Covid ICYMI

Good news for people struggling with sensory problems after a bout of COVID-19. Although mild cases of the disease often impair the ability to taste and smell, and the problem can drag on for months, a new study from Italy shows that most people return to their senses, as it were, within 3 years.

“In the vast majority of cases, the loss of the sense of smell is not irreversible,” said Paolo Boscolo-Rizzo, MD, a professor of medicine, surgery, and health sciences at the University of Trieste (Italy), and a co-author of the study, published as a research letter in JAMA Otolaryngology–Head & Neck Surgery.

Dr. Boscolo-Rizzo and his colleagues analyzed data from 88 adults with mild COVID-19, which was defined as having no lower respiratory disease and blood oxygen saturation of 94% or greater. Another group of 88 adults who never contracted the virus but sometimes had difficulties with smell and taste were also studied. In both groups, the average age was 49 years, all participants were White, and 58% were women.

The researchers tested participants’ sense of smell with sticks that contained different odors and checked their sense of taste with strips that had different tastes. Over time, fewer people had difficulty distinguishing odors. Three years after developing COVID-19, only 12 people had impaired smell, compared with 36 people at year 1 and 24 people at year 2. And at the 3-year mark, all participants had at least a partial ability to smell. 

The story was similar with sense of taste, with 10 of 88 people reporting impairments 3 years later. By then, people with COVID-19 were no more likely to have trouble with smell or taste than people who did not get the virus. 

A study this past June showed a strong correlation between severity of COVID-19 symptoms and impaired sense of taste and smell and estimated that millions of Americans maintained altered senses. More than 10% of people in the Italian study still had trouble with smell or taste 3 years later.
 

Emerging treatments, psychological concerns

“We’re seeing fewer people with this problem, but there are still people suffering from it,” said Fernando Carnavali, MD, an internal medicine physician and a site director for the Center for Post-COVID Care at the Icahn School of Medicine at Mount Sinai, New York City.

Dr. Carnavali wasn’t part of this study, but he did find the new results encouraging, and he called for similar studies in diverse populations that have experienced COVID-19. He also noted that an impaired sense of smell is distressing.

“It really has a significant psychological impact,” Dr. Carnavali said.

He recalled a patient crying in his office because her inability to smell made it impossible for her to cook. Dr. Carnavali recommended clinicians refer patients facing protracted loss of smell or taste to mental health professionals for support.

Treatments are emerging for COVID-19 smell loss. One approach is to inject platelet-rich plasma into a patient’s nasal cavities to help neurons related to smell repair themselves.

A randomized trial showed platelet-rich plasma significantly outperformed placebo in patients with smell loss up to a year after getting COVID-19.

“I wish more people would do it,” said Zara Patel, MD, an otolaryngologist at Stanford (Calif.) Medicine, who helped conduct that trial. She said some physicians may be nervous about injecting plasma so close to the skull and are therefore hesitant to try this approach. 

Another technique may help to address the olfactory condition known as parosmia, in which patients generally experience a benign odor as rancid, according to otolaryngologist Nyssa Farrell, MD, of Washington University School of Medicine, St. Louis. Dr. Farrell said around two-thirds of patients who contract COVID-19 develop the condition, and the rates of long-term parosmia range from 10%-50% depending on various studies.

“It is almost always foul; this can profoundly affect someone’s quality of life,” impairing their ability to eat or to be intimate with a partner who now smells unpleasant, said Dr. Farrell, who wasn’t associated with this research.

The treatment, called a stellate ganglion block, is provided through a shot into nerves in the neck. People with parosmia associated with COVID-19 often report that this method cures them. Dr. Patel said that may be because their psychological health is improving, not their sense of smell, because the area of the body where the stellate ganglion block is applied is not part of the olfactory system.

Earlier this year, Dr. Farrell and colleagues reported that parosmia linked to COVID-19 is associated with an increased risk for depression, anxiety, and suicidal ideation. 

One coauthor reported receiving grants from Smell and Taste Lab, Takasago, Baia Foods, and Frequency Therapeutics. The other authors reported no relevant financial relationships.

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

Good news for people struggling with sensory problems after a bout of COVID-19. Although mild cases of the disease often impair the ability to taste and smell, and the problem can drag on for months, a new study from Italy shows that most people return to their senses, as it were, within 3 years.

“In the vast majority of cases, the loss of the sense of smell is not irreversible,” said Paolo Boscolo-Rizzo, MD, a professor of medicine, surgery, and health sciences at the University of Trieste (Italy), and a co-author of the study, published as a research letter in JAMA Otolaryngology–Head & Neck Surgery.

Dr. Boscolo-Rizzo and his colleagues analyzed data from 88 adults with mild COVID-19, which was defined as having no lower respiratory disease and blood oxygen saturation of 94% or greater. Another group of 88 adults who never contracted the virus but sometimes had difficulties with smell and taste were also studied. In both groups, the average age was 49 years, all participants were White, and 58% were women.

The researchers tested participants’ sense of smell with sticks that contained different odors and checked their sense of taste with strips that had different tastes. Over time, fewer people had difficulty distinguishing odors. Three years after developing COVID-19, only 12 people had impaired smell, compared with 36 people at year 1 and 24 people at year 2. And at the 3-year mark, all participants had at least a partial ability to smell. 

The story was similar with sense of taste, with 10 of 88 people reporting impairments 3 years later. By then, people with COVID-19 were no more likely to have trouble with smell or taste than people who did not get the virus. 

A study this past June showed a strong correlation between severity of COVID-19 symptoms and impaired sense of taste and smell and estimated that millions of Americans maintained altered senses. More than 10% of people in the Italian study still had trouble with smell or taste 3 years later.
 

Emerging treatments, psychological concerns

“We’re seeing fewer people with this problem, but there are still people suffering from it,” said Fernando Carnavali, MD, an internal medicine physician and a site director for the Center for Post-COVID Care at the Icahn School of Medicine at Mount Sinai, New York City.

Dr. Carnavali wasn’t part of this study, but he did find the new results encouraging, and he called for similar studies in diverse populations that have experienced COVID-19. He also noted that an impaired sense of smell is distressing.

“It really has a significant psychological impact,” Dr. Carnavali said.

He recalled a patient crying in his office because her inability to smell made it impossible for her to cook. Dr. Carnavali recommended clinicians refer patients facing protracted loss of smell or taste to mental health professionals for support.

Treatments are emerging for COVID-19 smell loss. One approach is to inject platelet-rich plasma into a patient’s nasal cavities to help neurons related to smell repair themselves.

A randomized trial showed platelet-rich plasma significantly outperformed placebo in patients with smell loss up to a year after getting COVID-19.

“I wish more people would do it,” said Zara Patel, MD, an otolaryngologist at Stanford (Calif.) Medicine, who helped conduct that trial. She said some physicians may be nervous about injecting plasma so close to the skull and are therefore hesitant to try this approach. 

Another technique may help to address the olfactory condition known as parosmia, in which patients generally experience a benign odor as rancid, according to otolaryngologist Nyssa Farrell, MD, of Washington University School of Medicine, St. Louis. Dr. Farrell said around two-thirds of patients who contract COVID-19 develop the condition, and the rates of long-term parosmia range from 10%-50% depending on various studies.

“It is almost always foul; this can profoundly affect someone’s quality of life,” impairing their ability to eat or to be intimate with a partner who now smells unpleasant, said Dr. Farrell, who wasn’t associated with this research.

The treatment, called a stellate ganglion block, is provided through a shot into nerves in the neck. People with parosmia associated with COVID-19 often report that this method cures them. Dr. Patel said that may be because their psychological health is improving, not their sense of smell, because the area of the body where the stellate ganglion block is applied is not part of the olfactory system.

Earlier this year, Dr. Farrell and colleagues reported that parosmia linked to COVID-19 is associated with an increased risk for depression, anxiety, and suicidal ideation. 

One coauthor reported receiving grants from Smell and Taste Lab, Takasago, Baia Foods, and Frequency Therapeutics. The other authors reported no relevant financial relationships.

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

Good news for people struggling with sensory problems after a bout of COVID-19. Although mild cases of the disease often impair the ability to taste and smell, and the problem can drag on for months, a new study from Italy shows that most people return to their senses, as it were, within 3 years.

“In the vast majority of cases, the loss of the sense of smell is not irreversible,” said Paolo Boscolo-Rizzo, MD, a professor of medicine, surgery, and health sciences at the University of Trieste (Italy), and a co-author of the study, published as a research letter in JAMA Otolaryngology–Head & Neck Surgery.

Dr. Boscolo-Rizzo and his colleagues analyzed data from 88 adults with mild COVID-19, which was defined as having no lower respiratory disease and blood oxygen saturation of 94% or greater. Another group of 88 adults who never contracted the virus but sometimes had difficulties with smell and taste were also studied. In both groups, the average age was 49 years, all participants were White, and 58% were women.

The researchers tested participants’ sense of smell with sticks that contained different odors and checked their sense of taste with strips that had different tastes. Over time, fewer people had difficulty distinguishing odors. Three years after developing COVID-19, only 12 people had impaired smell, compared with 36 people at year 1 and 24 people at year 2. And at the 3-year mark, all participants had at least a partial ability to smell. 

The story was similar with sense of taste, with 10 of 88 people reporting impairments 3 years later. By then, people with COVID-19 were no more likely to have trouble with smell or taste than people who did not get the virus. 

A study this past June showed a strong correlation between severity of COVID-19 symptoms and impaired sense of taste and smell and estimated that millions of Americans maintained altered senses. More than 10% of people in the Italian study still had trouble with smell or taste 3 years later.
 

Emerging treatments, psychological concerns

“We’re seeing fewer people with this problem, but there are still people suffering from it,” said Fernando Carnavali, MD, an internal medicine physician and a site director for the Center for Post-COVID Care at the Icahn School of Medicine at Mount Sinai, New York City.

Dr. Carnavali wasn’t part of this study, but he did find the new results encouraging, and he called for similar studies in diverse populations that have experienced COVID-19. He also noted that an impaired sense of smell is distressing.

“It really has a significant psychological impact,” Dr. Carnavali said.

He recalled a patient crying in his office because her inability to smell made it impossible for her to cook. Dr. Carnavali recommended clinicians refer patients facing protracted loss of smell or taste to mental health professionals for support.

Treatments are emerging for COVID-19 smell loss. One approach is to inject platelet-rich plasma into a patient’s nasal cavities to help neurons related to smell repair themselves.

A randomized trial showed platelet-rich plasma significantly outperformed placebo in patients with smell loss up to a year after getting COVID-19.

“I wish more people would do it,” said Zara Patel, MD, an otolaryngologist at Stanford (Calif.) Medicine, who helped conduct that trial. She said some physicians may be nervous about injecting plasma so close to the skull and are therefore hesitant to try this approach. 

Another technique may help to address the olfactory condition known as parosmia, in which patients generally experience a benign odor as rancid, according to otolaryngologist Nyssa Farrell, MD, of Washington University School of Medicine, St. Louis. Dr. Farrell said around two-thirds of patients who contract COVID-19 develop the condition, and the rates of long-term parosmia range from 10%-50% depending on various studies.

“It is almost always foul; this can profoundly affect someone’s quality of life,” impairing their ability to eat or to be intimate with a partner who now smells unpleasant, said Dr. Farrell, who wasn’t associated with this research.

The treatment, called a stellate ganglion block, is provided through a shot into nerves in the neck. People with parosmia associated with COVID-19 often report that this method cures them. Dr. Patel said that may be because their psychological health is improving, not their sense of smell, because the area of the body where the stellate ganglion block is applied is not part of the olfactory system.

Earlier this year, Dr. Farrell and colleagues reported that parosmia linked to COVID-19 is associated with an increased risk for depression, anxiety, and suicidal ideation. 

One coauthor reported receiving grants from Smell and Taste Lab, Takasago, Baia Foods, and Frequency Therapeutics. The other authors reported no relevant financial relationships.

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

People infected multiple times with COVID-19 are more likely to develop long COVID, and most never fully recover from the condition. Those are two of the most striking findings of a comprehensive new research study of 138,000 veterans.

Lead researcher Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, spoke with this news organization about his team’s findings, what we know – and don’t – about long COVID, and what it means for physicians treating patients with the condition.

Excerpts of the interview follow.

Your research concluded that for those infected early in the pandemic, some long COVID symptoms declined over 2 years, but some did not. You have also concluded that long COVID is a chronic disease. Why?

We’ve been in this journey a little bit more than three and a half years. Some patients do experience some recovery. But that’s not the norm. Most people do not really fully recover. The health trajectory for people with long COVID is really very heterogeneous. There is no one-size-fits-all. There’s really no one line that I could give you that could cover all your patients. But it is very, very, very clear that a bunch of them experienced long COVID for sure; that’s really happening.

It happened in the pre-Delta era and in the Delta era, and with Omicron subvariants, even now. There are people who think, “This is a nothing-burger anymore,” or “It’s not an issue anymore.” It’s still happening with the current variants. Vaccines do reduce risk for long COVID, but do not completely eliminate the risk for long COVID.

You work with patients with long COVID in the clinic and also analyze data from thousands more. If long COVID does not go away, what should doctors look for in everyday practice that will help them recognize and help patients with long COVID?

Long COVID is not uncommon. We see it in the clinic in large numbers. Whatever clinic you’re running – if you’re running a cardiology clinic, or a nephrology clinic, or diabetes, or primary care – probably some of your people have it. You may not know about it. They may not tell you about it. You may not recognize it.

Not all long COVID is the same, and that’s really what makes it complex and makes it really hard to deal with in the clinic. But that’s the reality that we’re all dealing with. And it’s multisystemic; it’s not like it affects the heart only, the brain only, or the autonomic nervous system only. It does not behave in the same way in different individuals – they may have different manifestations, various health trajectories, and different outcomes. It’s important for doctors to get up to speed on long COVID as a multisystem illness.

Management at this point is really managing the symptoms. We don’t have a treatment for it; we don’t have a cure for it.

Some patients experience what you’ve described as partial recovery. What does that look like?

Some individuals do experience some recovery over time, but for most individuals, the recovery is long and arduous. Long COVID can last with them for many years. Some people may come back to the clinic and say, “I’m doing better,” but if you really flesh it out and dig deeper, they didn’t do better; they adjusted to a new baseline. They used to walk the dog three to four blocks, and now they walk the dog only half a block. They used to do an activity with their partner every Saturday or Sunday, and now they do half of that.

If you’re a physician, a primary care provider, or any other provider who is dealing with a patient with long COVID, know that this is really happening. It can happen even in vaccinated individuals. The presentation is heterogeneous. Some people may present to you with and say. “Well, before I had COVID I was mentally sharp and now having I’m having difficulty with memory, etc.” It can sometimes present as fatigue or postexertional malaise.

In some instances, it can present as sleep problems. It can present as what we call postural orthostatic tachycardia syndrome (POTS). Those people get a significant increase in heart rate with postural changes.

What the most important thing we can we learn from the emergence of long COVID?

This whole thing taught us that infections can cause chronic disease. That’s really the No. 1 lesson that I take from this pandemic – that infections can cause chronic disease.

Looking at only acute illness from COVID is really only looking at the tip of the iceberg. Beneath that tip of the iceberg lies this hidden toll of disease that we don’t really talk about that much.

This pandemic shone a very, very good light on the idea that there is really an intimate connection between infections and chronic disease. It was really hardwired into our medical training as doctors that most infections, when people get over the hump of the acute phase of the disease, it’s all behind them. I think long COVID has humbled us in many, many ways, but chief among those is the realization – the stark realization – that infections can cause chronic disease.

That’s really going back to your [first] question: What does it mean that some people are not recovering? They actually have chronic illness. I’m hoping that we will find a treatment, that we’ll start finding things that would help them get back to baseline. But at this point in time, what we’re dealing with is people with chronic illness or chronic disease that may continue to affect them for many years to come in the absence of a treatment or a cure.

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

People infected multiple times with COVID-19 are more likely to develop long COVID, and most never fully recover from the condition. Those are two of the most striking findings of a comprehensive new research study of 138,000 veterans.

Lead researcher Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, spoke with this news organization about his team’s findings, what we know – and don’t – about long COVID, and what it means for physicians treating patients with the condition.

Excerpts of the interview follow.

Your research concluded that for those infected early in the pandemic, some long COVID symptoms declined over 2 years, but some did not. You have also concluded that long COVID is a chronic disease. Why?

We’ve been in this journey a little bit more than three and a half years. Some patients do experience some recovery. But that’s not the norm. Most people do not really fully recover. The health trajectory for people with long COVID is really very heterogeneous. There is no one-size-fits-all. There’s really no one line that I could give you that could cover all your patients. But it is very, very, very clear that a bunch of them experienced long COVID for sure; that’s really happening.

It happened in the pre-Delta era and in the Delta era, and with Omicron subvariants, even now. There are people who think, “This is a nothing-burger anymore,” or “It’s not an issue anymore.” It’s still happening with the current variants. Vaccines do reduce risk for long COVID, but do not completely eliminate the risk for long COVID.

You work with patients with long COVID in the clinic and also analyze data from thousands more. If long COVID does not go away, what should doctors look for in everyday practice that will help them recognize and help patients with long COVID?

Long COVID is not uncommon. We see it in the clinic in large numbers. Whatever clinic you’re running – if you’re running a cardiology clinic, or a nephrology clinic, or diabetes, or primary care – probably some of your people have it. You may not know about it. They may not tell you about it. You may not recognize it.

Not all long COVID is the same, and that’s really what makes it complex and makes it really hard to deal with in the clinic. But that’s the reality that we’re all dealing with. And it’s multisystemic; it’s not like it affects the heart only, the brain only, or the autonomic nervous system only. It does not behave in the same way in different individuals – they may have different manifestations, various health trajectories, and different outcomes. It’s important for doctors to get up to speed on long COVID as a multisystem illness.

Management at this point is really managing the symptoms. We don’t have a treatment for it; we don’t have a cure for it.

Some patients experience what you’ve described as partial recovery. What does that look like?

Some individuals do experience some recovery over time, but for most individuals, the recovery is long and arduous. Long COVID can last with them for many years. Some people may come back to the clinic and say, “I’m doing better,” but if you really flesh it out and dig deeper, they didn’t do better; they adjusted to a new baseline. They used to walk the dog three to four blocks, and now they walk the dog only half a block. They used to do an activity with their partner every Saturday or Sunday, and now they do half of that.

If you’re a physician, a primary care provider, or any other provider who is dealing with a patient with long COVID, know that this is really happening. It can happen even in vaccinated individuals. The presentation is heterogeneous. Some people may present to you with and say. “Well, before I had COVID I was mentally sharp and now having I’m having difficulty with memory, etc.” It can sometimes present as fatigue or postexertional malaise.

In some instances, it can present as sleep problems. It can present as what we call postural orthostatic tachycardia syndrome (POTS). Those people get a significant increase in heart rate with postural changes.

What the most important thing we can we learn from the emergence of long COVID?

This whole thing taught us that infections can cause chronic disease. That’s really the No. 1 lesson that I take from this pandemic – that infections can cause chronic disease.

Looking at only acute illness from COVID is really only looking at the tip of the iceberg. Beneath that tip of the iceberg lies this hidden toll of disease that we don’t really talk about that much.

This pandemic shone a very, very good light on the idea that there is really an intimate connection between infections and chronic disease. It was really hardwired into our medical training as doctors that most infections, when people get over the hump of the acute phase of the disease, it’s all behind them. I think long COVID has humbled us in many, many ways, but chief among those is the realization – the stark realization – that infections can cause chronic disease.

That’s really going back to your [first] question: What does it mean that some people are not recovering? They actually have chronic illness. I’m hoping that we will find a treatment, that we’ll start finding things that would help them get back to baseline. But at this point in time, what we’re dealing with is people with chronic illness or chronic disease that may continue to affect them for many years to come in the absence of a treatment or a cure.

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

People infected multiple times with COVID-19 are more likely to develop long COVID, and most never fully recover from the condition. Those are two of the most striking findings of a comprehensive new research study of 138,000 veterans.

Lead researcher Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, spoke with this news organization about his team’s findings, what we know – and don’t – about long COVID, and what it means for physicians treating patients with the condition.

Excerpts of the interview follow.

Your research concluded that for those infected early in the pandemic, some long COVID symptoms declined over 2 years, but some did not. You have also concluded that long COVID is a chronic disease. Why?

We’ve been in this journey a little bit more than three and a half years. Some patients do experience some recovery. But that’s not the norm. Most people do not really fully recover. The health trajectory for people with long COVID is really very heterogeneous. There is no one-size-fits-all. There’s really no one line that I could give you that could cover all your patients. But it is very, very, very clear that a bunch of them experienced long COVID for sure; that’s really happening.

It happened in the pre-Delta era and in the Delta era, and with Omicron subvariants, even now. There are people who think, “This is a nothing-burger anymore,” or “It’s not an issue anymore.” It’s still happening with the current variants. Vaccines do reduce risk for long COVID, but do not completely eliminate the risk for long COVID.

You work with patients with long COVID in the clinic and also analyze data from thousands more. If long COVID does not go away, what should doctors look for in everyday practice that will help them recognize and help patients with long COVID?

Long COVID is not uncommon. We see it in the clinic in large numbers. Whatever clinic you’re running – if you’re running a cardiology clinic, or a nephrology clinic, or diabetes, or primary care – probably some of your people have it. You may not know about it. They may not tell you about it. You may not recognize it.

Not all long COVID is the same, and that’s really what makes it complex and makes it really hard to deal with in the clinic. But that’s the reality that we’re all dealing with. And it’s multisystemic; it’s not like it affects the heart only, the brain only, or the autonomic nervous system only. It does not behave in the same way in different individuals – they may have different manifestations, various health trajectories, and different outcomes. It’s important for doctors to get up to speed on long COVID as a multisystem illness.

Management at this point is really managing the symptoms. We don’t have a treatment for it; we don’t have a cure for it.

Some patients experience what you’ve described as partial recovery. What does that look like?

Some individuals do experience some recovery over time, but for most individuals, the recovery is long and arduous. Long COVID can last with them for many years. Some people may come back to the clinic and say, “I’m doing better,” but if you really flesh it out and dig deeper, they didn’t do better; they adjusted to a new baseline. They used to walk the dog three to four blocks, and now they walk the dog only half a block. They used to do an activity with their partner every Saturday or Sunday, and now they do half of that.

If you’re a physician, a primary care provider, or any other provider who is dealing with a patient with long COVID, know that this is really happening. It can happen even in vaccinated individuals. The presentation is heterogeneous. Some people may present to you with and say. “Well, before I had COVID I was mentally sharp and now having I’m having difficulty with memory, etc.” It can sometimes present as fatigue or postexertional malaise.

In some instances, it can present as sleep problems. It can present as what we call postural orthostatic tachycardia syndrome (POTS). Those people get a significant increase in heart rate with postural changes.

What the most important thing we can we learn from the emergence of long COVID?

This whole thing taught us that infections can cause chronic disease. That’s really the No. 1 lesson that I take from this pandemic – that infections can cause chronic disease.

Looking at only acute illness from COVID is really only looking at the tip of the iceberg. Beneath that tip of the iceberg lies this hidden toll of disease that we don’t really talk about that much.

This pandemic shone a very, very good light on the idea that there is really an intimate connection between infections and chronic disease. It was really hardwired into our medical training as doctors that most infections, when people get over the hump of the acute phase of the disease, it’s all behind them. I think long COVID has humbled us in many, many ways, but chief among those is the realization – the stark realization – that infections can cause chronic disease.

That’s really going back to your [first] question: What does it mean that some people are not recovering? They actually have chronic illness. I’m hoping that we will find a treatment, that we’ll start finding things that would help them get back to baseline. But at this point in time, what we’re dealing with is people with chronic illness or chronic disease that may continue to affect them for many years to come in the absence of a treatment or a cure.

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

A pair of new studies published about long COVID have shed more light on the sometimes-disabling condition that affects millions of people in the United States. 

Scientists worldwide have been working to understand the wide-ranging condition, from risk factors to causes to potential treatments. 

In the first study, 31 adults underwent lumbar puncture and blood draws to look for changes in their immune systems and also to look for changes in the nerve cells that could affect transmission of signals to the brain.

Among the participants, 25 people had neurocognitive symptoms of long COVID, such as memory loss or attention problems. Six participants had fully recovered from COVID, and 17 people had never had COVID. 

Those who had COVID were diagnosed between March 2020 and May 2021. Their fluid samples were drawn at least three months after their first symptoms.

The results were published in the Journal of Infectious Diseases. Study results showed that long COVID does not appear to be linked to the SARS-CoV-2 virus invading the brain or causing active brain damage.

According to a summary of the study from the University of Gothenburg (Sweden), where the researchers work, “there were no significant differences between the groups when analyzing blood and cerebrospinal fluid for immune activation or brain injury markers. The findings thus suggest that post-COVID condition is not the result of ongoing infection, immune activation, or brain damage.”

In the second study, Norwegian researchers compared the likelihood of having 17 different long COVID symptoms based on whether a person had been infected with COVID. The analysis included 53,846 people who were diagnosed with COVID between February 2020 and February 2021, as well as more than 485,000 people who were not infected. Most people had not been vaccinated against COVID-19 during the time of the study.

The results were published in the journal BMC Infectious Diseases. Study results showed that people who had COVID were more than twice as likely to experience shortness of breath or fatigue. They were also more likely to experience memory loss or headache compared to people who never had COVID. Researchers only looked at symptoms that occurred at least three months after a COVID diagnosis.

They also found that hospitalization increased the risk for experiencing long COVID symptoms of shortness of breath, fatigue, and memory loss.

The authors noted that a limitation of their study was that, often, not all symptoms reported during a visit with a general practice medical provider are recorded in Norway, which could have affected the results.

A version of this article appeared on Medscape.com.

A pair of new studies published about long COVID have shed more light on the sometimes-disabling condition that affects millions of people in the United States. 

Scientists worldwide have been working to understand the wide-ranging condition, from risk factors to causes to potential treatments. 

In the first study, 31 adults underwent lumbar puncture and blood draws to look for changes in their immune systems and also to look for changes in the nerve cells that could affect transmission of signals to the brain.

Among the participants, 25 people had neurocognitive symptoms of long COVID, such as memory loss or attention problems. Six participants had fully recovered from COVID, and 17 people had never had COVID. 

Those who had COVID were diagnosed between March 2020 and May 2021. Their fluid samples were drawn at least three months after their first symptoms.

The results were published in the Journal of Infectious Diseases. Study results showed that long COVID does not appear to be linked to the SARS-CoV-2 virus invading the brain or causing active brain damage.

According to a summary of the study from the University of Gothenburg (Sweden), where the researchers work, “there were no significant differences between the groups when analyzing blood and cerebrospinal fluid for immune activation or brain injury markers. The findings thus suggest that post-COVID condition is not the result of ongoing infection, immune activation, or brain damage.”

In the second study, Norwegian researchers compared the likelihood of having 17 different long COVID symptoms based on whether a person had been infected with COVID. The analysis included 53,846 people who were diagnosed with COVID between February 2020 and February 2021, as well as more than 485,000 people who were not infected. Most people had not been vaccinated against COVID-19 during the time of the study.

The results were published in the journal BMC Infectious Diseases. Study results showed that people who had COVID were more than twice as likely to experience shortness of breath or fatigue. They were also more likely to experience memory loss or headache compared to people who never had COVID. Researchers only looked at symptoms that occurred at least three months after a COVID diagnosis.

They also found that hospitalization increased the risk for experiencing long COVID symptoms of shortness of breath, fatigue, and memory loss.

The authors noted that a limitation of their study was that, often, not all symptoms reported during a visit with a general practice medical provider are recorded in Norway, which could have affected the results.

A version of this article appeared on Medscape.com.

A pair of new studies published about long COVID have shed more light on the sometimes-disabling condition that affects millions of people in the United States. 

Scientists worldwide have been working to understand the wide-ranging condition, from risk factors to causes to potential treatments. 

In the first study, 31 adults underwent lumbar puncture and blood draws to look for changes in their immune systems and also to look for changes in the nerve cells that could affect transmission of signals to the brain.

Among the participants, 25 people had neurocognitive symptoms of long COVID, such as memory loss or attention problems. Six participants had fully recovered from COVID, and 17 people had never had COVID. 

Those who had COVID were diagnosed between March 2020 and May 2021. Their fluid samples were drawn at least three months after their first symptoms.

The results were published in the Journal of Infectious Diseases. Study results showed that long COVID does not appear to be linked to the SARS-CoV-2 virus invading the brain or causing active brain damage.

According to a summary of the study from the University of Gothenburg (Sweden), where the researchers work, “there were no significant differences between the groups when analyzing blood and cerebrospinal fluid for immune activation or brain injury markers. The findings thus suggest that post-COVID condition is not the result of ongoing infection, immune activation, or brain damage.”

In the second study, Norwegian researchers compared the likelihood of having 17 different long COVID symptoms based on whether a person had been infected with COVID. The analysis included 53,846 people who were diagnosed with COVID between February 2020 and February 2021, as well as more than 485,000 people who were not infected. Most people had not been vaccinated against COVID-19 during the time of the study.

The results were published in the journal BMC Infectious Diseases. Study results showed that people who had COVID were more than twice as likely to experience shortness of breath or fatigue. They were also more likely to experience memory loss or headache compared to people who never had COVID. Researchers only looked at symptoms that occurred at least three months after a COVID diagnosis.

They also found that hospitalization increased the risk for experiencing long COVID symptoms of shortness of breath, fatigue, and memory loss.

The authors noted that a limitation of their study was that, often, not all symptoms reported during a visit with a general practice medical provider are recorded in Norway, which could have affected the results.

A version of this article appeared on Medscape.com.

Health care providers who give this year’s Moderna COVID-19 vaccine to children aged 6 months to 11 years should be sure they withdraw the correct volume of the vaccine from the vial to ensure a proper dose, the Food and Drug Administration said in a MedWatch issued Nov. 1, 2023.

That dose is 0.25 mL for children 6 months through 11 years. In the MedWatch, the FDA said that it “has become aware” that the single-dose vial for use in this age group “contains notably more than 0.25 mL of the vaccine.” It added: “Some healthcare providers may be withdrawing the entire contents of the vial to administer to an individual.”

The FDA revised the Fact Sheet for Healthcare Providers Administering Vaccine to clarify that the 0.25 mL should be withdrawn from the vial and that the vial and any excess then should be discarded. It is in a single-dose vial with a blue cap and a green label.

“It is common [for vaccine makers] to put in a little bit of extra vaccine just to make sure everyone gets enough,” said William Schaffner, MD, an infectious disease specialist at Vanderbilt University Medical Center, Nashville, Tenn. “The provider is supposed to be looking at the syringe when they withdraw it to make sure they get the right amount,” Dr. Schaffner said.

Recently, parents on social media had expressed concerns that their children may have gotten more than the recommended dose, with some parents noticing more reactions such as soreness and fever with the 2023-2024 vaccine dose than they did with their children’s previous COVID vaccinations.

“Since the beginning of the rollout, parents were telling us of cases where pharmacies accidentally gave their children a double dose, while doctors in our group were pointing out that their vials for children contained twice the amount than what was needed,” said Fatima Khan, a parent and cofounder of the group Protect Their Future, an organization that advocates for pediatric vaccine access. Members contacted the FDA and other officials. “We appreciate that the FDA took our concerns seriously and issued this safety update,” Ms. Khan said.

A spokesperson for Moderna is researching how much more vaccine the single-dose vials might contain.
 

No safety risks identified

“The FDA has not identified any safety risks associated with administration of the higher dose in individuals 6 months through 11 years of age and no serious adverse events were identified related to a dosing error for the vaccine,” Cherie Duvall-Jones, an FDA spokesperson, said in an email response.

“The FDA received questions from stakeholders about the dosing issue on Oct. 29, and contacted Moderna to discuss and better understand the issue,” Ms. Duvall-Jones said. The agency then alerted health care providers via the safety communication and other means to be sure the correct dosage is given to the children aged 12 years or younger.
 

One parent’s experience

Jane Jih, MD, an internist in San Francisco, took her 7-year-old daughter to a pharmacy to get the vaccine, and it was the first time the pharmacist had given a pediatric dose. “We both had to double check the dose,” Dr. Jih said. She observed that the vial had about 0.40 mL, which is 0.15 mL above the recommended dose.

A few weeks later, Dr. Jih could access the vaccine for her nearly-3-year-old son. The nurse practitioner who administered it had been giving many pediatric Moderna shots, she said, “so I felt more confident in the second scenario.”
 

Perhaps more reactions, no danger

“If you get a little bit more [than the recommended 0.25 mL], that certainly is not going to harm the child,” Dr. Schaffner said. “There may be a little bit more local reaction. In terms of the child’s immune system, there really isn’t any harm.”

If an entire adult dose is mistakenly given, he said, “I think the reaction locally in some children may be more evident, they may get more sore arms, redness, maybe a little bit more swelling and tenderness. Fever is also a possibility, but “these vaccines have not been associated with too much fever.”

Could a double dose do more harm than that? “It is unknown,” said Aaron Glatt, MD, chief of infectious diseases and hospital epidemiologist for Mount Sinai South Nassau, Oceanside, N.Y. “But there is the theoretical potential for some more complications. I do not know whether this [excess vaccine] would cause an increased likelihood of cardiac inflammatory problems like myocarditis or other rare complications to occur more frequently.”

The message for health care providers giving the vaccine, Dr. Schaffner said, is: “Look at your syringe to make sure the dose is appropriate.”

A version of this article appeared on Medscape.com.

Health care providers who give this year’s Moderna COVID-19 vaccine to children aged 6 months to 11 years should be sure they withdraw the correct volume of the vaccine from the vial to ensure a proper dose, the Food and Drug Administration said in a MedWatch issued Nov. 1, 2023.

That dose is 0.25 mL for children 6 months through 11 years. In the MedWatch, the FDA said that it “has become aware” that the single-dose vial for use in this age group “contains notably more than 0.25 mL of the vaccine.” It added: “Some healthcare providers may be withdrawing the entire contents of the vial to administer to an individual.”

The FDA revised the Fact Sheet for Healthcare Providers Administering Vaccine to clarify that the 0.25 mL should be withdrawn from the vial and that the vial and any excess then should be discarded. It is in a single-dose vial with a blue cap and a green label.

“It is common [for vaccine makers] to put in a little bit of extra vaccine just to make sure everyone gets enough,” said William Schaffner, MD, an infectious disease specialist at Vanderbilt University Medical Center, Nashville, Tenn. “The provider is supposed to be looking at the syringe when they withdraw it to make sure they get the right amount,” Dr. Schaffner said.

Recently, parents on social media had expressed concerns that their children may have gotten more than the recommended dose, with some parents noticing more reactions such as soreness and fever with the 2023-2024 vaccine dose than they did with their children’s previous COVID vaccinations.

“Since the beginning of the rollout, parents were telling us of cases where pharmacies accidentally gave their children a double dose, while doctors in our group were pointing out that their vials for children contained twice the amount than what was needed,” said Fatima Khan, a parent and cofounder of the group Protect Their Future, an organization that advocates for pediatric vaccine access. Members contacted the FDA and other officials. “We appreciate that the FDA took our concerns seriously and issued this safety update,” Ms. Khan said.

A spokesperson for Moderna is researching how much more vaccine the single-dose vials might contain.
 

No safety risks identified

“The FDA has not identified any safety risks associated with administration of the higher dose in individuals 6 months through 11 years of age and no serious adverse events were identified related to a dosing error for the vaccine,” Cherie Duvall-Jones, an FDA spokesperson, said in an email response.

“The FDA received questions from stakeholders about the dosing issue on Oct. 29, and contacted Moderna to discuss and better understand the issue,” Ms. Duvall-Jones said. The agency then alerted health care providers via the safety communication and other means to be sure the correct dosage is given to the children aged 12 years or younger.
 

One parent’s experience

Jane Jih, MD, an internist in San Francisco, took her 7-year-old daughter to a pharmacy to get the vaccine, and it was the first time the pharmacist had given a pediatric dose. “We both had to double check the dose,” Dr. Jih said. She observed that the vial had about 0.40 mL, which is 0.15 mL above the recommended dose.

A few weeks later, Dr. Jih could access the vaccine for her nearly-3-year-old son. The nurse practitioner who administered it had been giving many pediatric Moderna shots, she said, “so I felt more confident in the second scenario.”
 

Perhaps more reactions, no danger

“If you get a little bit more [than the recommended 0.25 mL], that certainly is not going to harm the child,” Dr. Schaffner said. “There may be a little bit more local reaction. In terms of the child’s immune system, there really isn’t any harm.”

If an entire adult dose is mistakenly given, he said, “I think the reaction locally in some children may be more evident, they may get more sore arms, redness, maybe a little bit more swelling and tenderness. Fever is also a possibility, but “these vaccines have not been associated with too much fever.”

Could a double dose do more harm than that? “It is unknown,” said Aaron Glatt, MD, chief of infectious diseases and hospital epidemiologist for Mount Sinai South Nassau, Oceanside, N.Y. “But there is the theoretical potential for some more complications. I do not know whether this [excess vaccine] would cause an increased likelihood of cardiac inflammatory problems like myocarditis or other rare complications to occur more frequently.”

The message for health care providers giving the vaccine, Dr. Schaffner said, is: “Look at your syringe to make sure the dose is appropriate.”

A version of this article appeared on Medscape.com.

Health care providers who give this year’s Moderna COVID-19 vaccine to children aged 6 months to 11 years should be sure they withdraw the correct volume of the vaccine from the vial to ensure a proper dose, the Food and Drug Administration said in a MedWatch issued Nov. 1, 2023.

That dose is 0.25 mL for children 6 months through 11 years. In the MedWatch, the FDA said that it “has become aware” that the single-dose vial for use in this age group “contains notably more than 0.25 mL of the vaccine.” It added: “Some healthcare providers may be withdrawing the entire contents of the vial to administer to an individual.”

The FDA revised the Fact Sheet for Healthcare Providers Administering Vaccine to clarify that the 0.25 mL should be withdrawn from the vial and that the vial and any excess then should be discarded. It is in a single-dose vial with a blue cap and a green label.

“It is common [for vaccine makers] to put in a little bit of extra vaccine just to make sure everyone gets enough,” said William Schaffner, MD, an infectious disease specialist at Vanderbilt University Medical Center, Nashville, Tenn. “The provider is supposed to be looking at the syringe when they withdraw it to make sure they get the right amount,” Dr. Schaffner said.

Recently, parents on social media had expressed concerns that their children may have gotten more than the recommended dose, with some parents noticing more reactions such as soreness and fever with the 2023-2024 vaccine dose than they did with their children’s previous COVID vaccinations.

“Since the beginning of the rollout, parents were telling us of cases where pharmacies accidentally gave their children a double dose, while doctors in our group were pointing out that their vials for children contained twice the amount than what was needed,” said Fatima Khan, a parent and cofounder of the group Protect Their Future, an organization that advocates for pediatric vaccine access. Members contacted the FDA and other officials. “We appreciate that the FDA took our concerns seriously and issued this safety update,” Ms. Khan said.

A spokesperson for Moderna is researching how much more vaccine the single-dose vials might contain.
 

No safety risks identified

“The FDA has not identified any safety risks associated with administration of the higher dose in individuals 6 months through 11 years of age and no serious adverse events were identified related to a dosing error for the vaccine,” Cherie Duvall-Jones, an FDA spokesperson, said in an email response.

“The FDA received questions from stakeholders about the dosing issue on Oct. 29, and contacted Moderna to discuss and better understand the issue,” Ms. Duvall-Jones said. The agency then alerted health care providers via the safety communication and other means to be sure the correct dosage is given to the children aged 12 years or younger.
 

One parent’s experience

Jane Jih, MD, an internist in San Francisco, took her 7-year-old daughter to a pharmacy to get the vaccine, and it was the first time the pharmacist had given a pediatric dose. “We both had to double check the dose,” Dr. Jih said. She observed that the vial had about 0.40 mL, which is 0.15 mL above the recommended dose.

A few weeks later, Dr. Jih could access the vaccine for her nearly-3-year-old son. The nurse practitioner who administered it had been giving many pediatric Moderna shots, she said, “so I felt more confident in the second scenario.”
 

Perhaps more reactions, no danger

“If you get a little bit more [than the recommended 0.25 mL], that certainly is not going to harm the child,” Dr. Schaffner said. “There may be a little bit more local reaction. In terms of the child’s immune system, there really isn’t any harm.”

If an entire adult dose is mistakenly given, he said, “I think the reaction locally in some children may be more evident, they may get more sore arms, redness, maybe a little bit more swelling and tenderness. Fever is also a possibility, but “these vaccines have not been associated with too much fever.”

Could a double dose do more harm than that? “It is unknown,” said Aaron Glatt, MD, chief of infectious diseases and hospital epidemiologist for Mount Sinai South Nassau, Oceanside, N.Y. “But there is the theoretical potential for some more complications. I do not know whether this [excess vaccine] would cause an increased likelihood of cardiac inflammatory problems like myocarditis or other rare complications to occur more frequently.”

The message for health care providers giving the vaccine, Dr. Schaffner said, is: “Look at your syringe to make sure the dose is appropriate.”

A version of this article appeared on Medscape.com.

TOPLINE:

Severe mental illness (SMI) has been linked to a 50% increased risk for all-cause mortality risk after COVID-19, a large population-based study suggests.

METHODOLOGY:

• Investigators analyzed data from the Clinical Practice Research Datalink database, which contains health information on 13.5 million patients receiving care from family practices in England and Northern Ireland.
• The study included participants with SMI, including schizophrenia, schizoaffective disorder, and bipolar disorder.
• Participants were aged 5 years or older with a SARS-CoV-2 infection recorded between Feb. 1, 2020, and March 31, 2021, spanning two waves of the pandemic.
• Death rates among participants with SMI and COVID-19 (n = 7,150; 56% female) were compared with those in a control group of participants without SMI who had been diagnosed with COVID-19 (n = 650,000; 55% female).

TAKEAWAY:

• Participants with SMI and COVID-19 had a 53% higher risk for death than those in the non-SMI control group (adjusted hazard ratio, 1.53; 95% confidence interval, 1.39-1.68).
• Black Caribbean/Black African participants were more likely than White participants to die of COVID-19 (aHR, 1.22; 95% CI, 1.12-1.34), although ethnicity was not recorded in 30% of participants.
• After SARS-CoV-2 infection, for every additional multimorbid condition, the aHR for death increased by 6% in the SMI group and 16% in the non-SMI group (P = .001). Some of these conditions included hypertension, heart disease, diabetes, kidney disease, depression, and anxiety.

IN PRACTICE:

“From a public health perspective, our study has emphasized the need for early and timely preventative interventions (e.g. vaccination) for the SMI population. Future studies are needed to disentangle the complex biological and psychosocial factors, and health care pathways, that have led to the greater mortality rates in the SMI population,” the authors write.

SOURCE:

Jayati Das-Munshi, MD, of Kings College London, led the study, which was published online in the British Journal of Psychiatry. The study was funded by the Health Foundation.

LIMITATIONS:

COVID-19 may have been underdiagnosed or underreported in the records studied. Also, investigators did not have information about cause of death.

DISCLOSURES:

One author received funding from Janssen, GSK, and Takeda. All other authors declared no conflicts of interest.

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

TOPLINE:

Severe mental illness (SMI) has been linked to a 50% increased risk for all-cause mortality risk after COVID-19, a large population-based study suggests.

METHODOLOGY:

• Investigators analyzed data from the Clinical Practice Research Datalink database, which contains health information on 13.5 million patients receiving care from family practices in England and Northern Ireland.
• The study included participants with SMI, including schizophrenia, schizoaffective disorder, and bipolar disorder.
• Participants were aged 5 years or older with a SARS-CoV-2 infection recorded between Feb. 1, 2020, and March 31, 2021, spanning two waves of the pandemic.
• Death rates among participants with SMI and COVID-19 (n = 7,150; 56% female) were compared with those in a control group of participants without SMI who had been diagnosed with COVID-19 (n = 650,000; 55% female).

TAKEAWAY:

• Participants with SMI and COVID-19 had a 53% higher risk for death than those in the non-SMI control group (adjusted hazard ratio, 1.53; 95% confidence interval, 1.39-1.68).
• Black Caribbean/Black African participants were more likely than White participants to die of COVID-19 (aHR, 1.22; 95% CI, 1.12-1.34), although ethnicity was not recorded in 30% of participants.
• After SARS-CoV-2 infection, for every additional multimorbid condition, the aHR for death increased by 6% in the SMI group and 16% in the non-SMI group (P = .001). Some of these conditions included hypertension, heart disease, diabetes, kidney disease, depression, and anxiety.

IN PRACTICE:

“From a public health perspective, our study has emphasized the need for early and timely preventative interventions (e.g. vaccination) for the SMI population. Future studies are needed to disentangle the complex biological and psychosocial factors, and health care pathways, that have led to the greater mortality rates in the SMI population,” the authors write.

SOURCE:

Jayati Das-Munshi, MD, of Kings College London, led the study, which was published online in the British Journal of Psychiatry. The study was funded by the Health Foundation.

LIMITATIONS:

COVID-19 may have been underdiagnosed or underreported in the records studied. Also, investigators did not have information about cause of death.

DISCLOSURES:

One author received funding from Janssen, GSK, and Takeda. All other authors declared no conflicts of interest.

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

TOPLINE:

Severe mental illness (SMI) has been linked to a 50% increased risk for all-cause mortality risk after COVID-19, a large population-based study suggests.

METHODOLOGY:

• Investigators analyzed data from the Clinical Practice Research Datalink database, which contains health information on 13.5 million patients receiving care from family practices in England and Northern Ireland.
• The study included participants with SMI, including schizophrenia, schizoaffective disorder, and bipolar disorder.
• Participants were aged 5 years or older with a SARS-CoV-2 infection recorded between Feb. 1, 2020, and March 31, 2021, spanning two waves of the pandemic.
• Death rates among participants with SMI and COVID-19 (n = 7,150; 56% female) were compared with those in a control group of participants without SMI who had been diagnosed with COVID-19 (n = 650,000; 55% female).

TAKEAWAY:

• Participants with SMI and COVID-19 had a 53% higher risk for death than those in the non-SMI control group (adjusted hazard ratio, 1.53; 95% confidence interval, 1.39-1.68).
• Black Caribbean/Black African participants were more likely than White participants to die of COVID-19 (aHR, 1.22; 95% CI, 1.12-1.34), although ethnicity was not recorded in 30% of participants.
• After SARS-CoV-2 infection, for every additional multimorbid condition, the aHR for death increased by 6% in the SMI group and 16% in the non-SMI group (P = .001). Some of these conditions included hypertension, heart disease, diabetes, kidney disease, depression, and anxiety.

IN PRACTICE:

“From a public health perspective, our study has emphasized the need for early and timely preventative interventions (e.g. vaccination) for the SMI population. Future studies are needed to disentangle the complex biological and psychosocial factors, and health care pathways, that have led to the greater mortality rates in the SMI population,” the authors write.

SOURCE:

Jayati Das-Munshi, MD, of Kings College London, led the study, which was published online in the British Journal of Psychiatry. The study was funded by the Health Foundation.

LIMITATIONS:

COVID-19 may have been underdiagnosed or underreported in the records studied. Also, investigators did not have information about cause of death.

DISCLOSURES:

One author received funding from Janssen, GSK, and Takeda. All other authors declared no conflicts of interest.

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

TOPLINE:

Nirmatrelvir-ritonavir doesn’t reduce the incidence of most post-COVID conditions, according to a new study. Thromboembolic events are the exception.
 

METHODOLOGY:

• A retrospective study of 9,593 veterans older than 65 years examined the impact of nirmatrelvir-ritonavir in comparison with no treatment on post–COVID-19 conditions (PCCs).
• Researchers coded 31 conditions, including those that fell into cardiac, pulmonary, renal, thromboembolic, gastrointestinal, neurologic, mental health, musculoskeletal, and endocrine categories.
• The incidence of PCCs was analyzed 31-180 days after treatment.

TAKEAWAY:

• The combined incidence of venous thromboembolism and pulmonary embolism was reduced among patients given nirmatrelvir-ritonavir.
• No statistically significant reduction of other conditions was found.
• Results differ from the conclusions of a smaller study that found that the incidence of 10 of 13 PCCs was lower.

IN PRACTICE:

“Our results suggest that considerations about PCCs may not be an important factor in COVID-19 treatment decisions,” the authors write.

SOURCE:

The study was funded by the Department of Veterans Affairs and was published online in Annals of Internal Medicine. George Ioannou, MD, director of hepatology at the VA Puget Sound Health Care System in Seattle, led the study.

LIMITATIONS:

A large number of outcomes were observed, so it’s possible that the association between treatment with nirmatrelvir-ritonavir and reduced incidence of thromboembolic events occurred by chance.

Data on COVID-19 treatments and PCCs may be incomplete. The long-term effects of PCCs may not have been fully captured by the ICD-10, which was used for diagnosis codes.

Electronic health records did not accurately capture the symptom burden or the date symptoms began. Patients in the treatment arm may have had more symptoms than matched control persons who were not treated.
 

DISCLOSURES:

The authors reported relationships with the Korean Diabetes Association, the American Diabetes Association, the International Society for the Diabetic Foot, Quality Insights, Brown University, and the Society for Women in Urology, among others.

A version of this article appeared on Medscape.com.

TOPLINE:

Nirmatrelvir-ritonavir doesn’t reduce the incidence of most post-COVID conditions, according to a new study. Thromboembolic events are the exception.
 

METHODOLOGY:

• A retrospective study of 9,593 veterans older than 65 years examined the impact of nirmatrelvir-ritonavir in comparison with no treatment on post–COVID-19 conditions (PCCs).
• Researchers coded 31 conditions, including those that fell into cardiac, pulmonary, renal, thromboembolic, gastrointestinal, neurologic, mental health, musculoskeletal, and endocrine categories.
• The incidence of PCCs was analyzed 31-180 days after treatment.

TAKEAWAY:

• The combined incidence of venous thromboembolism and pulmonary embolism was reduced among patients given nirmatrelvir-ritonavir.
• No statistically significant reduction of other conditions was found.
• Results differ from the conclusions of a smaller study that found that the incidence of 10 of 13 PCCs was lower.

IN PRACTICE:

“Our results suggest that considerations about PCCs may not be an important factor in COVID-19 treatment decisions,” the authors write.

SOURCE:

The study was funded by the Department of Veterans Affairs and was published online in Annals of Internal Medicine. George Ioannou, MD, director of hepatology at the VA Puget Sound Health Care System in Seattle, led the study.

LIMITATIONS:

A large number of outcomes were observed, so it’s possible that the association between treatment with nirmatrelvir-ritonavir and reduced incidence of thromboembolic events occurred by chance.

Data on COVID-19 treatments and PCCs may be incomplete. The long-term effects of PCCs may not have been fully captured by the ICD-10, which was used for diagnosis codes.

Electronic health records did not accurately capture the symptom burden or the date symptoms began. Patients in the treatment arm may have had more symptoms than matched control persons who were not treated.
 

DISCLOSURES:

The authors reported relationships with the Korean Diabetes Association, the American Diabetes Association, the International Society for the Diabetic Foot, Quality Insights, Brown University, and the Society for Women in Urology, among others.

A version of this article appeared on Medscape.com.

TOPLINE:

Nirmatrelvir-ritonavir doesn’t reduce the incidence of most post-COVID conditions, according to a new study. Thromboembolic events are the exception.
 

METHODOLOGY:

• A retrospective study of 9,593 veterans older than 65 years examined the impact of nirmatrelvir-ritonavir in comparison with no treatment on post–COVID-19 conditions (PCCs).
• Researchers coded 31 conditions, including those that fell into cardiac, pulmonary, renal, thromboembolic, gastrointestinal, neurologic, mental health, musculoskeletal, and endocrine categories.
• The incidence of PCCs was analyzed 31-180 days after treatment.

TAKEAWAY:

• The combined incidence of venous thromboembolism and pulmonary embolism was reduced among patients given nirmatrelvir-ritonavir.
• No statistically significant reduction of other conditions was found.
• Results differ from the conclusions of a smaller study that found that the incidence of 10 of 13 PCCs was lower.

IN PRACTICE:

“Our results suggest that considerations about PCCs may not be an important factor in COVID-19 treatment decisions,” the authors write.

SOURCE:

The study was funded by the Department of Veterans Affairs and was published online in Annals of Internal Medicine. George Ioannou, MD, director of hepatology at the VA Puget Sound Health Care System in Seattle, led the study.

LIMITATIONS:

A large number of outcomes were observed, so it’s possible that the association between treatment with nirmatrelvir-ritonavir and reduced incidence of thromboembolic events occurred by chance.

Data on COVID-19 treatments and PCCs may be incomplete. The long-term effects of PCCs may not have been fully captured by the ICD-10, which was used for diagnosis codes.

Electronic health records did not accurately capture the symptom burden or the date symptoms began. Patients in the treatment arm may have had more symptoms than matched control persons who were not treated.
 

DISCLOSURES:

The authors reported relationships with the Korean Diabetes Association, the American Diabetes Association, the International Society for the Diabetic Foot, Quality Insights, Brown University, and the Society for Women in Urology, among others.

A version of this article appeared on Medscape.com.

TOPLINE:

The risk for Guillain-Barré syndrome (GBS) is six times higher in people with COVID-19 in the 6 weeks following infection, according to a new study that also showed receipt of the Pfizer-BioNTech mRNA vaccine reduced GSB risk by 59%.

METHODOLOGY:

• The nested-case control study analyzed data from the largest healthcare provider in Israel for 3.2 million patients aged 16 years and older, with no history of GBS.
• GBS cases (n = 76) were identified based on hospital discharge data from January 2021 to June 2022.
• For every GBS case, investigators chose 10 controls at random, matched for age, gender, and follow-up duration (n = 760).
• Investigators examined the association between GBS and SARS-CoV-2 infection, established through documentation of prior positive SARS-CoV-2 test (PCR or antigen), and any COVID-19 vaccine administration.

TAKEAWAY:

• Among those diagnosed with GBS, 8 were exposed to SARS-CoV-2 infection only, 7 were exposed to COVID-19 vaccination only, and 1 patient was exposed to both SARS-CoV-2 infection and COVID-19 vaccination in the prior 6 weeks, leaving 60 GBS patients without exposure to either infection or vaccination.
• All COVID-19 vaccine doses administered in GBS cases within 6 weeks of the index date, and all but two doses administered in controls in the same timeframe, were Pfizer-BioNTech vaccines.
• Compared with people without GBS, those with the condition were more than six times as likely to have had SARS-CoV-2 infection within 6 weeks of GBS diagnosis (adjusted odds ratio, 6.30; 95% confidence interval, 2.55-15.56).
• People who received the COVID-19 vaccine were 59% less likely to develop GBS than those who did not get the vaccine (aOR, 0.41; 95% CI, 0.17-0.96).

IN PRACTICE:

“While Guillain-Barré is extremely rare, people should be aware that having a COVID infection can increase their risk of developing the disorder, and receiving an mRNA vaccine can decrease their risk,” study author Anat Arbel, MD, of Lady Davis Carmel Medical Center and the Technion-Israel Institute of Technology, Haifa, Israel, said in a press release.

SOURCE:

In addition to Dr. Arbel, the other lead author is Haya Bishara, MD, of Lady Davis Carmel Medical Center. The research was published online  in the journal Neurology.

LIMITATIONS:

There is a possibility of misclassification of SARS-CoV-2 infection, which could lead to an overestimation of the magnitude of association between infection and GBS. The diagnosis of GBS relied solely on ICD-9 coding, which has been shown in prior studies to contain errors.

DISCLOSURES:

The study was unfunded. Dr. Bishara and Dr. Arbel report no relevant financial relationships. One co-author, Eitan Auriel, MD, has received lecturer fees from Novo Nordisk, Pfizer, Boehringer Ingelheim, and Medison.

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

TOPLINE:

The risk for Guillain-Barré syndrome (GBS) is six times higher in people with COVID-19 in the 6 weeks following infection, according to a new study that also showed receipt of the Pfizer-BioNTech mRNA vaccine reduced GSB risk by 59%.

METHODOLOGY:

• The nested-case control study analyzed data from the largest healthcare provider in Israel for 3.2 million patients aged 16 years and older, with no history of GBS.
• GBS cases (n = 76) were identified based on hospital discharge data from January 2021 to June 2022.
• For every GBS case, investigators chose 10 controls at random, matched for age, gender, and follow-up duration (n = 760).
• Investigators examined the association between GBS and SARS-CoV-2 infection, established through documentation of prior positive SARS-CoV-2 test (PCR or antigen), and any COVID-19 vaccine administration.

TAKEAWAY:

• Among those diagnosed with GBS, 8 were exposed to SARS-CoV-2 infection only, 7 were exposed to COVID-19 vaccination only, and 1 patient was exposed to both SARS-CoV-2 infection and COVID-19 vaccination in the prior 6 weeks, leaving 60 GBS patients without exposure to either infection or vaccination.
• All COVID-19 vaccine doses administered in GBS cases within 6 weeks of the index date, and all but two doses administered in controls in the same timeframe, were Pfizer-BioNTech vaccines.
• Compared with people without GBS, those with the condition were more than six times as likely to have had SARS-CoV-2 infection within 6 weeks of GBS diagnosis (adjusted odds ratio, 6.30; 95% confidence interval, 2.55-15.56).
• People who received the COVID-19 vaccine were 59% less likely to develop GBS than those who did not get the vaccine (aOR, 0.41; 95% CI, 0.17-0.96).

IN PRACTICE:

“While Guillain-Barré is extremely rare, people should be aware that having a COVID infection can increase their risk of developing the disorder, and receiving an mRNA vaccine can decrease their risk,” study author Anat Arbel, MD, of Lady Davis Carmel Medical Center and the Technion-Israel Institute of Technology, Haifa, Israel, said in a press release.

SOURCE:

In addition to Dr. Arbel, the other lead author is Haya Bishara, MD, of Lady Davis Carmel Medical Center. The research was published online  in the journal Neurology.

LIMITATIONS:

There is a possibility of misclassification of SARS-CoV-2 infection, which could lead to an overestimation of the magnitude of association between infection and GBS. The diagnosis of GBS relied solely on ICD-9 coding, which has been shown in prior studies to contain errors.

DISCLOSURES:

The study was unfunded. Dr. Bishara and Dr. Arbel report no relevant financial relationships. One co-author, Eitan Auriel, MD, has received lecturer fees from Novo Nordisk, Pfizer, Boehringer Ingelheim, and Medison.

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

TOPLINE:

The risk for Guillain-Barré syndrome (GBS) is six times higher in people with COVID-19 in the 6 weeks following infection, according to a new study that also showed receipt of the Pfizer-BioNTech mRNA vaccine reduced GSB risk by 59%.

METHODOLOGY:

• The nested-case control study analyzed data from the largest healthcare provider in Israel for 3.2 million patients aged 16 years and older, with no history of GBS.
• GBS cases (n = 76) were identified based on hospital discharge data from January 2021 to June 2022.
• For every GBS case, investigators chose 10 controls at random, matched for age, gender, and follow-up duration (n = 760).
• Investigators examined the association between GBS and SARS-CoV-2 infection, established through documentation of prior positive SARS-CoV-2 test (PCR or antigen), and any COVID-19 vaccine administration.

TAKEAWAY:

• Among those diagnosed with GBS, 8 were exposed to SARS-CoV-2 infection only, 7 were exposed to COVID-19 vaccination only, and 1 patient was exposed to both SARS-CoV-2 infection and COVID-19 vaccination in the prior 6 weeks, leaving 60 GBS patients without exposure to either infection or vaccination.
• All COVID-19 vaccine doses administered in GBS cases within 6 weeks of the index date, and all but two doses administered in controls in the same timeframe, were Pfizer-BioNTech vaccines.
• Compared with people without GBS, those with the condition were more than six times as likely to have had SARS-CoV-2 infection within 6 weeks of GBS diagnosis (adjusted odds ratio, 6.30; 95% confidence interval, 2.55-15.56).
• People who received the COVID-19 vaccine were 59% less likely to develop GBS than those who did not get the vaccine (aOR, 0.41; 95% CI, 0.17-0.96).

IN PRACTICE:

“While Guillain-Barré is extremely rare, people should be aware that having a COVID infection can increase their risk of developing the disorder, and receiving an mRNA vaccine can decrease their risk,” study author Anat Arbel, MD, of Lady Davis Carmel Medical Center and the Technion-Israel Institute of Technology, Haifa, Israel, said in a press release.

SOURCE:

In addition to Dr. Arbel, the other lead author is Haya Bishara, MD, of Lady Davis Carmel Medical Center. The research was published online  in the journal Neurology.

LIMITATIONS:

There is a possibility of misclassification of SARS-CoV-2 infection, which could lead to an overestimation of the magnitude of association between infection and GBS. The diagnosis of GBS relied solely on ICD-9 coding, which has been shown in prior studies to contain errors.

DISCLOSURES:

The study was unfunded. Dr. Bishara and Dr. Arbel report no relevant financial relationships. One co-author, Eitan Auriel, MD, has received lecturer fees from Novo Nordisk, Pfizer, Boehringer Ingelheim, and Medison.

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

New evidence shows for the first time that the virus that causes COVID directly infects atherosclerotic plaques in the coronary arteries, producing a persistent inflammatory response.

The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.

“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.

Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”

Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.

“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.

Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.

“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.

Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”

Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.

Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
 

Heart disease after COVID

In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.

They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.

“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.

The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.

“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.

“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
 

Viral reservoirs

Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.

Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.

“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.

Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.

Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”

Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.

“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
 

Affecting more than lungs

Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.

“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”

Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.

“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.

Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.

Dr. Hotez says he believes these new findings will have implications for the future.

“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.

While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.

“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”

The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.

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

New evidence shows for the first time that the virus that causes COVID directly infects atherosclerotic plaques in the coronary arteries, producing a persistent inflammatory response.

The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.

“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.

Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”

Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.

“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.

Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.

“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.

Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”

Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.

Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
 

Heart disease after COVID

In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.

They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.

“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.

The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.

“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.

“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
 

Viral reservoirs

Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.

Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.

“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.

Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.

Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”

Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.

“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
 

Affecting more than lungs

Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.

“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”

Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.

“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.

Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.

Dr. Hotez says he believes these new findings will have implications for the future.

“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.

While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.

“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”

The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.

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

New evidence shows for the first time that the virus that causes COVID directly infects atherosclerotic plaques in the coronary arteries, producing a persistent inflammatory response.

The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.

“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.

Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”

Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.

“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.

Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.

“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.

Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”

Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.

Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
 

Heart disease after COVID

In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.

They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.

“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.

The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.

“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.

“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
 

Viral reservoirs

Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.

Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.

“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.

Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.

Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”

Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.

“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
 

Affecting more than lungs

Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.

“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”

Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.

“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.

Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.

Dr. Hotez says he believes these new findings will have implications for the future.

“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.

While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.

“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”

The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.

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

TOPLINE:

Half of kids with COVID-19 become noninfectious 3 days after testing positive, whether they were vaccinated or not, according to a new study. The findings indicate that return-to-school policies for infected children may not need to differ on the basis of vaccine or booster status.

METHODOLOGY:

• The study looked at 76 children, both vaccinated and unvaccinated, aged 7-18 years who had tested positive for COVID-19. 
• Researchers performed nasal swabs every other day for 10 days, sending the swab to a lab to be tested for cytopathic effect (CPE), or cell death, an indicator of infectivity.
• They took pictures of the lab cultures to look for signs of CPE starting at 6 days after the test, which corresponds to the 2nd day after testing positive.
• If CPE characteristics were present in at least 30% of images, children were considered infectious.

TAKEAWAY:

• By day 3, half of study participants were noninfectious, independent of whether they had been vaccinated.
• By day 5, less than 25% of children were infectious, regardless of vaccination status.
• Among vaccinated children, the duration of infectivity was similar for children who received a booster and for those who had not.
• The authors state that these results are consistent with those of a study in adults with the Omicron variant, which found no association between vaccination status and infectivity duration.

IN PRACTICE:

“Our findings suggest that current policies requiring isolation for 5 days after a positive test might be appropriate, as the majority of children were not infectious by day 5. Additionally, return-to-school policies may not need to discriminate by vaccine or booster status,” the authors wrote. 

SOURCE:

The study was led by Neeraj Sood, PhD, of the University of Southern California in Los Angeles, and was published in JAMA Pediatrics.

LIMITATIONS:

The sample size was small, and the authors identified the potential for nonresponse bias. The research did not include data from children who didn’t receive a test. CPE is the standard for estimating infectivity, but it can still carry inaccuracies.

DISCLOSURES:

The authors report no disclosures. The study was funded by RF Catalytic Capital.

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

TOPLINE:

Half of kids with COVID-19 become noninfectious 3 days after testing positive, whether they were vaccinated or not, according to a new study. The findings indicate that return-to-school policies for infected children may not need to differ on the basis of vaccine or booster status.

METHODOLOGY:

• The study looked at 76 children, both vaccinated and unvaccinated, aged 7-18 years who had tested positive for COVID-19. 
• Researchers performed nasal swabs every other day for 10 days, sending the swab to a lab to be tested for cytopathic effect (CPE), or cell death, an indicator of infectivity.
• They took pictures of the lab cultures to look for signs of CPE starting at 6 days after the test, which corresponds to the 2nd day after testing positive.
• If CPE characteristics were present in at least 30% of images, children were considered infectious.

TAKEAWAY:

• By day 3, half of study participants were noninfectious, independent of whether they had been vaccinated.
• By day 5, less than 25% of children were infectious, regardless of vaccination status.
• Among vaccinated children, the duration of infectivity was similar for children who received a booster and for those who had not.
• The authors state that these results are consistent with those of a study in adults with the Omicron variant, which found no association between vaccination status and infectivity duration.

IN PRACTICE:

“Our findings suggest that current policies requiring isolation for 5 days after a positive test might be appropriate, as the majority of children were not infectious by day 5. Additionally, return-to-school policies may not need to discriminate by vaccine or booster status,” the authors wrote. 

SOURCE:

The study was led by Neeraj Sood, PhD, of the University of Southern California in Los Angeles, and was published in JAMA Pediatrics.

LIMITATIONS:

The sample size was small, and the authors identified the potential for nonresponse bias. The research did not include data from children who didn’t receive a test. CPE is the standard for estimating infectivity, but it can still carry inaccuracies.

DISCLOSURES:

The authors report no disclosures. The study was funded by RF Catalytic Capital.

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

TOPLINE:

Half of kids with COVID-19 become noninfectious 3 days after testing positive, whether they were vaccinated or not, according to a new study. The findings indicate that return-to-school policies for infected children may not need to differ on the basis of vaccine or booster status.

METHODOLOGY:

• The study looked at 76 children, both vaccinated and unvaccinated, aged 7-18 years who had tested positive for COVID-19. 
• Researchers performed nasal swabs every other day for 10 days, sending the swab to a lab to be tested for cytopathic effect (CPE), or cell death, an indicator of infectivity.
• They took pictures of the lab cultures to look for signs of CPE starting at 6 days after the test, which corresponds to the 2nd day after testing positive.
• If CPE characteristics were present in at least 30% of images, children were considered infectious.

TAKEAWAY:

• By day 3, half of study participants were noninfectious, independent of whether they had been vaccinated.
• By day 5, less than 25% of children were infectious, regardless of vaccination status.
• Among vaccinated children, the duration of infectivity was similar for children who received a booster and for those who had not.
• The authors state that these results are consistent with those of a study in adults with the Omicron variant, which found no association between vaccination status and infectivity duration.

IN PRACTICE:

“Our findings suggest that current policies requiring isolation for 5 days after a positive test might be appropriate, as the majority of children were not infectious by day 5. Additionally, return-to-school policies may not need to discriminate by vaccine or booster status,” the authors wrote. 

SOURCE:

The study was led by Neeraj Sood, PhD, of the University of Southern California in Los Angeles, and was published in JAMA Pediatrics.

LIMITATIONS:

The sample size was small, and the authors identified the potential for nonresponse bias. The research did not include data from children who didn’t receive a test. CPE is the standard for estimating infectivity, but it can still carry inaccuracies.

DISCLOSURES:

The authors report no disclosures. The study was funded by RF Catalytic Capital.

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

SARS-CoV-2 infection is linked in men with increased incidence of urinary retention, urinary tract infection (UTI), and blood in the urine, a new study finds.

Authors of the study, led by Alex Qinyang Liu, of S.H. Ho Urology Centre, at The Chinese University of Hong Kong, highlighted the clinical implications.

“Clinicians should be aware of the significantly higher incidence of LUTS [lower urinary tract symptoms] complications with COVID-19 in this patient group and understand that these urological manifestations can occur regardless of COVID-19 severity,” the authors wrote.

Findings were published online in the Journal of Internal Medicine.

“This is the largest study demonstrating the detrimental urological effects of SARS-CoV-2 infection,” the authors wrote. They explained that current literature has included only small case series and observational studies assessing the connection between COVID-19 and male LUTS.
 

Nearly 18,000 patients in study

Included in this study were all male patients who used the public health care system in Hong Kong who received alpha-blocker monotherapy for LUTS from 2021 to 2022. After propensity score matching, 17,986 patients were included. Half had polymerase chain reaction–confirmed SARS-CoV-2 infection (n = 8,993).

The retrospective study compared urologic outcomes, including male benign prostatic hyperplasia (BPH) complications, and changes in medical treatment in the two groups. They compared male patients with SARS-CoV-2 infection who were taking baseline alpha blocker monotherapy for LUTS with a control group who had no SARS-CoV-2 infection.

They found that, compared with controls, the SARS-CoV-2–infected group had significantly higher incidence of retention of urine (4.55% vs. 0.86%, P < .001), hematuria (1.36% vs. 0.41%, P < .001), clinical UTI (4.31% vs. 1.49%, P < .001), culture-proven bacteriuria (9.02% vs. 1.97%, P < .001), and addition of 5-alpha reductase inhibitors (0.50% vs. 0.02%, P < .001).
 

Similar side effects even with asymptomatic infection

The researchers pointed out that similar incidence of retention of urine, hematuria, and addition of medication were seen even when patients had asymptomatic infection.

They added that their findings have biological plausibility because the coexpression of the proteins ACE2 and TMPRSS2 in the prostate makes it a target for SARS-CoV-2, which leads to inflammation and may help explain the primary outcomes.

“Given the high infectivity and unprecedented scale of the COVID-19 pandemic, these urological symptoms and complications represent a significant clinical burden that clinicians and urologists should be aware of,” the authors wrote.

The authors noted that the prevalence of BPH and LUTS rises with age and are among the most common urologic conditions affecting older men. “Incidentally, male patients of advanced age are also more significantly affected by COVID-19.”

The authors declare no relevant financial relationships.

SARS-CoV-2 infection is linked in men with increased incidence of urinary retention, urinary tract infection (UTI), and blood in the urine, a new study finds.

Authors of the study, led by Alex Qinyang Liu, of S.H. Ho Urology Centre, at The Chinese University of Hong Kong, highlighted the clinical implications.

“Clinicians should be aware of the significantly higher incidence of LUTS [lower urinary tract symptoms] complications with COVID-19 in this patient group and understand that these urological manifestations can occur regardless of COVID-19 severity,” the authors wrote.

Findings were published online in the Journal of Internal Medicine.

“This is the largest study demonstrating the detrimental urological effects of SARS-CoV-2 infection,” the authors wrote. They explained that current literature has included only small case series and observational studies assessing the connection between COVID-19 and male LUTS.
 

Nearly 18,000 patients in study

Included in this study were all male patients who used the public health care system in Hong Kong who received alpha-blocker monotherapy for LUTS from 2021 to 2022. After propensity score matching, 17,986 patients were included. Half had polymerase chain reaction–confirmed SARS-CoV-2 infection (n = 8,993).

The retrospective study compared urologic outcomes, including male benign prostatic hyperplasia (BPH) complications, and changes in medical treatment in the two groups. They compared male patients with SARS-CoV-2 infection who were taking baseline alpha blocker monotherapy for LUTS with a control group who had no SARS-CoV-2 infection.

They found that, compared with controls, the SARS-CoV-2–infected group had significantly higher incidence of retention of urine (4.55% vs. 0.86%, P < .001), hematuria (1.36% vs. 0.41%, P < .001), clinical UTI (4.31% vs. 1.49%, P < .001), culture-proven bacteriuria (9.02% vs. 1.97%, P < .001), and addition of 5-alpha reductase inhibitors (0.50% vs. 0.02%, P < .001).
 

Similar side effects even with asymptomatic infection

The researchers pointed out that similar incidence of retention of urine, hematuria, and addition of medication were seen even when patients had asymptomatic infection.

They added that their findings have biological plausibility because the coexpression of the proteins ACE2 and TMPRSS2 in the prostate makes it a target for SARS-CoV-2, which leads to inflammation and may help explain the primary outcomes.

“Given the high infectivity and unprecedented scale of the COVID-19 pandemic, these urological symptoms and complications represent a significant clinical burden that clinicians and urologists should be aware of,” the authors wrote.

The authors noted that the prevalence of BPH and LUTS rises with age and are among the most common urologic conditions affecting older men. “Incidentally, male patients of advanced age are also more significantly affected by COVID-19.”

The authors declare no relevant financial relationships.

SARS-CoV-2 infection is linked in men with increased incidence of urinary retention, urinary tract infection (UTI), and blood in the urine, a new study finds.

Authors of the study, led by Alex Qinyang Liu, of S.H. Ho Urology Centre, at The Chinese University of Hong Kong, highlighted the clinical implications.

“Clinicians should be aware of the significantly higher incidence of LUTS [lower urinary tract symptoms] complications with COVID-19 in this patient group and understand that these urological manifestations can occur regardless of COVID-19 severity,” the authors wrote.

Findings were published online in the Journal of Internal Medicine.

“This is the largest study demonstrating the detrimental urological effects of SARS-CoV-2 infection,” the authors wrote. They explained that current literature has included only small case series and observational studies assessing the connection between COVID-19 and male LUTS.
 

Nearly 18,000 patients in study

Included in this study were all male patients who used the public health care system in Hong Kong who received alpha-blocker monotherapy for LUTS from 2021 to 2022. After propensity score matching, 17,986 patients were included. Half had polymerase chain reaction–confirmed SARS-CoV-2 infection (n = 8,993).

The retrospective study compared urologic outcomes, including male benign prostatic hyperplasia (BPH) complications, and changes in medical treatment in the two groups. They compared male patients with SARS-CoV-2 infection who were taking baseline alpha blocker monotherapy for LUTS with a control group who had no SARS-CoV-2 infection.

They found that, compared with controls, the SARS-CoV-2–infected group had significantly higher incidence of retention of urine (4.55% vs. 0.86%, P < .001), hematuria (1.36% vs. 0.41%, P < .001), clinical UTI (4.31% vs. 1.49%, P < .001), culture-proven bacteriuria (9.02% vs. 1.97%, P < .001), and addition of 5-alpha reductase inhibitors (0.50% vs. 0.02%, P < .001).
 

Similar side effects even with asymptomatic infection

The researchers pointed out that similar incidence of retention of urine, hematuria, and addition of medication were seen even when patients had asymptomatic infection.

They added that their findings have biological plausibility because the coexpression of the proteins ACE2 and TMPRSS2 in the prostate makes it a target for SARS-CoV-2, which leads to inflammation and may help explain the primary outcomes.

“Given the high infectivity and unprecedented scale of the COVID-19 pandemic, these urological symptoms and complications represent a significant clinical burden that clinicians and urologists should be aware of,” the authors wrote.

The authors noted that the prevalence of BPH and LUTS rises with age and are among the most common urologic conditions affecting older men. “Incidentally, male patients of advanced age are also more significantly affected by COVID-19.”

The authors declare no relevant financial relationships.