MDedge Pediatrics

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

Maternal autoimmune diseases significantly increased the risk of ADHD in children, based on data from a large cohort study of more than 800,000 mothers and children and a subsequent meta-analysis.

“There is growing evidence that immune-related cells and proteins play a role in brain development and function and that maternal immune activation, including infection, autoimmune disease, and chronic inflammation during pregnancy, increases the risk of neurodevelopmental disorders among children,” wrote Timothy C. Nielsen, MPH, of the University of Sydney, and colleagues.

Previous research has examined a link between maternal autoimmune disorders and autism spectrum disorders in children, but associations with ADHD have not been well studied, they said.

In a population-based cohort study published in JAMA Pediatrics, the researchers identified 831,718 mothers and their 831,718 singleton infants in Australia. A total of 12,787 infants were born to mothers with an autoimmune diagnosis; 12,610 of them were matched to 50,440 control infants. ADHD was determined based on prescription for a stimulant treatment or a hospital diagnosis; children with a first ADHD event younger than 3 years were excluded.

In the total cohort of 63,050 infants, the presence of any maternal autoimmune disease was associated with a significantly increased risk of ADHD (hazard ratio, 1.30) as was the presence of several specific conditions: type 1 diabetes (HR, 2.23), psoriasis (HR, 1.66), and rheumatic fever or rheumatic carditis (HR, 1.75).

In addition, the researchers conducted a meta-analysis of the current study and four additional studies that yielded similar results. In the meta-analysis, the risk of ADHD was significantly associated with any maternal autoimmune disease in two studies (HR, 1.20); with maternal type 1 diabetes in four studies (HR, 1.53); with maternal hyperthyroidism in three studies (HR 1.15); and with maternal psoriasis in two studies (HR, 1.31).

Type 1 diabetes (T1D) had the highest HR and was the most often studied condition. However, “the observed association may also be related to nonimmune aspects of T1D, such as glycemic control, as nonautoimmune diabetes has been associated with ADHD among children,” the researchers wrote.

The study findings were limited by several factors, including the lack of outpatient and primary care records to identify maternal autoimmune disease, and lack of data on any medication used to managed diseases during pregnancy, as well as a lack of data on children with ADHD who might not have been treated with medication, the researchers noted. In addition, “given differences in study design and definitions, the pooled HRs presented in the meta-analysis need to be treated cautiously.”

However, the results were strengthened by the hybrid study design and large study population, and were generally consistent with previous research supporting an effect of maternal immune function on fetal neurodevelopment, they noted.

“Our study provides justification for future studies that examine the effect of maternal autoimmune diseases, including biomarkers, condition severity, and management in pregnancy and in the periconception period, on neurodevelopmental disorders in children,” they concluded.

Studies need to explore mechanism of action

The current study, with its hybrid design, adds support to the evidence of an association between any maternal autoimmune disease and ADHD in children, as well as an association between the specific conditions of type 1 diabetes, hyperthyroidism, and psoriasis in mothers and ADHD in children, Søren Dalsgaard, MD, of Aarhus (Denmark) University, wrote in an accompanying editorial.

“Importantly, Nielsen et al. emphasized in their article that, for the many different autoimmune diseases, different underlying mechanisms for the associations with disorders of the central nervous system were likely. They mentioned that, for T1D, low glycemic control may play a role, as type 2 diabetes has been associated with ADHD,” said Dr. Dalsgaard.

“Overall, these mechanisms are thought to include shared genetic and environmental risk factors or direct effects of maternal autoantibodies or cytokines crossing the placenta and altering the fetal immune response, which in turns leads to changes in the central nervous system,” Dr. Dalsgaard explained. However, the current study and previous studies have not identified the mechanisms to explain the association between ADHD in children and maternal autoimmune disease.

“To understand more about these associations, future studies should include researchers and data from different scientific disciplines, such as epidemiology, animal modeling, genetics, and neuroimmunology,” he concluded.
 

Association is not causality

Overall, the study findings add to the evidence of a correlation between autoimmune diseases and neurologic disease, said Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y., in an interview. “Anything that might contribute to behavioral problems is worth investigating.” However, it is important to remember that association is not causation.

“There is some literature and evidence that autoimmune disease is associated with mental health issues, but the mechanisms of action are unknown,” said Dr. Lessin. ADHD is highly heritable, so the association may be caused by a similar genetic predisposition, or it may be something related to autoimmunity that is impacting the fetus by passing through the placenta.

The current study’s strengths include the large size and hybrid design, but limitations such as the identification of ADHD based on medication prescriptions may have led to underreporting, and identifying maternal autoimmune disease via inpatient hospital diagnosis could have selected for more severe disease, he said.

From a clinical standpoint, the study suggests a correlation that should be noted in a family history and potentially used to inform a diagnosis, especially in cases of type 1 diabetes where the association was strongest, Dr. Lessin said. The findings also support the value of further research to look for mechanisms that might explain whether the association between autoimmune disease and ADHD is autoimmune system causality or shared genetic susceptibility.

The study received no outside funding. One coauthor disclosed receiving grants from the National Blood Authority Australia and the Australian National Health and Medical Research Council during the conduct of the study. Dr. Dalsgaard had no financial conflicts to disclose. Dr. Lessin disclosed serving as editor of the ADHD toolkit for the American Academy of Pediatrics and coauthor of the current ADHD clinical guidelines. He also serves in advisory capacity to Cognoa, a company involved in diagnosis of autism, and Corium/KemPharm, companies involved in the development of ADHD treatments.

Maternal autoimmune diseases significantly increased the risk of ADHD in children, based on data from a large cohort study of more than 800,000 mothers and children and a subsequent meta-analysis.

“There is growing evidence that immune-related cells and proteins play a role in brain development and function and that maternal immune activation, including infection, autoimmune disease, and chronic inflammation during pregnancy, increases the risk of neurodevelopmental disorders among children,” wrote Timothy C. Nielsen, MPH, of the University of Sydney, and colleagues.

Previous research has examined a link between maternal autoimmune disorders and autism spectrum disorders in children, but associations with ADHD have not been well studied, they said.

In a population-based cohort study published in JAMA Pediatrics, the researchers identified 831,718 mothers and their 831,718 singleton infants in Australia. A total of 12,787 infants were born to mothers with an autoimmune diagnosis; 12,610 of them were matched to 50,440 control infants. ADHD was determined based on prescription for a stimulant treatment or a hospital diagnosis; children with a first ADHD event younger than 3 years were excluded.

In the total cohort of 63,050 infants, the presence of any maternal autoimmune disease was associated with a significantly increased risk of ADHD (hazard ratio, 1.30) as was the presence of several specific conditions: type 1 diabetes (HR, 2.23), psoriasis (HR, 1.66), and rheumatic fever or rheumatic carditis (HR, 1.75).

In addition, the researchers conducted a meta-analysis of the current study and four additional studies that yielded similar results. In the meta-analysis, the risk of ADHD was significantly associated with any maternal autoimmune disease in two studies (HR, 1.20); with maternal type 1 diabetes in four studies (HR, 1.53); with maternal hyperthyroidism in three studies (HR 1.15); and with maternal psoriasis in two studies (HR, 1.31).

Type 1 diabetes (T1D) had the highest HR and was the most often studied condition. However, “the observed association may also be related to nonimmune aspects of T1D, such as glycemic control, as nonautoimmune diabetes has been associated with ADHD among children,” the researchers wrote.

The study findings were limited by several factors, including the lack of outpatient and primary care records to identify maternal autoimmune disease, and lack of data on any medication used to managed diseases during pregnancy, as well as a lack of data on children with ADHD who might not have been treated with medication, the researchers noted. In addition, “given differences in study design and definitions, the pooled HRs presented in the meta-analysis need to be treated cautiously.”

However, the results were strengthened by the hybrid study design and large study population, and were generally consistent with previous research supporting an effect of maternal immune function on fetal neurodevelopment, they noted.

“Our study provides justification for future studies that examine the effect of maternal autoimmune diseases, including biomarkers, condition severity, and management in pregnancy and in the periconception period, on neurodevelopmental disorders in children,” they concluded.

Studies need to explore mechanism of action

The current study, with its hybrid design, adds support to the evidence of an association between any maternal autoimmune disease and ADHD in children, as well as an association between the specific conditions of type 1 diabetes, hyperthyroidism, and psoriasis in mothers and ADHD in children, Søren Dalsgaard, MD, of Aarhus (Denmark) University, wrote in an accompanying editorial.

“Importantly, Nielsen et al. emphasized in their article that, for the many different autoimmune diseases, different underlying mechanisms for the associations with disorders of the central nervous system were likely. They mentioned that, for T1D, low glycemic control may play a role, as type 2 diabetes has been associated with ADHD,” said Dr. Dalsgaard.

“Overall, these mechanisms are thought to include shared genetic and environmental risk factors or direct effects of maternal autoantibodies or cytokines crossing the placenta and altering the fetal immune response, which in turns leads to changes in the central nervous system,” Dr. Dalsgaard explained. However, the current study and previous studies have not identified the mechanisms to explain the association between ADHD in children and maternal autoimmune disease.

“To understand more about these associations, future studies should include researchers and data from different scientific disciplines, such as epidemiology, animal modeling, genetics, and neuroimmunology,” he concluded.
 

Association is not causality

Overall, the study findings add to the evidence of a correlation between autoimmune diseases and neurologic disease, said Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y., in an interview. “Anything that might contribute to behavioral problems is worth investigating.” However, it is important to remember that association is not causation.

“There is some literature and evidence that autoimmune disease is associated with mental health issues, but the mechanisms of action are unknown,” said Dr. Lessin. ADHD is highly heritable, so the association may be caused by a similar genetic predisposition, or it may be something related to autoimmunity that is impacting the fetus by passing through the placenta.

The current study’s strengths include the large size and hybrid design, but limitations such as the identification of ADHD based on medication prescriptions may have led to underreporting, and identifying maternal autoimmune disease via inpatient hospital diagnosis could have selected for more severe disease, he said.

From a clinical standpoint, the study suggests a correlation that should be noted in a family history and potentially used to inform a diagnosis, especially in cases of type 1 diabetes where the association was strongest, Dr. Lessin said. The findings also support the value of further research to look for mechanisms that might explain whether the association between autoimmune disease and ADHD is autoimmune system causality or shared genetic susceptibility.

The study received no outside funding. One coauthor disclosed receiving grants from the National Blood Authority Australia and the Australian National Health and Medical Research Council during the conduct of the study. Dr. Dalsgaard had no financial conflicts to disclose. Dr. Lessin disclosed serving as editor of the ADHD toolkit for the American Academy of Pediatrics and coauthor of the current ADHD clinical guidelines. He also serves in advisory capacity to Cognoa, a company involved in diagnosis of autism, and Corium/KemPharm, companies involved in the development of ADHD treatments.

Maternal autoimmune diseases significantly increased the risk of ADHD in children, based on data from a large cohort study of more than 800,000 mothers and children and a subsequent meta-analysis.

“There is growing evidence that immune-related cells and proteins play a role in brain development and function and that maternal immune activation, including infection, autoimmune disease, and chronic inflammation during pregnancy, increases the risk of neurodevelopmental disorders among children,” wrote Timothy C. Nielsen, MPH, of the University of Sydney, and colleagues.

Previous research has examined a link between maternal autoimmune disorders and autism spectrum disorders in children, but associations with ADHD have not been well studied, they said.

In a population-based cohort study published in JAMA Pediatrics, the researchers identified 831,718 mothers and their 831,718 singleton infants in Australia. A total of 12,787 infants were born to mothers with an autoimmune diagnosis; 12,610 of them were matched to 50,440 control infants. ADHD was determined based on prescription for a stimulant treatment or a hospital diagnosis; children with a first ADHD event younger than 3 years were excluded.

In the total cohort of 63,050 infants, the presence of any maternal autoimmune disease was associated with a significantly increased risk of ADHD (hazard ratio, 1.30) as was the presence of several specific conditions: type 1 diabetes (HR, 2.23), psoriasis (HR, 1.66), and rheumatic fever or rheumatic carditis (HR, 1.75).

In addition, the researchers conducted a meta-analysis of the current study and four additional studies that yielded similar results. In the meta-analysis, the risk of ADHD was significantly associated with any maternal autoimmune disease in two studies (HR, 1.20); with maternal type 1 diabetes in four studies (HR, 1.53); with maternal hyperthyroidism in three studies (HR 1.15); and with maternal psoriasis in two studies (HR, 1.31).

Type 1 diabetes (T1D) had the highest HR and was the most often studied condition. However, “the observed association may also be related to nonimmune aspects of T1D, such as glycemic control, as nonautoimmune diabetes has been associated with ADHD among children,” the researchers wrote.

The study findings were limited by several factors, including the lack of outpatient and primary care records to identify maternal autoimmune disease, and lack of data on any medication used to managed diseases during pregnancy, as well as a lack of data on children with ADHD who might not have been treated with medication, the researchers noted. In addition, “given differences in study design and definitions, the pooled HRs presented in the meta-analysis need to be treated cautiously.”

However, the results were strengthened by the hybrid study design and large study population, and were generally consistent with previous research supporting an effect of maternal immune function on fetal neurodevelopment, they noted.

“Our study provides justification for future studies that examine the effect of maternal autoimmune diseases, including biomarkers, condition severity, and management in pregnancy and in the periconception period, on neurodevelopmental disorders in children,” they concluded.

Studies need to explore mechanism of action

The current study, with its hybrid design, adds support to the evidence of an association between any maternal autoimmune disease and ADHD in children, as well as an association between the specific conditions of type 1 diabetes, hyperthyroidism, and psoriasis in mothers and ADHD in children, Søren Dalsgaard, MD, of Aarhus (Denmark) University, wrote in an accompanying editorial.

“Importantly, Nielsen et al. emphasized in their article that, for the many different autoimmune diseases, different underlying mechanisms for the associations with disorders of the central nervous system were likely. They mentioned that, for T1D, low glycemic control may play a role, as type 2 diabetes has been associated with ADHD,” said Dr. Dalsgaard.

“Overall, these mechanisms are thought to include shared genetic and environmental risk factors or direct effects of maternal autoantibodies or cytokines crossing the placenta and altering the fetal immune response, which in turns leads to changes in the central nervous system,” Dr. Dalsgaard explained. However, the current study and previous studies have not identified the mechanisms to explain the association between ADHD in children and maternal autoimmune disease.

“To understand more about these associations, future studies should include researchers and data from different scientific disciplines, such as epidemiology, animal modeling, genetics, and neuroimmunology,” he concluded.
 

Association is not causality

Overall, the study findings add to the evidence of a correlation between autoimmune diseases and neurologic disease, said Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y., in an interview. “Anything that might contribute to behavioral problems is worth investigating.” However, it is important to remember that association is not causation.

“There is some literature and evidence that autoimmune disease is associated with mental health issues, but the mechanisms of action are unknown,” said Dr. Lessin. ADHD is highly heritable, so the association may be caused by a similar genetic predisposition, or it may be something related to autoimmunity that is impacting the fetus by passing through the placenta.

The current study’s strengths include the large size and hybrid design, but limitations such as the identification of ADHD based on medication prescriptions may have led to underreporting, and identifying maternal autoimmune disease via inpatient hospital diagnosis could have selected for more severe disease, he said.

From a clinical standpoint, the study suggests a correlation that should be noted in a family history and potentially used to inform a diagnosis, especially in cases of type 1 diabetes where the association was strongest, Dr. Lessin said. The findings also support the value of further research to look for mechanisms that might explain whether the association between autoimmune disease and ADHD is autoimmune system causality or shared genetic susceptibility.

The study received no outside funding. One coauthor disclosed receiving grants from the National Blood Authority Australia and the Australian National Health and Medical Research Council during the conduct of the study. Dr. Dalsgaard had no financial conflicts to disclose. Dr. Lessin disclosed serving as editor of the ADHD toolkit for the American Academy of Pediatrics and coauthor of the current ADHD clinical guidelines. He also serves in advisory capacity to Cognoa, a company involved in diagnosis of autism, and Corium/KemPharm, companies involved in the development of ADHD treatments.

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Are pediatric atopic dermatitis and atopic dermatitis the same disease?

“Maybe not,” Jonathan I. Silverberg, MD, PhD, MPH, said during the Revolutionizing Atopic Dermatitis symposium.

Dr. Silverberg, director of clinical research in the division of dermatology at George Washington University, Washington, based his comments largely on a review that he and his colleagues carried out to understand how features of atopic dermatitis (AD) vary by region globally as well as by age. They identified 101 studies with sufficient data for meta-analysis and stratified the results by pediatric and adult age groups.

Several signs and symptoms occurred with similar frequency among pediatric and adult patients, including pruritus, xerosis, flexural involvement, extensor involvement, early onset of disease, comorbid atopy, head and neck involvement, and ophthalmic comorbidities. However, adults were found to have more signs of chronic disease, more hand eczema, different patterns of hand eczema, and a stronger relationship of disease activity with emotional factors. Meanwhile, children were found to have more exudative or weeping lesions, more perifollicular eczema, and more pityriasis alba.

Dr. Silverberg showed photos of three adults with varied presentations of extensor involvement, including one “who had a lot of lichenification and thickening of the skin, but over knees where you might think about psoriasis,” he said. “All three of these patients were of Southeast Asian descent. That happens to be a region where this feature was reported much more commonly. It may even tie to some underlying immunopathophysiologic differences of the disease across different patient populations.”

AD signs that occur more commonly in adults than children include lichenification (100% vs. 48%), urticaria (32% vs. 20%), popular lichenoid lesions (46% vs. 8%), Hertoghe’s sign (25% vs. 2%), erythroderma (29% vs. 1%), and nodular prurigo (18% vs. 4%).

Hand eczema features also differ between adults and children, including hand or foot dermatitis (44% vs. 25%), dyshidrosis/pompholyx (21% vs. 3%), knuckle dermatitis (25% vs. 8%), nail involvement (15% vs. 8%), and fissured heels. However, ventral wrist dermatitis was found to be more than twice as common in children, compared with adults (34% vs. 15%).

Other signs of AD were more common in children, compared with adults, including exudative eczema (61% vs. 42%), pityriasis alba (28% vs. 18%), Dennie-Morgan infraorbital folds (47% vs. 36%), seborrheic dermatitis–like lesions (40% vs. 18%), and perifollicular accentuation (37% vs. 21%). “This is such an important sign to wrap your head around and get comfortable assessing,” he said. “I have seen patients who are erythrodermic with follicular eczema who were told that they were crazy and had psychogenic itch, and they should go to a shrink.”

AD triggers can differ between adults and children as well, including course influenced by emotions/environmental factors (72% vs. 32%), worsening itch worse (65% vs. 49%), course influenced by environment (62% vs. 37%), and course influenced by emotions (70% vs. 15%).

According to Dr. Silverberg, emerging research suggests that there may be differences in the immune pathways activated in pediatric versus adult AD. Specifically, more Th17 and interferon-gamma in AD lesions have been observed in children, compared with adults, and more Th22 and Th17 in nonlesional AD have been seen in children, compared with adults. “This leads to a question: Will children respond differently than adults to treatment?” Dr. Silverberg said. “We see that omalizumab doesn’t seem to help much in adults, yet a recent study suggested that it might work reasonably well for children. Dupilumab has different dosing requirements and potentially different responses between the pediatric and adult populations.”

Age differences in AD may also be related to differences in the skin microbiome. In 2016, researchers led by Richard L. Gallo, MD, PhD, professor of dermatology, University of California, San Diego, compared the skin microbiome between adults and children with AD by swabbing the volar forearm and performing 16S rRNA gene sequencing. The study included 59 young children, 13 teenagers, and 56 adults with AD as well as 68 age-matched non-atopic healthy controls. The researchers found a greater abundance of Streptococcus, Granulicatella, Gemella, Rothia, and Haemophilus in young children, compared with adults, while Propionibacterium, Corynebacterium, Staphylococcus, Lactobacillus, Finegoldia, and Anaerococcus were more abundant in adults, compared with children.

Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

[email protected]

Are pediatric atopic dermatitis and atopic dermatitis the same disease?

“Maybe not,” Jonathan I. Silverberg, MD, PhD, MPH, said during the Revolutionizing Atopic Dermatitis symposium.

Dr. Silverberg, director of clinical research in the division of dermatology at George Washington University, Washington, based his comments largely on a review that he and his colleagues carried out to understand how features of atopic dermatitis (AD) vary by region globally as well as by age. They identified 101 studies with sufficient data for meta-analysis and stratified the results by pediatric and adult age groups.

Several signs and symptoms occurred with similar frequency among pediatric and adult patients, including pruritus, xerosis, flexural involvement, extensor involvement, early onset of disease, comorbid atopy, head and neck involvement, and ophthalmic comorbidities. However, adults were found to have more signs of chronic disease, more hand eczema, different patterns of hand eczema, and a stronger relationship of disease activity with emotional factors. Meanwhile, children were found to have more exudative or weeping lesions, more perifollicular eczema, and more pityriasis alba.

Dr. Silverberg showed photos of three adults with varied presentations of extensor involvement, including one “who had a lot of lichenification and thickening of the skin, but over knees where you might think about psoriasis,” he said. “All three of these patients were of Southeast Asian descent. That happens to be a region where this feature was reported much more commonly. It may even tie to some underlying immunopathophysiologic differences of the disease across different patient populations.”

AD signs that occur more commonly in adults than children include lichenification (100% vs. 48%), urticaria (32% vs. 20%), popular lichenoid lesions (46% vs. 8%), Hertoghe’s sign (25% vs. 2%), erythroderma (29% vs. 1%), and nodular prurigo (18% vs. 4%).

Hand eczema features also differ between adults and children, including hand or foot dermatitis (44% vs. 25%), dyshidrosis/pompholyx (21% vs. 3%), knuckle dermatitis (25% vs. 8%), nail involvement (15% vs. 8%), and fissured heels. However, ventral wrist dermatitis was found to be more than twice as common in children, compared with adults (34% vs. 15%).

Other signs of AD were more common in children, compared with adults, including exudative eczema (61% vs. 42%), pityriasis alba (28% vs. 18%), Dennie-Morgan infraorbital folds (47% vs. 36%), seborrheic dermatitis–like lesions (40% vs. 18%), and perifollicular accentuation (37% vs. 21%). “This is such an important sign to wrap your head around and get comfortable assessing,” he said. “I have seen patients who are erythrodermic with follicular eczema who were told that they were crazy and had psychogenic itch, and they should go to a shrink.”

AD triggers can differ between adults and children as well, including course influenced by emotions/environmental factors (72% vs. 32%), worsening itch worse (65% vs. 49%), course influenced by environment (62% vs. 37%), and course influenced by emotions (70% vs. 15%).

According to Dr. Silverberg, emerging research suggests that there may be differences in the immune pathways activated in pediatric versus adult AD. Specifically, more Th17 and interferon-gamma in AD lesions have been observed in children, compared with adults, and more Th22 and Th17 in nonlesional AD have been seen in children, compared with adults. “This leads to a question: Will children respond differently than adults to treatment?” Dr. Silverberg said. “We see that omalizumab doesn’t seem to help much in adults, yet a recent study suggested that it might work reasonably well for children. Dupilumab has different dosing requirements and potentially different responses between the pediatric and adult populations.”

Age differences in AD may also be related to differences in the skin microbiome. In 2016, researchers led by Richard L. Gallo, MD, PhD, professor of dermatology, University of California, San Diego, compared the skin microbiome between adults and children with AD by swabbing the volar forearm and performing 16S rRNA gene sequencing. The study included 59 young children, 13 teenagers, and 56 adults with AD as well as 68 age-matched non-atopic healthy controls. The researchers found a greater abundance of Streptococcus, Granulicatella, Gemella, Rothia, and Haemophilus in young children, compared with adults, while Propionibacterium, Corynebacterium, Staphylococcus, Lactobacillus, Finegoldia, and Anaerococcus were more abundant in adults, compared with children.

Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

[email protected]

Are pediatric atopic dermatitis and atopic dermatitis the same disease?

“Maybe not,” Jonathan I. Silverberg, MD, PhD, MPH, said during the Revolutionizing Atopic Dermatitis symposium.

Dr. Silverberg, director of clinical research in the division of dermatology at George Washington University, Washington, based his comments largely on a review that he and his colleagues carried out to understand how features of atopic dermatitis (AD) vary by region globally as well as by age. They identified 101 studies with sufficient data for meta-analysis and stratified the results by pediatric and adult age groups.

Several signs and symptoms occurred with similar frequency among pediatric and adult patients, including pruritus, xerosis, flexural involvement, extensor involvement, early onset of disease, comorbid atopy, head and neck involvement, and ophthalmic comorbidities. However, adults were found to have more signs of chronic disease, more hand eczema, different patterns of hand eczema, and a stronger relationship of disease activity with emotional factors. Meanwhile, children were found to have more exudative or weeping lesions, more perifollicular eczema, and more pityriasis alba.

Dr. Silverberg showed photos of three adults with varied presentations of extensor involvement, including one “who had a lot of lichenification and thickening of the skin, but over knees where you might think about psoriasis,” he said. “All three of these patients were of Southeast Asian descent. That happens to be a region where this feature was reported much more commonly. It may even tie to some underlying immunopathophysiologic differences of the disease across different patient populations.”

AD signs that occur more commonly in adults than children include lichenification (100% vs. 48%), urticaria (32% vs. 20%), popular lichenoid lesions (46% vs. 8%), Hertoghe’s sign (25% vs. 2%), erythroderma (29% vs. 1%), and nodular prurigo (18% vs. 4%).

Hand eczema features also differ between adults and children, including hand or foot dermatitis (44% vs. 25%), dyshidrosis/pompholyx (21% vs. 3%), knuckle dermatitis (25% vs. 8%), nail involvement (15% vs. 8%), and fissured heels. However, ventral wrist dermatitis was found to be more than twice as common in children, compared with adults (34% vs. 15%).

Other signs of AD were more common in children, compared with adults, including exudative eczema (61% vs. 42%), pityriasis alba (28% vs. 18%), Dennie-Morgan infraorbital folds (47% vs. 36%), seborrheic dermatitis–like lesions (40% vs. 18%), and perifollicular accentuation (37% vs. 21%). “This is such an important sign to wrap your head around and get comfortable assessing,” he said. “I have seen patients who are erythrodermic with follicular eczema who were told that they were crazy and had psychogenic itch, and they should go to a shrink.”

AD triggers can differ between adults and children as well, including course influenced by emotions/environmental factors (72% vs. 32%), worsening itch worse (65% vs. 49%), course influenced by environment (62% vs. 37%), and course influenced by emotions (70% vs. 15%).

According to Dr. Silverberg, emerging research suggests that there may be differences in the immune pathways activated in pediatric versus adult AD. Specifically, more Th17 and interferon-gamma in AD lesions have been observed in children, compared with adults, and more Th22 and Th17 in nonlesional AD have been seen in children, compared with adults. “This leads to a question: Will children respond differently than adults to treatment?” Dr. Silverberg said. “We see that omalizumab doesn’t seem to help much in adults, yet a recent study suggested that it might work reasonably well for children. Dupilumab has different dosing requirements and potentially different responses between the pediatric and adult populations.”

Age differences in AD may also be related to differences in the skin microbiome. In 2016, researchers led by Richard L. Gallo, MD, PhD, professor of dermatology, University of California, San Diego, compared the skin microbiome between adults and children with AD by swabbing the volar forearm and performing 16S rRNA gene sequencing. The study included 59 young children, 13 teenagers, and 56 adults with AD as well as 68 age-matched non-atopic healthy controls. The researchers found a greater abundance of Streptococcus, Granulicatella, Gemella, Rothia, and Haemophilus in young children, compared with adults, while Propionibacterium, Corynebacterium, Staphylococcus, Lactobacillus, Finegoldia, and Anaerococcus were more abundant in adults, compared with children.

Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

[email protected]

Physician offices, which have been deemphasized in the COVID-19 vaccine rollout, should have a more prominent role in the effort going forward, said the Medical Group Management Association in a letter sent to President Joe Biden on Jan. 26.

“Due to our members’ role as community providers, we ask that the Administration include medical group practices in COVID-19 vaccine distribution strategies moving forward,” Halee Fischer-Wright, MD, president and CEO of MGMA, stated in the letter.

“Current vaccine efforts are haphazard at best and appear to rely on a passive first come first served approach with the public rushing to sign up for vaccines when scant supply becomes available,” MGMA noted. “This favors patients who can advocate for themselves or have family members able to do the same. Yet medical group practices already have patient relationships and experience vaccinating patients for influenza and other conditions.”

Moreover, physician practices have data on patient demographics, preexisting conditions, and risk factors. This is valuable information not available to hospitals, pharmacies, and state health departments, MGMA said.

“Furthermore, in a time of uncertainty and misinformation, patients are looking to their own physicians as a trusted source for information on vaccine safety and efficacy,” the letter stated. “Physician group practices can and should play a significant role in vaccine education.”

Despite these advantages of vaccinating patients in doctors’ offices, MGMA pointed out that “states have largely not leveraged physician practices in vaccine rollout efforts.”

In an MGMA survey conducted last week, 85% of independent practices and 45% of hospital- or health system–owned practices that sought COVID-19 vaccine for their patients were unable to obtain any. Of the practices able to get vaccine supplies, the majority said they had received only enough to vaccinate 1% or less of their patients.

Susan R. Bailey, MD, president of the American Medical Association commented in an interview that, “once enough supplies are available, we encourage the administration to ensure physician practices have an adequate supply of COVID-19 vaccines to vaccinate their patients. Physician practices will be an integral part of the vaccine administration process. Physicians are a trusted source of information for patients and their direct conversations and recommendations for patients to get vaccinated will help address hesitancy and result in more people getting vaccinated.”

Many groups, MGMA said, had been approved by their states to distribute the vaccine but received little or no inventory. Practice phone lines have been “flooded” by patients wanting to know why their physicians can’t vaccinate them.
 

Programs vary by state

In an interview, Dr. Fischer-Wright said that most practices want to vaccinate their patients. But only some states have set up programs that allow them to apply for the COVID-19 vaccines. “Most of our practices that were eligible for vaccination have applied for it,” she added.

The New York State Health Department is taking a different approach, according to Dial Hewlett Jr., MD, medical director for disease control services with the Westchester County Department of Health in White Plains, N.Y.. The state health department has designated specific sites across New York as vaccination hubs; in Westchester County, the hub is the Westchester Medical Center. When the hospital receives a vaccine shipment, it distributes some of it to smaller sites such as the county health department, which includes a vaccination clinic.

“So far, they haven’t gotten to the point where they’re distributing to pharmacies or doctors’ offices,” Dr. Hewlett said in an interview.

Right now, he said, the chief limiting factor is vaccine supply. When that expands, he said, physician offices will likely get more vaccine doses.

Both Dr. Hewlett and Dr. Fischer-Wright pointed out that physician offices are limited because they aren’t able to store the Pfizer vaccine, which requires ultracold freezers. “But now that we have the Moderna vaccine, 50% of the 200 million doses that have been promised can be delivered in a physician office,” said Dr. Fischer-Wright.

So why haven’t practices received more vaccine? Besides the inadequate supply across the nation, Dr. Fischer-Wright said, there have been difficulties in getting the vaccine to physician offices. Some MGMA members, she added, did receive vaccine supplies immediately. “These were independent practices that had over 200 physicians.”

Dr. Hewlett noted that some smaller practices have complained to the county department that they couldn’t obtain vaccine because they lacked the clout to compete with larger groups. “They’re not ordering enough product to make it a priority for whoever is involved with the distribution.”

Another problem – evident in the results of MGMA’s recent poll – is that health care systems that have vaccine supplies are sharing them with their own practices before they make any available to community practices.

“If you’re working for Northwell Health, you probably won’t have the kinds of challenges that the small mom-and-pop practice would have,” Dr. Hewlett said.
 

Overcoming vaccine hesitancy

More than a quarter of the U.S. population has indicated they are hesitant to get the COVID-19 vaccine. This is an area where Dr. Fischer-Wright believes physicians can help immensely.

“The benefit of having that type of activity occur in the physician office is that it’s a place where physicians have already established trust with patients,” she said. “And one of the reasons why some people don’t want a shot is that they don’t trust the vaccine. Having a human being that you have a relationship with provide you with the pros and cons is very compelling to get people to make an alternative choice.”

Physicians and their staff will also need to be educated before they administer the vaccine, Dr. Hewlett noted. “There will have to be education on the handling of the vaccine, but I think that can easily be done. Many practices have physician assistants and nurse practitioners who have been doing a lot of vaccinations in the office setting.”
 

Complex logistics

Based on the experience of his department’s vaccination clinic, which has been giving COVID-19 shots since Jan. 5, Dr. Hewlett said private practices have a lot to consider before they launch their own vaccination efforts.

To begin with, he said, “it’s a tricky situation with these vaccines that require two doses.” Before his clinic makes an appointment to vaccinate a patient, the scheduler has to make sure that the patient can return in 21 or 28 days, depending on whether they’re getting the Pfizer or Moderna vaccine.

“It’s difficult if they can’t show up 28 days after that date because we expect the same number of people to show up 28 days later for their second dose,” he said. “This is quite different from a standard medical practice. There aren’t too many situations where a person has to come back to the office after 28 days or 21 days.”

While the Centers for Disease Control and Prevention recently said the immunization schedule can be more flexible, Dr. Hewlett added, his clinic prefers to get patients back on the recommended schedule to make sure the vaccine will be maximally effective.

The clinic also has to follow state regulations requiring that all vaccines it receives be administered within a week of receipt. Right now, the clinic is open 6 days a week, giving about 300-400 shots a day. Each morning, a clerk records how many doses were administered the previous day, along with the lot numbers – and all data must be reported to the state.

The operation is fairly labor intensive. The clinic has a staff of about 30 people, most of whom are now engaged full time in the COVID-19 vaccination effort.

“We have people who check patients in and who screen to make sure no one has COVID symptoms. Other people escort patients to the vaccination stations. We have about 15 nurse practitioners and public health nurses who give the shots, and we have to make sure they’re accounting for every dose that’s given. And we have to make sure everybody getting a dose meets the eligibility criteria for shots,” he said. “We also have an area where patients are watched for 15 minutes after they’re vaccinated. Then there’s a group of five data entry people who locate appointment slots 28 days from today.”

It’s all still “a work in progress,” Dr. Hewlett said, but the staff who give COVID-19 shots and the patients who receive them are gratified to be making a difference.

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

Physician offices, which have been deemphasized in the COVID-19 vaccine rollout, should have a more prominent role in the effort going forward, said the Medical Group Management Association in a letter sent to President Joe Biden on Jan. 26.

“Due to our members’ role as community providers, we ask that the Administration include medical group practices in COVID-19 vaccine distribution strategies moving forward,” Halee Fischer-Wright, MD, president and CEO of MGMA, stated in the letter.

“Current vaccine efforts are haphazard at best and appear to rely on a passive first come first served approach with the public rushing to sign up for vaccines when scant supply becomes available,” MGMA noted. “This favors patients who can advocate for themselves or have family members able to do the same. Yet medical group practices already have patient relationships and experience vaccinating patients for influenza and other conditions.”

Moreover, physician practices have data on patient demographics, preexisting conditions, and risk factors. This is valuable information not available to hospitals, pharmacies, and state health departments, MGMA said.

“Furthermore, in a time of uncertainty and misinformation, patients are looking to their own physicians as a trusted source for information on vaccine safety and efficacy,” the letter stated. “Physician group practices can and should play a significant role in vaccine education.”

Despite these advantages of vaccinating patients in doctors’ offices, MGMA pointed out that “states have largely not leveraged physician practices in vaccine rollout efforts.”

In an MGMA survey conducted last week, 85% of independent practices and 45% of hospital- or health system–owned practices that sought COVID-19 vaccine for their patients were unable to obtain any. Of the practices able to get vaccine supplies, the majority said they had received only enough to vaccinate 1% or less of their patients.

Susan R. Bailey, MD, president of the American Medical Association commented in an interview that, “once enough supplies are available, we encourage the administration to ensure physician practices have an adequate supply of COVID-19 vaccines to vaccinate their patients. Physician practices will be an integral part of the vaccine administration process. Physicians are a trusted source of information for patients and their direct conversations and recommendations for patients to get vaccinated will help address hesitancy and result in more people getting vaccinated.”

Many groups, MGMA said, had been approved by their states to distribute the vaccine but received little or no inventory. Practice phone lines have been “flooded” by patients wanting to know why their physicians can’t vaccinate them.
 

Programs vary by state

In an interview, Dr. Fischer-Wright said that most practices want to vaccinate their patients. But only some states have set up programs that allow them to apply for the COVID-19 vaccines. “Most of our practices that were eligible for vaccination have applied for it,” she added.

The New York State Health Department is taking a different approach, according to Dial Hewlett Jr., MD, medical director for disease control services with the Westchester County Department of Health in White Plains, N.Y.. The state health department has designated specific sites across New York as vaccination hubs; in Westchester County, the hub is the Westchester Medical Center. When the hospital receives a vaccine shipment, it distributes some of it to smaller sites such as the county health department, which includes a vaccination clinic.

“So far, they haven’t gotten to the point where they’re distributing to pharmacies or doctors’ offices,” Dr. Hewlett said in an interview.

Right now, he said, the chief limiting factor is vaccine supply. When that expands, he said, physician offices will likely get more vaccine doses.

Both Dr. Hewlett and Dr. Fischer-Wright pointed out that physician offices are limited because they aren’t able to store the Pfizer vaccine, which requires ultracold freezers. “But now that we have the Moderna vaccine, 50% of the 200 million doses that have been promised can be delivered in a physician office,” said Dr. Fischer-Wright.

So why haven’t practices received more vaccine? Besides the inadequate supply across the nation, Dr. Fischer-Wright said, there have been difficulties in getting the vaccine to physician offices. Some MGMA members, she added, did receive vaccine supplies immediately. “These were independent practices that had over 200 physicians.”

Dr. Hewlett noted that some smaller practices have complained to the county department that they couldn’t obtain vaccine because they lacked the clout to compete with larger groups. “They’re not ordering enough product to make it a priority for whoever is involved with the distribution.”

Another problem – evident in the results of MGMA’s recent poll – is that health care systems that have vaccine supplies are sharing them with their own practices before they make any available to community practices.

“If you’re working for Northwell Health, you probably won’t have the kinds of challenges that the small mom-and-pop practice would have,” Dr. Hewlett said.
 

Overcoming vaccine hesitancy

More than a quarter of the U.S. population has indicated they are hesitant to get the COVID-19 vaccine. This is an area where Dr. Fischer-Wright believes physicians can help immensely.

“The benefit of having that type of activity occur in the physician office is that it’s a place where physicians have already established trust with patients,” she said. “And one of the reasons why some people don’t want a shot is that they don’t trust the vaccine. Having a human being that you have a relationship with provide you with the pros and cons is very compelling to get people to make an alternative choice.”

Physicians and their staff will also need to be educated before they administer the vaccine, Dr. Hewlett noted. “There will have to be education on the handling of the vaccine, but I think that can easily be done. Many practices have physician assistants and nurse practitioners who have been doing a lot of vaccinations in the office setting.”
 

Complex logistics

Based on the experience of his department’s vaccination clinic, which has been giving COVID-19 shots since Jan. 5, Dr. Hewlett said private practices have a lot to consider before they launch their own vaccination efforts.

To begin with, he said, “it’s a tricky situation with these vaccines that require two doses.” Before his clinic makes an appointment to vaccinate a patient, the scheduler has to make sure that the patient can return in 21 or 28 days, depending on whether they’re getting the Pfizer or Moderna vaccine.

“It’s difficult if they can’t show up 28 days after that date because we expect the same number of people to show up 28 days later for their second dose,” he said. “This is quite different from a standard medical practice. There aren’t too many situations where a person has to come back to the office after 28 days or 21 days.”

While the Centers for Disease Control and Prevention recently said the immunization schedule can be more flexible, Dr. Hewlett added, his clinic prefers to get patients back on the recommended schedule to make sure the vaccine will be maximally effective.

The clinic also has to follow state regulations requiring that all vaccines it receives be administered within a week of receipt. Right now, the clinic is open 6 days a week, giving about 300-400 shots a day. Each morning, a clerk records how many doses were administered the previous day, along with the lot numbers – and all data must be reported to the state.

The operation is fairly labor intensive. The clinic has a staff of about 30 people, most of whom are now engaged full time in the COVID-19 vaccination effort.

“We have people who check patients in and who screen to make sure no one has COVID symptoms. Other people escort patients to the vaccination stations. We have about 15 nurse practitioners and public health nurses who give the shots, and we have to make sure they’re accounting for every dose that’s given. And we have to make sure everybody getting a dose meets the eligibility criteria for shots,” he said. “We also have an area where patients are watched for 15 minutes after they’re vaccinated. Then there’s a group of five data entry people who locate appointment slots 28 days from today.”

It’s all still “a work in progress,” Dr. Hewlett said, but the staff who give COVID-19 shots and the patients who receive them are gratified to be making a difference.

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

Physician offices, which have been deemphasized in the COVID-19 vaccine rollout, should have a more prominent role in the effort going forward, said the Medical Group Management Association in a letter sent to President Joe Biden on Jan. 26.

“Due to our members’ role as community providers, we ask that the Administration include medical group practices in COVID-19 vaccine distribution strategies moving forward,” Halee Fischer-Wright, MD, president and CEO of MGMA, stated in the letter.

“Current vaccine efforts are haphazard at best and appear to rely on a passive first come first served approach with the public rushing to sign up for vaccines when scant supply becomes available,” MGMA noted. “This favors patients who can advocate for themselves or have family members able to do the same. Yet medical group practices already have patient relationships and experience vaccinating patients for influenza and other conditions.”

Moreover, physician practices have data on patient demographics, preexisting conditions, and risk factors. This is valuable information not available to hospitals, pharmacies, and state health departments, MGMA said.

“Furthermore, in a time of uncertainty and misinformation, patients are looking to their own physicians as a trusted source for information on vaccine safety and efficacy,” the letter stated. “Physician group practices can and should play a significant role in vaccine education.”

Despite these advantages of vaccinating patients in doctors’ offices, MGMA pointed out that “states have largely not leveraged physician practices in vaccine rollout efforts.”

In an MGMA survey conducted last week, 85% of independent practices and 45% of hospital- or health system–owned practices that sought COVID-19 vaccine for their patients were unable to obtain any. Of the practices able to get vaccine supplies, the majority said they had received only enough to vaccinate 1% or less of their patients.

Susan R. Bailey, MD, president of the American Medical Association commented in an interview that, “once enough supplies are available, we encourage the administration to ensure physician practices have an adequate supply of COVID-19 vaccines to vaccinate their patients. Physician practices will be an integral part of the vaccine administration process. Physicians are a trusted source of information for patients and their direct conversations and recommendations for patients to get vaccinated will help address hesitancy and result in more people getting vaccinated.”

Many groups, MGMA said, had been approved by their states to distribute the vaccine but received little or no inventory. Practice phone lines have been “flooded” by patients wanting to know why their physicians can’t vaccinate them.
 

Programs vary by state

In an interview, Dr. Fischer-Wright said that most practices want to vaccinate their patients. But only some states have set up programs that allow them to apply for the COVID-19 vaccines. “Most of our practices that were eligible for vaccination have applied for it,” she added.

The New York State Health Department is taking a different approach, according to Dial Hewlett Jr., MD, medical director for disease control services with the Westchester County Department of Health in White Plains, N.Y.. The state health department has designated specific sites across New York as vaccination hubs; in Westchester County, the hub is the Westchester Medical Center. When the hospital receives a vaccine shipment, it distributes some of it to smaller sites such as the county health department, which includes a vaccination clinic.

“So far, they haven’t gotten to the point where they’re distributing to pharmacies or doctors’ offices,” Dr. Hewlett said in an interview.

Right now, he said, the chief limiting factor is vaccine supply. When that expands, he said, physician offices will likely get more vaccine doses.

Both Dr. Hewlett and Dr. Fischer-Wright pointed out that physician offices are limited because they aren’t able to store the Pfizer vaccine, which requires ultracold freezers. “But now that we have the Moderna vaccine, 50% of the 200 million doses that have been promised can be delivered in a physician office,” said Dr. Fischer-Wright.

So why haven’t practices received more vaccine? Besides the inadequate supply across the nation, Dr. Fischer-Wright said, there have been difficulties in getting the vaccine to physician offices. Some MGMA members, she added, did receive vaccine supplies immediately. “These were independent practices that had over 200 physicians.”

Dr. Hewlett noted that some smaller practices have complained to the county department that they couldn’t obtain vaccine because they lacked the clout to compete with larger groups. “They’re not ordering enough product to make it a priority for whoever is involved with the distribution.”

Another problem – evident in the results of MGMA’s recent poll – is that health care systems that have vaccine supplies are sharing them with their own practices before they make any available to community practices.

“If you’re working for Northwell Health, you probably won’t have the kinds of challenges that the small mom-and-pop practice would have,” Dr. Hewlett said.
 

Overcoming vaccine hesitancy

More than a quarter of the U.S. population has indicated they are hesitant to get the COVID-19 vaccine. This is an area where Dr. Fischer-Wright believes physicians can help immensely.

“The benefit of having that type of activity occur in the physician office is that it’s a place where physicians have already established trust with patients,” she said. “And one of the reasons why some people don’t want a shot is that they don’t trust the vaccine. Having a human being that you have a relationship with provide you with the pros and cons is very compelling to get people to make an alternative choice.”

Physicians and their staff will also need to be educated before they administer the vaccine, Dr. Hewlett noted. “There will have to be education on the handling of the vaccine, but I think that can easily be done. Many practices have physician assistants and nurse practitioners who have been doing a lot of vaccinations in the office setting.”
 

Complex logistics

Based on the experience of his department’s vaccination clinic, which has been giving COVID-19 shots since Jan. 5, Dr. Hewlett said private practices have a lot to consider before they launch their own vaccination efforts.

To begin with, he said, “it’s a tricky situation with these vaccines that require two doses.” Before his clinic makes an appointment to vaccinate a patient, the scheduler has to make sure that the patient can return in 21 or 28 days, depending on whether they’re getting the Pfizer or Moderna vaccine.

“It’s difficult if they can’t show up 28 days after that date because we expect the same number of people to show up 28 days later for their second dose,” he said. “This is quite different from a standard medical practice. There aren’t too many situations where a person has to come back to the office after 28 days or 21 days.”

While the Centers for Disease Control and Prevention recently said the immunization schedule can be more flexible, Dr. Hewlett added, his clinic prefers to get patients back on the recommended schedule to make sure the vaccine will be maximally effective.

The clinic also has to follow state regulations requiring that all vaccines it receives be administered within a week of receipt. Right now, the clinic is open 6 days a week, giving about 300-400 shots a day. Each morning, a clerk records how many doses were administered the previous day, along with the lot numbers – and all data must be reported to the state.

The operation is fairly labor intensive. The clinic has a staff of about 30 people, most of whom are now engaged full time in the COVID-19 vaccination effort.

“We have people who check patients in and who screen to make sure no one has COVID symptoms. Other people escort patients to the vaccination stations. We have about 15 nurse practitioners and public health nurses who give the shots, and we have to make sure they’re accounting for every dose that’s given. And we have to make sure everybody getting a dose meets the eligibility criteria for shots,” he said. “We also have an area where patients are watched for 15 minutes after they’re vaccinated. Then there’s a group of five data entry people who locate appointment slots 28 days from today.”

It’s all still “a work in progress,” Dr. Hewlett said, but the staff who give COVID-19 shots and the patients who receive them are gratified to be making a difference.

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

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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

The United States is nearly 6 weeks into its historic campaign to vaccinate Americans against the virus that causes COVID-19, and so far, the two vaccines in use look remarkably low risk, according to new data presented today at a meeting of vaccine experts that advise the Centers for Disease Control and Prevention.

With 23.5 million doses of the Pfizer and Moderna vaccines now given, there have been very few serious side effects. In addition, deaths reported after people got the vaccine do not seem to be related to it.

The most common symptoms reported after vaccination were pain where people got the shot, fatigue, headache, and muscle soreness. These were more common after the second dose. In addition, about one in four people reported fever and chills after the second shot.

“On the whole, I thought it was very reassuring,” said William Schaffner, MD, an infectious disease expert with Vanderbilt University, Nashville, Tenn., who listened to the presentations.

The CDC is collecting safety information through multiple channels. These include a new smartphone-based app called V-Safe, which collects daily information from people who’ve been vaccinated; the federal Vaccine Adverse Event Reporting System, which accepts reports from anyone; and the Vaccine Safety Datalink, which is a collaboration between the CDC and nine major hospital systems. There’s also the Clinical Immunization Safety Assessment Project, a collaboration between the CDC and vaccine safety experts.

After surveying these systems, experts heading the safety committee for the CDC’s Advisory Committee on Immunization Practices said there have been few serious side effects reported.

Very rarely, severe allergic reactions – called anaphylaxis – have occurred after vaccination. There have been 50 of these cases reported after the Pfizer vaccine and 21 cases reported after the Moderna vaccine to date. Nearly all of them – 94% of the anaphylaxis cases after Pfizer vaccines and 100% of those after Moderna’s vaccine – have been in women, though it’s not clear why.

That translates to a rate of about five cases of anaphylaxis for every million doses of the Pfizer vaccine and about three for every million doses of the Moderna vaccine. Most of these occur within 15 minutes after getting a vaccine dose, with one reported as long as 20 hours after the shot.

The CDC suspects these may be related to an ingredient called polyethylene glycol (PEG). PEG is a part of the particles that slip the vaccines’ mRNA into cells with instructions to make the spike protein of the virus. Cells then express these spikes on their surfaces so the immune system can learn to recognize them and make defenses against them. PEG is a common ingredient in many drugs and occasionally triggers anaphylaxis.
 

Reported deaths seem unrelated to vaccines

Through Jan. 18, 196 people have died after getting a vaccine.

Most of these deaths (129) were in patients in long term care facilities. These deaths are still being investigated, but when they were compared with the number of deaths that might be expected over the same period because of natural causes, they seemed to be coincidental and not caused by the vaccine, said Tom Shimabukuro, MD, deputy director of the Immunization Safety Office at the CDC, who studied the data.

In fact, death rates were lower among vaccinated nursing home residents, compared with those who had not been vaccinated.

“These findings suggest that short-term mortality rates appear unrelated to vaccination for COVID-19,” Dr. Shimabukuro said.

This also appeared to be true for younger adults who died after their shots.

There were 28 people aged under 65 years who died after being vaccinated. Most of these deaths were heart related, according to autopsy reports. When investigators compared the number of sudden cardiac deaths expected to occur in this population naturally, they found people who were vaccinated had a lower rate than would have been expected without vaccination. This suggests that these deaths were also unrelated to the vaccine.
 

More vaccines on the horizon

The panel also heard an update from drug company AstraZeneca on its vaccine. It’s being used in 18 countries but has not yet been authorized in the United States.

That vaccine is currently in phase 3 of its U.S. clinical trials, and more than 26,000 people who have volunteered to get the shot had received their second dose as of Jan. 21, the company said.

The Food and Drug Administration requires at least 2 months of follow-up before it will evaluate a vaccine for an emergency-use authorization, which means the company would be ready to submit by the end of March, with a possible approval by April.

The AstraZeneca vaccine uses a more traditional method to create immunity, slipping a key part of the virus that causes COVID-19 into the shell of an adenovirus – a virus that causes cold-like symptoms – that normally infects monkeys. When the immune system sees the virus, it generates protective defenses against it.

The two-dose vaccine can be stored in a regular refrigerator for up to 6 months, which makes it easier to handle than the mRNA vaccines, which require much colder storage. Another advantage appears to be that it’s less likely to trigger severe allergic reactions. So far, there have been no cases of anaphylaxis reported after this shot.

In total, four serious side effects have been reported with the AstraZeneca vaccine, including two cases of transverse myelitis, a serious condition that causes swelling of the spinal cord, leading to pain, muscle weakness, and paralysis. One of these was in the group that got the placebo. The reports paused the trial, but it was allowed to continue after a safety review.

This vaccine also appears to be less effective than the mRNA shots. Data presented to the panel show it appears to cut the risk of developing a COVID infection that has symptoms by 62%. That’s over the 50% threshold the FDA set for approval but less than seen with the mRNA vaccines, which are more than 90% effective at preventing infections.

“Is the average person going to want to take the AstraZeneca shot? What role is this going to play in our vaccination program?” Dr. Schaffner said.

Johnson & Johnson will have enough data from its clinical trials to submit it to the FDA within the next week, the company said in a call with shareholders on Tuesday. So far, its one-dose shots looks to be about as effective as both the Pfizer and Moderna vaccines.

“It could be that we wind up with four vaccines: Three that can run very fast, and one that’s not so fast,” Dr. Schaffner said.

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

The United States is nearly 6 weeks into its historic campaign to vaccinate Americans against the virus that causes COVID-19, and so far, the two vaccines in use look remarkably low risk, according to new data presented today at a meeting of vaccine experts that advise the Centers for Disease Control and Prevention.

With 23.5 million doses of the Pfizer and Moderna vaccines now given, there have been very few serious side effects. In addition, deaths reported after people got the vaccine do not seem to be related to it.

The most common symptoms reported after vaccination were pain where people got the shot, fatigue, headache, and muscle soreness. These were more common after the second dose. In addition, about one in four people reported fever and chills after the second shot.

“On the whole, I thought it was very reassuring,” said William Schaffner, MD, an infectious disease expert with Vanderbilt University, Nashville, Tenn., who listened to the presentations.

The CDC is collecting safety information through multiple channels. These include a new smartphone-based app called V-Safe, which collects daily information from people who’ve been vaccinated; the federal Vaccine Adverse Event Reporting System, which accepts reports from anyone; and the Vaccine Safety Datalink, which is a collaboration between the CDC and nine major hospital systems. There’s also the Clinical Immunization Safety Assessment Project, a collaboration between the CDC and vaccine safety experts.

After surveying these systems, experts heading the safety committee for the CDC’s Advisory Committee on Immunization Practices said there have been few serious side effects reported.

Very rarely, severe allergic reactions – called anaphylaxis – have occurred after vaccination. There have been 50 of these cases reported after the Pfizer vaccine and 21 cases reported after the Moderna vaccine to date. Nearly all of them – 94% of the anaphylaxis cases after Pfizer vaccines and 100% of those after Moderna’s vaccine – have been in women, though it’s not clear why.

That translates to a rate of about five cases of anaphylaxis for every million doses of the Pfizer vaccine and about three for every million doses of the Moderna vaccine. Most of these occur within 15 minutes after getting a vaccine dose, with one reported as long as 20 hours after the shot.

The CDC suspects these may be related to an ingredient called polyethylene glycol (PEG). PEG is a part of the particles that slip the vaccines’ mRNA into cells with instructions to make the spike protein of the virus. Cells then express these spikes on their surfaces so the immune system can learn to recognize them and make defenses against them. PEG is a common ingredient in many drugs and occasionally triggers anaphylaxis.
 

Reported deaths seem unrelated to vaccines

Through Jan. 18, 196 people have died after getting a vaccine.

Most of these deaths (129) were in patients in long term care facilities. These deaths are still being investigated, but when they were compared with the number of deaths that might be expected over the same period because of natural causes, they seemed to be coincidental and not caused by the vaccine, said Tom Shimabukuro, MD, deputy director of the Immunization Safety Office at the CDC, who studied the data.

In fact, death rates were lower among vaccinated nursing home residents, compared with those who had not been vaccinated.

“These findings suggest that short-term mortality rates appear unrelated to vaccination for COVID-19,” Dr. Shimabukuro said.

This also appeared to be true for younger adults who died after their shots.

There were 28 people aged under 65 years who died after being vaccinated. Most of these deaths were heart related, according to autopsy reports. When investigators compared the number of sudden cardiac deaths expected to occur in this population naturally, they found people who were vaccinated had a lower rate than would have been expected without vaccination. This suggests that these deaths were also unrelated to the vaccine.
 

More vaccines on the horizon

The panel also heard an update from drug company AstraZeneca on its vaccine. It’s being used in 18 countries but has not yet been authorized in the United States.

That vaccine is currently in phase 3 of its U.S. clinical trials, and more than 26,000 people who have volunteered to get the shot had received their second dose as of Jan. 21, the company said.

The Food and Drug Administration requires at least 2 months of follow-up before it will evaluate a vaccine for an emergency-use authorization, which means the company would be ready to submit by the end of March, with a possible approval by April.

The AstraZeneca vaccine uses a more traditional method to create immunity, slipping a key part of the virus that causes COVID-19 into the shell of an adenovirus – a virus that causes cold-like symptoms – that normally infects monkeys. When the immune system sees the virus, it generates protective defenses against it.

The two-dose vaccine can be stored in a regular refrigerator for up to 6 months, which makes it easier to handle than the mRNA vaccines, which require much colder storage. Another advantage appears to be that it’s less likely to trigger severe allergic reactions. So far, there have been no cases of anaphylaxis reported after this shot.

In total, four serious side effects have been reported with the AstraZeneca vaccine, including two cases of transverse myelitis, a serious condition that causes swelling of the spinal cord, leading to pain, muscle weakness, and paralysis. One of these was in the group that got the placebo. The reports paused the trial, but it was allowed to continue after a safety review.

This vaccine also appears to be less effective than the mRNA shots. Data presented to the panel show it appears to cut the risk of developing a COVID infection that has symptoms by 62%. That’s over the 50% threshold the FDA set for approval but less than seen with the mRNA vaccines, which are more than 90% effective at preventing infections.

“Is the average person going to want to take the AstraZeneca shot? What role is this going to play in our vaccination program?” Dr. Schaffner said.

Johnson & Johnson will have enough data from its clinical trials to submit it to the FDA within the next week, the company said in a call with shareholders on Tuesday. So far, its one-dose shots looks to be about as effective as both the Pfizer and Moderna vaccines.

“It could be that we wind up with four vaccines: Three that can run very fast, and one that’s not so fast,” Dr. Schaffner said.

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

The United States is nearly 6 weeks into its historic campaign to vaccinate Americans against the virus that causes COVID-19, and so far, the two vaccines in use look remarkably low risk, according to new data presented today at a meeting of vaccine experts that advise the Centers for Disease Control and Prevention.

With 23.5 million doses of the Pfizer and Moderna vaccines now given, there have been very few serious side effects. In addition, deaths reported after people got the vaccine do not seem to be related to it.

The most common symptoms reported after vaccination were pain where people got the shot, fatigue, headache, and muscle soreness. These were more common after the second dose. In addition, about one in four people reported fever and chills after the second shot.

“On the whole, I thought it was very reassuring,” said William Schaffner, MD, an infectious disease expert with Vanderbilt University, Nashville, Tenn., who listened to the presentations.

The CDC is collecting safety information through multiple channels. These include a new smartphone-based app called V-Safe, which collects daily information from people who’ve been vaccinated; the federal Vaccine Adverse Event Reporting System, which accepts reports from anyone; and the Vaccine Safety Datalink, which is a collaboration between the CDC and nine major hospital systems. There’s also the Clinical Immunization Safety Assessment Project, a collaboration between the CDC and vaccine safety experts.

After surveying these systems, experts heading the safety committee for the CDC’s Advisory Committee on Immunization Practices said there have been few serious side effects reported.

Very rarely, severe allergic reactions – called anaphylaxis – have occurred after vaccination. There have been 50 of these cases reported after the Pfizer vaccine and 21 cases reported after the Moderna vaccine to date. Nearly all of them – 94% of the anaphylaxis cases after Pfizer vaccines and 100% of those after Moderna’s vaccine – have been in women, though it’s not clear why.

That translates to a rate of about five cases of anaphylaxis for every million doses of the Pfizer vaccine and about three for every million doses of the Moderna vaccine. Most of these occur within 15 minutes after getting a vaccine dose, with one reported as long as 20 hours after the shot.

The CDC suspects these may be related to an ingredient called polyethylene glycol (PEG). PEG is a part of the particles that slip the vaccines’ mRNA into cells with instructions to make the spike protein of the virus. Cells then express these spikes on their surfaces so the immune system can learn to recognize them and make defenses against them. PEG is a common ingredient in many drugs and occasionally triggers anaphylaxis.
 

Reported deaths seem unrelated to vaccines

Through Jan. 18, 196 people have died after getting a vaccine.

Most of these deaths (129) were in patients in long term care facilities. These deaths are still being investigated, but when they were compared with the number of deaths that might be expected over the same period because of natural causes, they seemed to be coincidental and not caused by the vaccine, said Tom Shimabukuro, MD, deputy director of the Immunization Safety Office at the CDC, who studied the data.

In fact, death rates were lower among vaccinated nursing home residents, compared with those who had not been vaccinated.

“These findings suggest that short-term mortality rates appear unrelated to vaccination for COVID-19,” Dr. Shimabukuro said.

This also appeared to be true for younger adults who died after their shots.

There were 28 people aged under 65 years who died after being vaccinated. Most of these deaths were heart related, according to autopsy reports. When investigators compared the number of sudden cardiac deaths expected to occur in this population naturally, they found people who were vaccinated had a lower rate than would have been expected without vaccination. This suggests that these deaths were also unrelated to the vaccine.
 

More vaccines on the horizon

The panel also heard an update from drug company AstraZeneca on its vaccine. It’s being used in 18 countries but has not yet been authorized in the United States.

That vaccine is currently in phase 3 of its U.S. clinical trials, and more than 26,000 people who have volunteered to get the shot had received their second dose as of Jan. 21, the company said.

The Food and Drug Administration requires at least 2 months of follow-up before it will evaluate a vaccine for an emergency-use authorization, which means the company would be ready to submit by the end of March, with a possible approval by April.

The AstraZeneca vaccine uses a more traditional method to create immunity, slipping a key part of the virus that causes COVID-19 into the shell of an adenovirus – a virus that causes cold-like symptoms – that normally infects monkeys. When the immune system sees the virus, it generates protective defenses against it.

The two-dose vaccine can be stored in a regular refrigerator for up to 6 months, which makes it easier to handle than the mRNA vaccines, which require much colder storage. Another advantage appears to be that it’s less likely to trigger severe allergic reactions. So far, there have been no cases of anaphylaxis reported after this shot.

In total, four serious side effects have been reported with the AstraZeneca vaccine, including two cases of transverse myelitis, a serious condition that causes swelling of the spinal cord, leading to pain, muscle weakness, and paralysis. One of these was in the group that got the placebo. The reports paused the trial, but it was allowed to continue after a safety review.

This vaccine also appears to be less effective than the mRNA shots. Data presented to the panel show it appears to cut the risk of developing a COVID infection that has symptoms by 62%. That’s over the 50% threshold the FDA set for approval but less than seen with the mRNA vaccines, which are more than 90% effective at preventing infections.

“Is the average person going to want to take the AstraZeneca shot? What role is this going to play in our vaccination program?” Dr. Schaffner said.

Johnson & Johnson will have enough data from its clinical trials to submit it to the FDA within the next week, the company said in a call with shareholders on Tuesday. So far, its one-dose shots looks to be about as effective as both the Pfizer and Moderna vaccines.

“It could be that we wind up with four vaccines: Three that can run very fast, and one that’s not so fast,” Dr. Schaffner said.

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

A follow-up look at an international registry suggests that some people may have persistent, long-lasting dermatologic manifestations – especially so-called “COVID toes” – as a result of infection with or exposure to the SARS-CoV-2 virus, but some dermatologists question if the skin signs and symptoms are truly related.

In their commentary in the Lancet Infectious Diseases, Esther P. Freeman, MD, PhD, and colleagues who lead and participate in the American Academy of Dermatology’s international registry said their analysis “revealed a previously unreported subset of patients who experience long-haul symptoms in dermatology-dominant COVID-19.”

Some of the data was presented at the 29th European Academy of Dermatology and Venereology in late October 2020, but has since been updated with more cases.

Dermatologists who spoke with this news organization said it has not been settled that some skin manifestations – such as pernio/chilblains rashes, seen primarily in nonhospitalized patients, and described in the registry – are definitively caused by COVID. They also noted that in some cases, patients who initially test negative for COVID-19 by polymerase chain reaction (PCR) sometimes do not ever develop antibodies, which could mean they were never actually exposed to SARS-CoV-2.

M. Alexander Otto/MDedge News

“I still question whether the perniosis is directly related to infection with SARS-CoV-2 or not,” said Anthony Fernandez, MD, PhD, director of medical and inpatient dermatology and assistant professor of dermatopathology at the Cleveland Clinic. His uncertainty is driven by the lack of seroconversion and that few cases were seen over the summer in the United States – suggesting that it may still be a result of cold temperatures.

“I’m not sure there is a definitive correct answer, definitely not that everyone would agree on,” said Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Conn.

Dr. Freeman, however, believed that pernio and especially persistent lesions are caused by an immune response to COVID.

In an interview, she noted the multiple cases of patients in the registry who did seroconvert and that, while a registry is not a perfect means of getting an answer, it is good for generating questions. Taken collectively, the cases in the registry can “tell a story for further hypotheses,” said Dr. Freeman, who is director of global health dermatology at Massachusetts General Hospital and assistant professor of dermatology at Harvard University, both in Boston.

“We were noticing this signal across the world” that patients “developed these toe lesions and they never got better,” said Dr. Freeman. Generally, people who experience pernio, also described as COVID toes or “COVID fingers,” recover in 4-8 weeks. But in the registry, “we did have this subset of patients who really were experiencing these very longstanding symptoms,” she added.

Two patients with lab-confirmed COVID have had long-lasting pernio of 133 days and 150 days. “I’m caring for a cohort in Boston who have had long COVID of the skin and symptoms for over 10 months,” Dr. Freeman said.
 

Pernio dominates

The registry – a collaboration between the AAD and the International League of Dermatological Societies – was launched in April 2020. Any medical professional can enter case information. From April to October, 1,030 total cases and 331 laboratory-confirmed or suspected COVID-19 cases with dermatological manifestations were entered from 41 countries.

Most of the cases were just recorded at a single time point, which is an acknowledged limitation of the study.

Dr. Freeman and colleagues reached out to registry participants in June and August to get updates on COVID lab test results and sign and symptom duration. Overall, 234 total and 96 lab-confirmed COVID infections had more lengthy data about sign and symptom duration.

Pernio lasted a median of 15 days in patients with suspected disease and 12 days for those with lab-confirmed COVID, compared with a median of 7 days for morbilliform eruptions, 4 days for urticarial eruptions, and 20 days for papulosquamous eruptions – all in patients with lab-confirmed disease.

Of the 103 cases of pernio, 7 had symptoms lasting more than 60 days. Only two of those seven patients had lab-confirmed COVID. Initially, the one patient tested negative with nasopharyngeal PCR, and serum IgM and IgG. Six weeks after pernio onset, the patient – still experiencing fatigue and pernio – seroconverted to anti–SARS-CoV-2 IgM positivity.

The other long-haul patient, after a negative PCR, tested positive for SARS-CoV-2 serum IgG 1 month after pernio onset.

Robust immune response?

Dr. Freeman said these patients might have a very high interferon response initially to the virus, which makes for a mild to nonexistent disease, but could create inflammation elsewhere. “I almost view the toes as an innocent bystander of a robust immune response to SARS-CoV-2.”

Although he has not seen extended pernio or other skin manifestations in his patients, Dr. Fernandez said the interferon hypothesis is “fair,” and “the best that’s out there.” Dr. Fernandez is currently studying cutaneous manifestations of COVID-19 as a principal investigator of a trial sponsored by the Clinical and Translational Science Collaborative of Cleveland.

Dr. Ko said in an interview that she has not observed long-haul skin issues in her patients, but Yale colleagues have.

In a study, she and Yale colleagues published in September, SARS-CoV-2 spike protein was detected in perniotic lesions, but not nuclear protein or viral RNA. The test they used – immunohistochemistry – can be nonspecific, which muddied results.

She does not think there is replicating virus in the skin or the lesions. Instead, said Dr. Ko, “either there is viral spike protein that has somehow become disassociated from actively replicating virus that somehow got deposited in endothelial cells,” or the staining “was spurious,” or some other protein is cross-reacting. “And the people who are unlucky enough to have that protein in their endothelial cells can manifest this COVID-toe, COVID-finger phenomenon.”

To her, it’s an unsolved mystery. “The weird thing is, we’ve never before had this much perniosis,” Dr. Ko said.

Dr. Fernandez is not convinced yet, noting that, in Cleveland, more pernio cases were observed in March and April than in the summer. “If it is a manifestation of the infection then you also need the right environment, the cold weather for this manifestation to present,” he said. “Or, it really isn’t a direct manifestation of COVID-19 but may be more related to other factors,” such as lifestyle changes related to limitations implemented to help mitigate the spread of the disease.

“To me the jury is still out whether or not the perniotic lesions really can tell us something about a patient’s exposure and infection with SARS-CoV-2,” he said.

Dr. Freeman reported receiving a grant from the International League of Dermatological Societies and nonfinancial support from the AAD for the study. Dr. Ko reported no conflicts. Dr. Fernadnez had no disclosures.

A follow-up look at an international registry suggests that some people may have persistent, long-lasting dermatologic manifestations – especially so-called “COVID toes” – as a result of infection with or exposure to the SARS-CoV-2 virus, but some dermatologists question if the skin signs and symptoms are truly related.

In their commentary in the Lancet Infectious Diseases, Esther P. Freeman, MD, PhD, and colleagues who lead and participate in the American Academy of Dermatology’s international registry said their analysis “revealed a previously unreported subset of patients who experience long-haul symptoms in dermatology-dominant COVID-19.”

Some of the data was presented at the 29th European Academy of Dermatology and Venereology in late October 2020, but has since been updated with more cases.

Dermatologists who spoke with this news organization said it has not been settled that some skin manifestations – such as pernio/chilblains rashes, seen primarily in nonhospitalized patients, and described in the registry – are definitively caused by COVID. They also noted that in some cases, patients who initially test negative for COVID-19 by polymerase chain reaction (PCR) sometimes do not ever develop antibodies, which could mean they were never actually exposed to SARS-CoV-2.

M. Alexander Otto/MDedge News

“I still question whether the perniosis is directly related to infection with SARS-CoV-2 or not,” said Anthony Fernandez, MD, PhD, director of medical and inpatient dermatology and assistant professor of dermatopathology at the Cleveland Clinic. His uncertainty is driven by the lack of seroconversion and that few cases were seen over the summer in the United States – suggesting that it may still be a result of cold temperatures.

“I’m not sure there is a definitive correct answer, definitely not that everyone would agree on,” said Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Conn.

Dr. Freeman, however, believed that pernio and especially persistent lesions are caused by an immune response to COVID.

In an interview, she noted the multiple cases of patients in the registry who did seroconvert and that, while a registry is not a perfect means of getting an answer, it is good for generating questions. Taken collectively, the cases in the registry can “tell a story for further hypotheses,” said Dr. Freeman, who is director of global health dermatology at Massachusetts General Hospital and assistant professor of dermatology at Harvard University, both in Boston.

“We were noticing this signal across the world” that patients “developed these toe lesions and they never got better,” said Dr. Freeman. Generally, people who experience pernio, also described as COVID toes or “COVID fingers,” recover in 4-8 weeks. But in the registry, “we did have this subset of patients who really were experiencing these very longstanding symptoms,” she added.

Two patients with lab-confirmed COVID have had long-lasting pernio of 133 days and 150 days. “I’m caring for a cohort in Boston who have had long COVID of the skin and symptoms for over 10 months,” Dr. Freeman said.
 

Pernio dominates

The registry – a collaboration between the AAD and the International League of Dermatological Societies – was launched in April 2020. Any medical professional can enter case information. From April to October, 1,030 total cases and 331 laboratory-confirmed or suspected COVID-19 cases with dermatological manifestations were entered from 41 countries.

Most of the cases were just recorded at a single time point, which is an acknowledged limitation of the study.

Dr. Freeman and colleagues reached out to registry participants in June and August to get updates on COVID lab test results and sign and symptom duration. Overall, 234 total and 96 lab-confirmed COVID infections had more lengthy data about sign and symptom duration.

Pernio lasted a median of 15 days in patients with suspected disease and 12 days for those with lab-confirmed COVID, compared with a median of 7 days for morbilliform eruptions, 4 days for urticarial eruptions, and 20 days for papulosquamous eruptions – all in patients with lab-confirmed disease.

Of the 103 cases of pernio, 7 had symptoms lasting more than 60 days. Only two of those seven patients had lab-confirmed COVID. Initially, the one patient tested negative with nasopharyngeal PCR, and serum IgM and IgG. Six weeks after pernio onset, the patient – still experiencing fatigue and pernio – seroconverted to anti–SARS-CoV-2 IgM positivity.

The other long-haul patient, after a negative PCR, tested positive for SARS-CoV-2 serum IgG 1 month after pernio onset.

Robust immune response?

Dr. Freeman said these patients might have a very high interferon response initially to the virus, which makes for a mild to nonexistent disease, but could create inflammation elsewhere. “I almost view the toes as an innocent bystander of a robust immune response to SARS-CoV-2.”

Although he has not seen extended pernio or other skin manifestations in his patients, Dr. Fernandez said the interferon hypothesis is “fair,” and “the best that’s out there.” Dr. Fernandez is currently studying cutaneous manifestations of COVID-19 as a principal investigator of a trial sponsored by the Clinical and Translational Science Collaborative of Cleveland.

Dr. Ko said in an interview that she has not observed long-haul skin issues in her patients, but Yale colleagues have.

In a study, she and Yale colleagues published in September, SARS-CoV-2 spike protein was detected in perniotic lesions, but not nuclear protein or viral RNA. The test they used – immunohistochemistry – can be nonspecific, which muddied results.

She does not think there is replicating virus in the skin or the lesions. Instead, said Dr. Ko, “either there is viral spike protein that has somehow become disassociated from actively replicating virus that somehow got deposited in endothelial cells,” or the staining “was spurious,” or some other protein is cross-reacting. “And the people who are unlucky enough to have that protein in their endothelial cells can manifest this COVID-toe, COVID-finger phenomenon.”

To her, it’s an unsolved mystery. “The weird thing is, we’ve never before had this much perniosis,” Dr. Ko said.

Dr. Fernandez is not convinced yet, noting that, in Cleveland, more pernio cases were observed in March and April than in the summer. “If it is a manifestation of the infection then you also need the right environment, the cold weather for this manifestation to present,” he said. “Or, it really isn’t a direct manifestation of COVID-19 but may be more related to other factors,” such as lifestyle changes related to limitations implemented to help mitigate the spread of the disease.

“To me the jury is still out whether or not the perniotic lesions really can tell us something about a patient’s exposure and infection with SARS-CoV-2,” he said.

Dr. Freeman reported receiving a grant from the International League of Dermatological Societies and nonfinancial support from the AAD for the study. Dr. Ko reported no conflicts. Dr. Fernadnez had no disclosures.

A follow-up look at an international registry suggests that some people may have persistent, long-lasting dermatologic manifestations – especially so-called “COVID toes” – as a result of infection with or exposure to the SARS-CoV-2 virus, but some dermatologists question if the skin signs and symptoms are truly related.

In their commentary in the Lancet Infectious Diseases, Esther P. Freeman, MD, PhD, and colleagues who lead and participate in the American Academy of Dermatology’s international registry said their analysis “revealed a previously unreported subset of patients who experience long-haul symptoms in dermatology-dominant COVID-19.”

Some of the data was presented at the 29th European Academy of Dermatology and Venereology in late October 2020, but has since been updated with more cases.

Dermatologists who spoke with this news organization said it has not been settled that some skin manifestations – such as pernio/chilblains rashes, seen primarily in nonhospitalized patients, and described in the registry – are definitively caused by COVID. They also noted that in some cases, patients who initially test negative for COVID-19 by polymerase chain reaction (PCR) sometimes do not ever develop antibodies, which could mean they were never actually exposed to SARS-CoV-2.

M. Alexander Otto/MDedge News

“I still question whether the perniosis is directly related to infection with SARS-CoV-2 or not,” said Anthony Fernandez, MD, PhD, director of medical and inpatient dermatology and assistant professor of dermatopathology at the Cleveland Clinic. His uncertainty is driven by the lack of seroconversion and that few cases were seen over the summer in the United States – suggesting that it may still be a result of cold temperatures.

“I’m not sure there is a definitive correct answer, definitely not that everyone would agree on,” said Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Conn.

Dr. Freeman, however, believed that pernio and especially persistent lesions are caused by an immune response to COVID.

In an interview, she noted the multiple cases of patients in the registry who did seroconvert and that, while a registry is not a perfect means of getting an answer, it is good for generating questions. Taken collectively, the cases in the registry can “tell a story for further hypotheses,” said Dr. Freeman, who is director of global health dermatology at Massachusetts General Hospital and assistant professor of dermatology at Harvard University, both in Boston.

“We were noticing this signal across the world” that patients “developed these toe lesions and they never got better,” said Dr. Freeman. Generally, people who experience pernio, also described as COVID toes or “COVID fingers,” recover in 4-8 weeks. But in the registry, “we did have this subset of patients who really were experiencing these very longstanding symptoms,” she added.

Two patients with lab-confirmed COVID have had long-lasting pernio of 133 days and 150 days. “I’m caring for a cohort in Boston who have had long COVID of the skin and symptoms for over 10 months,” Dr. Freeman said.
 

Pernio dominates

The registry – a collaboration between the AAD and the International League of Dermatological Societies – was launched in April 2020. Any medical professional can enter case information. From April to October, 1,030 total cases and 331 laboratory-confirmed or suspected COVID-19 cases with dermatological manifestations were entered from 41 countries.

Most of the cases were just recorded at a single time point, which is an acknowledged limitation of the study.

Dr. Freeman and colleagues reached out to registry participants in June and August to get updates on COVID lab test results and sign and symptom duration. Overall, 234 total and 96 lab-confirmed COVID infections had more lengthy data about sign and symptom duration.

Pernio lasted a median of 15 days in patients with suspected disease and 12 days for those with lab-confirmed COVID, compared with a median of 7 days for morbilliform eruptions, 4 days for urticarial eruptions, and 20 days for papulosquamous eruptions – all in patients with lab-confirmed disease.

Of the 103 cases of pernio, 7 had symptoms lasting more than 60 days. Only two of those seven patients had lab-confirmed COVID. Initially, the one patient tested negative with nasopharyngeal PCR, and serum IgM and IgG. Six weeks after pernio onset, the patient – still experiencing fatigue and pernio – seroconverted to anti–SARS-CoV-2 IgM positivity.

The other long-haul patient, after a negative PCR, tested positive for SARS-CoV-2 serum IgG 1 month after pernio onset.

Robust immune response?

Dr. Freeman said these patients might have a very high interferon response initially to the virus, which makes for a mild to nonexistent disease, but could create inflammation elsewhere. “I almost view the toes as an innocent bystander of a robust immune response to SARS-CoV-2.”

Although he has not seen extended pernio or other skin manifestations in his patients, Dr. Fernandez said the interferon hypothesis is “fair,” and “the best that’s out there.” Dr. Fernandez is currently studying cutaneous manifestations of COVID-19 as a principal investigator of a trial sponsored by the Clinical and Translational Science Collaborative of Cleveland.

Dr. Ko said in an interview that she has not observed long-haul skin issues in her patients, but Yale colleagues have.

In a study, she and Yale colleagues published in September, SARS-CoV-2 spike protein was detected in perniotic lesions, but not nuclear protein or viral RNA. The test they used – immunohistochemistry – can be nonspecific, which muddied results.

She does not think there is replicating virus in the skin or the lesions. Instead, said Dr. Ko, “either there is viral spike protein that has somehow become disassociated from actively replicating virus that somehow got deposited in endothelial cells,” or the staining “was spurious,” or some other protein is cross-reacting. “And the people who are unlucky enough to have that protein in their endothelial cells can manifest this COVID-toe, COVID-finger phenomenon.”

To her, it’s an unsolved mystery. “The weird thing is, we’ve never before had this much perniosis,” Dr. Ko said.

Dr. Fernandez is not convinced yet, noting that, in Cleveland, more pernio cases were observed in March and April than in the summer. “If it is a manifestation of the infection then you also need the right environment, the cold weather for this manifestation to present,” he said. “Or, it really isn’t a direct manifestation of COVID-19 but may be more related to other factors,” such as lifestyle changes related to limitations implemented to help mitigate the spread of the disease.

“To me the jury is still out whether or not the perniotic lesions really can tell us something about a patient’s exposure and infection with SARS-CoV-2,” he said.

Dr. Freeman reported receiving a grant from the International League of Dermatological Societies and nonfinancial support from the AAD for the study. Dr. Ko reported no conflicts. Dr. Fernadnez had no disclosures.

Among the more than 320 million people in the United States, there was a prevalence estimate of 67.6 million sexually transmitted infections at the time of assessment in 2018, according to the results of an epidemiologic study using multiple data sources, including the National Health and Nutrition Examination Survey (NHANES).

In addition, almost half of the incident STIs occurred in the 15- to 24-year age bracket, according to a report published online in Sexually Transmitted Diseases. Researchers estimated the combined number of prevalent and incident infections of eight STIs in the United States in 2018: chlamydia, gonorrhea, trichomoniasis, syphilis, genital herpes (caused by herpes simplex virus type 2 [HSV-2]), human papillomavirus (HPV), sexually transmitted hepatitis B virus (HBV), and sexually transmitted HIV.

The estimated incidences of these STIs in this update, the first since 2008, were made using more recent data and improved estimation methods to provide updated STI prevalence and incidence estimates for 2018, both overall and by disease. “Having a combined estimate is crucial for policy purposes to illustrate the importance of STIs in the United States,” according to Kristen M. Kreisel, PhD, an epidemiologist at the Centers for Disease Control and Prevention, division of STD prevention, and colleagues.

The number of prevalent and incident infections were obtained by multiplying each STI’s updated per capita estimates by the 2018 full resident population estimates from the American Community Survey.
 

Detailed results

Chlamydia. The prevalence of chlamydia was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. There were an estimated 2.4 million prevalent urogenital chlamydial infections among persons aged 15-39 years in 2018; 1.1 and 1.3 million infections among men and women, respectively. Individuals aged 15-24 years comprised 56.7% and 75.8% of all infections in men and women respectively.

Gonorrhea. The prevalence of gonorrhea was estimated using ordinary differential equation based modeling. The number of prevalent urogenital gonococcal infections in 2018 among 15- to 39-year-olds was 209,000 overall; 50,000 in men and 155,000 in women. Of these, 113,000 (54.1%) occurred in 15- to 24-year-olds.

Trichomoniasis. The prevalence of trichomoniasis was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. The number of prevalent Trichomonas infections among 15- to 59-year-olds was 2.6 million, with 470,000 in men and 2.1 million in women. Persons aged 15-24 years comprised 15.6% of all prevalent infections, according to the authors.

Syphilis. The number of estimated prevalent syphilitic infections (all stages) among 14- to 49-year-old persons in 2018 was 156,000, with infections in men comprising 71.8% of all infections. Infections in both men and women aged 14-24 years accounted for about 25% of all infections, with 36,000 total prevalent syphilitic infections among 14- to 24-year-olds in 2018.

Genital herpes. The prevalence of genital herpes (caused by HSV-2) was estimated using 2015-2018 NHANES data, according to the authors. In persons aged 15-49 years in 2018, there were 18.6 million prevalent HSV-2 infections; 6.4 million among men and 12.2 million among women. Infections in 15- to 24-year-olds comprised 7.1% of all prevalent HSV-2 infections.

HPV. The prevalence of HPV was estimated using 2013-2016 NHANES data, which was assumed to reflect stable prevalence in 2018, according to the authors. Among 15- to 59-year-olds, the estimated number of persons, men, and women infected with one or more disease-associated HPV types in 2018 was 42.5, 23.4, and 19.2 million, respectively, with an estimated 9.0 million (21%) 15- to 24-year-olds infected,

HBV. NHANES 2013-2018 data were used to estimate the prevalence of sexually transmitted chronic HBV infections in 2018, according to the authors. The estimated number of infections among persons aged 15 years and older in 2018 was 103,000 (51,000 men and 52,000 women). There small sample size of individuals aged 15-24 years in the NHANES database made it impossible to obtain an accurate estimate for this group, according to the authors.

HIV. Data from the National HIV Surveillance System were used to estimate the prevalence and incidence of sexually transmitted HIV infections for persons aged 13 years and older in 2018. A total of 984,000 individuals aged 13 years and older were estimated to be living with sexually transmitted HIV at the end of 2018, according to the authors. Nearly 80% were men. In the 13- to 24-year-old age bracket, there were an estimated 45,400 living with sexually transmitted HIV.

Billions in costs

Commenting on the study by the CDC researchers, Raul Romaguera, acting director for CDC’s division of STD prevention, stated in a press release: “There are significant human and financial costs associated with these infections, and we know from other studies that cuts in STI prevention efforts result in higher costs down the road. Preventing STIs could save billions in medical costs, but more importantly, prevention would improve the health and lives of millions of people.”

“About 20% of the total U.S. population had an STI at a given point in 2018, while nearly half of all incident infections occurred in people aged 15-24 years. Focusing STI prevention efforts on the 15- to 24-year-old population may be key to lowering the STI burden in the U.S.,” the researchers concluded.

The authors reported that they had no disclosures.

[email protected]

Among the more than 320 million people in the United States, there was a prevalence estimate of 67.6 million sexually transmitted infections at the time of assessment in 2018, according to the results of an epidemiologic study using multiple data sources, including the National Health and Nutrition Examination Survey (NHANES).

In addition, almost half of the incident STIs occurred in the 15- to 24-year age bracket, according to a report published online in Sexually Transmitted Diseases. Researchers estimated the combined number of prevalent and incident infections of eight STIs in the United States in 2018: chlamydia, gonorrhea, trichomoniasis, syphilis, genital herpes (caused by herpes simplex virus type 2 [HSV-2]), human papillomavirus (HPV), sexually transmitted hepatitis B virus (HBV), and sexually transmitted HIV.

The estimated incidences of these STIs in this update, the first since 2008, were made using more recent data and improved estimation methods to provide updated STI prevalence and incidence estimates for 2018, both overall and by disease. “Having a combined estimate is crucial for policy purposes to illustrate the importance of STIs in the United States,” according to Kristen M. Kreisel, PhD, an epidemiologist at the Centers for Disease Control and Prevention, division of STD prevention, and colleagues.

The number of prevalent and incident infections were obtained by multiplying each STI’s updated per capita estimates by the 2018 full resident population estimates from the American Community Survey.
 

Detailed results

Chlamydia. The prevalence of chlamydia was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. There were an estimated 2.4 million prevalent urogenital chlamydial infections among persons aged 15-39 years in 2018; 1.1 and 1.3 million infections among men and women, respectively. Individuals aged 15-24 years comprised 56.7% and 75.8% of all infections in men and women respectively.

Gonorrhea. The prevalence of gonorrhea was estimated using ordinary differential equation based modeling. The number of prevalent urogenital gonococcal infections in 2018 among 15- to 39-year-olds was 209,000 overall; 50,000 in men and 155,000 in women. Of these, 113,000 (54.1%) occurred in 15- to 24-year-olds.

Trichomoniasis. The prevalence of trichomoniasis was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. The number of prevalent Trichomonas infections among 15- to 59-year-olds was 2.6 million, with 470,000 in men and 2.1 million in women. Persons aged 15-24 years comprised 15.6% of all prevalent infections, according to the authors.

Syphilis. The number of estimated prevalent syphilitic infections (all stages) among 14- to 49-year-old persons in 2018 was 156,000, with infections in men comprising 71.8% of all infections. Infections in both men and women aged 14-24 years accounted for about 25% of all infections, with 36,000 total prevalent syphilitic infections among 14- to 24-year-olds in 2018.

Genital herpes. The prevalence of genital herpes (caused by HSV-2) was estimated using 2015-2018 NHANES data, according to the authors. In persons aged 15-49 years in 2018, there were 18.6 million prevalent HSV-2 infections; 6.4 million among men and 12.2 million among women. Infections in 15- to 24-year-olds comprised 7.1% of all prevalent HSV-2 infections.

HPV. The prevalence of HPV was estimated using 2013-2016 NHANES data, which was assumed to reflect stable prevalence in 2018, according to the authors. Among 15- to 59-year-olds, the estimated number of persons, men, and women infected with one or more disease-associated HPV types in 2018 was 42.5, 23.4, and 19.2 million, respectively, with an estimated 9.0 million (21%) 15- to 24-year-olds infected,

HBV. NHANES 2013-2018 data were used to estimate the prevalence of sexually transmitted chronic HBV infections in 2018, according to the authors. The estimated number of infections among persons aged 15 years and older in 2018 was 103,000 (51,000 men and 52,000 women). There small sample size of individuals aged 15-24 years in the NHANES database made it impossible to obtain an accurate estimate for this group, according to the authors.

HIV. Data from the National HIV Surveillance System were used to estimate the prevalence and incidence of sexually transmitted HIV infections for persons aged 13 years and older in 2018. A total of 984,000 individuals aged 13 years and older were estimated to be living with sexually transmitted HIV at the end of 2018, according to the authors. Nearly 80% were men. In the 13- to 24-year-old age bracket, there were an estimated 45,400 living with sexually transmitted HIV.

Billions in costs

Commenting on the study by the CDC researchers, Raul Romaguera, acting director for CDC’s division of STD prevention, stated in a press release: “There are significant human and financial costs associated with these infections, and we know from other studies that cuts in STI prevention efforts result in higher costs down the road. Preventing STIs could save billions in medical costs, but more importantly, prevention would improve the health and lives of millions of people.”

“About 20% of the total U.S. population had an STI at a given point in 2018, while nearly half of all incident infections occurred in people aged 15-24 years. Focusing STI prevention efforts on the 15- to 24-year-old population may be key to lowering the STI burden in the U.S.,” the researchers concluded.

The authors reported that they had no disclosures.

[email protected]

Among the more than 320 million people in the United States, there was a prevalence estimate of 67.6 million sexually transmitted infections at the time of assessment in 2018, according to the results of an epidemiologic study using multiple data sources, including the National Health and Nutrition Examination Survey (NHANES).

In addition, almost half of the incident STIs occurred in the 15- to 24-year age bracket, according to a report published online in Sexually Transmitted Diseases. Researchers estimated the combined number of prevalent and incident infections of eight STIs in the United States in 2018: chlamydia, gonorrhea, trichomoniasis, syphilis, genital herpes (caused by herpes simplex virus type 2 [HSV-2]), human papillomavirus (HPV), sexually transmitted hepatitis B virus (HBV), and sexually transmitted HIV.

The estimated incidences of these STIs in this update, the first since 2008, were made using more recent data and improved estimation methods to provide updated STI prevalence and incidence estimates for 2018, both overall and by disease. “Having a combined estimate is crucial for policy purposes to illustrate the importance of STIs in the United States,” according to Kristen M. Kreisel, PhD, an epidemiologist at the Centers for Disease Control and Prevention, division of STD prevention, and colleagues.

The number of prevalent and incident infections were obtained by multiplying each STI’s updated per capita estimates by the 2018 full resident population estimates from the American Community Survey.
 

Detailed results

Chlamydia. The prevalence of chlamydia was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. There were an estimated 2.4 million prevalent urogenital chlamydial infections among persons aged 15-39 years in 2018; 1.1 and 1.3 million infections among men and women, respectively. Individuals aged 15-24 years comprised 56.7% and 75.8% of all infections in men and women respectively.

Gonorrhea. The prevalence of gonorrhea was estimated using ordinary differential equation based modeling. The number of prevalent urogenital gonococcal infections in 2018 among 15- to 39-year-olds was 209,000 overall; 50,000 in men and 155,000 in women. Of these, 113,000 (54.1%) occurred in 15- to 24-year-olds.

Trichomoniasis. The prevalence of trichomoniasis was estimated using 2015-2018 NHANES data, which was then used to create a modeled prevalence in 2018, according to the authors. The number of prevalent Trichomonas infections among 15- to 59-year-olds was 2.6 million, with 470,000 in men and 2.1 million in women. Persons aged 15-24 years comprised 15.6% of all prevalent infections, according to the authors.

Syphilis. The number of estimated prevalent syphilitic infections (all stages) among 14- to 49-year-old persons in 2018 was 156,000, with infections in men comprising 71.8% of all infections. Infections in both men and women aged 14-24 years accounted for about 25% of all infections, with 36,000 total prevalent syphilitic infections among 14- to 24-year-olds in 2018.

Genital herpes. The prevalence of genital herpes (caused by HSV-2) was estimated using 2015-2018 NHANES data, according to the authors. In persons aged 15-49 years in 2018, there were 18.6 million prevalent HSV-2 infections; 6.4 million among men and 12.2 million among women. Infections in 15- to 24-year-olds comprised 7.1% of all prevalent HSV-2 infections.

HPV. The prevalence of HPV was estimated using 2013-2016 NHANES data, which was assumed to reflect stable prevalence in 2018, according to the authors. Among 15- to 59-year-olds, the estimated number of persons, men, and women infected with one or more disease-associated HPV types in 2018 was 42.5, 23.4, and 19.2 million, respectively, with an estimated 9.0 million (21%) 15- to 24-year-olds infected,

HBV. NHANES 2013-2018 data were used to estimate the prevalence of sexually transmitted chronic HBV infections in 2018, according to the authors. The estimated number of infections among persons aged 15 years and older in 2018 was 103,000 (51,000 men and 52,000 women). There small sample size of individuals aged 15-24 years in the NHANES database made it impossible to obtain an accurate estimate for this group, according to the authors.

HIV. Data from the National HIV Surveillance System were used to estimate the prevalence and incidence of sexually transmitted HIV infections for persons aged 13 years and older in 2018. A total of 984,000 individuals aged 13 years and older were estimated to be living with sexually transmitted HIV at the end of 2018, according to the authors. Nearly 80% were men. In the 13- to 24-year-old age bracket, there were an estimated 45,400 living with sexually transmitted HIV.

Billions in costs

Commenting on the study by the CDC researchers, Raul Romaguera, acting director for CDC’s division of STD prevention, stated in a press release: “There are significant human and financial costs associated with these infections, and we know from other studies that cuts in STI prevention efforts result in higher costs down the road. Preventing STIs could save billions in medical costs, but more importantly, prevention would improve the health and lives of millions of people.”

“About 20% of the total U.S. population had an STI at a given point in 2018, while nearly half of all incident infections occurred in people aged 15-24 years. Focusing STI prevention efforts on the 15- to 24-year-old population may be key to lowering the STI burden in the U.S.,” the researchers concluded.

The authors reported that they had no disclosures.

[email protected]