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COVID-19 doesn’t spike A1c levels
Key takeaways
Results from a retrospective, observational, case-control study of more than 20,000 people from a single U.S. medical center showed a statistically significant but clinically insignificant increase in A1c in people following COVID-19 infection, in both those with and without diabetes.
After people received a diagnosis of COVID-19 infection, they were 40% more likely to also receive a diagnosis of type 2 diabetes, compared with people who tested negative for COVID-19, a difference that was significant and could be explained by the increased medical care received by people who test positive for COVID-19.
The risk of incident diabetic ketoacidosis (DKA) among people who tested positive for COVID-19 was significantly higher among those with pre-existing type 2 diabetes, those using insulin, and among Black individuals.
Why this matters
The authors said that their study is the first report of evidence that infection with COVID-19 affects A1c levels in a large, real-world clinical cohort.
Until now, the impact of COVID-19 infection on A1c remained unclear. Results from previous studies indicated that COVID-19 infection may increase A1c levels, but the studied cohorts were small and lacked uninfected controls.
The current study included 8,755 people infected with COVID-19, had data from both before and after the infection on diabetes status and A1c levels, and also included many matched, uninfected people who served as controls.
Study design
Data came from a Cleveland Clinic registry that included 81,093 people who tested positive for COVID-19 between March 2020 and May 2021 and 153,034 matched individuals who tested negative for COVID-19 during the same period.
The researchers retrospectively selected patients with an A1c recorded within 12 months before their COVID-19 test, as well as a second A1c value recorded within 12 months after COVID-19 testing. This produced a study cohort of 8,755 COVID-positive people and 11,998 matched people who tested negative for COVID-19.
To evaluate the risk of DKA onset after COVID-19 infection, the authors identified two sub-cohorts that excluded those with a history of DKA. The sub-cohorts were 701 people with type 1 diabetes and 21,830 with type 2 diabetes.
Key results
The investigators found a statistically significant but clinically insignificant A1c increase following a positive COVID-19 test, an average A1c increase of 0.06 percentage points. Those who tested negative for COVID-19 had a clinically insignificant change in their average A1c level that was of borderline statistical significance, an average increase of 0.02 percentage points (P = .05).
The statistically significant but clinically insignificant increase in A1c following infection with COVID-19 was similar in people with and without type 2 diabetes prior to infection.
In patients with type 2 diabetes who became infected with COVID-19, the researchers saw significant positive associations between higher A1c levels before infection and time to hospitalization (hazard ratio, 1.07), need for assisted breathing (HR, 1.06), and ICU admission (HR, 1.07).
Following a COVID-19 infection, people were 40% more likely to receive a diagnosis of incident type 2 diabetes, compared with matched uninfected people. The authors said a possible explanation is that after diagnosis of COVID-19, infected people in general received more intensified care that led to better identification of those with underlying type 2 diabetes.
The 701 people included with pre-existing type 1 diabetes showed no significant difference in their rate of developing DKA between those infected and not infected with COVID-19.
Among the 21,830 people with pre-existing type 2 diabetes, the DKA risk was a significant 35% greater for those who were infected with COVID-19, compared with those who were uninfected. The magnitude of this increased relative risk was even higher among the patients with type 2 diabetes who used insulin as part of their treatment.
The difference in DKA risk didn’t differ between Black and White patients who were not infected with COVID-19, but among those infected by COVID-19, Black patients were more than twice as likely to be diagnosed with DKA, compared with White patients, a significant difference.
Black patients with type 2 diabetes who became infected with COVID-19 had a significant (63%) increased rate of DKA compared with Black patients with type 2 diabetes who remained uninfected.
Limitations
The study included patients with A1c measurements made up to 12 months prior to their COVID-19 test, and hence comorbid conditions, medication changes during this period, or other factors may have affected subsequent A1c levels. To address this, the authors also assessed outcomes at 3- and 6-month intervals, which produced results consistent with the 12-month findings.
The researchers did not have A1c values for many of the more than 234,000 people in the entire registry who underwent COVID-19 testing from March 2020-May 2021 at the Cleveland Clinic, omissions that may have biased the study cohort.
This was a single-center study. Some patients may have received care outside of the center, hence records of those episodes could not be included.
Disclosures
The study received no commercial funding. Four authors received consulting and speaker honoraria and research funding from AstraZeneca, Bayer, Boehringer Ingelheim, Corcept Therapeutics, Diasome, Eli Lilly, Merck, Novo Nordisk, and Sanofi. Three authors have intellectual property related to treatment decisionmaking in the context of type 2 diabetes.
This is a summary of a preprint research study “Impacts of COVID-19 on glycemia and risk of diabetic ketoacidosis,” written by researchers at the Cleveland Clinic on medRxiv. The study has not yet been peer reviewed. The full text of the study can be found on medRxiv.org.
A version of this article first appeared on Medscape.com.
Key takeaways
Results from a retrospective, observational, case-control study of more than 20,000 people from a single U.S. medical center showed a statistically significant but clinically insignificant increase in A1c in people following COVID-19 infection, in both those with and without diabetes.
After people received a diagnosis of COVID-19 infection, they were 40% more likely to also receive a diagnosis of type 2 diabetes, compared with people who tested negative for COVID-19, a difference that was significant and could be explained by the increased medical care received by people who test positive for COVID-19.
The risk of incident diabetic ketoacidosis (DKA) among people who tested positive for COVID-19 was significantly higher among those with pre-existing type 2 diabetes, those using insulin, and among Black individuals.
Why this matters
The authors said that their study is the first report of evidence that infection with COVID-19 affects A1c levels in a large, real-world clinical cohort.
Until now, the impact of COVID-19 infection on A1c remained unclear. Results from previous studies indicated that COVID-19 infection may increase A1c levels, but the studied cohorts were small and lacked uninfected controls.
The current study included 8,755 people infected with COVID-19, had data from both before and after the infection on diabetes status and A1c levels, and also included many matched, uninfected people who served as controls.
Study design
Data came from a Cleveland Clinic registry that included 81,093 people who tested positive for COVID-19 between March 2020 and May 2021 and 153,034 matched individuals who tested negative for COVID-19 during the same period.
The researchers retrospectively selected patients with an A1c recorded within 12 months before their COVID-19 test, as well as a second A1c value recorded within 12 months after COVID-19 testing. This produced a study cohort of 8,755 COVID-positive people and 11,998 matched people who tested negative for COVID-19.
To evaluate the risk of DKA onset after COVID-19 infection, the authors identified two sub-cohorts that excluded those with a history of DKA. The sub-cohorts were 701 people with type 1 diabetes and 21,830 with type 2 diabetes.
Key results
The investigators found a statistically significant but clinically insignificant A1c increase following a positive COVID-19 test, an average A1c increase of 0.06 percentage points. Those who tested negative for COVID-19 had a clinically insignificant change in their average A1c level that was of borderline statistical significance, an average increase of 0.02 percentage points (P = .05).
The statistically significant but clinically insignificant increase in A1c following infection with COVID-19 was similar in people with and without type 2 diabetes prior to infection.
In patients with type 2 diabetes who became infected with COVID-19, the researchers saw significant positive associations between higher A1c levels before infection and time to hospitalization (hazard ratio, 1.07), need for assisted breathing (HR, 1.06), and ICU admission (HR, 1.07).
Following a COVID-19 infection, people were 40% more likely to receive a diagnosis of incident type 2 diabetes, compared with matched uninfected people. The authors said a possible explanation is that after diagnosis of COVID-19, infected people in general received more intensified care that led to better identification of those with underlying type 2 diabetes.
The 701 people included with pre-existing type 1 diabetes showed no significant difference in their rate of developing DKA between those infected and not infected with COVID-19.
Among the 21,830 people with pre-existing type 2 diabetes, the DKA risk was a significant 35% greater for those who were infected with COVID-19, compared with those who were uninfected. The magnitude of this increased relative risk was even higher among the patients with type 2 diabetes who used insulin as part of their treatment.
The difference in DKA risk didn’t differ between Black and White patients who were not infected with COVID-19, but among those infected by COVID-19, Black patients were more than twice as likely to be diagnosed with DKA, compared with White patients, a significant difference.
Black patients with type 2 diabetes who became infected with COVID-19 had a significant (63%) increased rate of DKA compared with Black patients with type 2 diabetes who remained uninfected.
Limitations
The study included patients with A1c measurements made up to 12 months prior to their COVID-19 test, and hence comorbid conditions, medication changes during this period, or other factors may have affected subsequent A1c levels. To address this, the authors also assessed outcomes at 3- and 6-month intervals, which produced results consistent with the 12-month findings.
The researchers did not have A1c values for many of the more than 234,000 people in the entire registry who underwent COVID-19 testing from March 2020-May 2021 at the Cleveland Clinic, omissions that may have biased the study cohort.
This was a single-center study. Some patients may have received care outside of the center, hence records of those episodes could not be included.
Disclosures
The study received no commercial funding. Four authors received consulting and speaker honoraria and research funding from AstraZeneca, Bayer, Boehringer Ingelheim, Corcept Therapeutics, Diasome, Eli Lilly, Merck, Novo Nordisk, and Sanofi. Three authors have intellectual property related to treatment decisionmaking in the context of type 2 diabetes.
This is a summary of a preprint research study “Impacts of COVID-19 on glycemia and risk of diabetic ketoacidosis,” written by researchers at the Cleveland Clinic on medRxiv. The study has not yet been peer reviewed. The full text of the study can be found on medRxiv.org.
A version of this article first appeared on Medscape.com.
Key takeaways
Results from a retrospective, observational, case-control study of more than 20,000 people from a single U.S. medical center showed a statistically significant but clinically insignificant increase in A1c in people following COVID-19 infection, in both those with and without diabetes.
After people received a diagnosis of COVID-19 infection, they were 40% more likely to also receive a diagnosis of type 2 diabetes, compared with people who tested negative for COVID-19, a difference that was significant and could be explained by the increased medical care received by people who test positive for COVID-19.
The risk of incident diabetic ketoacidosis (DKA) among people who tested positive for COVID-19 was significantly higher among those with pre-existing type 2 diabetes, those using insulin, and among Black individuals.
Why this matters
The authors said that their study is the first report of evidence that infection with COVID-19 affects A1c levels in a large, real-world clinical cohort.
Until now, the impact of COVID-19 infection on A1c remained unclear. Results from previous studies indicated that COVID-19 infection may increase A1c levels, but the studied cohorts were small and lacked uninfected controls.
The current study included 8,755 people infected with COVID-19, had data from both before and after the infection on diabetes status and A1c levels, and also included many matched, uninfected people who served as controls.
Study design
Data came from a Cleveland Clinic registry that included 81,093 people who tested positive for COVID-19 between March 2020 and May 2021 and 153,034 matched individuals who tested negative for COVID-19 during the same period.
The researchers retrospectively selected patients with an A1c recorded within 12 months before their COVID-19 test, as well as a second A1c value recorded within 12 months after COVID-19 testing. This produced a study cohort of 8,755 COVID-positive people and 11,998 matched people who tested negative for COVID-19.
To evaluate the risk of DKA onset after COVID-19 infection, the authors identified two sub-cohorts that excluded those with a history of DKA. The sub-cohorts were 701 people with type 1 diabetes and 21,830 with type 2 diabetes.
Key results
The investigators found a statistically significant but clinically insignificant A1c increase following a positive COVID-19 test, an average A1c increase of 0.06 percentage points. Those who tested negative for COVID-19 had a clinically insignificant change in their average A1c level that was of borderline statistical significance, an average increase of 0.02 percentage points (P = .05).
The statistically significant but clinically insignificant increase in A1c following infection with COVID-19 was similar in people with and without type 2 diabetes prior to infection.
In patients with type 2 diabetes who became infected with COVID-19, the researchers saw significant positive associations between higher A1c levels before infection and time to hospitalization (hazard ratio, 1.07), need for assisted breathing (HR, 1.06), and ICU admission (HR, 1.07).
Following a COVID-19 infection, people were 40% more likely to receive a diagnosis of incident type 2 diabetes, compared with matched uninfected people. The authors said a possible explanation is that after diagnosis of COVID-19, infected people in general received more intensified care that led to better identification of those with underlying type 2 diabetes.
The 701 people included with pre-existing type 1 diabetes showed no significant difference in their rate of developing DKA between those infected and not infected with COVID-19.
Among the 21,830 people with pre-existing type 2 diabetes, the DKA risk was a significant 35% greater for those who were infected with COVID-19, compared with those who were uninfected. The magnitude of this increased relative risk was even higher among the patients with type 2 diabetes who used insulin as part of their treatment.
The difference in DKA risk didn’t differ between Black and White patients who were not infected with COVID-19, but among those infected by COVID-19, Black patients were more than twice as likely to be diagnosed with DKA, compared with White patients, a significant difference.
Black patients with type 2 diabetes who became infected with COVID-19 had a significant (63%) increased rate of DKA compared with Black patients with type 2 diabetes who remained uninfected.
Limitations
The study included patients with A1c measurements made up to 12 months prior to their COVID-19 test, and hence comorbid conditions, medication changes during this period, or other factors may have affected subsequent A1c levels. To address this, the authors also assessed outcomes at 3- and 6-month intervals, which produced results consistent with the 12-month findings.
The researchers did not have A1c values for many of the more than 234,000 people in the entire registry who underwent COVID-19 testing from March 2020-May 2021 at the Cleveland Clinic, omissions that may have biased the study cohort.
This was a single-center study. Some patients may have received care outside of the center, hence records of those episodes could not be included.
Disclosures
The study received no commercial funding. Four authors received consulting and speaker honoraria and research funding from AstraZeneca, Bayer, Boehringer Ingelheim, Corcept Therapeutics, Diasome, Eli Lilly, Merck, Novo Nordisk, and Sanofi. Three authors have intellectual property related to treatment decisionmaking in the context of type 2 diabetes.
This is a summary of a preprint research study “Impacts of COVID-19 on glycemia and risk of diabetic ketoacidosis,” written by researchers at the Cleveland Clinic on medRxiv. The study has not yet been peer reviewed. The full text of the study can be found on medRxiv.org.
A version of this article first appeared on Medscape.com.
Yes, Russian docs should be shut out of medical associations, says ethicist
This transcript has been edited for clarity.
Hi. I’m Art Caplan. I’m at the division of medical ethics at the NYU Grossman School of Medicine.
There are many difficult moral issues that are being fueled by the terrible war that Russia is waging against Ukraine. I think there is no way to justify anything that the Russians are doing. Ukraine did not do anything to violate Russian integrity, Russian territorial integrity, or anything by way of being aggressive toward Russia.
Russia decided at some point it wanted the Ukraine back. Putin has a dream, as the long-standing leader of Russia, to restore the Soviet empire, and Ukraine is top of the list of the places that he wants back for a variety of reasons.
We’re not here to debate the merits and demerits of this terrible act of war.
The European Society of Cardiology made a decision very recently to drop, as members, both Russia and Belarus, Russia’s ally in this aggressive war against Ukraine. They basically found it intolerable to have business as usual with these subsidiary cardiology societies as part of the ongoing activities of the European group.
The sole goal of this overarching European group is to reduce the health burden of cardiovascular disease. It doesn’t have political goals. It doesn’t have much to say about anything other than, “Let’s get evidence-based medicine used to try and prevent heart disease or treat heart disease.” So there’s noble intent.
Many of its members asked, “What are we doing in politics? Why are we punishing Russian and Belarussian cardiologists, acting as if somehow they are responsible for what the Russian army is doing or for what Putin has decided to do? Why are we acting against them? They are just trying to fight heart disease. That’s a legitimate goal for any doctor, public health official, or scientist.” They didn’t see, as members, why this exclusion had taken place.
I believe the exclusion is appropriate and some of the membership, obviously, in the European Society of Cardiology, agrees. It’s not because they’re holding doctors or scientists directly accountable for Putin’s war crimes, ethnic cleansing assault, or bombing and shelling of hospitals, maternity hospitals, and civilians.
They understand that these scientists and doctors have little to do with such things, but we are in a new form of warfare, and that warfare is basically economic and sociologic: turning Russia, as an inexcusably aggressive state, into a pariah.
The reason to break the ties is that that is the way to bring pressure upon Putin and his kleptocratic, oligarchic advisers to stop the attack, to try and bring down their economy, to say, “Business is not going to go on as usual. You will be excluded from normal scientific and medical commerce. We’re not going to be holding conferences or exchanging ideas,” and in my view, extending it to say, “We’re not taking your papers, we’re not publishing anything you do. We’re not even having you speak at our meetings until this war, this aggressive invasion, and these war crimes come to a halt.”
There is actually a basis for this action. It isn’t in the organization’s own bylaws, which as I said, are very simple — reduce cardiovascular disease burden — but they are a member of a broader group, the Biomedical Alliance in Europe, which does have a very explicit code of ethics.
I’m going to read you a little bit from that code. It says healthcare organizations should uphold and promote equality, diversity and inclusion, accountability, transparency, and equality. They also say that all members, including the European Society of Cardiology, should be committed both to the Declaration of Helsinki, a fundamental medical ethics document, and the Declaration of Geneva. These rules refer to the highest respect of human beings, responsible resource allocation, and preservation of the environment, among other things.
What the organization is doing is consistent with the code of ethics that the broader organization of all the medical societies of Europe say that these individual groups should be doing. You can’t collaborate with war criminals. You can’t act as if business as usual is going on. That’s not inclusive. That’s not respect for diversity.
I think the Ukrainian medical societies of cardiology and other specialties would find it grimly ironic to say that keeping Russian and Belarus members makes sense, given what’s going on in their country and what is happening to them. They’re under attack. They’re being killed. Their healthcare institutions are being indiscriminately shelled and bombed.
It’s very hard — and I understand that — to say we’re going to punish scientists. We’re going to, perhaps, even cause public health problems in Russia because we’re not going to collaborate right now with doctors and scientists in cardiology or any other medical specialty. I think it’s what has to be done.
We’re in a new era of trying to combat what is basically organized, international ethnic terrorism, complete with war crimes. We fight financially. We fight by isolating. We fight by excluding. It’s painful. It’s difficult. It’s somewhat unfair to individuals.
Only through that kind of pain are we going to get the kind of pressure that will achieve justice. I think that is a goal that we have to commend the European Society of Cardiology for honoring.
Dr. Caplan is director of the division of medical ethics at New York University. He is the author or editor of 35 books and 750 peer-reviewed articles as well as a frequent commentator in the media on bioethical issues. He has served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (an unpaid position), and is a contributing author and adviser for Medscape. A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Hi. I’m Art Caplan. I’m at the division of medical ethics at the NYU Grossman School of Medicine.
There are many difficult moral issues that are being fueled by the terrible war that Russia is waging against Ukraine. I think there is no way to justify anything that the Russians are doing. Ukraine did not do anything to violate Russian integrity, Russian territorial integrity, or anything by way of being aggressive toward Russia.
Russia decided at some point it wanted the Ukraine back. Putin has a dream, as the long-standing leader of Russia, to restore the Soviet empire, and Ukraine is top of the list of the places that he wants back for a variety of reasons.
We’re not here to debate the merits and demerits of this terrible act of war.
The European Society of Cardiology made a decision very recently to drop, as members, both Russia and Belarus, Russia’s ally in this aggressive war against Ukraine. They basically found it intolerable to have business as usual with these subsidiary cardiology societies as part of the ongoing activities of the European group.
The sole goal of this overarching European group is to reduce the health burden of cardiovascular disease. It doesn’t have political goals. It doesn’t have much to say about anything other than, “Let’s get evidence-based medicine used to try and prevent heart disease or treat heart disease.” So there’s noble intent.
Many of its members asked, “What are we doing in politics? Why are we punishing Russian and Belarussian cardiologists, acting as if somehow they are responsible for what the Russian army is doing or for what Putin has decided to do? Why are we acting against them? They are just trying to fight heart disease. That’s a legitimate goal for any doctor, public health official, or scientist.” They didn’t see, as members, why this exclusion had taken place.
I believe the exclusion is appropriate and some of the membership, obviously, in the European Society of Cardiology, agrees. It’s not because they’re holding doctors or scientists directly accountable for Putin’s war crimes, ethnic cleansing assault, or bombing and shelling of hospitals, maternity hospitals, and civilians.
They understand that these scientists and doctors have little to do with such things, but we are in a new form of warfare, and that warfare is basically economic and sociologic: turning Russia, as an inexcusably aggressive state, into a pariah.
The reason to break the ties is that that is the way to bring pressure upon Putin and his kleptocratic, oligarchic advisers to stop the attack, to try and bring down their economy, to say, “Business is not going to go on as usual. You will be excluded from normal scientific and medical commerce. We’re not going to be holding conferences or exchanging ideas,” and in my view, extending it to say, “We’re not taking your papers, we’re not publishing anything you do. We’re not even having you speak at our meetings until this war, this aggressive invasion, and these war crimes come to a halt.”
There is actually a basis for this action. It isn’t in the organization’s own bylaws, which as I said, are very simple — reduce cardiovascular disease burden — but they are a member of a broader group, the Biomedical Alliance in Europe, which does have a very explicit code of ethics.
I’m going to read you a little bit from that code. It says healthcare organizations should uphold and promote equality, diversity and inclusion, accountability, transparency, and equality. They also say that all members, including the European Society of Cardiology, should be committed both to the Declaration of Helsinki, a fundamental medical ethics document, and the Declaration of Geneva. These rules refer to the highest respect of human beings, responsible resource allocation, and preservation of the environment, among other things.
What the organization is doing is consistent with the code of ethics that the broader organization of all the medical societies of Europe say that these individual groups should be doing. You can’t collaborate with war criminals. You can’t act as if business as usual is going on. That’s not inclusive. That’s not respect for diversity.
I think the Ukrainian medical societies of cardiology and other specialties would find it grimly ironic to say that keeping Russian and Belarus members makes sense, given what’s going on in their country and what is happening to them. They’re under attack. They’re being killed. Their healthcare institutions are being indiscriminately shelled and bombed.
It’s very hard — and I understand that — to say we’re going to punish scientists. We’re going to, perhaps, even cause public health problems in Russia because we’re not going to collaborate right now with doctors and scientists in cardiology or any other medical specialty. I think it’s what has to be done.
We’re in a new era of trying to combat what is basically organized, international ethnic terrorism, complete with war crimes. We fight financially. We fight by isolating. We fight by excluding. It’s painful. It’s difficult. It’s somewhat unfair to individuals.
Only through that kind of pain are we going to get the kind of pressure that will achieve justice. I think that is a goal that we have to commend the European Society of Cardiology for honoring.
Dr. Caplan is director of the division of medical ethics at New York University. He is the author or editor of 35 books and 750 peer-reviewed articles as well as a frequent commentator in the media on bioethical issues. He has served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (an unpaid position), and is a contributing author and adviser for Medscape. A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Hi. I’m Art Caplan. I’m at the division of medical ethics at the NYU Grossman School of Medicine.
There are many difficult moral issues that are being fueled by the terrible war that Russia is waging against Ukraine. I think there is no way to justify anything that the Russians are doing. Ukraine did not do anything to violate Russian integrity, Russian territorial integrity, or anything by way of being aggressive toward Russia.
Russia decided at some point it wanted the Ukraine back. Putin has a dream, as the long-standing leader of Russia, to restore the Soviet empire, and Ukraine is top of the list of the places that he wants back for a variety of reasons.
We’re not here to debate the merits and demerits of this terrible act of war.
The European Society of Cardiology made a decision very recently to drop, as members, both Russia and Belarus, Russia’s ally in this aggressive war against Ukraine. They basically found it intolerable to have business as usual with these subsidiary cardiology societies as part of the ongoing activities of the European group.
The sole goal of this overarching European group is to reduce the health burden of cardiovascular disease. It doesn’t have political goals. It doesn’t have much to say about anything other than, “Let’s get evidence-based medicine used to try and prevent heart disease or treat heart disease.” So there’s noble intent.
Many of its members asked, “What are we doing in politics? Why are we punishing Russian and Belarussian cardiologists, acting as if somehow they are responsible for what the Russian army is doing or for what Putin has decided to do? Why are we acting against them? They are just trying to fight heart disease. That’s a legitimate goal for any doctor, public health official, or scientist.” They didn’t see, as members, why this exclusion had taken place.
I believe the exclusion is appropriate and some of the membership, obviously, in the European Society of Cardiology, agrees. It’s not because they’re holding doctors or scientists directly accountable for Putin’s war crimes, ethnic cleansing assault, or bombing and shelling of hospitals, maternity hospitals, and civilians.
They understand that these scientists and doctors have little to do with such things, but we are in a new form of warfare, and that warfare is basically economic and sociologic: turning Russia, as an inexcusably aggressive state, into a pariah.
The reason to break the ties is that that is the way to bring pressure upon Putin and his kleptocratic, oligarchic advisers to stop the attack, to try and bring down their economy, to say, “Business is not going to go on as usual. You will be excluded from normal scientific and medical commerce. We’re not going to be holding conferences or exchanging ideas,” and in my view, extending it to say, “We’re not taking your papers, we’re not publishing anything you do. We’re not even having you speak at our meetings until this war, this aggressive invasion, and these war crimes come to a halt.”
There is actually a basis for this action. It isn’t in the organization’s own bylaws, which as I said, are very simple — reduce cardiovascular disease burden — but they are a member of a broader group, the Biomedical Alliance in Europe, which does have a very explicit code of ethics.
I’m going to read you a little bit from that code. It says healthcare organizations should uphold and promote equality, diversity and inclusion, accountability, transparency, and equality. They also say that all members, including the European Society of Cardiology, should be committed both to the Declaration of Helsinki, a fundamental medical ethics document, and the Declaration of Geneva. These rules refer to the highest respect of human beings, responsible resource allocation, and preservation of the environment, among other things.
What the organization is doing is consistent with the code of ethics that the broader organization of all the medical societies of Europe say that these individual groups should be doing. You can’t collaborate with war criminals. You can’t act as if business as usual is going on. That’s not inclusive. That’s not respect for diversity.
I think the Ukrainian medical societies of cardiology and other specialties would find it grimly ironic to say that keeping Russian and Belarus members makes sense, given what’s going on in their country and what is happening to them. They’re under attack. They’re being killed. Their healthcare institutions are being indiscriminately shelled and bombed.
It’s very hard — and I understand that — to say we’re going to punish scientists. We’re going to, perhaps, even cause public health problems in Russia because we’re not going to collaborate right now with doctors and scientists in cardiology or any other medical specialty. I think it’s what has to be done.
We’re in a new era of trying to combat what is basically organized, international ethnic terrorism, complete with war crimes. We fight financially. We fight by isolating. We fight by excluding. It’s painful. It’s difficult. It’s somewhat unfair to individuals.
Only through that kind of pain are we going to get the kind of pressure that will achieve justice. I think that is a goal that we have to commend the European Society of Cardiology for honoring.
Dr. Caplan is director of the division of medical ethics at New York University. He is the author or editor of 35 books and 750 peer-reviewed articles as well as a frequent commentator in the media on bioethical issues. He has served as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (an unpaid position), and is a contributing author and adviser for Medscape. A version of this article first appeared on Medscape.com.
‘It’s about transparency’: Indiana law prohibits misleading medical titles
While several health care professionals can perform some of the same functions as physicians, at the end of the day, they are not MDs or DOs, nor do they have the education and training to earn the right to present themselves to patients as such. That’s the reasoning behind Senate Bill 239, recently signed into law by Indiana Gov. Eric J. Holcomb.
“It’s about transparency. Health care professionals at every level should be proud of their profession and want to help patients make an informed choice when seeking out options for treatment,” Carrie Davis, MD, a Bloomington, Ind.–based dermatologist and member of the Indiana State Medical Association’s commission on legislation, told this news organization. “When this law goes into effect, a patient will be able to seek that treatment with confidence knowing they can trust the education, training, and license of the health care expert they’ve chosen to see.”
such as anesthesiologist, cardiologist, dermatologist, and others by professionals who have not graduated from medical school and completed the necessary training to adopt the physician title. It also prohibits health care professionals from using deceptive or misleading advertising that misrepresents or falsely describes their profession, education, or skills.
“Using the medical term ‘anesthesiologist’ for nurse anesthetists, confuses patients who deserve to be fully informed of their health care provider’s qualifications,” Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA), said in a statement. “This new law affirms the most fundamental right of patients to know the qualifications of their health care professional.”
What’s in a title?
The problem stretches far beyond professional turf battles, as patients are often confused about the differences between various types of health care providers, according to the American Medical Association’s Truth in Advertising Campaign. Often, patients mistakenly believe they are meeting with medical doctors or doctors of osteopathic medicine when they are not.
Seung Sim, MD, an Indiana anesthesiologist and the immediate past president of the Indiana Society of Anesthesiologists, said in an interview that every member of the medical team plays an important role in high-quality patient care, but among that team, education and training differs.
“The threat to patient safety comes by nonphysicians marketing themselves in a way that is confusing to patients, and misleading, making the patient believe they’re seeing a physician when they’re not,” said Dr. Sim. “That patient deserves to know who is providing their health care and what level of education and training they have, so the patient can make the best decision for their treatment.”
Medical groups speak out
Several professional medical groups have voiced their opposition to medical title misappropriation.
Perhaps most notably, the ASA has been spearheading efforts that prohibit medical professionals to identify as physicians for several years. In 2019, the ASA authored Resolution 228, which calls on the AMA to oppose and work with state medical societies to prevent the misappropriation of medical specialties’ titles.
The resolution, which was adopted by the AMA in June 2019, also reaffirms support of the Scope of Practice Partnership’s Truth in Advertising Campaign to ensure patients receive accurate information about who is providing their care.
In addition, in 2021, the ASA condemned the decision by the American Association of Nurse Anesthetists to change its name to the American Association of Nurse Anesthesiology (AANA) – pointing out that the term “nurse anesthesiologist” could confuse patients and create discord in the care setting, ultimately risking patient safety.
While the ASA and other professional groups support team-based models of care, they are quick to point out that health care professionals need to know their place in the lineup.
A statement from the American Osteopathic Association (AOA), for instance, points out that only DOs and MDs can be licensed to practice medicine – and, therefore, “physician-led” should not mean “physician-optional.” In fact, only professionals who have earned the right to practice medicine through completion of medical school and accredited residency/fellowship training and who have achieved board certification in their chosen specialty/subspecialty should take the helm of these multidisciplinary teams, according to the AOA.
The AANA cast the controversy in a completely different light, characterizing its name change as part of a rebranding effort to advance the science of nurse anesthesiology and advocate for certified registered nurse anesthetists. In 2021, the AANA asserted: “The notion of being pushed by the American Society of Anesthesiologists that rebranding and changing the name of the AANA will somehow mislead or harm patients or create discord among providers is absurd at best and false and inflammatory fearmongering at worst.”
A version of this article first appeared on Medscape.com.
While several health care professionals can perform some of the same functions as physicians, at the end of the day, they are not MDs or DOs, nor do they have the education and training to earn the right to present themselves to patients as such. That’s the reasoning behind Senate Bill 239, recently signed into law by Indiana Gov. Eric J. Holcomb.
“It’s about transparency. Health care professionals at every level should be proud of their profession and want to help patients make an informed choice when seeking out options for treatment,” Carrie Davis, MD, a Bloomington, Ind.–based dermatologist and member of the Indiana State Medical Association’s commission on legislation, told this news organization. “When this law goes into effect, a patient will be able to seek that treatment with confidence knowing they can trust the education, training, and license of the health care expert they’ve chosen to see.”
such as anesthesiologist, cardiologist, dermatologist, and others by professionals who have not graduated from medical school and completed the necessary training to adopt the physician title. It also prohibits health care professionals from using deceptive or misleading advertising that misrepresents or falsely describes their profession, education, or skills.
“Using the medical term ‘anesthesiologist’ for nurse anesthetists, confuses patients who deserve to be fully informed of their health care provider’s qualifications,” Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA), said in a statement. “This new law affirms the most fundamental right of patients to know the qualifications of their health care professional.”
What’s in a title?
The problem stretches far beyond professional turf battles, as patients are often confused about the differences between various types of health care providers, according to the American Medical Association’s Truth in Advertising Campaign. Often, patients mistakenly believe they are meeting with medical doctors or doctors of osteopathic medicine when they are not.
Seung Sim, MD, an Indiana anesthesiologist and the immediate past president of the Indiana Society of Anesthesiologists, said in an interview that every member of the medical team plays an important role in high-quality patient care, but among that team, education and training differs.
“The threat to patient safety comes by nonphysicians marketing themselves in a way that is confusing to patients, and misleading, making the patient believe they’re seeing a physician when they’re not,” said Dr. Sim. “That patient deserves to know who is providing their health care and what level of education and training they have, so the patient can make the best decision for their treatment.”
Medical groups speak out
Several professional medical groups have voiced their opposition to medical title misappropriation.
Perhaps most notably, the ASA has been spearheading efforts that prohibit medical professionals to identify as physicians for several years. In 2019, the ASA authored Resolution 228, which calls on the AMA to oppose and work with state medical societies to prevent the misappropriation of medical specialties’ titles.
The resolution, which was adopted by the AMA in June 2019, also reaffirms support of the Scope of Practice Partnership’s Truth in Advertising Campaign to ensure patients receive accurate information about who is providing their care.
In addition, in 2021, the ASA condemned the decision by the American Association of Nurse Anesthetists to change its name to the American Association of Nurse Anesthesiology (AANA) – pointing out that the term “nurse anesthesiologist” could confuse patients and create discord in the care setting, ultimately risking patient safety.
While the ASA and other professional groups support team-based models of care, they are quick to point out that health care professionals need to know their place in the lineup.
A statement from the American Osteopathic Association (AOA), for instance, points out that only DOs and MDs can be licensed to practice medicine – and, therefore, “physician-led” should not mean “physician-optional.” In fact, only professionals who have earned the right to practice medicine through completion of medical school and accredited residency/fellowship training and who have achieved board certification in their chosen specialty/subspecialty should take the helm of these multidisciplinary teams, according to the AOA.
The AANA cast the controversy in a completely different light, characterizing its name change as part of a rebranding effort to advance the science of nurse anesthesiology and advocate for certified registered nurse anesthetists. In 2021, the AANA asserted: “The notion of being pushed by the American Society of Anesthesiologists that rebranding and changing the name of the AANA will somehow mislead or harm patients or create discord among providers is absurd at best and false and inflammatory fearmongering at worst.”
A version of this article first appeared on Medscape.com.
While several health care professionals can perform some of the same functions as physicians, at the end of the day, they are not MDs or DOs, nor do they have the education and training to earn the right to present themselves to patients as such. That’s the reasoning behind Senate Bill 239, recently signed into law by Indiana Gov. Eric J. Holcomb.
“It’s about transparency. Health care professionals at every level should be proud of their profession and want to help patients make an informed choice when seeking out options for treatment,” Carrie Davis, MD, a Bloomington, Ind.–based dermatologist and member of the Indiana State Medical Association’s commission on legislation, told this news organization. “When this law goes into effect, a patient will be able to seek that treatment with confidence knowing they can trust the education, training, and license of the health care expert they’ve chosen to see.”
such as anesthesiologist, cardiologist, dermatologist, and others by professionals who have not graduated from medical school and completed the necessary training to adopt the physician title. It also prohibits health care professionals from using deceptive or misleading advertising that misrepresents or falsely describes their profession, education, or skills.
“Using the medical term ‘anesthesiologist’ for nurse anesthetists, confuses patients who deserve to be fully informed of their health care provider’s qualifications,” Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA), said in a statement. “This new law affirms the most fundamental right of patients to know the qualifications of their health care professional.”
What’s in a title?
The problem stretches far beyond professional turf battles, as patients are often confused about the differences between various types of health care providers, according to the American Medical Association’s Truth in Advertising Campaign. Often, patients mistakenly believe they are meeting with medical doctors or doctors of osteopathic medicine when they are not.
Seung Sim, MD, an Indiana anesthesiologist and the immediate past president of the Indiana Society of Anesthesiologists, said in an interview that every member of the medical team plays an important role in high-quality patient care, but among that team, education and training differs.
“The threat to patient safety comes by nonphysicians marketing themselves in a way that is confusing to patients, and misleading, making the patient believe they’re seeing a physician when they’re not,” said Dr. Sim. “That patient deserves to know who is providing their health care and what level of education and training they have, so the patient can make the best decision for their treatment.”
Medical groups speak out
Several professional medical groups have voiced their opposition to medical title misappropriation.
Perhaps most notably, the ASA has been spearheading efforts that prohibit medical professionals to identify as physicians for several years. In 2019, the ASA authored Resolution 228, which calls on the AMA to oppose and work with state medical societies to prevent the misappropriation of medical specialties’ titles.
The resolution, which was adopted by the AMA in June 2019, also reaffirms support of the Scope of Practice Partnership’s Truth in Advertising Campaign to ensure patients receive accurate information about who is providing their care.
In addition, in 2021, the ASA condemned the decision by the American Association of Nurse Anesthetists to change its name to the American Association of Nurse Anesthesiology (AANA) – pointing out that the term “nurse anesthesiologist” could confuse patients and create discord in the care setting, ultimately risking patient safety.
While the ASA and other professional groups support team-based models of care, they are quick to point out that health care professionals need to know their place in the lineup.
A statement from the American Osteopathic Association (AOA), for instance, points out that only DOs and MDs can be licensed to practice medicine – and, therefore, “physician-led” should not mean “physician-optional.” In fact, only professionals who have earned the right to practice medicine through completion of medical school and accredited residency/fellowship training and who have achieved board certification in their chosen specialty/subspecialty should take the helm of these multidisciplinary teams, according to the AOA.
The AANA cast the controversy in a completely different light, characterizing its name change as part of a rebranding effort to advance the science of nurse anesthesiology and advocate for certified registered nurse anesthetists. In 2021, the AANA asserted: “The notion of being pushed by the American Society of Anesthesiologists that rebranding and changing the name of the AANA will somehow mislead or harm patients or create discord among providers is absurd at best and false and inflammatory fearmongering at worst.”
A version of this article first appeared on Medscape.com.
U.S. health officials tracking COVID-19 increase in U.K.
according to NPR.
Daily cases counts have increased 38% in the past week, according to the latest data from the U.K. Health Security Agency. Hospitalizations are up about 25% as well.
“Over the last year or so, what happens in the U.K. usually happens here a few weeks later,” Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, told NPR.
“And right now, the U.K. is seeing somewhat of a rebound in cases,” he said.
Health officials in the United Kingdom have noted the latest increase is likely due to the contagious BA.2 Omicron subvariant, the recent loosening of coronavirus restrictions, and waning immunity from vaccinations and infections.
“All three of those factors we have here in the United States,” Dr. Fauci said. “So I would not be surprised if, in the next few weeks, we see either a plateauing … of cases or even [the curve] rebounds and slightly goes up.”
Right now, COVID-19 cases in the United Stastes have dropped to their lowest levels since July 2021, according to the latest Centers for Disease Control and Prevention data, with fewer than 30,000 daily cases. At the same time, the rate of decline in cases has slowed significantly and is beginning to plateau.
Public health experts are also pointing to wastewater surveillance data that shows an uptick in viral activity across the country. The CDC’s wastewater dashboard indicates that about 35% of sites that monitor wastewater are seeing an increase, with consistent growth in Florida, Rhode Island, and West Virginia.
“The power of wastewater surveillance is that it’s an early warning system,” Amy Kirby, the program lead for the CDC’s National Wastewater Surveillance System, told NPR.
“We are seeing evidence of increases in some communities across the country,” she said. “What looked like noise at the beginning of the week is starting to look like a true signal here at the end of the week.”
The wastewater system doesn’t distinguish between Omicron and subvariants such as BA.2. However, other CDC data has found an increase in BA.2 cases in the United States, making up about a quarter of new COVID-19 cases.
The BA.2 variant has roughly doubled each week for the last month, which means it could become the dominant coronavirus strain in the United States in coming weeks, according to USA Today. Cases appear to be spreading more quickly in the Northeast and West, making up about 39% of cases in New York and New Jersey last week.
BA.2 also accounts for nearly 39% of cases across the Northeast, including Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island and Vermont, USA Today reported. In the West, which includes Arizona, California and Nevada, the subvariant makes up about 28% of new cases. In the upper West, which includes Alaska, Oregon and Washington, about 26% of cases are BA.2.
The good news is that BA.2 “doesn’t seem to evade our vaccines or immunity any more than the prior Omicron [variant]. And it doesn’t seem to lead to any more increased severity of disease,” Rochelle Walensky, MD, the CDC director, told NPR’s Morning Edition on March 18.
The effects of BA.2 will likely depend on the immunity profile in the United States, including how long it’s been since someone was vaccinated, boosted, or recovered from an infection, she said.
Health officials are watching other countries with BA.2 increases, such as Germany, Italy, and the Netherlands. Many European countries have been reporting an uptick but not implementing major restrictions or shutdowns, USA Today reported.
The BA.2 variant likely won’t lead to a major surge in severe disease or strict COVID-19 measures, Dr. Fauci told NPR, but some coronavirus protocols may need to be implemented again if cases grow dramatically.
“We must be ready to pivot and, if necessary, to go back to stricter mitigation with regard to masks,” he said.
A version of this article first appeared on WebMD.com.
according to NPR.
Daily cases counts have increased 38% in the past week, according to the latest data from the U.K. Health Security Agency. Hospitalizations are up about 25% as well.
“Over the last year or so, what happens in the U.K. usually happens here a few weeks later,” Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, told NPR.
“And right now, the U.K. is seeing somewhat of a rebound in cases,” he said.
Health officials in the United Kingdom have noted the latest increase is likely due to the contagious BA.2 Omicron subvariant, the recent loosening of coronavirus restrictions, and waning immunity from vaccinations and infections.
“All three of those factors we have here in the United States,” Dr. Fauci said. “So I would not be surprised if, in the next few weeks, we see either a plateauing … of cases or even [the curve] rebounds and slightly goes up.”
Right now, COVID-19 cases in the United Stastes have dropped to their lowest levels since July 2021, according to the latest Centers for Disease Control and Prevention data, with fewer than 30,000 daily cases. At the same time, the rate of decline in cases has slowed significantly and is beginning to plateau.
Public health experts are also pointing to wastewater surveillance data that shows an uptick in viral activity across the country. The CDC’s wastewater dashboard indicates that about 35% of sites that monitor wastewater are seeing an increase, with consistent growth in Florida, Rhode Island, and West Virginia.
“The power of wastewater surveillance is that it’s an early warning system,” Amy Kirby, the program lead for the CDC’s National Wastewater Surveillance System, told NPR.
“We are seeing evidence of increases in some communities across the country,” she said. “What looked like noise at the beginning of the week is starting to look like a true signal here at the end of the week.”
The wastewater system doesn’t distinguish between Omicron and subvariants such as BA.2. However, other CDC data has found an increase in BA.2 cases in the United States, making up about a quarter of new COVID-19 cases.
The BA.2 variant has roughly doubled each week for the last month, which means it could become the dominant coronavirus strain in the United States in coming weeks, according to USA Today. Cases appear to be spreading more quickly in the Northeast and West, making up about 39% of cases in New York and New Jersey last week.
BA.2 also accounts for nearly 39% of cases across the Northeast, including Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island and Vermont, USA Today reported. In the West, which includes Arizona, California and Nevada, the subvariant makes up about 28% of new cases. In the upper West, which includes Alaska, Oregon and Washington, about 26% of cases are BA.2.
The good news is that BA.2 “doesn’t seem to evade our vaccines or immunity any more than the prior Omicron [variant]. And it doesn’t seem to lead to any more increased severity of disease,” Rochelle Walensky, MD, the CDC director, told NPR’s Morning Edition on March 18.
The effects of BA.2 will likely depend on the immunity profile in the United States, including how long it’s been since someone was vaccinated, boosted, or recovered from an infection, she said.
Health officials are watching other countries with BA.2 increases, such as Germany, Italy, and the Netherlands. Many European countries have been reporting an uptick but not implementing major restrictions or shutdowns, USA Today reported.
The BA.2 variant likely won’t lead to a major surge in severe disease or strict COVID-19 measures, Dr. Fauci told NPR, but some coronavirus protocols may need to be implemented again if cases grow dramatically.
“We must be ready to pivot and, if necessary, to go back to stricter mitigation with regard to masks,” he said.
A version of this article first appeared on WebMD.com.
according to NPR.
Daily cases counts have increased 38% in the past week, according to the latest data from the U.K. Health Security Agency. Hospitalizations are up about 25% as well.
“Over the last year or so, what happens in the U.K. usually happens here a few weeks later,” Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, told NPR.
“And right now, the U.K. is seeing somewhat of a rebound in cases,” he said.
Health officials in the United Kingdom have noted the latest increase is likely due to the contagious BA.2 Omicron subvariant, the recent loosening of coronavirus restrictions, and waning immunity from vaccinations and infections.
“All three of those factors we have here in the United States,” Dr. Fauci said. “So I would not be surprised if, in the next few weeks, we see either a plateauing … of cases or even [the curve] rebounds and slightly goes up.”
Right now, COVID-19 cases in the United Stastes have dropped to their lowest levels since July 2021, according to the latest Centers for Disease Control and Prevention data, with fewer than 30,000 daily cases. At the same time, the rate of decline in cases has slowed significantly and is beginning to plateau.
Public health experts are also pointing to wastewater surveillance data that shows an uptick in viral activity across the country. The CDC’s wastewater dashboard indicates that about 35% of sites that monitor wastewater are seeing an increase, with consistent growth in Florida, Rhode Island, and West Virginia.
“The power of wastewater surveillance is that it’s an early warning system,” Amy Kirby, the program lead for the CDC’s National Wastewater Surveillance System, told NPR.
“We are seeing evidence of increases in some communities across the country,” she said. “What looked like noise at the beginning of the week is starting to look like a true signal here at the end of the week.”
The wastewater system doesn’t distinguish between Omicron and subvariants such as BA.2. However, other CDC data has found an increase in BA.2 cases in the United States, making up about a quarter of new COVID-19 cases.
The BA.2 variant has roughly doubled each week for the last month, which means it could become the dominant coronavirus strain in the United States in coming weeks, according to USA Today. Cases appear to be spreading more quickly in the Northeast and West, making up about 39% of cases in New York and New Jersey last week.
BA.2 also accounts for nearly 39% of cases across the Northeast, including Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island and Vermont, USA Today reported. In the West, which includes Arizona, California and Nevada, the subvariant makes up about 28% of new cases. In the upper West, which includes Alaska, Oregon and Washington, about 26% of cases are BA.2.
The good news is that BA.2 “doesn’t seem to evade our vaccines or immunity any more than the prior Omicron [variant]. And it doesn’t seem to lead to any more increased severity of disease,” Rochelle Walensky, MD, the CDC director, told NPR’s Morning Edition on March 18.
The effects of BA.2 will likely depend on the immunity profile in the United States, including how long it’s been since someone was vaccinated, boosted, or recovered from an infection, she said.
Health officials are watching other countries with BA.2 increases, such as Germany, Italy, and the Netherlands. Many European countries have been reporting an uptick but not implementing major restrictions or shutdowns, USA Today reported.
The BA.2 variant likely won’t lead to a major surge in severe disease or strict COVID-19 measures, Dr. Fauci told NPR, but some coronavirus protocols may need to be implemented again if cases grow dramatically.
“We must be ready to pivot and, if necessary, to go back to stricter mitigation with regard to masks,” he said.
A version of this article first appeared on WebMD.com.
New test for Lp(a) allows more accurate LDL-cholesterol results
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
Walking 10,000 steps a day: Desirable goal or urban myth?
Some myths never die. The idea of taking 10,000 steps a day is one of them. What started as a catchy marketing slogan has become a mantra for anyone promoting physical activity.
It all began in 1965 when the Japanese company Yamasa Tokei began selling a new step-counter which they called manpo-kei (ten-thousand steps meter). They coupled the product launch with an ad campaign – “Let’s walk 10,000 steps a day!” – in a bid to encourage physical activity. The threshold was always somewhat arbitrary, but the idea of 10,000 steps cemented itself in the public consciousness from that point forward.
To be fair, there is nothing wrong with taking 10,000 steps a day, and it does roughly correlate with the generally recommended amount of physical activity. Most people will take somewhere between 5,000 and 7,500 steps a day even if they lead largely sedentary lives. If you add 30 minutes of walking to your daily routine, that will account for an extra 3,000-4,000 steps and bring you close to that 10,000-step threshold. As such, setting a 10,000-step target is a potentially useful shorthand for people aspiring to achieve ideal levels of physical activity.
But walking fewer steps still has a benefit. A study in JAMA Network Open followed a cohort of 2,110 adults from the CARDIA study and found, rather unsurprisingly, that those with more steps per day had lower rates of all-cause mortality. But interestingly, those who averaged 7,000-10,000 steps per day did just as well as those who walked more than 10,000 steps, suggesting that the lower threshold was probably the inflection point.
Other research has shown that improving your step count is probably more important than achieving any specific threshold. In one Canadian study, patients with diabetes were randomized to usual care or to an exercise prescription from their physicians. The intervention group improved their daily step count from around 5,000 steps per day to about 6,200 steps per day. While the increase was less than the researchers had hoped for, it still resulted in improvements in blood sugar control. In another study, a 24-week walking program reduced blood pressure by 11 points in postmenopausal women, even though their increased daily step counts fell shy of the 10,000 goal at about 9,000 steps. Similarly, a small Japanese study found that enrolling postmenopausal women in a weekly exercise program helped improve their lipid profile even though they only increased their daily step count from 6,800 to 8,500 steps per day. And an analysis of U.S. NHANES data showed a mortality benefit when individuals taking more than 8,000 steps were compared with those taking fewer than 4,000 steps per day. The benefits largely plateaued beyond 9,000-10,000 steps.
The reality is that walking 10,000 steps a day is a laudable goal and is almost certainly beneficial. But even lower levels of physical activity have benefits. The trick is not so much to aim for some theoretical ideal but to improve upon your current baseline. Encouraging patients to get into the habit of taking a daily walk (be it in the morning, during lunchtime, or in the evening) is going to pay dividends regardless of their daily step count. The point is that when it comes to physical activity, the greatest benefit seems to be when we go from doing nothing to doing something.
Dr. Labos is a cardiologist at Queen Elizabeth Health Complex, Montreal. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Some myths never die. The idea of taking 10,000 steps a day is one of them. What started as a catchy marketing slogan has become a mantra for anyone promoting physical activity.
It all began in 1965 when the Japanese company Yamasa Tokei began selling a new step-counter which they called manpo-kei (ten-thousand steps meter). They coupled the product launch with an ad campaign – “Let’s walk 10,000 steps a day!” – in a bid to encourage physical activity. The threshold was always somewhat arbitrary, but the idea of 10,000 steps cemented itself in the public consciousness from that point forward.
To be fair, there is nothing wrong with taking 10,000 steps a day, and it does roughly correlate with the generally recommended amount of physical activity. Most people will take somewhere between 5,000 and 7,500 steps a day even if they lead largely sedentary lives. If you add 30 minutes of walking to your daily routine, that will account for an extra 3,000-4,000 steps and bring you close to that 10,000-step threshold. As such, setting a 10,000-step target is a potentially useful shorthand for people aspiring to achieve ideal levels of physical activity.
But walking fewer steps still has a benefit. A study in JAMA Network Open followed a cohort of 2,110 adults from the CARDIA study and found, rather unsurprisingly, that those with more steps per day had lower rates of all-cause mortality. But interestingly, those who averaged 7,000-10,000 steps per day did just as well as those who walked more than 10,000 steps, suggesting that the lower threshold was probably the inflection point.
Other research has shown that improving your step count is probably more important than achieving any specific threshold. In one Canadian study, patients with diabetes were randomized to usual care or to an exercise prescription from their physicians. The intervention group improved their daily step count from around 5,000 steps per day to about 6,200 steps per day. While the increase was less than the researchers had hoped for, it still resulted in improvements in blood sugar control. In another study, a 24-week walking program reduced blood pressure by 11 points in postmenopausal women, even though their increased daily step counts fell shy of the 10,000 goal at about 9,000 steps. Similarly, a small Japanese study found that enrolling postmenopausal women in a weekly exercise program helped improve their lipid profile even though they only increased their daily step count from 6,800 to 8,500 steps per day. And an analysis of U.S. NHANES data showed a mortality benefit when individuals taking more than 8,000 steps were compared with those taking fewer than 4,000 steps per day. The benefits largely plateaued beyond 9,000-10,000 steps.
The reality is that walking 10,000 steps a day is a laudable goal and is almost certainly beneficial. But even lower levels of physical activity have benefits. The trick is not so much to aim for some theoretical ideal but to improve upon your current baseline. Encouraging patients to get into the habit of taking a daily walk (be it in the morning, during lunchtime, or in the evening) is going to pay dividends regardless of their daily step count. The point is that when it comes to physical activity, the greatest benefit seems to be when we go from doing nothing to doing something.
Dr. Labos is a cardiologist at Queen Elizabeth Health Complex, Montreal. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Some myths never die. The idea of taking 10,000 steps a day is one of them. What started as a catchy marketing slogan has become a mantra for anyone promoting physical activity.
It all began in 1965 when the Japanese company Yamasa Tokei began selling a new step-counter which they called manpo-kei (ten-thousand steps meter). They coupled the product launch with an ad campaign – “Let’s walk 10,000 steps a day!” – in a bid to encourage physical activity. The threshold was always somewhat arbitrary, but the idea of 10,000 steps cemented itself in the public consciousness from that point forward.
To be fair, there is nothing wrong with taking 10,000 steps a day, and it does roughly correlate with the generally recommended amount of physical activity. Most people will take somewhere between 5,000 and 7,500 steps a day even if they lead largely sedentary lives. If you add 30 minutes of walking to your daily routine, that will account for an extra 3,000-4,000 steps and bring you close to that 10,000-step threshold. As such, setting a 10,000-step target is a potentially useful shorthand for people aspiring to achieve ideal levels of physical activity.
But walking fewer steps still has a benefit. A study in JAMA Network Open followed a cohort of 2,110 adults from the CARDIA study and found, rather unsurprisingly, that those with more steps per day had lower rates of all-cause mortality. But interestingly, those who averaged 7,000-10,000 steps per day did just as well as those who walked more than 10,000 steps, suggesting that the lower threshold was probably the inflection point.
Other research has shown that improving your step count is probably more important than achieving any specific threshold. In one Canadian study, patients with diabetes were randomized to usual care or to an exercise prescription from their physicians. The intervention group improved their daily step count from around 5,000 steps per day to about 6,200 steps per day. While the increase was less than the researchers had hoped for, it still resulted in improvements in blood sugar control. In another study, a 24-week walking program reduced blood pressure by 11 points in postmenopausal women, even though their increased daily step counts fell shy of the 10,000 goal at about 9,000 steps. Similarly, a small Japanese study found that enrolling postmenopausal women in a weekly exercise program helped improve their lipid profile even though they only increased their daily step count from 6,800 to 8,500 steps per day. And an analysis of U.S. NHANES data showed a mortality benefit when individuals taking more than 8,000 steps were compared with those taking fewer than 4,000 steps per day. The benefits largely plateaued beyond 9,000-10,000 steps.
The reality is that walking 10,000 steps a day is a laudable goal and is almost certainly beneficial. But even lower levels of physical activity have benefits. The trick is not so much to aim for some theoretical ideal but to improve upon your current baseline. Encouraging patients to get into the habit of taking a daily walk (be it in the morning, during lunchtime, or in the evening) is going to pay dividends regardless of their daily step count. The point is that when it comes to physical activity, the greatest benefit seems to be when we go from doing nothing to doing something.
Dr. Labos is a cardiologist at Queen Elizabeth Health Complex, Montreal. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Empagliflozin scores topline win in EMPA-KIDNEY trial
Researchers running the EMPA-KIDNEY trial that’s been testing the safety and efficacy of the SGLT2 inhibitor empagliflozin (Jardiance) in about 6,600 patients with chronic kidney disease (CKD) announced on March 16 that they had stopped the trial early because of positive efficacy that met the study’s prespecified threshold for early termination.
EMPA-KIDNEY is the third major trial of an agent from the sodium-glucose cotransport 2 (SGLT2) inhibitor class tested in patients with CKD to be stopped early because of positive results that met a prespecified termination rule.
In 2020, the DAPA-CKD trial of dapagliflozin (Farxiga) stopped early, after a median follow-up of 2.4 years, because of positive efficacy results. In 2019, the same thing happened in the CREDENCE trial of canagliflozin (Invokana), with the unexpected halt coming after a median follow-up of 2.62 years.
The announcement about EMPA-KIDNEY did not include information on median follow-up, but enrollment into the trial ran from May 2019 to April 2021, which means that the longest that enrolled patients could have been in the study was about 2.85 years.
The primary efficacy endpoint in EMPA-KIDNEY was a composite of a sustained decline in estimated glomerular filtration rate (eGFR) to less than 10 mL/min/1.73 m2, renal death, a sustained decline of at least 40% in eGFR from baseline, or cardiovascular death. The announcement of the trial’s early termination provided no details on the efficacy results.
EMPA-KIDNEY enrolled a wider range of patients
EMPA-KIDNEY expands the scope of types of patients with CKD now shown to benefit from treatment with an SGLT2 inhibitor. CREDENCE tested canagliflozin only in patients with type 2 diabetes and diabetic nephropathy, and in DAPA-CKD, two-thirds of enrolled patients had type 2 diabetes, and all had CKD. In EMPA-KIDNEY, 46% of the 6,609 enrolled patients had diabetes (including a very small number with type 1 diabetes).
Another departure from prior studies of an SGLT2 inhibitor for patients selected primarily for having CKD was that in EMPA-KIDNEY, 20% of patients did not have albuminuria, and for 34%, eGFR at entry was less than 30 mL/min/1.73 m2, with all enrolled patients required to have an eGFR at entry of greater than or equal to 20 mL/min/1.73 m2. Average eGFR in EMPA-KIDNEY was about 38 mL/min/1.73 m2. To be included in the trial, patients were not required to have albuminuria, except those whose eGFR was greater than or equal to 45 mL/min/1.73 m2.
In DAPA-CKD, the minimum eGFR at entry had to be greater than or equal to 25 mL/min/1.73 m2, and roughly 14% of enrolled patients had an eGFR of less than 30 mL/min/1.73 m2. The average eGFR in DAPA-CKD was about 43 mL/min/1.73 m2. In addition, all patients had at least microalbuminuria, with a minimum urinary albumin-to-creatinine ratio of 200. In CREDENCE, the minimum eGFR for enrollment was 30 mL/min/1.73 m2, and the average eGFR was about 56 mL/min/1.73 m2. All patients in CREDENCE had to have macroalbuminuria, with a urinary albumin-to-creatinine ratio of more than 300.
According to the researchers who designed EMPA-KIDNEY, the trial enrollment criteria aimed to include adults with CKD “who are frequently seen in practice but were under-represented in previous SGLT2 inhibitor trials.”
Indications for empagliflozin are expanding
The success of empagliflozin in EMPA-KIDNEY follows its positive results in both the EMPEROR-Reduced and EMPEROR-Preserved trials, which collectively proved the efficacy of the agent for patients with heart failure regardless of their left ventricular ejection fraction and regardless of whether they also had diabetes.
These results led the U.S. Food and Drug Administration to recently expand the labeled indication for empagliflozin to all patients with heart failure. Empagliflozin also has labeled indications for glycemic control in patients with type 2 diabetes and to reduce the risk of cardiovascular death in adults with type 2 diabetes and established cardiovascular disease.
As of today, empagliflozin has no labeled indication for treating patients with CKD. Dapagliflozin received that indication in April 2021, and canagliflozin received an indication for treating patients with type 2 diabetes, diabetic nephropathy, and albuminuria in September 2019.
EMPA-KIDNEY is sponsored by Boehringer Ingelheim and Lilly, the two companies that jointly market empagliflozin (Jardiance).
A version of this article first appeared on Medscape.com.
Researchers running the EMPA-KIDNEY trial that’s been testing the safety and efficacy of the SGLT2 inhibitor empagliflozin (Jardiance) in about 6,600 patients with chronic kidney disease (CKD) announced on March 16 that they had stopped the trial early because of positive efficacy that met the study’s prespecified threshold for early termination.
EMPA-KIDNEY is the third major trial of an agent from the sodium-glucose cotransport 2 (SGLT2) inhibitor class tested in patients with CKD to be stopped early because of positive results that met a prespecified termination rule.
In 2020, the DAPA-CKD trial of dapagliflozin (Farxiga) stopped early, after a median follow-up of 2.4 years, because of positive efficacy results. In 2019, the same thing happened in the CREDENCE trial of canagliflozin (Invokana), with the unexpected halt coming after a median follow-up of 2.62 years.
The announcement about EMPA-KIDNEY did not include information on median follow-up, but enrollment into the trial ran from May 2019 to April 2021, which means that the longest that enrolled patients could have been in the study was about 2.85 years.
The primary efficacy endpoint in EMPA-KIDNEY was a composite of a sustained decline in estimated glomerular filtration rate (eGFR) to less than 10 mL/min/1.73 m2, renal death, a sustained decline of at least 40% in eGFR from baseline, or cardiovascular death. The announcement of the trial’s early termination provided no details on the efficacy results.
EMPA-KIDNEY enrolled a wider range of patients
EMPA-KIDNEY expands the scope of types of patients with CKD now shown to benefit from treatment with an SGLT2 inhibitor. CREDENCE tested canagliflozin only in patients with type 2 diabetes and diabetic nephropathy, and in DAPA-CKD, two-thirds of enrolled patients had type 2 diabetes, and all had CKD. In EMPA-KIDNEY, 46% of the 6,609 enrolled patients had diabetes (including a very small number with type 1 diabetes).
Another departure from prior studies of an SGLT2 inhibitor for patients selected primarily for having CKD was that in EMPA-KIDNEY, 20% of patients did not have albuminuria, and for 34%, eGFR at entry was less than 30 mL/min/1.73 m2, with all enrolled patients required to have an eGFR at entry of greater than or equal to 20 mL/min/1.73 m2. Average eGFR in EMPA-KIDNEY was about 38 mL/min/1.73 m2. To be included in the trial, patients were not required to have albuminuria, except those whose eGFR was greater than or equal to 45 mL/min/1.73 m2.
In DAPA-CKD, the minimum eGFR at entry had to be greater than or equal to 25 mL/min/1.73 m2, and roughly 14% of enrolled patients had an eGFR of less than 30 mL/min/1.73 m2. The average eGFR in DAPA-CKD was about 43 mL/min/1.73 m2. In addition, all patients had at least microalbuminuria, with a minimum urinary albumin-to-creatinine ratio of 200. In CREDENCE, the minimum eGFR for enrollment was 30 mL/min/1.73 m2, and the average eGFR was about 56 mL/min/1.73 m2. All patients in CREDENCE had to have macroalbuminuria, with a urinary albumin-to-creatinine ratio of more than 300.
According to the researchers who designed EMPA-KIDNEY, the trial enrollment criteria aimed to include adults with CKD “who are frequently seen in practice but were under-represented in previous SGLT2 inhibitor trials.”
Indications for empagliflozin are expanding
The success of empagliflozin in EMPA-KIDNEY follows its positive results in both the EMPEROR-Reduced and EMPEROR-Preserved trials, which collectively proved the efficacy of the agent for patients with heart failure regardless of their left ventricular ejection fraction and regardless of whether they also had diabetes.
These results led the U.S. Food and Drug Administration to recently expand the labeled indication for empagliflozin to all patients with heart failure. Empagliflozin also has labeled indications for glycemic control in patients with type 2 diabetes and to reduce the risk of cardiovascular death in adults with type 2 diabetes and established cardiovascular disease.
As of today, empagliflozin has no labeled indication for treating patients with CKD. Dapagliflozin received that indication in April 2021, and canagliflozin received an indication for treating patients with type 2 diabetes, diabetic nephropathy, and albuminuria in September 2019.
EMPA-KIDNEY is sponsored by Boehringer Ingelheim and Lilly, the two companies that jointly market empagliflozin (Jardiance).
A version of this article first appeared on Medscape.com.
Researchers running the EMPA-KIDNEY trial that’s been testing the safety and efficacy of the SGLT2 inhibitor empagliflozin (Jardiance) in about 6,600 patients with chronic kidney disease (CKD) announced on March 16 that they had stopped the trial early because of positive efficacy that met the study’s prespecified threshold for early termination.
EMPA-KIDNEY is the third major trial of an agent from the sodium-glucose cotransport 2 (SGLT2) inhibitor class tested in patients with CKD to be stopped early because of positive results that met a prespecified termination rule.
In 2020, the DAPA-CKD trial of dapagliflozin (Farxiga) stopped early, after a median follow-up of 2.4 years, because of positive efficacy results. In 2019, the same thing happened in the CREDENCE trial of canagliflozin (Invokana), with the unexpected halt coming after a median follow-up of 2.62 years.
The announcement about EMPA-KIDNEY did not include information on median follow-up, but enrollment into the trial ran from May 2019 to April 2021, which means that the longest that enrolled patients could have been in the study was about 2.85 years.
The primary efficacy endpoint in EMPA-KIDNEY was a composite of a sustained decline in estimated glomerular filtration rate (eGFR) to less than 10 mL/min/1.73 m2, renal death, a sustained decline of at least 40% in eGFR from baseline, or cardiovascular death. The announcement of the trial’s early termination provided no details on the efficacy results.
EMPA-KIDNEY enrolled a wider range of patients
EMPA-KIDNEY expands the scope of types of patients with CKD now shown to benefit from treatment with an SGLT2 inhibitor. CREDENCE tested canagliflozin only in patients with type 2 diabetes and diabetic nephropathy, and in DAPA-CKD, two-thirds of enrolled patients had type 2 diabetes, and all had CKD. In EMPA-KIDNEY, 46% of the 6,609 enrolled patients had diabetes (including a very small number with type 1 diabetes).
Another departure from prior studies of an SGLT2 inhibitor for patients selected primarily for having CKD was that in EMPA-KIDNEY, 20% of patients did not have albuminuria, and for 34%, eGFR at entry was less than 30 mL/min/1.73 m2, with all enrolled patients required to have an eGFR at entry of greater than or equal to 20 mL/min/1.73 m2. Average eGFR in EMPA-KIDNEY was about 38 mL/min/1.73 m2. To be included in the trial, patients were not required to have albuminuria, except those whose eGFR was greater than or equal to 45 mL/min/1.73 m2.
In DAPA-CKD, the minimum eGFR at entry had to be greater than or equal to 25 mL/min/1.73 m2, and roughly 14% of enrolled patients had an eGFR of less than 30 mL/min/1.73 m2. The average eGFR in DAPA-CKD was about 43 mL/min/1.73 m2. In addition, all patients had at least microalbuminuria, with a minimum urinary albumin-to-creatinine ratio of 200. In CREDENCE, the minimum eGFR for enrollment was 30 mL/min/1.73 m2, and the average eGFR was about 56 mL/min/1.73 m2. All patients in CREDENCE had to have macroalbuminuria, with a urinary albumin-to-creatinine ratio of more than 300.
According to the researchers who designed EMPA-KIDNEY, the trial enrollment criteria aimed to include adults with CKD “who are frequently seen in practice but were under-represented in previous SGLT2 inhibitor trials.”
Indications for empagliflozin are expanding
The success of empagliflozin in EMPA-KIDNEY follows its positive results in both the EMPEROR-Reduced and EMPEROR-Preserved trials, which collectively proved the efficacy of the agent for patients with heart failure regardless of their left ventricular ejection fraction and regardless of whether they also had diabetes.
These results led the U.S. Food and Drug Administration to recently expand the labeled indication for empagliflozin to all patients with heart failure. Empagliflozin also has labeled indications for glycemic control in patients with type 2 diabetes and to reduce the risk of cardiovascular death in adults with type 2 diabetes and established cardiovascular disease.
As of today, empagliflozin has no labeled indication for treating patients with CKD. Dapagliflozin received that indication in April 2021, and canagliflozin received an indication for treating patients with type 2 diabetes, diabetic nephropathy, and albuminuria in September 2019.
EMPA-KIDNEY is sponsored by Boehringer Ingelheim and Lilly, the two companies that jointly market empagliflozin (Jardiance).
A version of this article first appeared on Medscape.com.
Kawasaki disease guideline highlights rheumatology angles
All Kawasaki disease (KD) patients should be treated first with intravenous immunoglobulin, according to an updated guideline issued jointly by the American College of Rheumatology and the Vasculitis Foundation.
KD has low mortality when treated appropriately, guideline first author Mark Gorelik, MD, assistant professor of pediatrics at Columbia University, New York, and colleagues wrote.
The update is important at this time because new evidence continues to emerge in the clinical management of KD, Dr. Gorelik said in an interview.
“In addition, this guideline approaches Kawasaki disease from a perspective of acting as an adjunct to the already existing and excellent American Heart Association guidelines by adding information in areas that rheumatologists may play a role,” Dr. Gorelik said. “This is specifically regarding patients who may require additional therapy beyond standard IVIg, such as patients who may be at higher risk of morbidity from disease and patients who have refractory disease,” he explained.
The guideline, published in Arthritis & Rheumatology, includes 11 recommendations, 1 good practice statement, and 1 ungraded position statement. The good practice statement emphasizes that all patients with KD should be initially treated with IVIg.
The position statement advises that either nonglucocorticoid immunosuppressive therapy or glucocorticoids may be used for patients with acute KD whose fever persists despite repeated IVIg treatment. No clinical evidence currently supports the superiority of either nonglucocorticoid immunosuppressive therapy or glucocorticoids; therefore, the authors support the use of either based on what is appropriate in any given clinical situation. Although optimal dosage and duration of glucocorticoids have yet to be determined in a U.S. population, the authors described a typical glucocorticoid dosage as starting prednisone at 2 mg/kg per day, with a maximum of 60 mg/day, and dose tapering over 15 days.
The 11 recommendations consist of 7 strong and 4 conditional recommendations. The strong recommendations focus on prompt treatment of incomplete KD, treatment with aspirin, and obtaining an echocardiogram in patients with unexplained macrophage activation syndrome or shock. The conditional recommendations support using established therapy promptly at disease onset, then identifying cases in which additional therapy is needed.
Dr. Gorelik highlighted four clinical takeaways from the guideline. First, “patients with higher risk for complications do exist in Kawasaki disease, and that these patients can be treated more aggressively,” he said. “Specifically, patients with aneurysms seen at first ultrasound, and patients who are under 6 months, are more likely to have progressive and/or refractory disease; these patients can be treated with an adjunctive short course of corticosteroids.”
Second, “the use of high-dose aspirin for patients with Kawasaki disease does not have strong basis in evidence. While aspirin itself of some dose is necessary for patients with Kawasaki disease, use of either high- or low-dose aspirin has the same outcome for patients, and a physician may choose either of these in practice,” he said.
Third, “we continue to recommend that refractory patients with Kawasaki disease be treated with a second dose of IVIg; however, there are many scenarios in which a physician may choose either corticosteroids [either a single high dose of >10 mg/kg, or a short moderate-dose course of 2 mg/kg per day for 5-7 days] or a biologic agent such as infliximab. ... These are valid choices for therapy in patients with refractory Kawasaki disease,” he emphasized.
Fourth, “physicians should discard the idea of treating before [and conversely, not treating after] 10 days of fever,” Dr. Gorelik said. “Patients with Kawasaki disease should be treated as soon as the diagnosis is made, regardless of whether this patient is on day 5, day 12, or day 20 of symptoms.”
Update incorporates emerging evidence
Potential barriers to implementing the guideline in practice include the challenge of weaning doctors from practices that are habitual in medicine, Dr. Gorelik said. “One of these is the use of high-dose aspirin for Kawasaki disease; a number of studies have shown over the past decade or more that high-dose aspirin has no greater effect than lower-dose aspirin for Kawasaki disease. Despite all of these studies, the use of high-dose aspirin continued. High-dose aspirin for Kawasaki disease was used in the era prior to use of IVIg as an anti-inflammatory agent. However, it has poor efficacy in this regard, and the true benefit for aspirin is for anticoagulation for patients at risk of a clot, and this is just as effective in lower doses. Expressing this in a guideline could help to change practices by helping physicians understand not only what they are guided to do, but why.”
Additional research is needed to better identify high-risk patients in non-Japanese populations, he noted. “While studies from Japan suggest that higher-risk patients can be identified based on various parameters, these have not been well replicated in non-Japanese populations. Good research that identifies which patients may be more at risk in other populations would be helpful to more precisely target high-risk therapy.”
Other research needs include a clearer understanding of the best therapies for refractory patients, Dr. Gorelik said. “One area of the most difficulty was determining whether patients with refractory disease should have repeated IVIg or a switch to glucocorticoids and biologic agents. Some of this research is underway, and some was published just as these guidelines were being drawn, and this particular area is one that is likely to change significantly. While currently we recommend a repeated dose of IVIg, it is likely that over the very near term, the use of repeated IVIg in KD will be curtailed” because of concerns such as the relatively high rate of hemolysis. Research to identify which therapy has a noninferior effect with a superior risk profile is needed; such research “will likely result in a future iteration of these guidelines specifically related to this question,” he concluded.
The KD guideline is the final companion to three additional ACR/VF vasculitis guidelines that were released in July 2021. The guideline research received no outside funding. The researchers had no financial conflicts to disclose.
All Kawasaki disease (KD) patients should be treated first with intravenous immunoglobulin, according to an updated guideline issued jointly by the American College of Rheumatology and the Vasculitis Foundation.
KD has low mortality when treated appropriately, guideline first author Mark Gorelik, MD, assistant professor of pediatrics at Columbia University, New York, and colleagues wrote.
The update is important at this time because new evidence continues to emerge in the clinical management of KD, Dr. Gorelik said in an interview.
“In addition, this guideline approaches Kawasaki disease from a perspective of acting as an adjunct to the already existing and excellent American Heart Association guidelines by adding information in areas that rheumatologists may play a role,” Dr. Gorelik said. “This is specifically regarding patients who may require additional therapy beyond standard IVIg, such as patients who may be at higher risk of morbidity from disease and patients who have refractory disease,” he explained.
The guideline, published in Arthritis & Rheumatology, includes 11 recommendations, 1 good practice statement, and 1 ungraded position statement. The good practice statement emphasizes that all patients with KD should be initially treated with IVIg.
The position statement advises that either nonglucocorticoid immunosuppressive therapy or glucocorticoids may be used for patients with acute KD whose fever persists despite repeated IVIg treatment. No clinical evidence currently supports the superiority of either nonglucocorticoid immunosuppressive therapy or glucocorticoids; therefore, the authors support the use of either based on what is appropriate in any given clinical situation. Although optimal dosage and duration of glucocorticoids have yet to be determined in a U.S. population, the authors described a typical glucocorticoid dosage as starting prednisone at 2 mg/kg per day, with a maximum of 60 mg/day, and dose tapering over 15 days.
The 11 recommendations consist of 7 strong and 4 conditional recommendations. The strong recommendations focus on prompt treatment of incomplete KD, treatment with aspirin, and obtaining an echocardiogram in patients with unexplained macrophage activation syndrome or shock. The conditional recommendations support using established therapy promptly at disease onset, then identifying cases in which additional therapy is needed.
Dr. Gorelik highlighted four clinical takeaways from the guideline. First, “patients with higher risk for complications do exist in Kawasaki disease, and that these patients can be treated more aggressively,” he said. “Specifically, patients with aneurysms seen at first ultrasound, and patients who are under 6 months, are more likely to have progressive and/or refractory disease; these patients can be treated with an adjunctive short course of corticosteroids.”
Second, “the use of high-dose aspirin for patients with Kawasaki disease does not have strong basis in evidence. While aspirin itself of some dose is necessary for patients with Kawasaki disease, use of either high- or low-dose aspirin has the same outcome for patients, and a physician may choose either of these in practice,” he said.
Third, “we continue to recommend that refractory patients with Kawasaki disease be treated with a second dose of IVIg; however, there are many scenarios in which a physician may choose either corticosteroids [either a single high dose of >10 mg/kg, or a short moderate-dose course of 2 mg/kg per day for 5-7 days] or a biologic agent such as infliximab. ... These are valid choices for therapy in patients with refractory Kawasaki disease,” he emphasized.
Fourth, “physicians should discard the idea of treating before [and conversely, not treating after] 10 days of fever,” Dr. Gorelik said. “Patients with Kawasaki disease should be treated as soon as the diagnosis is made, regardless of whether this patient is on day 5, day 12, or day 20 of symptoms.”
Update incorporates emerging evidence
Potential barriers to implementing the guideline in practice include the challenge of weaning doctors from practices that are habitual in medicine, Dr. Gorelik said. “One of these is the use of high-dose aspirin for Kawasaki disease; a number of studies have shown over the past decade or more that high-dose aspirin has no greater effect than lower-dose aspirin for Kawasaki disease. Despite all of these studies, the use of high-dose aspirin continued. High-dose aspirin for Kawasaki disease was used in the era prior to use of IVIg as an anti-inflammatory agent. However, it has poor efficacy in this regard, and the true benefit for aspirin is for anticoagulation for patients at risk of a clot, and this is just as effective in lower doses. Expressing this in a guideline could help to change practices by helping physicians understand not only what they are guided to do, but why.”
Additional research is needed to better identify high-risk patients in non-Japanese populations, he noted. “While studies from Japan suggest that higher-risk patients can be identified based on various parameters, these have not been well replicated in non-Japanese populations. Good research that identifies which patients may be more at risk in other populations would be helpful to more precisely target high-risk therapy.”
Other research needs include a clearer understanding of the best therapies for refractory patients, Dr. Gorelik said. “One area of the most difficulty was determining whether patients with refractory disease should have repeated IVIg or a switch to glucocorticoids and biologic agents. Some of this research is underway, and some was published just as these guidelines were being drawn, and this particular area is one that is likely to change significantly. While currently we recommend a repeated dose of IVIg, it is likely that over the very near term, the use of repeated IVIg in KD will be curtailed” because of concerns such as the relatively high rate of hemolysis. Research to identify which therapy has a noninferior effect with a superior risk profile is needed; such research “will likely result in a future iteration of these guidelines specifically related to this question,” he concluded.
The KD guideline is the final companion to three additional ACR/VF vasculitis guidelines that were released in July 2021. The guideline research received no outside funding. The researchers had no financial conflicts to disclose.
All Kawasaki disease (KD) patients should be treated first with intravenous immunoglobulin, according to an updated guideline issued jointly by the American College of Rheumatology and the Vasculitis Foundation.
KD has low mortality when treated appropriately, guideline first author Mark Gorelik, MD, assistant professor of pediatrics at Columbia University, New York, and colleagues wrote.
The update is important at this time because new evidence continues to emerge in the clinical management of KD, Dr. Gorelik said in an interview.
“In addition, this guideline approaches Kawasaki disease from a perspective of acting as an adjunct to the already existing and excellent American Heart Association guidelines by adding information in areas that rheumatologists may play a role,” Dr. Gorelik said. “This is specifically regarding patients who may require additional therapy beyond standard IVIg, such as patients who may be at higher risk of morbidity from disease and patients who have refractory disease,” he explained.
The guideline, published in Arthritis & Rheumatology, includes 11 recommendations, 1 good practice statement, and 1 ungraded position statement. The good practice statement emphasizes that all patients with KD should be initially treated with IVIg.
The position statement advises that either nonglucocorticoid immunosuppressive therapy or glucocorticoids may be used for patients with acute KD whose fever persists despite repeated IVIg treatment. No clinical evidence currently supports the superiority of either nonglucocorticoid immunosuppressive therapy or glucocorticoids; therefore, the authors support the use of either based on what is appropriate in any given clinical situation. Although optimal dosage and duration of glucocorticoids have yet to be determined in a U.S. population, the authors described a typical glucocorticoid dosage as starting prednisone at 2 mg/kg per day, with a maximum of 60 mg/day, and dose tapering over 15 days.
The 11 recommendations consist of 7 strong and 4 conditional recommendations. The strong recommendations focus on prompt treatment of incomplete KD, treatment with aspirin, and obtaining an echocardiogram in patients with unexplained macrophage activation syndrome or shock. The conditional recommendations support using established therapy promptly at disease onset, then identifying cases in which additional therapy is needed.
Dr. Gorelik highlighted four clinical takeaways from the guideline. First, “patients with higher risk for complications do exist in Kawasaki disease, and that these patients can be treated more aggressively,” he said. “Specifically, patients with aneurysms seen at first ultrasound, and patients who are under 6 months, are more likely to have progressive and/or refractory disease; these patients can be treated with an adjunctive short course of corticosteroids.”
Second, “the use of high-dose aspirin for patients with Kawasaki disease does not have strong basis in evidence. While aspirin itself of some dose is necessary for patients with Kawasaki disease, use of either high- or low-dose aspirin has the same outcome for patients, and a physician may choose either of these in practice,” he said.
Third, “we continue to recommend that refractory patients with Kawasaki disease be treated with a second dose of IVIg; however, there are many scenarios in which a physician may choose either corticosteroids [either a single high dose of >10 mg/kg, or a short moderate-dose course of 2 mg/kg per day for 5-7 days] or a biologic agent such as infliximab. ... These are valid choices for therapy in patients with refractory Kawasaki disease,” he emphasized.
Fourth, “physicians should discard the idea of treating before [and conversely, not treating after] 10 days of fever,” Dr. Gorelik said. “Patients with Kawasaki disease should be treated as soon as the diagnosis is made, regardless of whether this patient is on day 5, day 12, or day 20 of symptoms.”
Update incorporates emerging evidence
Potential barriers to implementing the guideline in practice include the challenge of weaning doctors from practices that are habitual in medicine, Dr. Gorelik said. “One of these is the use of high-dose aspirin for Kawasaki disease; a number of studies have shown over the past decade or more that high-dose aspirin has no greater effect than lower-dose aspirin for Kawasaki disease. Despite all of these studies, the use of high-dose aspirin continued. High-dose aspirin for Kawasaki disease was used in the era prior to use of IVIg as an anti-inflammatory agent. However, it has poor efficacy in this regard, and the true benefit for aspirin is for anticoagulation for patients at risk of a clot, and this is just as effective in lower doses. Expressing this in a guideline could help to change practices by helping physicians understand not only what they are guided to do, but why.”
Additional research is needed to better identify high-risk patients in non-Japanese populations, he noted. “While studies from Japan suggest that higher-risk patients can be identified based on various parameters, these have not been well replicated in non-Japanese populations. Good research that identifies which patients may be more at risk in other populations would be helpful to more precisely target high-risk therapy.”
Other research needs include a clearer understanding of the best therapies for refractory patients, Dr. Gorelik said. “One area of the most difficulty was determining whether patients with refractory disease should have repeated IVIg or a switch to glucocorticoids and biologic agents. Some of this research is underway, and some was published just as these guidelines were being drawn, and this particular area is one that is likely to change significantly. While currently we recommend a repeated dose of IVIg, it is likely that over the very near term, the use of repeated IVIg in KD will be curtailed” because of concerns such as the relatively high rate of hemolysis. Research to identify which therapy has a noninferior effect with a superior risk profile is needed; such research “will likely result in a future iteration of these guidelines specifically related to this question,” he concluded.
The KD guideline is the final companion to three additional ACR/VF vasculitis guidelines that were released in July 2021. The guideline research received no outside funding. The researchers had no financial conflicts to disclose.
FROM ARTHRITIS & RHEUMATOLOGY
COVID surge in Western Europe puts U.S. health experts on alert
, even as states and cities continue to lift restrictions amid low case numbers.
Infectious disease experts are watching BA.2, the Omicron subvariant that appears to be more transmissible than the original strain. BA.2 is fueling outbreaks across Europe and is growing in dominance across the United States.
“It’s picking up steam. It’s across at least 12 countries … from Finland to Greece,” Eric Topol, MD, director of the Scripps Research Translational Institute, told The Washington Post.
He has been following the surge and has posted recent charts of the outbreak on Twitter. Hospitalizations appear to be increasing in some places as well, he noted, despite the higher vaccination rates of many Western European countries.
“There’s no question there’s a significant wave there,” Dr. Topol said.
Germany recorded more than 260,000 new cases on March 15, according to the data tracker from the New York Times, but coronavirus restrictions are still being lifted this week. The U.K. is reporting more than 75,000 daily cases, and the Netherlands is reporting more than 60,000 daily cases, which are considered major numbers, compared to their population sizes. Meanwhile, France, Italy, and Switzerland are also reporting large increases in infections.
During the past 2 years, widespread outbreaks in Europe have been followed by similar surges in the U.S. weeks later. Most experts interviewed by the Post predicted that it’s likely to happen again.
In the United States, the BA.2 subvariant accounted for 23% of new COVID-19 cases for the week ending March 12, according to the latest estimate from the Centers for Disease Control and Prevention, while the original Omicron strain made up about 66% of cases. The BA.2 percentage is up from 13.7% of new cases for the week ending March 5, 7.1% the previous week, and 4.1% the week before that. In parts of the Northeast and New England, BA.2 makes up more than 38% of new cases.
At the same time, the 7 -day average of COVID-19 cases continues to drop in the United States, with about 31,000 daily cases currently, the New York Times data tracker shows. About 25,000 COVID-19 patients are hospitalized across the country, which has fallen 44% in the past 2 weeks, and about 1,200 deaths are being reported daily.
Several variables could affect the course of a future surge, the Post reported. Vaccination rates, coronavirus safety protocols, and access to antiviral medications could dictate how another wave unfolds across the country.
About 82% of the eligible U.S. population has received at least one vaccine dose, and 69% is fully vaccinated, according to the latest CDC data. About half of those who are eligible for booster doses have received one. In Germany, nearly 76% of people are fully vaccinated, the newspaper reported, and in the United Kingdom, about 74% are fully vaccinated.
Health experts are also considering how natural immunity from a previous infection could affect a BA.2 surge. Millions of Americans were infected with the original Omicron strain, BA.1, which could provide protection. That said, researchers aren’t quite sure whether BA.1 infection protects against BA.2.
“It’s like a weather alert. Right now, the skies are sunny and bright, and we hope they stay that way,” Michael Osterholm, PhD, director of the University of Minnesota’s Center for Infectious Disease Research and Policy, told CNN.
“But we could have some bad weather by evening,” he said. “We just don’t know.”
A version of this article first appeared on WebMD.com.
, even as states and cities continue to lift restrictions amid low case numbers.
Infectious disease experts are watching BA.2, the Omicron subvariant that appears to be more transmissible than the original strain. BA.2 is fueling outbreaks across Europe and is growing in dominance across the United States.
“It’s picking up steam. It’s across at least 12 countries … from Finland to Greece,” Eric Topol, MD, director of the Scripps Research Translational Institute, told The Washington Post.
He has been following the surge and has posted recent charts of the outbreak on Twitter. Hospitalizations appear to be increasing in some places as well, he noted, despite the higher vaccination rates of many Western European countries.
“There’s no question there’s a significant wave there,” Dr. Topol said.
Germany recorded more than 260,000 new cases on March 15, according to the data tracker from the New York Times, but coronavirus restrictions are still being lifted this week. The U.K. is reporting more than 75,000 daily cases, and the Netherlands is reporting more than 60,000 daily cases, which are considered major numbers, compared to their population sizes. Meanwhile, France, Italy, and Switzerland are also reporting large increases in infections.
During the past 2 years, widespread outbreaks in Europe have been followed by similar surges in the U.S. weeks later. Most experts interviewed by the Post predicted that it’s likely to happen again.
In the United States, the BA.2 subvariant accounted for 23% of new COVID-19 cases for the week ending March 12, according to the latest estimate from the Centers for Disease Control and Prevention, while the original Omicron strain made up about 66% of cases. The BA.2 percentage is up from 13.7% of new cases for the week ending March 5, 7.1% the previous week, and 4.1% the week before that. In parts of the Northeast and New England, BA.2 makes up more than 38% of new cases.
At the same time, the 7 -day average of COVID-19 cases continues to drop in the United States, with about 31,000 daily cases currently, the New York Times data tracker shows. About 25,000 COVID-19 patients are hospitalized across the country, which has fallen 44% in the past 2 weeks, and about 1,200 deaths are being reported daily.
Several variables could affect the course of a future surge, the Post reported. Vaccination rates, coronavirus safety protocols, and access to antiviral medications could dictate how another wave unfolds across the country.
About 82% of the eligible U.S. population has received at least one vaccine dose, and 69% is fully vaccinated, according to the latest CDC data. About half of those who are eligible for booster doses have received one. In Germany, nearly 76% of people are fully vaccinated, the newspaper reported, and in the United Kingdom, about 74% are fully vaccinated.
Health experts are also considering how natural immunity from a previous infection could affect a BA.2 surge. Millions of Americans were infected with the original Omicron strain, BA.1, which could provide protection. That said, researchers aren’t quite sure whether BA.1 infection protects against BA.2.
“It’s like a weather alert. Right now, the skies are sunny and bright, and we hope they stay that way,” Michael Osterholm, PhD, director of the University of Minnesota’s Center for Infectious Disease Research and Policy, told CNN.
“But we could have some bad weather by evening,” he said. “We just don’t know.”
A version of this article first appeared on WebMD.com.
, even as states and cities continue to lift restrictions amid low case numbers.
Infectious disease experts are watching BA.2, the Omicron subvariant that appears to be more transmissible than the original strain. BA.2 is fueling outbreaks across Europe and is growing in dominance across the United States.
“It’s picking up steam. It’s across at least 12 countries … from Finland to Greece,” Eric Topol, MD, director of the Scripps Research Translational Institute, told The Washington Post.
He has been following the surge and has posted recent charts of the outbreak on Twitter. Hospitalizations appear to be increasing in some places as well, he noted, despite the higher vaccination rates of many Western European countries.
“There’s no question there’s a significant wave there,” Dr. Topol said.
Germany recorded more than 260,000 new cases on March 15, according to the data tracker from the New York Times, but coronavirus restrictions are still being lifted this week. The U.K. is reporting more than 75,000 daily cases, and the Netherlands is reporting more than 60,000 daily cases, which are considered major numbers, compared to their population sizes. Meanwhile, France, Italy, and Switzerland are also reporting large increases in infections.
During the past 2 years, widespread outbreaks in Europe have been followed by similar surges in the U.S. weeks later. Most experts interviewed by the Post predicted that it’s likely to happen again.
In the United States, the BA.2 subvariant accounted for 23% of new COVID-19 cases for the week ending March 12, according to the latest estimate from the Centers for Disease Control and Prevention, while the original Omicron strain made up about 66% of cases. The BA.2 percentage is up from 13.7% of new cases for the week ending March 5, 7.1% the previous week, and 4.1% the week before that. In parts of the Northeast and New England, BA.2 makes up more than 38% of new cases.
At the same time, the 7 -day average of COVID-19 cases continues to drop in the United States, with about 31,000 daily cases currently, the New York Times data tracker shows. About 25,000 COVID-19 patients are hospitalized across the country, which has fallen 44% in the past 2 weeks, and about 1,200 deaths are being reported daily.
Several variables could affect the course of a future surge, the Post reported. Vaccination rates, coronavirus safety protocols, and access to antiviral medications could dictate how another wave unfolds across the country.
About 82% of the eligible U.S. population has received at least one vaccine dose, and 69% is fully vaccinated, according to the latest CDC data. About half of those who are eligible for booster doses have received one. In Germany, nearly 76% of people are fully vaccinated, the newspaper reported, and in the United Kingdom, about 74% are fully vaccinated.
Health experts are also considering how natural immunity from a previous infection could affect a BA.2 surge. Millions of Americans were infected with the original Omicron strain, BA.1, which could provide protection. That said, researchers aren’t quite sure whether BA.1 infection protects against BA.2.
“It’s like a weather alert. Right now, the skies are sunny and bright, and we hope they stay that way,” Michael Osterholm, PhD, director of the University of Minnesota’s Center for Infectious Disease Research and Policy, told CNN.
“But we could have some bad weather by evening,” he said. “We just don’t know.”
A version of this article first appeared on WebMD.com.
Obesity linked to combined OSA syndrome and severe asthma
Almost all patients with both obstructive sleep apnea syndrome and severe asthma fell into the obesity phenotype, not the allergy phenotype, based on data from nearly 1,500 adults.
Both asthma and sleep-disordered breathing are common conditions worldwide, and previous research suggests that obstructive sleep apnea syndrome (OSAS) and severe asthma in particular could be associated, wrote Laurent Portel, MD, of Centre Hospitalier de Libourne, France, and colleagues.
“Even if the underlying mechanisms are not well established, it is clear that both OSAS and obesity act to aggravate existing asthma, making it more difficult to control,” they said. However, the pathology of this relationship is not well-understood, and data on severe asthma phenotypes and OSAS are limited, they said.
In a study published in Respiratory Medicine and Research, the investigators reviewed data from 1,465 patients older than 18 years with severe asthma who were part of a larger, prospective multicenter study of the management of asthma patients. The larger study, developed by the Collège des Pneumologues des Hôpitaux Généraux (CPHG) is known as the FASE-CPHG (France Asthme SEvère-CPHG) and includes 104 nonacademic hospitals in France.
Diagnosis of OSAS was reported by physicians; diagnosis of severe asthma was based on the Global Initiative for Asthma criteria. The average age of the patients was 54.4 years, 63% were women, and 60% were nonsmokers.
A total of 161 patients were diagnosed with OSAS. The researchers conducted a cluster analysis on 1,424 patients, including 156 of the OSAS patients. They identified five clusters: early-onset atopic asthma (690 patients), obese asthma (153 patients), late-onset asthma (299 patients), eosinophilic asthma (143 patients), and aspirin sensitivity asthma (139 patients).
All 153 patients in the obese asthma cluster had OSAS, by contrast, none of the patients in the early atopic asthma cluster had OSAS.
Overall, obesity, male sex, high blood pressure, depression, late-onset asthma, and early-onset atopic asthma were independently associated with OSAS, with odds ratios of 5.782, 3.047, 2.875, 2.552, 1.789, and 0.622, respectively.
Notably, OSAS patients were more frequently treated with long-term oral corticosteroids than those without OSAS (30% vs. 15%, P < .0001), the researchers said. “It is possible that this treatment may be responsible for obesity, and it represents a well-known risk factor for developing OSAS,” they wrote.
Uncontrolled asthma was significantly more common in OSAS patients than in those without OSAS (77.7% vs. 69%, P = .03), and significantly more OSAS patients reported no or occasional physical activity (79.8% vs. 68.2%, P ≤ .001).
The study findings were limited by several factors including the lack of patients from primary care or university hospitals, which may limit the generalizability of the results, the reliance on physician statements for diagnosis of OSAS, and the lack of data on OSAS severity or treatment, the researchers noted.
However, the results fill a needed gap in the literature because of the limited data on severe asthma patients in real life, and identifying severe asthma patients by phenotype may help identify those at greatest risk for OSAS, they said.
“Identified patients could more easily benefit from specific examinations such as poly(somno)graphy and, consequently, could benefit from a better management of both asthma and OSAS,” they emphasized.
The larger FASE-CPHG study was supported in part by ALK, AstraZeneca, Boehringer Ingelheim, GSK, and Le Nouveau Souffle. The researchers had no financial conflicts to disclose.
Almost all patients with both obstructive sleep apnea syndrome and severe asthma fell into the obesity phenotype, not the allergy phenotype, based on data from nearly 1,500 adults.
Both asthma and sleep-disordered breathing are common conditions worldwide, and previous research suggests that obstructive sleep apnea syndrome (OSAS) and severe asthma in particular could be associated, wrote Laurent Portel, MD, of Centre Hospitalier de Libourne, France, and colleagues.
“Even if the underlying mechanisms are not well established, it is clear that both OSAS and obesity act to aggravate existing asthma, making it more difficult to control,” they said. However, the pathology of this relationship is not well-understood, and data on severe asthma phenotypes and OSAS are limited, they said.
In a study published in Respiratory Medicine and Research, the investigators reviewed data from 1,465 patients older than 18 years with severe asthma who were part of a larger, prospective multicenter study of the management of asthma patients. The larger study, developed by the Collège des Pneumologues des Hôpitaux Généraux (CPHG) is known as the FASE-CPHG (France Asthme SEvère-CPHG) and includes 104 nonacademic hospitals in France.
Diagnosis of OSAS was reported by physicians; diagnosis of severe asthma was based on the Global Initiative for Asthma criteria. The average age of the patients was 54.4 years, 63% were women, and 60% were nonsmokers.
A total of 161 patients were diagnosed with OSAS. The researchers conducted a cluster analysis on 1,424 patients, including 156 of the OSAS patients. They identified five clusters: early-onset atopic asthma (690 patients), obese asthma (153 patients), late-onset asthma (299 patients), eosinophilic asthma (143 patients), and aspirin sensitivity asthma (139 patients).
All 153 patients in the obese asthma cluster had OSAS, by contrast, none of the patients in the early atopic asthma cluster had OSAS.
Overall, obesity, male sex, high blood pressure, depression, late-onset asthma, and early-onset atopic asthma were independently associated with OSAS, with odds ratios of 5.782, 3.047, 2.875, 2.552, 1.789, and 0.622, respectively.
Notably, OSAS patients were more frequently treated with long-term oral corticosteroids than those without OSAS (30% vs. 15%, P < .0001), the researchers said. “It is possible that this treatment may be responsible for obesity, and it represents a well-known risk factor for developing OSAS,” they wrote.
Uncontrolled asthma was significantly more common in OSAS patients than in those without OSAS (77.7% vs. 69%, P = .03), and significantly more OSAS patients reported no or occasional physical activity (79.8% vs. 68.2%, P ≤ .001).
The study findings were limited by several factors including the lack of patients from primary care or university hospitals, which may limit the generalizability of the results, the reliance on physician statements for diagnosis of OSAS, and the lack of data on OSAS severity or treatment, the researchers noted.
However, the results fill a needed gap in the literature because of the limited data on severe asthma patients in real life, and identifying severe asthma patients by phenotype may help identify those at greatest risk for OSAS, they said.
“Identified patients could more easily benefit from specific examinations such as poly(somno)graphy and, consequently, could benefit from a better management of both asthma and OSAS,” they emphasized.
The larger FASE-CPHG study was supported in part by ALK, AstraZeneca, Boehringer Ingelheim, GSK, and Le Nouveau Souffle. The researchers had no financial conflicts to disclose.
Almost all patients with both obstructive sleep apnea syndrome and severe asthma fell into the obesity phenotype, not the allergy phenotype, based on data from nearly 1,500 adults.
Both asthma and sleep-disordered breathing are common conditions worldwide, and previous research suggests that obstructive sleep apnea syndrome (OSAS) and severe asthma in particular could be associated, wrote Laurent Portel, MD, of Centre Hospitalier de Libourne, France, and colleagues.
“Even if the underlying mechanisms are not well established, it is clear that both OSAS and obesity act to aggravate existing asthma, making it more difficult to control,” they said. However, the pathology of this relationship is not well-understood, and data on severe asthma phenotypes and OSAS are limited, they said.
In a study published in Respiratory Medicine and Research, the investigators reviewed data from 1,465 patients older than 18 years with severe asthma who were part of a larger, prospective multicenter study of the management of asthma patients. The larger study, developed by the Collège des Pneumologues des Hôpitaux Généraux (CPHG) is known as the FASE-CPHG (France Asthme SEvère-CPHG) and includes 104 nonacademic hospitals in France.
Diagnosis of OSAS was reported by physicians; diagnosis of severe asthma was based on the Global Initiative for Asthma criteria. The average age of the patients was 54.4 years, 63% were women, and 60% were nonsmokers.
A total of 161 patients were diagnosed with OSAS. The researchers conducted a cluster analysis on 1,424 patients, including 156 of the OSAS patients. They identified five clusters: early-onset atopic asthma (690 patients), obese asthma (153 patients), late-onset asthma (299 patients), eosinophilic asthma (143 patients), and aspirin sensitivity asthma (139 patients).
All 153 patients in the obese asthma cluster had OSAS, by contrast, none of the patients in the early atopic asthma cluster had OSAS.
Overall, obesity, male sex, high blood pressure, depression, late-onset asthma, and early-onset atopic asthma were independently associated with OSAS, with odds ratios of 5.782, 3.047, 2.875, 2.552, 1.789, and 0.622, respectively.
Notably, OSAS patients were more frequently treated with long-term oral corticosteroids than those without OSAS (30% vs. 15%, P < .0001), the researchers said. “It is possible that this treatment may be responsible for obesity, and it represents a well-known risk factor for developing OSAS,” they wrote.
Uncontrolled asthma was significantly more common in OSAS patients than in those without OSAS (77.7% vs. 69%, P = .03), and significantly more OSAS patients reported no or occasional physical activity (79.8% vs. 68.2%, P ≤ .001).
The study findings were limited by several factors including the lack of patients from primary care or university hospitals, which may limit the generalizability of the results, the reliance on physician statements for diagnosis of OSAS, and the lack of data on OSAS severity or treatment, the researchers noted.
However, the results fill a needed gap in the literature because of the limited data on severe asthma patients in real life, and identifying severe asthma patients by phenotype may help identify those at greatest risk for OSAS, they said.
“Identified patients could more easily benefit from specific examinations such as poly(somno)graphy and, consequently, could benefit from a better management of both asthma and OSAS,” they emphasized.
The larger FASE-CPHG study was supported in part by ALK, AstraZeneca, Boehringer Ingelheim, GSK, and Le Nouveau Souffle. The researchers had no financial conflicts to disclose.
FROM RESPIRATORY MEDICINE AND RESEARCH