitor for patients with HF regardless of left ventricular function.

In the trial, which included more than 6,200 patients, dapagliflozin led to a statistically significant and clinically meaningful early reduction in the primary composite endpoint of cardiovascular (CV) death or worsening HF for patients with HFmrEF or HFpEFF.

In addition, results of a pooled analysis of the DAPA-HF and DELIVER phase 3 trials showed a consistent benefit from dapagliflozin treatment in significantly reducing the combined endpoint of CV death or HF hospitalization across the range of LVEF.

The European Commission expanded the indication for dapagliflozin (Forxiga) to include HF across the full spectrum of LVEF in February.

The SGLT2 inhibitor is also approved for use by patients with chronic kidney disease. It was first approved in 2014 to improve glycemic control for patients with diabetes mellitus.

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

The Food and Drug Administration has expanded the indication of dapagliflozin (Farxiga, AstraZeneca) to include treatment of heart failure across the full spectrum of left ventricular ejection fraction (LVEF) – including HF with mildly reduced ejection fraction (HFmrEF) and with preserved ejection fraction (HFpEF).

The sodium-glucose cotransporter 2 (SGLT2) inhibitor was previously approved in the United States for adults with heart failure with reduced ejection fraction (HFrEF).

The expanded indication is based on data from the phase 3 DELIVER trial, which showed clear clinical benefits of the SGLT2 inhibitor for patients with HF regardless of left ventricular function.

In the trial, which included more than 6,200 patients, dapagliflozin led to a statistically significant and clinically meaningful early reduction in the primary composite endpoint of cardiovascular (CV) death or worsening HF for patients with HFmrEF or HFpEFF.

In addition, results of a pooled analysis of the DAPA-HF and DELIVER phase 3 trials showed a consistent benefit from dapagliflozin treatment in significantly reducing the combined endpoint of CV death or HF hospitalization across the range of LVEF.

The European Commission expanded the indication for dapagliflozin (Forxiga) to include HF across the full spectrum of LVEF in February.

The SGLT2 inhibitor is also approved for use by patients with chronic kidney disease. It was first approved in 2014 to improve glycemic control for patients with diabetes mellitus.

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

The Food and Drug Administration has expanded the indication of dapagliflozin (Farxiga, AstraZeneca) to include treatment of heart failure across the full spectrum of left ventricular ejection fraction (LVEF) – including HF with mildly reduced ejection fraction (HFmrEF) and with preserved ejection fraction (HFpEF).

The sodium-glucose cotransporter 2 (SGLT2) inhibitor was previously approved in the United States for adults with heart failure with reduced ejection fraction (HFrEF).

The expanded indication is based on data from the phase 3 DELIVER trial, which showed clear clinical benefits of the SGLT2 inhibitor for patients with HF regardless of left ventricular function.

In the trial, which included more than 6,200 patients, dapagliflozin led to a statistically significant and clinically meaningful early reduction in the primary composite endpoint of cardiovascular (CV) death or worsening HF for patients with HFmrEF or HFpEFF.

In addition, results of a pooled analysis of the DAPA-HF and DELIVER phase 3 trials showed a consistent benefit from dapagliflozin treatment in significantly reducing the combined endpoint of CV death or HF hospitalization across the range of LVEF.

The European Commission expanded the indication for dapagliflozin (Forxiga) to include HF across the full spectrum of LVEF in February.

The SGLT2 inhibitor is also approved for use by patients with chronic kidney disease. It was first approved in 2014 to improve glycemic control for patients with diabetes mellitus.

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

Based on discussions during PancreasFest 2021, a group of experts and key opinion leaders have proposed a new definition of exocrine pancreatic insufficiency (EPI) and best practices for diagnosis and management, according to a recent report in Gastro Hep Advances

Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.

University of Pittsburgh

“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.

EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.

Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.

In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.

The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.

Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.

Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.

“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.

After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.

PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.

For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.

For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.

“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”

PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.

Based on discussions during PancreasFest 2021, a group of experts and key opinion leaders have proposed a new definition of exocrine pancreatic insufficiency (EPI) and best practices for diagnosis and management, according to a recent report in Gastro Hep Advances

Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.

University of Pittsburgh

“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.

EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.

Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.

In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.

The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.

Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.

Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.

“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.

After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.

PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.

For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.

For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.

“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”

PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.

Based on discussions during PancreasFest 2021, a group of experts and key opinion leaders have proposed a new definition of exocrine pancreatic insufficiency (EPI) and best practices for diagnosis and management, according to a recent report in Gastro Hep Advances

Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.

University of Pittsburgh

“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.

EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.

Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.

In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.

The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.

Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.

Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.

“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.

After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.

PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.

For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.

For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.

“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”

PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.

CHICAGO – The total annual waste generated by a single, large academic endoscopy unit over 2 months could cover about two football fields, according to Madhav Desai, MD, MPH, assistant professor of medicine at the University of Minnesota, Minneapolis. About 20% of the waste, most of which went to landfills, was potentially recyclable, he said in a presentation given at the annual Digestive Disease Week® meeting.

Gastrointestinal endoscopies are critical for the screening, diagnosis, and treatment of a variety of gastrointestinal conditions. But like other medical procedures, endoscopies are a source of environmental waste, including plastic, sharps, personal protective equipment (PPE), and cleaning supplies, and also energy waste.

Walter Alexander/MDedge News

“This all goes back to the damage that mankind is inflicting on the environment in general, with the health care sector as one of the top contributors to plastic waste generation, landfills and water wastage,” Dr. Desai said. “Endoscopies, with their numerous benefits, substantially increase waste generation through landfill waste and liquid consumption and waste through the cleaning of endoscopes. We have a responsibility to look into this topic.”

To prospectively assess total waste generation from their institution, Dr. Desai, who was with the Kansas City (Mo.) Veterans Administration Medical Center, when the research was conducted, collected data on the items used in 450 consecutive procedures from May to June 2022. The data included procedure type, accessory use, intravenous tubing, numbers of biopsy jars, linens, PPE, and more, beginning at the point of patient entry to the endoscopy unit until discharge. They also collected data on waste generation related to reprocessing after each procedure and daily energy use (including endoscopy equipment, lights, and computers). With an eye toward finding opportunities to improve and maximize waste recycling, they stratified waste into the three categories of biohazardous, nonbiohazardous, or potentially recyclable.

“We found that the total waste generated during the time period was 1,398.6 kg, with more than half of it, 61.6%, going directly to landfill,” Dr. Desai said in an interview. “That’s an amount that an average family in the U.S. would use for 2 months. That’s a huge amount.”
 

Most waste consists of sharps

Exactly one-third was biohazard waste and 5.1% was sharps, they found. A single procedure, on average, sent 2.19 kg of waste to landfill. Extrapolated to 1 year, the waste total amounts to 9,189 kg (equivalent to just over 10 U.S. tons) and per 100 procedures to 219 kg (about 483 pounds).

They estimated 20% of the landfill waste was potentially recyclable (such as plastic CO₂ tubing, O₂ connector, syringes, etc.), which could reduce the total landfill burden by 8.6 kg per day or 2,580 kg per year (or 61 kg per 100 procedures). Reprocessing endoscopes generated 194 gallons of liquid waste (735.26 kg) per day or 1,385 gallons per 100 procedures.

Turning to energy consumption, Dr. Desai reported that daily use in the endoscopy unit was 277.1 kW-hours (equivalent to 8.2 gallons of gasoline), adding up to about 1,980 kW per 100 procedures. “That 100-procedure amount is the equivalent of the energy used for an average fuel efficiency car to travel 1,200 miles, the distance from Seattle to San Diego,” he said.

“One next step,” Dr. Desai said, “is getting help from GI societies to come together and have endoscopy units track their own performance. You need benchmarks so that you can determine how good an endoscopist you are with respect to waste.”

He commented further:“We all owe it to the environment. And, we have all witnessed what Mother Nature can do to you.”

Working on the potentially recyclable materials that account for 20% of the total waste would be a simple initial step to reduce waste going to landfills, Dr. Desai and colleagues concluded in the meeting abstract. “These data could serve as an actionable model for health systems to reduce total waste generation and move toward environmentally sustainable endoscopy units,” they wrote.

The authors reported no disclosures.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – The total annual waste generated by a single, large academic endoscopy unit over 2 months could cover about two football fields, according to Madhav Desai, MD, MPH, assistant professor of medicine at the University of Minnesota, Minneapolis. About 20% of the waste, most of which went to landfills, was potentially recyclable, he said in a presentation given at the annual Digestive Disease Week® meeting.

Gastrointestinal endoscopies are critical for the screening, diagnosis, and treatment of a variety of gastrointestinal conditions. But like other medical procedures, endoscopies are a source of environmental waste, including plastic, sharps, personal protective equipment (PPE), and cleaning supplies, and also energy waste.

Walter Alexander/MDedge News

“This all goes back to the damage that mankind is inflicting on the environment in general, with the health care sector as one of the top contributors to plastic waste generation, landfills and water wastage,” Dr. Desai said. “Endoscopies, with their numerous benefits, substantially increase waste generation through landfill waste and liquid consumption and waste through the cleaning of endoscopes. We have a responsibility to look into this topic.”

To prospectively assess total waste generation from their institution, Dr. Desai, who was with the Kansas City (Mo.) Veterans Administration Medical Center, when the research was conducted, collected data on the items used in 450 consecutive procedures from May to June 2022. The data included procedure type, accessory use, intravenous tubing, numbers of biopsy jars, linens, PPE, and more, beginning at the point of patient entry to the endoscopy unit until discharge. They also collected data on waste generation related to reprocessing after each procedure and daily energy use (including endoscopy equipment, lights, and computers). With an eye toward finding opportunities to improve and maximize waste recycling, they stratified waste into the three categories of biohazardous, nonbiohazardous, or potentially recyclable.

“We found that the total waste generated during the time period was 1,398.6 kg, with more than half of it, 61.6%, going directly to landfill,” Dr. Desai said in an interview. “That’s an amount that an average family in the U.S. would use for 2 months. That’s a huge amount.”
 

Most waste consists of sharps

Exactly one-third was biohazard waste and 5.1% was sharps, they found. A single procedure, on average, sent 2.19 kg of waste to landfill. Extrapolated to 1 year, the waste total amounts to 9,189 kg (equivalent to just over 10 U.S. tons) and per 100 procedures to 219 kg (about 483 pounds).

They estimated 20% of the landfill waste was potentially recyclable (such as plastic CO₂ tubing, O₂ connector, syringes, etc.), which could reduce the total landfill burden by 8.6 kg per day or 2,580 kg per year (or 61 kg per 100 procedures). Reprocessing endoscopes generated 194 gallons of liquid waste (735.26 kg) per day or 1,385 gallons per 100 procedures.

Turning to energy consumption, Dr. Desai reported that daily use in the endoscopy unit was 277.1 kW-hours (equivalent to 8.2 gallons of gasoline), adding up to about 1,980 kW per 100 procedures. “That 100-procedure amount is the equivalent of the energy used for an average fuel efficiency car to travel 1,200 miles, the distance from Seattle to San Diego,” he said.

“One next step,” Dr. Desai said, “is getting help from GI societies to come together and have endoscopy units track their own performance. You need benchmarks so that you can determine how good an endoscopist you are with respect to waste.”

He commented further:“We all owe it to the environment. And, we have all witnessed what Mother Nature can do to you.”

Working on the potentially recyclable materials that account for 20% of the total waste would be a simple initial step to reduce waste going to landfills, Dr. Desai and colleagues concluded in the meeting abstract. “These data could serve as an actionable model for health systems to reduce total waste generation and move toward environmentally sustainable endoscopy units,” they wrote.

The authors reported no disclosures.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – The total annual waste generated by a single, large academic endoscopy unit over 2 months could cover about two football fields, according to Madhav Desai, MD, MPH, assistant professor of medicine at the University of Minnesota, Minneapolis. About 20% of the waste, most of which went to landfills, was potentially recyclable, he said in a presentation given at the annual Digestive Disease Week® meeting.

Gastrointestinal endoscopies are critical for the screening, diagnosis, and treatment of a variety of gastrointestinal conditions. But like other medical procedures, endoscopies are a source of environmental waste, including plastic, sharps, personal protective equipment (PPE), and cleaning supplies, and also energy waste.

Walter Alexander/MDedge News

“This all goes back to the damage that mankind is inflicting on the environment in general, with the health care sector as one of the top contributors to plastic waste generation, landfills and water wastage,” Dr. Desai said. “Endoscopies, with their numerous benefits, substantially increase waste generation through landfill waste and liquid consumption and waste through the cleaning of endoscopes. We have a responsibility to look into this topic.”

To prospectively assess total waste generation from their institution, Dr. Desai, who was with the Kansas City (Mo.) Veterans Administration Medical Center, when the research was conducted, collected data on the items used in 450 consecutive procedures from May to June 2022. The data included procedure type, accessory use, intravenous tubing, numbers of biopsy jars, linens, PPE, and more, beginning at the point of patient entry to the endoscopy unit until discharge. They also collected data on waste generation related to reprocessing after each procedure and daily energy use (including endoscopy equipment, lights, and computers). With an eye toward finding opportunities to improve and maximize waste recycling, they stratified waste into the three categories of biohazardous, nonbiohazardous, or potentially recyclable.

“We found that the total waste generated during the time period was 1,398.6 kg, with more than half of it, 61.6%, going directly to landfill,” Dr. Desai said in an interview. “That’s an amount that an average family in the U.S. would use for 2 months. That’s a huge amount.”
 

Most waste consists of sharps

Exactly one-third was biohazard waste and 5.1% was sharps, they found. A single procedure, on average, sent 2.19 kg of waste to landfill. Extrapolated to 1 year, the waste total amounts to 9,189 kg (equivalent to just over 10 U.S. tons) and per 100 procedures to 219 kg (about 483 pounds).

They estimated 20% of the landfill waste was potentially recyclable (such as plastic CO₂ tubing, O₂ connector, syringes, etc.), which could reduce the total landfill burden by 8.6 kg per day or 2,580 kg per year (or 61 kg per 100 procedures). Reprocessing endoscopes generated 194 gallons of liquid waste (735.26 kg) per day or 1,385 gallons per 100 procedures.

Turning to energy consumption, Dr. Desai reported that daily use in the endoscopy unit was 277.1 kW-hours (equivalent to 8.2 gallons of gasoline), adding up to about 1,980 kW per 100 procedures. “That 100-procedure amount is the equivalent of the energy used for an average fuel efficiency car to travel 1,200 miles, the distance from Seattle to San Diego,” he said.

“One next step,” Dr. Desai said, “is getting help from GI societies to come together and have endoscopy units track their own performance. You need benchmarks so that you can determine how good an endoscopist you are with respect to waste.”

He commented further:“We all owe it to the environment. And, we have all witnessed what Mother Nature can do to you.”

Working on the potentially recyclable materials that account for 20% of the total waste would be a simple initial step to reduce waste going to landfills, Dr. Desai and colleagues concluded in the meeting abstract. “These data could serve as an actionable model for health systems to reduce total waste generation and move toward environmentally sustainable endoscopy units,” they wrote.

The authors reported no disclosures.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

The VA MISSION Act of 2018 expanded options for veterans to receive government-paid health care from private sector community health care practitioners. The act tasked the US Department of Veterans Affairs (VA) to develop rules that determine eligibility for outside care based on appointment wait times or distance to the nearest VA facility. As a part of those standards, VA opted not to include the availability of VA telehealth in its wait time calculations—a decision that we believe was a gross misjudgment with far-reaching consequences for veterans. Excluding telehealth from the guidelines has unnecessarily restricted veterans’ access to high-quality health care and has squandered large sums of taxpayer dollars.

The VA has reviewed its initial MISSION Act eligibility standards and proposed a correction that recognizes telehealth as a valid means of providing health care to veterans who prefer that option.¹ Telehealth may not have been an essential component of health care before the COVID-19 pandemic, but now it is clear that the best action VA can take is to swiftly enact its recommended change, stipulating that both VA telehealth and in-person health care constitute access to treatment. If implemented, this correction would save taxpayers an astronomical sum—according to a VA report to Congress, about $1.1 billion in fiscal year 2021 alone.² The cost savings from this proposed correction is reason enough to implement it. But just as importantly, increased use of VA telehealth also means higher quality, quicker, and more convenient care for veterans.

The VA is the recognized world leader in providing telehealth that is effective, timely, and veteran centric. Veterans across the country have access to telehealth services in more than 30 specialties.³ To ensure accessibility, the VA has established partnerships with major mobile broadband carriers so that veterans can receive telehealth at home without additional charges.⁴ The VA project Accessing Telehealth through Local Area Stations (ATLAS) brings VA telehealth to areas where existing internet infrastructure may not be adequate to support video telehealth. ATLAS is a collaboration with private organizations, including Veterans of Foreign Wars, The American Legion, and Walmart.⁴ The agency also provides tablets to veterans who might not have access to telehealth, fostering higher access and patient satisfaction.⁴

The VA can initiate telehealth care rapidly. The “Anywhere to Anywhere” VA Health Care initiative and telecare hubs eliminate geographic constraints, allowing clinicians to provide team-based services across county and state lines to veterans’ homes and communities.

VA’s telehealth effort maximizes convenience for veterans. It reduces travel time, travel expenses, depletion of sick leave, and the need for childcare. Veterans with posttraumatic stress disorder or military sexual trauma who are triggered by traffic and waiting rooms, those with mobility issues, or those facing the stigma of mental health treatment often prefer to receive care in the familiarity of their home. Nonetheless, any veteran who desires an in-person appointment would continue to have that option under the proposed VA rule change.

VA telehealth is often used for mental health care, using the same evidence-based psychotherapies that VA has championed and are superior to that available in the private sector.^5,6 This advantage is largely due to VA’s rigorous training, consultation, case review, care delivery, measurement standards, and integrated care model. In a recent survey of veterans engaged in mental health care, 80% reported that VA virtual care via video and/or telephone is as helpful or more helpful than in‐person services.⁷ And yet, because of existing regulations, VA telemental health (TMH) does not qualify as access, resulting in hundreds of thousands of TMH visits being outsourced yearly to community practitioners that could be quickly and beneficially furnished by VA clinicians.

Telehealth has been shown to be as clinically effective as in-person care. A recent review of 38 meta-analyses covering telehealth with 10 medical disciplines found that for all disciplines, telehealth was as effective, if not more so, than conventional care.⁸ And because the likelihood of not showing up for telehealth appointments is lower than for in-person appointments, continuity of care is uninterrupted, and health care outcomes are improved.

Telehealth is health care. The VA must end the double standard that has handicapped it from including telehealth availability in determinations of eligibility for community care. The VA has voiced its intention to seek stakeholder input before implementing its proposed correction. The change is long overdue. It will save the VA a billion dollars annually while ensuring that veterans have quicker access to better treatment.

The VA MISSION Act of 2018 expanded options for veterans to receive government-paid health care from private sector community health care practitioners. The act tasked the US Department of Veterans Affairs (VA) to develop rules that determine eligibility for outside care based on appointment wait times or distance to the nearest VA facility. As a part of those standards, VA opted not to include the availability of VA telehealth in its wait time calculations—a decision that we believe was a gross misjudgment with far-reaching consequences for veterans. Excluding telehealth from the guidelines has unnecessarily restricted veterans’ access to high-quality health care and has squandered large sums of taxpayer dollars.

The VA has reviewed its initial MISSION Act eligibility standards and proposed a correction that recognizes telehealth as a valid means of providing health care to veterans who prefer that option.¹ Telehealth may not have been an essential component of health care before the COVID-19 pandemic, but now it is clear that the best action VA can take is to swiftly enact its recommended change, stipulating that both VA telehealth and in-person health care constitute access to treatment. If implemented, this correction would save taxpayers an astronomical sum—according to a VA report to Congress, about $1.1 billion in fiscal year 2021 alone.² The cost savings from this proposed correction is reason enough to implement it. But just as importantly, increased use of VA telehealth also means higher quality, quicker, and more convenient care for veterans.

The VA is the recognized world leader in providing telehealth that is effective, timely, and veteran centric. Veterans across the country have access to telehealth services in more than 30 specialties.³ To ensure accessibility, the VA has established partnerships with major mobile broadband carriers so that veterans can receive telehealth at home without additional charges.⁴ The VA project Accessing Telehealth through Local Area Stations (ATLAS) brings VA telehealth to areas where existing internet infrastructure may not be adequate to support video telehealth. ATLAS is a collaboration with private organizations, including Veterans of Foreign Wars, The American Legion, and Walmart.⁴ The agency also provides tablets to veterans who might not have access to telehealth, fostering higher access and patient satisfaction.⁴

The VA can initiate telehealth care rapidly. The “Anywhere to Anywhere” VA Health Care initiative and telecare hubs eliminate geographic constraints, allowing clinicians to provide team-based services across county and state lines to veterans’ homes and communities.

VA’s telehealth effort maximizes convenience for veterans. It reduces travel time, travel expenses, depletion of sick leave, and the need for childcare. Veterans with posttraumatic stress disorder or military sexual trauma who are triggered by traffic and waiting rooms, those with mobility issues, or those facing the stigma of mental health treatment often prefer to receive care in the familiarity of their home. Nonetheless, any veteran who desires an in-person appointment would continue to have that option under the proposed VA rule change.

VA telehealth is often used for mental health care, using the same evidence-based psychotherapies that VA has championed and are superior to that available in the private sector.^5,6 This advantage is largely due to VA’s rigorous training, consultation, case review, care delivery, measurement standards, and integrated care model. In a recent survey of veterans engaged in mental health care, 80% reported that VA virtual care via video and/or telephone is as helpful or more helpful than in‐person services.⁷ And yet, because of existing regulations, VA telemental health (TMH) does not qualify as access, resulting in hundreds of thousands of TMH visits being outsourced yearly to community practitioners that could be quickly and beneficially furnished by VA clinicians.

Telehealth has been shown to be as clinically effective as in-person care. A recent review of 38 meta-analyses covering telehealth with 10 medical disciplines found that for all disciplines, telehealth was as effective, if not more so, than conventional care.⁸ And because the likelihood of not showing up for telehealth appointments is lower than for in-person appointments, continuity of care is uninterrupted, and health care outcomes are improved.

Telehealth is health care. The VA must end the double standard that has handicapped it from including telehealth availability in determinations of eligibility for community care. The VA has voiced its intention to seek stakeholder input before implementing its proposed correction. The change is long overdue. It will save the VA a billion dollars annually while ensuring that veterans have quicker access to better treatment.

The VA MISSION Act of 2018 expanded options for veterans to receive government-paid health care from private sector community health care practitioners. The act tasked the US Department of Veterans Affairs (VA) to develop rules that determine eligibility for outside care based on appointment wait times or distance to the nearest VA facility. As a part of those standards, VA opted not to include the availability of VA telehealth in its wait time calculations—a decision that we believe was a gross misjudgment with far-reaching consequences for veterans. Excluding telehealth from the guidelines has unnecessarily restricted veterans’ access to high-quality health care and has squandered large sums of taxpayer dollars.

The VA has reviewed its initial MISSION Act eligibility standards and proposed a correction that recognizes telehealth as a valid means of providing health care to veterans who prefer that option.¹ Telehealth may not have been an essential component of health care before the COVID-19 pandemic, but now it is clear that the best action VA can take is to swiftly enact its recommended change, stipulating that both VA telehealth and in-person health care constitute access to treatment. If implemented, this correction would save taxpayers an astronomical sum—according to a VA report to Congress, about $1.1 billion in fiscal year 2021 alone.² The cost savings from this proposed correction is reason enough to implement it. But just as importantly, increased use of VA telehealth also means higher quality, quicker, and more convenient care for veterans.

The VA is the recognized world leader in providing telehealth that is effective, timely, and veteran centric. Veterans across the country have access to telehealth services in more than 30 specialties.³ To ensure accessibility, the VA has established partnerships with major mobile broadband carriers so that veterans can receive telehealth at home without additional charges.⁴ The VA project Accessing Telehealth through Local Area Stations (ATLAS) brings VA telehealth to areas where existing internet infrastructure may not be adequate to support video telehealth. ATLAS is a collaboration with private organizations, including Veterans of Foreign Wars, The American Legion, and Walmart.⁴ The agency also provides tablets to veterans who might not have access to telehealth, fostering higher access and patient satisfaction.⁴

The VA can initiate telehealth care rapidly. The “Anywhere to Anywhere” VA Health Care initiative and telecare hubs eliminate geographic constraints, allowing clinicians to provide team-based services across county and state lines to veterans’ homes and communities.

VA’s telehealth effort maximizes convenience for veterans. It reduces travel time, travel expenses, depletion of sick leave, and the need for childcare. Veterans with posttraumatic stress disorder or military sexual trauma who are triggered by traffic and waiting rooms, those with mobility issues, or those facing the stigma of mental health treatment often prefer to receive care in the familiarity of their home. Nonetheless, any veteran who desires an in-person appointment would continue to have that option under the proposed VA rule change.

VA telehealth is often used for mental health care, using the same evidence-based psychotherapies that VA has championed and are superior to that available in the private sector.^5,6 This advantage is largely due to VA’s rigorous training, consultation, case review, care delivery, measurement standards, and integrated care model. In a recent survey of veterans engaged in mental health care, 80% reported that VA virtual care via video and/or telephone is as helpful or more helpful than in‐person services.⁷ And yet, because of existing regulations, VA telemental health (TMH) does not qualify as access, resulting in hundreds of thousands of TMH visits being outsourced yearly to community practitioners that could be quickly and beneficially furnished by VA clinicians.

Telehealth has been shown to be as clinically effective as in-person care. A recent review of 38 meta-analyses covering telehealth with 10 medical disciplines found that for all disciplines, telehealth was as effective, if not more so, than conventional care.⁸ And because the likelihood of not showing up for telehealth appointments is lower than for in-person appointments, continuity of care is uninterrupted, and health care outcomes are improved.

Telehealth is health care. The VA must end the double standard that has handicapped it from including telehealth availability in determinations of eligibility for community care. The VA has voiced its intention to seek stakeholder input before implementing its proposed correction. The change is long overdue. It will save the VA a billion dollars annually while ensuring that veterans have quicker access to better treatment.

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

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

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

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

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

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

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.

Of note, investigators estimate that roughly 15% of schizophrenia cases among young males may be preventable by avoiding cannabis use disorder (CUD).

“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.

“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.

The study was published online in Psychological Medicine.
 

A modifiable risk factor

The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.

A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.

The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).

The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.

For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.

“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
 

Legalization sends the wrong message

In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”

In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.

“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.

“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.

The study received no specific funding. The authors disclosed no relevant financial relationships.

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

A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.

Of note, investigators estimate that roughly 15% of schizophrenia cases among young males may be preventable by avoiding cannabis use disorder (CUD).

“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.

“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.

The study was published online in Psychological Medicine.
 

A modifiable risk factor

The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.

A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.

The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).

The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.

For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.

“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
 

Legalization sends the wrong message

In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”

In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.

“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.

“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.

The study received no specific funding. The authors disclosed no relevant financial relationships.

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

A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.

Of note, investigators estimate that roughly 15% of schizophrenia cases among young males may be preventable by avoiding cannabis use disorder (CUD).

“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.

“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.

The study was published online in Psychological Medicine.
 

A modifiable risk factor

The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.

A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.

The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).

The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.

For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.

“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
 

Legalization sends the wrong message

In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”

In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.

“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.

“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.

The study received no specific funding. The authors disclosed no relevant financial relationships.

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

For adults with acute hypoxemic respiratory failure (AHRF), treatment using a helmet interface is likely superior to a face mask interface, according to a systematic review of recent randomized controlled trials examining different noninvasive oxygenation strategies for AHRF treatment.

The meta-analysis of 36 trials) found also that helmet interface probably lowers mortality and risk of mechanical intervention, and reduces hospital and ICU stay.

The COVID-19 pandemic has underscored the benefits of optimizing noninvasive strategies to avoid unnecessary intubation. Intubation may be avoided in patients with AHRF through noninvasive oxygenation strategies, including high flow nasal cannula (HFNC), continuous positive airway pressure (CPAP) and noninvasive bilevel ventilation, noted Tyler Pitre, MD, department of medicine, McMaster University, Hamilton, Ont., and colleagues. CPAP and bilevel ventilation can be delivered through different interfaces, most commonly face mask or helmet. While research has shown noninvasive strategies to be associated with reductions in risk for invasive mechanical ventilation, mortality assessments and analyses comparing specific modalities (i.e., CPAP vs. bilevel ventilation) have been limited. The incremental reduction in diaphragmatic effort and improved gas exchange demonstrated for bilevel ventilation compared with CPAP in COPD patients suggests that responses in AHRF may differ for CPAP and bilevel ventilation, state Dr. Pitre and colleagues. On the other hand, the increased drive pressure of bilevel ventilation may compound patient self-induced lung injury with concomitant lung inflammation and need for prolonged respiratory support. New evidence from several large, high quality randomized controlled trials (RCTs) in COVID-19-related AHRF offered an opportunity to reassess comparative efficacies, the researchers noted.

The retrospective study encompassed RCTs with all types of AHRF, including COVID-19 related, with a total of 7,046 patients whose median age was 59.4 years (61.4% were males). Thirty of the 36 RCTs reported on mortality (6,114 patients and 1,539 deaths). The study’s analysis showed with moderate certainty that helmet CPAP reduces mortality (231 fewer deaths per 1,000 [95% confidence interval (CI), 126-273]) while the 63 fewer deaths per 1,000 (95% CI, 15-102) indicated with low certainty that HFNC may reduce mortality compared with standard oxygen therapy (SOT). The analysis showed also that face mask bilevel (36 fewer deaths per 1,000 [84.0 fewer to 24.0 more]) and helmet bilevel ventilation (129.0 fewer deaths per 1,000 [195.0 to 24.0 fewer]) may reduce death compared with SOT (all low certainty). The mortality benefit for face mask CPAP compared with SOT was uncertain (very low certainty) (9 fewer deaths per 1,000 [81 fewer deaths to 84 more]). For helmet CPAP vs. HFNC ventilation, the mortality benefit had moderate certainty (198.1 fewer events per 1,000 [95% CI, 69.75-248.31].