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Tirzepatide superior to semaglutide for A1c control, weight loss
, results from a meta-analysis of 22 randomized controlled trials show.
“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.
“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.
The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.
While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.
For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.
Overall, 18,472 participants were included in the studies.
All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
Blood glucose reduction
Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).
All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.
Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
Body weight reduction comparisons
The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).
In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
Adverse events: Increased GI events with highest tirzepatide dose
Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.
There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).
In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).
There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
Real-world applications, comparisons
Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.
“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.
Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.
Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.
Among other issues of comparison with the two drugs is cost.
In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.
Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.
Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.
Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.
Dr. Karagiannis reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, results from a meta-analysis of 22 randomized controlled trials show.
“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.
“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.
The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.
While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.
For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.
Overall, 18,472 participants were included in the studies.
All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
Blood glucose reduction
Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).
All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.
Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
Body weight reduction comparisons
The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).
In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
Adverse events: Increased GI events with highest tirzepatide dose
Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.
There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).
In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).
There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
Real-world applications, comparisons
Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.
“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.
Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.
Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.
Among other issues of comparison with the two drugs is cost.
In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.
Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.
Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.
Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.
Dr. Karagiannis reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, results from a meta-analysis of 22 randomized controlled trials show.
“The results indicate tirzepatide’s superior performance over subcutaneous semaglutide in managing blood sugar and achieving weight loss, making it a promising option in the pharmaceutical management of type 2 diabetes,” first author Thomas Karagiannis, MD, PhD, Aristotle University of Thessaloniki, Greece, said in an interview.
“In clinical context, the most potent doses of each drug revealed a clear difference regarding weight loss, with tirzepatide resulting in an average weight reduction that exceeded that of semaglutide by 5.7 kg (12.6 pounds),” he said.
The study is scheduled to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in early October.
While a multitude of studies have been conducted for tirzepatide, a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 (GLP-1) receptor agonist, and semaglutide, a selective GLP-1 agonist, studies comparing the two drugs directly are lacking.
For a more comprehensive understanding of how the drugs compare, Dr. Karagiannis and colleagues conducted the meta-analysis of 22 trials, including two direct comparisons, the SURPASS-2 trial and a smaller trial, and 20 other studies comparing either semaglutide or tirzepatide with a common comparator, such as placebo, basal insulin, or other GLP-RA-1 drugs.
Overall, 18,472 participants were included in the studies.
All included studies had assessed a maintenance dose of tirzepatide of either 5, 10, or 15 mg once weekly or semaglutide at doses of 0.5, 1.0, or 2.0 mg once weekly for at least 12 weeks. All comparisons were for subcutaneous injection formulations (semaglutide can also be taken orally).
Blood glucose reduction
Tirzepatide at 15 mg was found to have the highest efficacy in the reduction of A1c compared with placebo, with a mean difference of –2.00%, followed by tirzepatide 10 mg (–1.86%) and semaglutide 2.0 mg (–1.62%).
All three of the tirzepatide doses had greater reductions in A1c compared with the respective low, medium, and high doses of semaglutide.
Dr. Karagiannis noted that the differences are significant: “An A1c reduction even by 0.5% is often deemed clinically important,” he said.
Body weight reduction comparisons
The reductions in body weight across the three drug doses were greater with tirzepatide (–10.96 kg [24.2 pounds], –8.75 kg [19.3 pounds], and –6.16 kg [13.6 pounds] for 15, 10, and 5 mg, respectively) compared with semaglutide (–5.24 kg [11.6 pounds], –4.44 kg [9.8 pounds], and –2.72 kg [6 pounds] for semaglutide 2.0, 1.0, and 0.5 mg, respectively).
In terms of drug-to-drug comparisons, tirzepatide 15 mg had a mean of 5.72 kg (12.6 pounds) greater reduction in body weight vs. semaglutide 2.0 mg; tirzepatide 10 mg had a mean of 3.52 kg (7.8 pounds) reduction vs. semaglutide 2.0 mg; and tirzepatide 5 mg had a mean of a 1.72 kg (3.8 pounds) greater reduction vs. semaglutide 1.0 mg.
Adverse events: Increased GI events with highest tirzepatide dose
Regarding the gastrointestinal adverse events associated with the drugs, tirzepatide 15 mg had the highest rate of the two drugs at their various doses, with a risk ratio (RR) of 3.57 compared with placebo for nausea, an RR of 4.35 for vomiting, and 2.04 for diarrhea.
There were no significant differences between the two drugs for the gastrointestinal events, with the exception of the highest dose of tirzepatide, 15 mg, which had a higher risk of vomiting vs. semaglutide 1.0 (RR 1.39) and semaglutide 0.5 mg (RR 1.85).
In addition, tirzepatide 15 mg had a higher risk vs. semaglutide 0.5 mg for nausea (RR 1.45).
There were no significant differences between the two drugs and placebo in the risk of serious adverse events.
Real-world applications, comparisons
Dr. Karagiannis noted that the results indicate that benefits of the efficacy of the higher tirzepatide dose need to be balanced with those potential side effects.
“Although the efficacy of the high tirzepatide dose might make it a favorable choice, its real-world application can be affected on an individual’s ability to tolerate these side effects in case they occur,” he explained.
Ultimately, “some patients may prioritize tolerability over enhanced efficacy,” he added.
Furthermore, while all three maintenance doses of tirzepatide analyzed have received marketing authorization, “to get a clearer picture of the real-world tolerance to these doses outside the context of randomized controlled trials, well-designed observational studies would be necessary,” Dr. Karagiannis said.
Among other issues of comparison with the two drugs is cost.
In a recent analysis, the cost per 1% of body weight reduction was reported to be $1,197 for high-dose tirzepatide (15 mg) vs. $1,511 for semaglutide 2.4 mg, with an overall cost of 72 weeks of therapy with tirzepatide at $17,527 compared with $22,878 for semaglutide.
Overall, patients and clinicians should consider the full range of differences and similarities between the medications, “from [their] efficacy and side effects to cost-effectiveness, long-term safety, and cardiovascular profile,” Dr. Karagiannis said.
Semaglutide is currently approved by the Food and Drug Administration for treatment of type 2 diabetes and obesity/weight loss management.
Tirzepatide has also received approval for the treatment of type 2 diabetes and its manufacturers have submitted applications for its approval for obesity/weight loss management.
Dr. Karagiannis reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM EASD 2023
Patients with rheumatism have premature immune system aging
LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.
“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”
“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.
While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
‘Inflamm-aging’
“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.
As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.
The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.
With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.
This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
‘Bad old T cells’
Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”
In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
Power sources fail
In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”
At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.
T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”
Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
Inflammatory cell death
In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”
In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.
Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”
Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.
When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”
This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.
LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.
“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”
“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.
While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
‘Inflamm-aging’
“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.
As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.
The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.
With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.
This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
‘Bad old T cells’
Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”
In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
Power sources fail
In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”
At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.
T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”
Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
Inflammatory cell death
In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”
In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.
Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”
Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.
When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”
This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.
LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.
“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”
“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.
While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
‘Inflamm-aging’
“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.
As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.
The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.
With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.
This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
‘Bad old T cells’
Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”
In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
Power sources fail
In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”
At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.
T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”
Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
Inflammatory cell death
In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”
In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.
Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”
Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.
When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”
This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.
Heart societies ready to split from ABIM over long-standing MOC disputes
What if cardiology were no longer an internal medicine subspecialty?
As envisioned, the new “independent, self-governed” entity would supplant the ABIM’s long-standing and widely criticized MOC system and establish cardiology as its own specialty with its own subspecialties. Long in coming, it is only the latest response to many in the field who for years have charged that the MOC system is needlessly burdensome and expensive.
“It’s time to have a dedicated cardiovascular medicine board of our own,” said B. Hadley Wilson, MD, in the group’s announcement. “Cardiology is a distinct medical specialty, and physicians want and deserve a clinical competency and continuous certification program that is meaningful to their practice and patients.”
Hadley Wilson, Sanger Heart & Vascular Institute Vascular Kenilworth, Charlotte, N.C., is president of the American College of Cardiology, one of the four societies spearheading the initiative along with the Heart Failure Society of America, the Heart Rhythm Society, and the Society for Cardiovascular Angiography & Interventions.
Their Sept. 21 statement says that the consortium will apply to the American Board of Medical Specialties to request an independent cardiology board that follows a “new competency-based approach to continuous certification – one that harnesses the knowledge, skills, and attitudes required to sustain professional excellence and care for cardiovascular patients effectively.”
It continues, “The new board requirements will de-emphasize timed, high stakes performance exams in the continuous certification process and instead will focus on learning assessments to identify gaps in current knowledge or skills.”
“The new board’s focus on competence in the pursuit of continuous certification is a needed paradigm shift for the field,” states HFSA President John R. Teerlink, MD, University of California, San Francisco, and the San Francisco VA Medical Center, in the announcement.
“I commend these professional cardiovascular societies for taking on this important challenge,” Deepak L. Bhatt, MD, MPH, Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, New York City, told this news organization by email.
“This is an incredible opportunity to redefine what ongoing cardiovascular education means to the contemporary practicing cardiologist in a way that is relevant to improving the care of actual patients,” said Dr. Bhatt, who chairs the ACC Accreditation Oversight Committee.
“There needs to be an agile, personalized, convenient, and effective system to assist practitioners to stay current with new knowledge and demonstrate the necessary competencies,” Harlan Krumholz, MD, said in an email.
“There is a deep sense in the profession that the current approaches do not meet the needs of clinicians or society,” said Dr. Krumholz, Yale School of Medicine, New Haven, Conn., who has sat on the ABIM board of directors.
“This effort, which now will create competition, has the potential to spark innovation,” he said. “The key is that any approach needs to ask the question, ‘Is the cost and effort producing benefit for patients and society?’ If it is not, we have not found the right system.”
In a statement in response to the new development, ABIM said it plans to continue “offering and administering” its existing MOC programs across all specialties.
“Any physician choosing to maintain their ABIM certification in these disciplines will continue to have a pathway with ABIM to do so,” it says. “Questions about the cardiovascular organizations’ announcement and how it may affect individual physicians are best answered by those organizations.”
The process of approving the heart societies’ application to ABMS “is expected to take several months,” their announcement states. If approval is granted, “it will then take several additional months before initial certification and continuous certification and competency programs would begin.”
Medscape provides educational content including MOC. Medscape’s editorial content, including news and features, is developed independently of the educational content available on Medscape.
A version of this article first appeared on Medscape.com.
What if cardiology were no longer an internal medicine subspecialty?
As envisioned, the new “independent, self-governed” entity would supplant the ABIM’s long-standing and widely criticized MOC system and establish cardiology as its own specialty with its own subspecialties. Long in coming, it is only the latest response to many in the field who for years have charged that the MOC system is needlessly burdensome and expensive.
“It’s time to have a dedicated cardiovascular medicine board of our own,” said B. Hadley Wilson, MD, in the group’s announcement. “Cardiology is a distinct medical specialty, and physicians want and deserve a clinical competency and continuous certification program that is meaningful to their practice and patients.”
Hadley Wilson, Sanger Heart & Vascular Institute Vascular Kenilworth, Charlotte, N.C., is president of the American College of Cardiology, one of the four societies spearheading the initiative along with the Heart Failure Society of America, the Heart Rhythm Society, and the Society for Cardiovascular Angiography & Interventions.
Their Sept. 21 statement says that the consortium will apply to the American Board of Medical Specialties to request an independent cardiology board that follows a “new competency-based approach to continuous certification – one that harnesses the knowledge, skills, and attitudes required to sustain professional excellence and care for cardiovascular patients effectively.”
It continues, “The new board requirements will de-emphasize timed, high stakes performance exams in the continuous certification process and instead will focus on learning assessments to identify gaps in current knowledge or skills.”
“The new board’s focus on competence in the pursuit of continuous certification is a needed paradigm shift for the field,” states HFSA President John R. Teerlink, MD, University of California, San Francisco, and the San Francisco VA Medical Center, in the announcement.
“I commend these professional cardiovascular societies for taking on this important challenge,” Deepak L. Bhatt, MD, MPH, Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, New York City, told this news organization by email.
“This is an incredible opportunity to redefine what ongoing cardiovascular education means to the contemporary practicing cardiologist in a way that is relevant to improving the care of actual patients,” said Dr. Bhatt, who chairs the ACC Accreditation Oversight Committee.
“There needs to be an agile, personalized, convenient, and effective system to assist practitioners to stay current with new knowledge and demonstrate the necessary competencies,” Harlan Krumholz, MD, said in an email.
“There is a deep sense in the profession that the current approaches do not meet the needs of clinicians or society,” said Dr. Krumholz, Yale School of Medicine, New Haven, Conn., who has sat on the ABIM board of directors.
“This effort, which now will create competition, has the potential to spark innovation,” he said. “The key is that any approach needs to ask the question, ‘Is the cost and effort producing benefit for patients and society?’ If it is not, we have not found the right system.”
In a statement in response to the new development, ABIM said it plans to continue “offering and administering” its existing MOC programs across all specialties.
“Any physician choosing to maintain their ABIM certification in these disciplines will continue to have a pathway with ABIM to do so,” it says. “Questions about the cardiovascular organizations’ announcement and how it may affect individual physicians are best answered by those organizations.”
The process of approving the heart societies’ application to ABMS “is expected to take several months,” their announcement states. If approval is granted, “it will then take several additional months before initial certification and continuous certification and competency programs would begin.”
Medscape provides educational content including MOC. Medscape’s editorial content, including news and features, is developed independently of the educational content available on Medscape.
A version of this article first appeared on Medscape.com.
What if cardiology were no longer an internal medicine subspecialty?
As envisioned, the new “independent, self-governed” entity would supplant the ABIM’s long-standing and widely criticized MOC system and establish cardiology as its own specialty with its own subspecialties. Long in coming, it is only the latest response to many in the field who for years have charged that the MOC system is needlessly burdensome and expensive.
“It’s time to have a dedicated cardiovascular medicine board of our own,” said B. Hadley Wilson, MD, in the group’s announcement. “Cardiology is a distinct medical specialty, and physicians want and deserve a clinical competency and continuous certification program that is meaningful to their practice and patients.”
Hadley Wilson, Sanger Heart & Vascular Institute Vascular Kenilworth, Charlotte, N.C., is president of the American College of Cardiology, one of the four societies spearheading the initiative along with the Heart Failure Society of America, the Heart Rhythm Society, and the Society for Cardiovascular Angiography & Interventions.
Their Sept. 21 statement says that the consortium will apply to the American Board of Medical Specialties to request an independent cardiology board that follows a “new competency-based approach to continuous certification – one that harnesses the knowledge, skills, and attitudes required to sustain professional excellence and care for cardiovascular patients effectively.”
It continues, “The new board requirements will de-emphasize timed, high stakes performance exams in the continuous certification process and instead will focus on learning assessments to identify gaps in current knowledge or skills.”
“The new board’s focus on competence in the pursuit of continuous certification is a needed paradigm shift for the field,” states HFSA President John R. Teerlink, MD, University of California, San Francisco, and the San Francisco VA Medical Center, in the announcement.
“I commend these professional cardiovascular societies for taking on this important challenge,” Deepak L. Bhatt, MD, MPH, Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, New York City, told this news organization by email.
“This is an incredible opportunity to redefine what ongoing cardiovascular education means to the contemporary practicing cardiologist in a way that is relevant to improving the care of actual patients,” said Dr. Bhatt, who chairs the ACC Accreditation Oversight Committee.
“There needs to be an agile, personalized, convenient, and effective system to assist practitioners to stay current with new knowledge and demonstrate the necessary competencies,” Harlan Krumholz, MD, said in an email.
“There is a deep sense in the profession that the current approaches do not meet the needs of clinicians or society,” said Dr. Krumholz, Yale School of Medicine, New Haven, Conn., who has sat on the ABIM board of directors.
“This effort, which now will create competition, has the potential to spark innovation,” he said. “The key is that any approach needs to ask the question, ‘Is the cost and effort producing benefit for patients and society?’ If it is not, we have not found the right system.”
In a statement in response to the new development, ABIM said it plans to continue “offering and administering” its existing MOC programs across all specialties.
“Any physician choosing to maintain their ABIM certification in these disciplines will continue to have a pathway with ABIM to do so,” it says. “Questions about the cardiovascular organizations’ announcement and how it may affect individual physicians are best answered by those organizations.”
The process of approving the heart societies’ application to ABMS “is expected to take several months,” their announcement states. If approval is granted, “it will then take several additional months before initial certification and continuous certification and competency programs would begin.”
Medscape provides educational content including MOC. Medscape’s editorial content, including news and features, is developed independently of the educational content available on Medscape.
A version of this article first appeared on Medscape.com.
Echocardiography boosts prognostic power in T1D
AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.
Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.
The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.
Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
‘Trying to figure out’ the type 1 diabetes link
“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.
The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.
The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.
This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.
Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
MPI reflects left ventricular function
MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.
“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”
The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.
The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.
Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.
The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.
Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
‘Trying to figure out’ the type 1 diabetes link
“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.
The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.
The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.
This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.
Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
MPI reflects left ventricular function
MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.
“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”
The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.
The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
AMSTERDAM – Calculating a patient’s myocardial performance index (MPI) and adding it to a standard risk-prediction model significantly increased prognostic accuracy for major adverse cardiovascular events (MACE), especially heart failure, in people with type 1 but not type 2 diabetes, an analysis of data from about 2,000 Danish patients shows.
Hashmat S.Z. Bahrami, MD, said at the annual congress of the European Society of Cardiology.
The primary analysis he reported showed a significantly elevated adjusted hazard ratio of 1.2 among people with either type 1 or type 2 diabetes and an elevated MPI, compared with those with diabetes but a lower MPI value.
Further analysis divided the study cohort into the 1,093 people with type 1 diabetes and the 1,030 with type 2 diabetes and showed that the significant association of elevated MPI with increased MACE was entirely confined to the type 1 diabetes subgroup, again with a hazard ratio of 1.2, but without any significant association among those with type 2 diabetes, said Dr. Bahrami, a cardiology researcher at Copenhagen University Hospital.
‘Trying to figure out’ the type 1 diabetes link
“We’re still trying to figure out” the explanation for this difference based on diabetes type, Dr. Bahrami said. He speculated that it might relate to a higher incidence of heart failure among those with type 1 diabetes, or to longer duration of diabetes in the type 1 subgroup.
The ability of elevated MPI to predict an increased risk specifically for heart failure was apparent in another analysis he presented that divided MACE events into the individual components of this composite. Elevated MPI significantly linked with a 1.3-fold elevated risk for heart failure in those with type 1 diabetes, but high MPI had no significant association with any of the other event types included in the MACE composite.
The researchers also assessed the incremental impact from adding MPI data to an established cardiovascular disease (CVD) risk calculator for people with type 1 diabetes, the Steno Type 1 Risk Engine, which includes nine parameters such as age, sex, blood pressure, diabetes duration, and two different measures of renal function.
This analysis showed that adding MPI significantly boosted the attributable CVD risk from an area-under-the-curve of 0.77 to an AUC of 0.79. Including MPI also boosted the AUC for risk of future heart failure from 0.77 with the existing Steno Type 1 Risk Engine to 0.83, also a significant increase.
Simultaneously with his talk at the Congress, a report on the findings was published online in the European Heart Journal Cardiovascular Imaging.
MPI reflects left ventricular function
MPI is calculated by adding a person’s isovolumic cardiac relaxation time to their isovolumic cardiac contraction time and dividing this by their ejection time. These time measurements come from examination with tissue Doppler M-mode echocardiography, Dr. Bahrami explained, and when assessed together reflect left ventricular function during both systolic and diastolic phases.
“MPI has been around for many years, but our technique is rather novel” and has high intra- and inter-observer reproducibility, he said. “It’s highly reproducible and feasible.”
The study included data collected prospectively from Danish adults without any known CVD enrolled in the Thousand & 1 study of people with type 1 diabetes and the Thousand & 2 study of people with type 2 diabetes. The analyses that Dr. Bahrami reported included CVD events during a median 5.3 years of follow-up.
The study received funding from Novo Nordisk. Dr. Bahrami has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
AT ESC 2023
NPs and PAs handling increasingly more primary care visits: New studies
When patients seek primary care, it’s becoming more likely that they’ll see a nurse practitioner or physician assistant.
Health care visits to NPs and PAs, also known as advanced practice providers, have been rising in recent years compared with doctor visits, according to the latest studies. The proportion of Medicare visits that NPs and PAs delivered nearly doubled in the 7-year period 2013-2019 (14% in 2013 to 26% in 2019), according to research published this month in the BMJ. Among study participants, 42% had at least one visit with an NP or PA. Meanwhile, primary care visits with a physician decreased by 18%, the study showed.
Medicare accounts for roughly 20% of the U.S. population and 23% of health care spending, according to 2023 data cited in the report. Study authors surveyed a random sample, 20% of Medicare recipients who sought care through in-person and telemedicine visits to outpatient and nursing facilities before the COVID-19 pandemic.
Medical clinics have turned to NPs and PAs to offset a shortage of primary care doctors, with the United States having fewer physicians per capita than other industrialized nations, according to Ateev Mehrotra, MD, MPH, professor of health care policy at Harvard Medical School and one of the authors of the BMJ report.
Nursing schools also struggle to meet the growing demand for NPs. In more than half of U.S. states, NPs can work independently without physician supervision, while PAs face more restrictions.
Another study earlier this year also found a rise in APP care. FAIR Health reported that nearly one in three patients received care between 2016 and 2022 from someone other than a physician, with NPs providing 27% of primary care visits and PAs, 15%.
The trend isn’t new. But for many years, claims data from Medicare or commercial payers masked the impact of advanced practitioners because their care was billed under a supervising physician, explained Michael L. Powe, vice president of reimbursement and professional advocacy for the American Academy of Physician Assistants, which represents PAs.
NPs and PAs are more likely to see patients with lower incomes, those who live in rural communities, or those who have disabilities, according to the BMJ study, suggesting that these providers may improve access to health care.
They already comprise about half of the primary care professionals in rural areas, said Stephen Ferrara, DNP, president of the American Association of Nurse Practitioners, citing a 2022 report by the Medicare Payment Advisory Commission.
The BMJ study also found that NPs and PAs were more likely to see patients for certain conditions. For example, they handled 42% of visits for respiratory infections and 37% of visits for anxiety, compared with only 13% of visits for eye problems and 20% of visits for hypertension.
Dr. Mehrotra said patients, in general, are still unlikely to see only an NP for many conditions, particularly chronic illness. “You might see the physician one time and then the nurse practitioner, and then the PA. And you might see another physician in the practice.”
He said health care leaders need to decide how to set up teams to best serve patients. From a health policy perspective, they should also consider whether to boost funding for NP and PA education or primary care residencies.
Meanwhile, the growth of advanced practitioners continues. The Bureau of Labor Statistics estimates that the number of NPs will increase to 359,000 in 2031 (80% growth from 2019) and the number of PAs will increase to 178,000 (48% growth).
A version of this article first appeared on Medscape.com.
When patients seek primary care, it’s becoming more likely that they’ll see a nurse practitioner or physician assistant.
Health care visits to NPs and PAs, also known as advanced practice providers, have been rising in recent years compared with doctor visits, according to the latest studies. The proportion of Medicare visits that NPs and PAs delivered nearly doubled in the 7-year period 2013-2019 (14% in 2013 to 26% in 2019), according to research published this month in the BMJ. Among study participants, 42% had at least one visit with an NP or PA. Meanwhile, primary care visits with a physician decreased by 18%, the study showed.
Medicare accounts for roughly 20% of the U.S. population and 23% of health care spending, according to 2023 data cited in the report. Study authors surveyed a random sample, 20% of Medicare recipients who sought care through in-person and telemedicine visits to outpatient and nursing facilities before the COVID-19 pandemic.
Medical clinics have turned to NPs and PAs to offset a shortage of primary care doctors, with the United States having fewer physicians per capita than other industrialized nations, according to Ateev Mehrotra, MD, MPH, professor of health care policy at Harvard Medical School and one of the authors of the BMJ report.
Nursing schools also struggle to meet the growing demand for NPs. In more than half of U.S. states, NPs can work independently without physician supervision, while PAs face more restrictions.
Another study earlier this year also found a rise in APP care. FAIR Health reported that nearly one in three patients received care between 2016 and 2022 from someone other than a physician, with NPs providing 27% of primary care visits and PAs, 15%.
The trend isn’t new. But for many years, claims data from Medicare or commercial payers masked the impact of advanced practitioners because their care was billed under a supervising physician, explained Michael L. Powe, vice president of reimbursement and professional advocacy for the American Academy of Physician Assistants, which represents PAs.
NPs and PAs are more likely to see patients with lower incomes, those who live in rural communities, or those who have disabilities, according to the BMJ study, suggesting that these providers may improve access to health care.
They already comprise about half of the primary care professionals in rural areas, said Stephen Ferrara, DNP, president of the American Association of Nurse Practitioners, citing a 2022 report by the Medicare Payment Advisory Commission.
The BMJ study also found that NPs and PAs were more likely to see patients for certain conditions. For example, they handled 42% of visits for respiratory infections and 37% of visits for anxiety, compared with only 13% of visits for eye problems and 20% of visits for hypertension.
Dr. Mehrotra said patients, in general, are still unlikely to see only an NP for many conditions, particularly chronic illness. “You might see the physician one time and then the nurse practitioner, and then the PA. And you might see another physician in the practice.”
He said health care leaders need to decide how to set up teams to best serve patients. From a health policy perspective, they should also consider whether to boost funding for NP and PA education or primary care residencies.
Meanwhile, the growth of advanced practitioners continues. The Bureau of Labor Statistics estimates that the number of NPs will increase to 359,000 in 2031 (80% growth from 2019) and the number of PAs will increase to 178,000 (48% growth).
A version of this article first appeared on Medscape.com.
When patients seek primary care, it’s becoming more likely that they’ll see a nurse practitioner or physician assistant.
Health care visits to NPs and PAs, also known as advanced practice providers, have been rising in recent years compared with doctor visits, according to the latest studies. The proportion of Medicare visits that NPs and PAs delivered nearly doubled in the 7-year period 2013-2019 (14% in 2013 to 26% in 2019), according to research published this month in the BMJ. Among study participants, 42% had at least one visit with an NP or PA. Meanwhile, primary care visits with a physician decreased by 18%, the study showed.
Medicare accounts for roughly 20% of the U.S. population and 23% of health care spending, according to 2023 data cited in the report. Study authors surveyed a random sample, 20% of Medicare recipients who sought care through in-person and telemedicine visits to outpatient and nursing facilities before the COVID-19 pandemic.
Medical clinics have turned to NPs and PAs to offset a shortage of primary care doctors, with the United States having fewer physicians per capita than other industrialized nations, according to Ateev Mehrotra, MD, MPH, professor of health care policy at Harvard Medical School and one of the authors of the BMJ report.
Nursing schools also struggle to meet the growing demand for NPs. In more than half of U.S. states, NPs can work independently without physician supervision, while PAs face more restrictions.
Another study earlier this year also found a rise in APP care. FAIR Health reported that nearly one in three patients received care between 2016 and 2022 from someone other than a physician, with NPs providing 27% of primary care visits and PAs, 15%.
The trend isn’t new. But for many years, claims data from Medicare or commercial payers masked the impact of advanced practitioners because their care was billed under a supervising physician, explained Michael L. Powe, vice president of reimbursement and professional advocacy for the American Academy of Physician Assistants, which represents PAs.
NPs and PAs are more likely to see patients with lower incomes, those who live in rural communities, or those who have disabilities, according to the BMJ study, suggesting that these providers may improve access to health care.
They already comprise about half of the primary care professionals in rural areas, said Stephen Ferrara, DNP, president of the American Association of Nurse Practitioners, citing a 2022 report by the Medicare Payment Advisory Commission.
The BMJ study also found that NPs and PAs were more likely to see patients for certain conditions. For example, they handled 42% of visits for respiratory infections and 37% of visits for anxiety, compared with only 13% of visits for eye problems and 20% of visits for hypertension.
Dr. Mehrotra said patients, in general, are still unlikely to see only an NP for many conditions, particularly chronic illness. “You might see the physician one time and then the nurse practitioner, and then the PA. And you might see another physician in the practice.”
He said health care leaders need to decide how to set up teams to best serve patients. From a health policy perspective, they should also consider whether to boost funding for NP and PA education or primary care residencies.
Meanwhile, the growth of advanced practitioners continues. The Bureau of Labor Statistics estimates that the number of NPs will increase to 359,000 in 2031 (80% growth from 2019) and the number of PAs will increase to 178,000 (48% growth).
A version of this article first appeared on Medscape.com.
Ginger consumption may mitigate neutrophil dysfunction and inflammation
TOPLINE:
Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.
METHODOLOGY:
- Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
- Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
- The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.
TAKEAWAY:
- Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
- Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
- The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
- Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.
IN PRACTICE:
The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.
SOURCE:
First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.
LIMITATIONS:
More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.
DISCLOSURES:
The study received no outside funding. The researchers report no relevant financial relationships.
A version of this article appeared on Medscape.com.
TOPLINE:
Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.
METHODOLOGY:
- Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
- Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
- The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.
TAKEAWAY:
- Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
- Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
- The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
- Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.
IN PRACTICE:
The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.
SOURCE:
First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.
LIMITATIONS:
More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.
DISCLOSURES:
The study received no outside funding. The researchers report no relevant financial relationships.
A version of this article appeared on Medscape.com.
TOPLINE:
Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.
METHODOLOGY:
- Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
- Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
- The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.
TAKEAWAY:
- Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
- Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
- The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
- Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.
IN PRACTICE:
The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.
SOURCE:
First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.
LIMITATIONS:
More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.
DISCLOSURES:
The study received no outside funding. The researchers report no relevant financial relationships.
A version of this article appeared on Medscape.com.
Fremanezumab reduces medication overuse in chronic migraine
Key clinical point: Fremanezumab was effective as a preventive treatment in patients with chronic migraine (CM) with or without medication overuse (MO) and showed potential benefits in reducing MO.
Major finding: During a 12-week follow-up period, the administration of monthly and quarterly fremanezumab vs placebo led to significantly reduced average number of monthly headache days of moderate or greater severity in patients with MO (monthly: mean change [∆] −2.0, P = .0012; and quarterly: ∆ −1.8, P = .0042) and without MO (monthly: ∆ −1.6, P = .0437; and quarterly: ∆ −1.5, P = .0441). A greater proportion of patients receiving fremanezumab vs placebo reverted to no MO (P ≤ .05).
Study details: This post hoc analysis of a phase 2b/3 trial included 479 Japanese patients with CM who were randomly assigned to receive monthly fremanezumab (n = 159), quarterly fremanezumab (n = 159), or placebo (n = 161), and of whom 320 patients reported MO.
Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Several authors declared being full-time employees of Otsuka Pharmaceutical Co., Ltd., and N Imai declared ties with various other sources.
Source: Imai N et al. Effects of fremanezumab on medication overuse in Japanese chronic migraine patients: Post hoc analysis of a multicenter, randomized, double-blind, placebo-controlled trial. Neurol Ther. 2023 (Sep 11). doi: 10.1007/s40120-023-00531-3
Key clinical point: Fremanezumab was effective as a preventive treatment in patients with chronic migraine (CM) with or without medication overuse (MO) and showed potential benefits in reducing MO.
Major finding: During a 12-week follow-up period, the administration of monthly and quarterly fremanezumab vs placebo led to significantly reduced average number of monthly headache days of moderate or greater severity in patients with MO (monthly: mean change [∆] −2.0, P = .0012; and quarterly: ∆ −1.8, P = .0042) and without MO (monthly: ∆ −1.6, P = .0437; and quarterly: ∆ −1.5, P = .0441). A greater proportion of patients receiving fremanezumab vs placebo reverted to no MO (P ≤ .05).
Study details: This post hoc analysis of a phase 2b/3 trial included 479 Japanese patients with CM who were randomly assigned to receive monthly fremanezumab (n = 159), quarterly fremanezumab (n = 159), or placebo (n = 161), and of whom 320 patients reported MO.
Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Several authors declared being full-time employees of Otsuka Pharmaceutical Co., Ltd., and N Imai declared ties with various other sources.
Source: Imai N et al. Effects of fremanezumab on medication overuse in Japanese chronic migraine patients: Post hoc analysis of a multicenter, randomized, double-blind, placebo-controlled trial. Neurol Ther. 2023 (Sep 11). doi: 10.1007/s40120-023-00531-3
Key clinical point: Fremanezumab was effective as a preventive treatment in patients with chronic migraine (CM) with or without medication overuse (MO) and showed potential benefits in reducing MO.
Major finding: During a 12-week follow-up period, the administration of monthly and quarterly fremanezumab vs placebo led to significantly reduced average number of monthly headache days of moderate or greater severity in patients with MO (monthly: mean change [∆] −2.0, P = .0012; and quarterly: ∆ −1.8, P = .0042) and without MO (monthly: ∆ −1.6, P = .0437; and quarterly: ∆ −1.5, P = .0441). A greater proportion of patients receiving fremanezumab vs placebo reverted to no MO (P ≤ .05).
Study details: This post hoc analysis of a phase 2b/3 trial included 479 Japanese patients with CM who were randomly assigned to receive monthly fremanezumab (n = 159), quarterly fremanezumab (n = 159), or placebo (n = 161), and of whom 320 patients reported MO.
Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Several authors declared being full-time employees of Otsuka Pharmaceutical Co., Ltd., and N Imai declared ties with various other sources.
Source: Imai N et al. Effects of fremanezumab on medication overuse in Japanese chronic migraine patients: Post hoc analysis of a multicenter, randomized, double-blind, placebo-controlled trial. Neurol Ther. 2023 (Sep 11). doi: 10.1007/s40120-023-00531-3
Responders to anti-CGRP mAb show improvement in migraine-attack-associated symptoms
Key clinical point: Patients with migraine who achieved ≥ 50% reduction in headache days at 6 months (responders) with anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) showed an even greater reduction in the number of days per month with photophobia, phonophobia, and aura ratios.
Major finding: Monthly headache days reduced significantly by 9.4 days/month (P < .001) and 2.2 days/month (P = .004) among responders and non-responders, respectively, with responders having additional significant reductions in photophobia (−19.5%; P < .001), phonophobia (−12.1%; P = .010), and aura (−25.1%; P = .008) ratios. Higher basal photophobia ratios were predictors of increased response rates between months 3 and 6 (incidence risk ratio 0.928; P = .040).
Study details: This prospective observational study included 158 patients with migraine treated with anti-CGRP mAb, of whom 43.7% were responders.
Disclosures: This study did not receive any funding. A Alpuente, E Caronna, M Torres-Ferrús, and P Pozo-Rosich declared receiving honoraria as consultants or speakers from various sources.
Source: Alpuente A et al. Impact of anti-CGRP monoclonal antibodies on migraine attack accompanying symptoms: A real-world evidence study. Cephalalgia. 2023;43(8):3331024231177636 (Aug 9). doi: 10.1177/03331024231177636
Key clinical point: Patients with migraine who achieved ≥ 50% reduction in headache days at 6 months (responders) with anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) showed an even greater reduction in the number of days per month with photophobia, phonophobia, and aura ratios.
Major finding: Monthly headache days reduced significantly by 9.4 days/month (P < .001) and 2.2 days/month (P = .004) among responders and non-responders, respectively, with responders having additional significant reductions in photophobia (−19.5%; P < .001), phonophobia (−12.1%; P = .010), and aura (−25.1%; P = .008) ratios. Higher basal photophobia ratios were predictors of increased response rates between months 3 and 6 (incidence risk ratio 0.928; P = .040).
Study details: This prospective observational study included 158 patients with migraine treated with anti-CGRP mAb, of whom 43.7% were responders.
Disclosures: This study did not receive any funding. A Alpuente, E Caronna, M Torres-Ferrús, and P Pozo-Rosich declared receiving honoraria as consultants or speakers from various sources.
Source: Alpuente A et al. Impact of anti-CGRP monoclonal antibodies on migraine attack accompanying symptoms: A real-world evidence study. Cephalalgia. 2023;43(8):3331024231177636 (Aug 9). doi: 10.1177/03331024231177636
Key clinical point: Patients with migraine who achieved ≥ 50% reduction in headache days at 6 months (responders) with anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) showed an even greater reduction in the number of days per month with photophobia, phonophobia, and aura ratios.
Major finding: Monthly headache days reduced significantly by 9.4 days/month (P < .001) and 2.2 days/month (P = .004) among responders and non-responders, respectively, with responders having additional significant reductions in photophobia (−19.5%; P < .001), phonophobia (−12.1%; P = .010), and aura (−25.1%; P = .008) ratios. Higher basal photophobia ratios were predictors of increased response rates between months 3 and 6 (incidence risk ratio 0.928; P = .040).
Study details: This prospective observational study included 158 patients with migraine treated with anti-CGRP mAb, of whom 43.7% were responders.
Disclosures: This study did not receive any funding. A Alpuente, E Caronna, M Torres-Ferrús, and P Pozo-Rosich declared receiving honoraria as consultants or speakers from various sources.
Source: Alpuente A et al. Impact of anti-CGRP monoclonal antibodies on migraine attack accompanying symptoms: A real-world evidence study. Cephalalgia. 2023;43(8):3331024231177636 (Aug 9). doi: 10.1177/03331024231177636
Migraine history and COVID-19 risk in older women: Is there a link?
Key clinical point: No appreciable association was observed between a history of migraine or its subtypes and an increase in the risk for COVID-19, including hospitalization for COVID-19, in older women.
Major finding: No significant association was observed between a history of migraine and the risk of developing COVID-19 (odds ratio [OR] 1.08; 95% CI 0.95-1.22) or being hospitalized for COVID-19 (OR 1.20; 95% CI 0.86-1.68) among older women. Similarly, other migraine statuses, including migraine with aura, showed no association with the risk for COVID-19.
Study details: This prospective cohort study included 16,492 women (age ≥ 45 years) enrolled in the Women’s Health Study, of whom 28.9% had a history of migraine and 7.7% reported positive SARS-CoV-2 test results, a diagnosis of COVID-19, or hospitalization for COVID-19.
Disclosures: The Women’s Health Study was funded by grants from the US National Cancer Institute and the US National Heart, Lung, and Blood Institute. T Kurth declared receiving research grants and personal compensation from various sources. The other authors declared no conflicts of interest.
Source: Rist PM et al. History of migraine and risk of COVID-19: A cohort study. Am J Med. 2023 (Aug 18). doi: 10.1016/j.amjmed.2023.07.021
Key clinical point: No appreciable association was observed between a history of migraine or its subtypes and an increase in the risk for COVID-19, including hospitalization for COVID-19, in older women.
Major finding: No significant association was observed between a history of migraine and the risk of developing COVID-19 (odds ratio [OR] 1.08; 95% CI 0.95-1.22) or being hospitalized for COVID-19 (OR 1.20; 95% CI 0.86-1.68) among older women. Similarly, other migraine statuses, including migraine with aura, showed no association with the risk for COVID-19.
Study details: This prospective cohort study included 16,492 women (age ≥ 45 years) enrolled in the Women’s Health Study, of whom 28.9% had a history of migraine and 7.7% reported positive SARS-CoV-2 test results, a diagnosis of COVID-19, or hospitalization for COVID-19.
Disclosures: The Women’s Health Study was funded by grants from the US National Cancer Institute and the US National Heart, Lung, and Blood Institute. T Kurth declared receiving research grants and personal compensation from various sources. The other authors declared no conflicts of interest.
Source: Rist PM et al. History of migraine and risk of COVID-19: A cohort study. Am J Med. 2023 (Aug 18). doi: 10.1016/j.amjmed.2023.07.021
Key clinical point: No appreciable association was observed between a history of migraine or its subtypes and an increase in the risk for COVID-19, including hospitalization for COVID-19, in older women.
Major finding: No significant association was observed between a history of migraine and the risk of developing COVID-19 (odds ratio [OR] 1.08; 95% CI 0.95-1.22) or being hospitalized for COVID-19 (OR 1.20; 95% CI 0.86-1.68) among older women. Similarly, other migraine statuses, including migraine with aura, showed no association with the risk for COVID-19.
Study details: This prospective cohort study included 16,492 women (age ≥ 45 years) enrolled in the Women’s Health Study, of whom 28.9% had a history of migraine and 7.7% reported positive SARS-CoV-2 test results, a diagnosis of COVID-19, or hospitalization for COVID-19.
Disclosures: The Women’s Health Study was funded by grants from the US National Cancer Institute and the US National Heart, Lung, and Blood Institute. T Kurth declared receiving research grants and personal compensation from various sources. The other authors declared no conflicts of interest.
Source: Rist PM et al. History of migraine and risk of COVID-19: A cohort study. Am J Med. 2023 (Aug 18). doi: 10.1016/j.amjmed.2023.07.021
Meta-analysis evaluates risk for migraine among patients with multiple sclerosis
Key clinical point: Nearly 24% of patients with multiple sclerosis (MS) experience migraine, with the odds of migraine occurrence being approximately 2-fold higher in patients with MS compared with control individuals.
Major finding: The overall prevalence rate of migraine among patients with MS was 0.24 (95% CI 0.21-0.28). Moreover, patients with MS vs control participants without MS had a ~2-fold greater risk of experiencing migraine (odds ratio 1.96; 95% CI 1.20-3.20).
Study details: This meta-analysis of 35 studies included 279,620 patients with MS and 279,603 control participants without MS.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.
Source: Mohammadi M et al. The association between multiple sclerosis and migraine: A meta-analysis. Mult Scler Relat Disord. 2023;79:104954 (Aug 30). doi: 10.1016/j.msard.2023.104954
Key clinical point: Nearly 24% of patients with multiple sclerosis (MS) experience migraine, with the odds of migraine occurrence being approximately 2-fold higher in patients with MS compared with control individuals.
Major finding: The overall prevalence rate of migraine among patients with MS was 0.24 (95% CI 0.21-0.28). Moreover, patients with MS vs control participants without MS had a ~2-fold greater risk of experiencing migraine (odds ratio 1.96; 95% CI 1.20-3.20).
Study details: This meta-analysis of 35 studies included 279,620 patients with MS and 279,603 control participants without MS.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.
Source: Mohammadi M et al. The association between multiple sclerosis and migraine: A meta-analysis. Mult Scler Relat Disord. 2023;79:104954 (Aug 30). doi: 10.1016/j.msard.2023.104954
Key clinical point: Nearly 24% of patients with multiple sclerosis (MS) experience migraine, with the odds of migraine occurrence being approximately 2-fold higher in patients with MS compared with control individuals.
Major finding: The overall prevalence rate of migraine among patients with MS was 0.24 (95% CI 0.21-0.28). Moreover, patients with MS vs control participants without MS had a ~2-fold greater risk of experiencing migraine (odds ratio 1.96; 95% CI 1.20-3.20).
Study details: This meta-analysis of 35 studies included 279,620 patients with MS and 279,603 control participants without MS.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.
Source: Mohammadi M et al. The association between multiple sclerosis and migraine: A meta-analysis. Mult Scler Relat Disord. 2023;79:104954 (Aug 30). doi: 10.1016/j.msard.2023.104954