Journal of Clinical Outcomes Management

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

TOPLINE:

Two doses of an mRNA COVID-19 vaccine slashes COVID-19-related hospitalizations and emergency department (ED) visits in children aged 6 months to 4 years by 40%, according to a new study by the Centers for Disease Control and Prevention (CDC).

METHODOLOGY:

• SARS-CoV-2 infection can severely affect children who have certain chronic conditions.
• Researchers assessed the effectiveness of COVID-19 vaccines in preventing emergency ED visits and hospitalizations associated with the illness from July 2022 to September 2023.
• They drew data from the New Vaccine Surveillance Network, which conducts population-based, prospective surveillance for acute respiratory illness in children at seven pediatric medical centers.
• The period assessed was the first year vaccines were authorized for children aged 6 months to 4 years; during that period, several Omicron subvariants arose.
• Researchers used data from 7,434 infants and children; data included patients’ vaccine status and their test results for SARS-CoV-2.

TAKEAWAY:

• Of the 7,434 infants and children who had an acute respiratory illness and were hospitalized or visited the ED, 387 had COVID-19.
• Children who received two doses of a COVID-19 vaccine were 40% less likely to have a COVID-19-associated hospitalization or ED visit compared with unvaccinated youth.
• One dose of a COVID-19 vaccine reduced ED visits and hospitalizations by 31%.

IN PRACTICE:

“The findings in this report support the recommendation for COVID-19 vaccination for all children aged ≥6 months and highlight the importance of completion of a primary series for young children,” the researchers reported.

SOURCE:

The study was led by Heidi L. Moline, MD, of the CDC.

LIMITATIONS:

Because the number of children with antibodies and immunity against SARS-CoV-2 has grown, vaccine effectiveness rates in the study may no longer be as relevant. Children with preexisting chronic conditions may be more likely to be vaccinated and receive medical attention. The low rates of vaccination may have prevented researchers from conducting a more detailed analysis. The Pfizer-BioNTech vaccine requires three doses, whereas Moderna’s requires two doses; this may have skewed the estimated efficacy of the Pfizer-BioNTech vaccine.

DISCLOSURES:

The authors report a variety of potential conflicts of interest, which are detailed in the article.

A version of this article appeared on Medscape.com.

One of the biggest challenges facing clinicians who treat long COVID is a lack of consensus when it comes to recognizing and diagnosing the condition. But a new study suggests testing for certain biomarkers may identify long COVID with accuracy approaching 80%.

Effective diagnostic testing would be a game-changer in the long COVID fight, for it’s not just the fatigue, brain fog, heart palpitations, and other persistent symptoms that affect patients. Two out of three people with long COVID also suffer mental health challenges like depression and anxiety. Some patients say their symptoms are not taken seriously by their doctors. And as many as 12% of long COVID patients are unemployed because of the severity of their illness and their employers may be skeptical of their condition.

Quick, accurate diagnosis would eliminate all that. Now a new preprint study suggests that the elevation of certain immune system proteins are a commonality in long COVID patients and identifying them may be an accurate way to diagnose the condition.

Researchers at Cardiff (Wales) University, tracked 166 patients, 79 of whom had been diagnosed with long COVID and 87 who had not. All participants had recovered from a severe bout of acute COVID-19.

In an analysis of the blood plasma of the study participants, researchers found elevated levels of certain components. Four proteins in particular – Ba, iC3b, C5a, and TCC – predicted the presence of long COVID with 78.5% accuracy.

“I was gobsmacked by the results. We’re seeing a massive dysregulation in those four biomarkers,” says study author Wioleta Zelek, PhD, a research fellow at Cardiff University. “It’s a combination that we showed was predictive of long COVID.” 

The study revealed that long COVID was associated with inflammation of the immune system causing these complement proteins to remain dysregulated. Proteins like C3, C4, and C5 are important parts of the immune system because they recruit phagocytes, cells that attack and engulf bacteria and viruses at the site of infection to destroy pathogens like SARS-coV-2. 

In the case of long COVID, these proteins remain chronically elevated. While the symptoms of long COVID have seemed largely unrelated to one another, researchers point to elevated inflammation as a connecting factor that causes various systems in the body to go haywire.

“Anything that could help to better diagnose patients with long COVID is research we’re greatly appreciative of within the clinical community,” said Nisha Viswanathan, MD, director of the University of California, Los Angeles, Long COVID program at UCLA Health. 

Testing for biomarkers highlighted in the study, as well as others like serotonin and cortisol, may help doctors separate patients who have long COVID from patients who have similar symptoms caused by other conditions, said Dr. Viswanathan. For example, a recent study published in the journal Cell found lower serotonin levels in long COVID patients, compared with patients who were diagnosed with acute COVID-19 but recovered from the condition.

Dr. Viswanathan cautions that the biomarker test does not answer all the questions about diagnosing long COVID. For example, Dr. Viswanathan said scientists don’t know whether complement dysregulation is caused by long COVID and not another underlying medical issue that patients had prior to infection, because “we don’t know where patients’ levels were prior to developing long COVID.” For example, those with autoimmune issues are more likely to develop long COVID, which means their levels could have been elevated prior to a COVID infection.

It is increasingly likely, said Dr. Viswanathan, that long COVID is an umbrella term for a host of conditions that could be caused by different impacts of the virus. Other research has pointed to the different phenotypes of long COVID. For example, some are focused on cardiopulmonary issues and others on fatigue and gastrointestinal problems. 

“It looks like these different phenotypes have a different mechanism for disease,” she said. This means that it’s less likely to be a one-size-fits-all condition and the next step in the research should be identifying which biomarker is aligned with which phenotype of the disease. 

Better diagnostics will open the door to better treatments, Dr. Zelek said. The more doctors understand about the mechanism causing immune dysregulation in long COVID patients, the more they can treat it with existing medications. Dr. Zelek’s lab has been studying certain medications like pegcetacoplan (C3 blocker), danicopan (anti-factor D), and iptacopan (anti-factor B) that can be used to break the body’s cycle of inflammation and reduce symptoms experienced in those with long COVID. 

These drugs are approved by the U.S. Food and Drug Administration for the treatment of a rare blood disease called paroxysmal nocturnal hemoglobinuria. The C5 inhibitor zilucoplan has also been used in patients hospitalized with COVID-19 and researchers have found that the drug lowered serum C5 and interleukin-8 concentration in the blood, seeming to reduce certain aspects of the immune system’s inflammatory response to the virus. 

The Cardiff University research is one of the most detailed studies to highlight long COVID biomarkers to date, said infectious disease specialist Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. The research needs to be duplicated in a larger study population that might include the other biomarkers like serotonin and cortisol to see if they’re related, she said. 

Researchers are learning more everyday about the various biomarkers that may be linked to long COVID, she added. This Cardiff study showed that a huge percentage of those patients had elevated levels of certain complements. The next step, said Dr. McComsey, “is to put all these puzzle pieces together” so that clinicians have a common diagnostic tool or tools that provide patients with some peace of mind in starting their road to recovery.

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

One of the biggest challenges facing clinicians who treat long COVID is a lack of consensus when it comes to recognizing and diagnosing the condition. But a new study suggests testing for certain biomarkers may identify long COVID with accuracy approaching 80%.

Effective diagnostic testing would be a game-changer in the long COVID fight, for it’s not just the fatigue, brain fog, heart palpitations, and other persistent symptoms that affect patients. Two out of three people with long COVID also suffer mental health challenges like depression and anxiety. Some patients say their symptoms are not taken seriously by their doctors. And as many as 12% of long COVID patients are unemployed because of the severity of their illness and their employers may be skeptical of their condition.

Quick, accurate diagnosis would eliminate all that. Now a new preprint study suggests that the elevation of certain immune system proteins are a commonality in long COVID patients and identifying them may be an accurate way to diagnose the condition.

Researchers at Cardiff (Wales) University, tracked 166 patients, 79 of whom had been diagnosed with long COVID and 87 who had not. All participants had recovered from a severe bout of acute COVID-19.

In an analysis of the blood plasma of the study participants, researchers found elevated levels of certain components. Four proteins in particular – Ba, iC3b, C5a, and TCC – predicted the presence of long COVID with 78.5% accuracy.

“I was gobsmacked by the results. We’re seeing a massive dysregulation in those four biomarkers,” says study author Wioleta Zelek, PhD, a research fellow at Cardiff University. “It’s a combination that we showed was predictive of long COVID.” 

The study revealed that long COVID was associated with inflammation of the immune system causing these complement proteins to remain dysregulated. Proteins like C3, C4, and C5 are important parts of the immune system because they recruit phagocytes, cells that attack and engulf bacteria and viruses at the site of infection to destroy pathogens like SARS-coV-2. 

In the case of long COVID, these proteins remain chronically elevated. While the symptoms of long COVID have seemed largely unrelated to one another, researchers point to elevated inflammation as a connecting factor that causes various systems in the body to go haywire.

“Anything that could help to better diagnose patients with long COVID is research we’re greatly appreciative of within the clinical community,” said Nisha Viswanathan, MD, director of the University of California, Los Angeles, Long COVID program at UCLA Health. 

Testing for biomarkers highlighted in the study, as well as others like serotonin and cortisol, may help doctors separate patients who have long COVID from patients who have similar symptoms caused by other conditions, said Dr. Viswanathan. For example, a recent study published in the journal Cell found lower serotonin levels in long COVID patients, compared with patients who were diagnosed with acute COVID-19 but recovered from the condition.

Dr. Viswanathan cautions that the biomarker test does not answer all the questions about diagnosing long COVID. For example, Dr. Viswanathan said scientists don’t know whether complement dysregulation is caused by long COVID and not another underlying medical issue that patients had prior to infection, because “we don’t know where patients’ levels were prior to developing long COVID.” For example, those with autoimmune issues are more likely to develop long COVID, which means their levels could have been elevated prior to a COVID infection.

It is increasingly likely, said Dr. Viswanathan, that long COVID is an umbrella term for a host of conditions that could be caused by different impacts of the virus. Other research has pointed to the different phenotypes of long COVID. For example, some are focused on cardiopulmonary issues and others on fatigue and gastrointestinal problems. 

“It looks like these different phenotypes have a different mechanism for disease,” she said. This means that it’s less likely to be a one-size-fits-all condition and the next step in the research should be identifying which biomarker is aligned with which phenotype of the disease. 

Better diagnostics will open the door to better treatments, Dr. Zelek said. The more doctors understand about the mechanism causing immune dysregulation in long COVID patients, the more they can treat it with existing medications. Dr. Zelek’s lab has been studying certain medications like pegcetacoplan (C3 blocker), danicopan (anti-factor D), and iptacopan (anti-factor B) that can be used to break the body’s cycle of inflammation and reduce symptoms experienced in those with long COVID. 

These drugs are approved by the U.S. Food and Drug Administration for the treatment of a rare blood disease called paroxysmal nocturnal hemoglobinuria. The C5 inhibitor zilucoplan has also been used in patients hospitalized with COVID-19 and researchers have found that the drug lowered serum C5 and interleukin-8 concentration in the blood, seeming to reduce certain aspects of the immune system’s inflammatory response to the virus. 

The Cardiff University research is one of the most detailed studies to highlight long COVID biomarkers to date, said infectious disease specialist Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. The research needs to be duplicated in a larger study population that might include the other biomarkers like serotonin and cortisol to see if they’re related, she said. 

Researchers are learning more everyday about the various biomarkers that may be linked to long COVID, she added. This Cardiff study showed that a huge percentage of those patients had elevated levels of certain complements. The next step, said Dr. McComsey, “is to put all these puzzle pieces together” so that clinicians have a common diagnostic tool or tools that provide patients with some peace of mind in starting their road to recovery.

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

One of the biggest challenges facing clinicians who treat long COVID is a lack of consensus when it comes to recognizing and diagnosing the condition. But a new study suggests testing for certain biomarkers may identify long COVID with accuracy approaching 80%.

Effective diagnostic testing would be a game-changer in the long COVID fight, for it’s not just the fatigue, brain fog, heart palpitations, and other persistent symptoms that affect patients. Two out of three people with long COVID also suffer mental health challenges like depression and anxiety. Some patients say their symptoms are not taken seriously by their doctors. And as many as 12% of long COVID patients are unemployed because of the severity of their illness and their employers may be skeptical of their condition.

Quick, accurate diagnosis would eliminate all that. Now a new preprint study suggests that the elevation of certain immune system proteins are a commonality in long COVID patients and identifying them may be an accurate way to diagnose the condition.

Researchers at Cardiff (Wales) University, tracked 166 patients, 79 of whom had been diagnosed with long COVID and 87 who had not. All participants had recovered from a severe bout of acute COVID-19.

In an analysis of the blood plasma of the study participants, researchers found elevated levels of certain components. Four proteins in particular – Ba, iC3b, C5a, and TCC – predicted the presence of long COVID with 78.5% accuracy.

“I was gobsmacked by the results. We’re seeing a massive dysregulation in those four biomarkers,” says study author Wioleta Zelek, PhD, a research fellow at Cardiff University. “It’s a combination that we showed was predictive of long COVID.” 

The study revealed that long COVID was associated with inflammation of the immune system causing these complement proteins to remain dysregulated. Proteins like C3, C4, and C5 are important parts of the immune system because they recruit phagocytes, cells that attack and engulf bacteria and viruses at the site of infection to destroy pathogens like SARS-coV-2. 

In the case of long COVID, these proteins remain chronically elevated. While the symptoms of long COVID have seemed largely unrelated to one another, researchers point to elevated inflammation as a connecting factor that causes various systems in the body to go haywire.

“Anything that could help to better diagnose patients with long COVID is research we’re greatly appreciative of within the clinical community,” said Nisha Viswanathan, MD, director of the University of California, Los Angeles, Long COVID program at UCLA Health. 

Testing for biomarkers highlighted in the study, as well as others like serotonin and cortisol, may help doctors separate patients who have long COVID from patients who have similar symptoms caused by other conditions, said Dr. Viswanathan. For example, a recent study published in the journal Cell found lower serotonin levels in long COVID patients, compared with patients who were diagnosed with acute COVID-19 but recovered from the condition.

Dr. Viswanathan cautions that the biomarker test does not answer all the questions about diagnosing long COVID. For example, Dr. Viswanathan said scientists don’t know whether complement dysregulation is caused by long COVID and not another underlying medical issue that patients had prior to infection, because “we don’t know where patients’ levels were prior to developing long COVID.” For example, those with autoimmune issues are more likely to develop long COVID, which means their levels could have been elevated prior to a COVID infection.

It is increasingly likely, said Dr. Viswanathan, that long COVID is an umbrella term for a host of conditions that could be caused by different impacts of the virus. Other research has pointed to the different phenotypes of long COVID. For example, some are focused on cardiopulmonary issues and others on fatigue and gastrointestinal problems. 

“It looks like these different phenotypes have a different mechanism for disease,” she said. This means that it’s less likely to be a one-size-fits-all condition and the next step in the research should be identifying which biomarker is aligned with which phenotype of the disease. 

Better diagnostics will open the door to better treatments, Dr. Zelek said. The more doctors understand about the mechanism causing immune dysregulation in long COVID patients, the more they can treat it with existing medications. Dr. Zelek’s lab has been studying certain medications like pegcetacoplan (C3 blocker), danicopan (anti-factor D), and iptacopan (anti-factor B) that can be used to break the body’s cycle of inflammation and reduce symptoms experienced in those with long COVID. 

These drugs are approved by the U.S. Food and Drug Administration for the treatment of a rare blood disease called paroxysmal nocturnal hemoglobinuria. The C5 inhibitor zilucoplan has also been used in patients hospitalized with COVID-19 and researchers have found that the drug lowered serum C5 and interleukin-8 concentration in the blood, seeming to reduce certain aspects of the immune system’s inflammatory response to the virus. 

The Cardiff University research is one of the most detailed studies to highlight long COVID biomarkers to date, said infectious disease specialist Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. The research needs to be duplicated in a larger study population that might include the other biomarkers like serotonin and cortisol to see if they’re related, she said. 

Researchers are learning more everyday about the various biomarkers that may be linked to long COVID, she added. This Cardiff study showed that a huge percentage of those patients had elevated levels of certain complements. The next step, said Dr. McComsey, “is to put all these puzzle pieces together” so that clinicians have a common diagnostic tool or tools that provide patients with some peace of mind in starting their road to recovery.

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

TOPLINE:

In individuals with low B-cell counts, T cells have enhanced responses to COVID-19 vaccination and may help prevent severe disease after infection.

METHODOLOGY:

• How the immune systems of B cell–deficient patients respond to SARS-CoV-2 infection and vaccination is not fully understood.
• Researchers evaluated anti–SARS-CoV-2 T-cell responses in 33 patients treated with rituximab (RTX), 12 patients with common variable immune deficiency, and 44 controls.
• The study analyzed effector and memory CD4+ and CD8+ T-cell responses to SARS-CoV-2 after infection and vaccination.

TAKEAWAY: 

• All B cell–deficient individuals (those treated with RTX or those with a diagnosis of common variable immune deficiency) had increased effector and memory T-cell responses after SARS-CoV-2 vaccination, compared with controls.
• Patients treated with RTX who were vaccinated against COVID-19 had 4.8-fold reduced odds of moderate or severe disease. (These data were not available for patients with common variable immune deficiency.)
• RTX treatment was associated with a decrease in preexisting T-cell immunity in unvaccinated patients, regardless of prior infection with SARS-CoV-2.
• This association was not found in vaccinated patients treated with RTX.

IN PRACTICE:

“[These findings] provide support for vaccination in this vulnerable population and demonstrate the potential benefit of vaccine-induced CD8+ T-cell responses on reducing disease severity from SARS-CoV-2 infection in the absence of spike protein–specific antibodies,” the authors wrote.

SOURCE:

The study was published online on November 29 in Science Translational Medicine. The first author is Reza Zonozi, MD, who conducted the research while at Massachusetts General Hospital, Boston, and is now in private practice in northern Virginia. 

LIMITATIONS:

Researchers did not obtain specimens from patients with common variable immune deficiency after SARS-CoV-2 infection. Only a small subset of immunophenotyped participants had subsequent SARS-CoV-2 infection.

DISCLOSURES:

The research was supported by grants from the National Institutes of Health, the Centers for Disease Control and Prevention, the Howard Hughes Medical Institute, the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard Medical School, the Mark and Lisa Schwartz Foundation and E. Schwartz; the Lambertus Family Foundation; and S. Edgerly and P. Edgerly. Four authors reported relationships with pharmaceutical companies including AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Gilead Sciences, Merck, and Pfizer.

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

TOPLINE:

In individuals with low B-cell counts, T cells have enhanced responses to COVID-19 vaccination and may help prevent severe disease after infection.

METHODOLOGY:

• How the immune systems of B cell–deficient patients respond to SARS-CoV-2 infection and vaccination is not fully understood.
• Researchers evaluated anti–SARS-CoV-2 T-cell responses in 33 patients treated with rituximab (RTX), 12 patients with common variable immune deficiency, and 44 controls.
• The study analyzed effector and memory CD4+ and CD8+ T-cell responses to SARS-CoV-2 after infection and vaccination.

TAKEAWAY: 

• All B cell–deficient individuals (those treated with RTX or those with a diagnosis of common variable immune deficiency) had increased effector and memory T-cell responses after SARS-CoV-2 vaccination, compared with controls.
• Patients treated with RTX who were vaccinated against COVID-19 had 4.8-fold reduced odds of moderate or severe disease. (These data were not available for patients with common variable immune deficiency.)
• RTX treatment was associated with a decrease in preexisting T-cell immunity in unvaccinated patients, regardless of prior infection with SARS-CoV-2.
• This association was not found in vaccinated patients treated with RTX.

IN PRACTICE:

“[These findings] provide support for vaccination in this vulnerable population and demonstrate the potential benefit of vaccine-induced CD8+ T-cell responses on reducing disease severity from SARS-CoV-2 infection in the absence of spike protein–specific antibodies,” the authors wrote.

SOURCE:

The study was published online on November 29 in Science Translational Medicine. The first author is Reza Zonozi, MD, who conducted the research while at Massachusetts General Hospital, Boston, and is now in private practice in northern Virginia. 

LIMITATIONS:

Researchers did not obtain specimens from patients with common variable immune deficiency after SARS-CoV-2 infection. Only a small subset of immunophenotyped participants had subsequent SARS-CoV-2 infection.

DISCLOSURES:

The research was supported by grants from the National Institutes of Health, the Centers for Disease Control and Prevention, the Howard Hughes Medical Institute, the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard Medical School, the Mark and Lisa Schwartz Foundation and E. Schwartz; the Lambertus Family Foundation; and S. Edgerly and P. Edgerly. Four authors reported relationships with pharmaceutical companies including AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Gilead Sciences, Merck, and Pfizer.

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

TOPLINE:

In individuals with low B-cell counts, T cells have enhanced responses to COVID-19 vaccination and may help prevent severe disease after infection.

METHODOLOGY:

• How the immune systems of B cell–deficient patients respond to SARS-CoV-2 infection and vaccination is not fully understood.
• Researchers evaluated anti–SARS-CoV-2 T-cell responses in 33 patients treated with rituximab (RTX), 12 patients with common variable immune deficiency, and 44 controls.
• The study analyzed effector and memory CD4+ and CD8+ T-cell responses to SARS-CoV-2 after infection and vaccination.

TAKEAWAY: 

• All B cell–deficient individuals (those treated with RTX or those with a diagnosis of common variable immune deficiency) had increased effector and memory T-cell responses after SARS-CoV-2 vaccination, compared with controls.
• Patients treated with RTX who were vaccinated against COVID-19 had 4.8-fold reduced odds of moderate or severe disease. (These data were not available for patients with common variable immune deficiency.)
• RTX treatment was associated with a decrease in preexisting T-cell immunity in unvaccinated patients, regardless of prior infection with SARS-CoV-2.
• This association was not found in vaccinated patients treated with RTX.

IN PRACTICE:

“[These findings] provide support for vaccination in this vulnerable population and demonstrate the potential benefit of vaccine-induced CD8+ T-cell responses on reducing disease severity from SARS-CoV-2 infection in the absence of spike protein–specific antibodies,” the authors wrote.

SOURCE:

The study was published online on November 29 in Science Translational Medicine. The first author is Reza Zonozi, MD, who conducted the research while at Massachusetts General Hospital, Boston, and is now in private practice in northern Virginia. 

LIMITATIONS:

Researchers did not obtain specimens from patients with common variable immune deficiency after SARS-CoV-2 infection. Only a small subset of immunophenotyped participants had subsequent SARS-CoV-2 infection.

DISCLOSURES:

The research was supported by grants from the National Institutes of Health, the Centers for Disease Control and Prevention, the Howard Hughes Medical Institute, the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard Medical School, the Mark and Lisa Schwartz Foundation and E. Schwartz; the Lambertus Family Foundation; and S. Edgerly and P. Edgerly. Four authors reported relationships with pharmaceutical companies including AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Gilead Sciences, Merck, and Pfizer.

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

An emerging variant of COVID-19 called BA.2.86 that caused alarm in the summer of 2023 has landed on the Center for Disease Control and Prevention’s radar again.

The variant accounted for nearly 9% of cases during the 2-week period ending Nov. 25, up from 3% during the previous 2 weeks, according to data published Nov. 27 by the CDC. The estimates are not exact, and the CDC indicated the actual percentage of cases may range from 5% to 15%.

The CDC took the unusual step of publishing a specific statement about the rise in BA.2.86 cases. The variant drew worldwide attention during the summer because of how different its makeup is, compared with other prominent variants of the virus that causes COVID-19, raising the potential for the new variant to be more capable of causing infection. But after a flurry of interest in BA.2.86, it didn’t end up being as widespread as expected, so for months it wasn’t listed as a standalone variant on the CDC’s variant tracker list.

“At this time, BA.2.86 does not appear to be driving increases in infections or hospitalizations in the United States,” the CDC wrote in its advisory. “It is not possible at this time to know whether BA.2.86 infection produces different symptoms from other variants. In general, symptoms of COVID-19 tend to be similar across variants. The types of symptoms and how severe they are usually depend more on a person’s immunity than which variant causes the infection.”

BA.2.86 is now the third-most prominent variant circulating the United States, behind HV.1 and EG.5, which combined account for about 45% of all U.S. COVID-19 cases. All three are from the Omicron lineage of the virus.

About 8% of all COVID tests reported to the CDC were positive for the week ending Nov. 18, which is a decline, compared with recent weeks. But indicators for severe cases of the illness have ticked up lately, including rises among ED visits for COVID, hospitalizations, and deaths.

A version of this article appeared on WebMD.com.

An emerging variant of COVID-19 called BA.2.86 that caused alarm in the summer of 2023 has landed on the Center for Disease Control and Prevention’s radar again.

The variant accounted for nearly 9% of cases during the 2-week period ending Nov. 25, up from 3% during the previous 2 weeks, according to data published Nov. 27 by the CDC. The estimates are not exact, and the CDC indicated the actual percentage of cases may range from 5% to 15%.

The CDC took the unusual step of publishing a specific statement about the rise in BA.2.86 cases. The variant drew worldwide attention during the summer because of how different its makeup is, compared with other prominent variants of the virus that causes COVID-19, raising the potential for the new variant to be more capable of causing infection. But after a flurry of interest in BA.2.86, it didn’t end up being as widespread as expected, so for months it wasn’t listed as a standalone variant on the CDC’s variant tracker list.

“At this time, BA.2.86 does not appear to be driving increases in infections or hospitalizations in the United States,” the CDC wrote in its advisory. “It is not possible at this time to know whether BA.2.86 infection produces different symptoms from other variants. In general, symptoms of COVID-19 tend to be similar across variants. The types of symptoms and how severe they are usually depend more on a person’s immunity than which variant causes the infection.”

BA.2.86 is now the third-most prominent variant circulating the United States, behind HV.1 and EG.5, which combined account for about 45% of all U.S. COVID-19 cases. All three are from the Omicron lineage of the virus.

About 8% of all COVID tests reported to the CDC were positive for the week ending Nov. 18, which is a decline, compared with recent weeks. But indicators for severe cases of the illness have ticked up lately, including rises among ED visits for COVID, hospitalizations, and deaths.

A version of this article appeared on WebMD.com.

An emerging variant of COVID-19 called BA.2.86 that caused alarm in the summer of 2023 has landed on the Center for Disease Control and Prevention’s radar again.

The variant accounted for nearly 9% of cases during the 2-week period ending Nov. 25, up from 3% during the previous 2 weeks, according to data published Nov. 27 by the CDC. The estimates are not exact, and the CDC indicated the actual percentage of cases may range from 5% to 15%.

The CDC took the unusual step of publishing a specific statement about the rise in BA.2.86 cases. The variant drew worldwide attention during the summer because of how different its makeup is, compared with other prominent variants of the virus that causes COVID-19, raising the potential for the new variant to be more capable of causing infection. But after a flurry of interest in BA.2.86, it didn’t end up being as widespread as expected, so for months it wasn’t listed as a standalone variant on the CDC’s variant tracker list.

“At this time, BA.2.86 does not appear to be driving increases in infections or hospitalizations in the United States,” the CDC wrote in its advisory. “It is not possible at this time to know whether BA.2.86 infection produces different symptoms from other variants. In general, symptoms of COVID-19 tend to be similar across variants. The types of symptoms and how severe they are usually depend more on a person’s immunity than which variant causes the infection.”

BA.2.86 is now the third-most prominent variant circulating the United States, behind HV.1 and EG.5, which combined account for about 45% of all U.S. COVID-19 cases. All three are from the Omicron lineage of the virus.

About 8% of all COVID tests reported to the CDC were positive for the week ending Nov. 18, which is a decline, compared with recent weeks. But indicators for severe cases of the illness have ticked up lately, including rises among ED visits for COVID, hospitalizations, and deaths.

A version of this article appeared on WebMD.com.

As many as 87% of patients experience symptoms after COVID-19 infection that last 2 months or more, one of the most common being chest pain. And chronic chest discomfort may persist in some individuals for years after COVID, warranting future studies of reliable treatments and pain management in this population, a new study shows.

“Recent studies have shown that chest pain occurs in as many as 89% of patients who qualify as having long COVID,” said Ansley Poole, an undergraduate student at the University of South Florida, Tampa, who conducted the research under the supervision of Christine Hunt, DO, and her colleagues at Mayo Clinic, Jacksonville, Fla.

The findings, though preliminary, shed light on the prevalence, current treatments, and ongoing challenges in managing symptoms of long COVID, said Ms. Poole, who presented the research at the annual Pain Medicine Meeting sponsored by the American Society of Regional Anesthesia and Pain Medicine.

Long COVID, which affects an estimated 18 million Americans, manifests approximately 12 weeks after the initial infection and can persist for 2 months or more. Ms. Poole and her team set out to identify risk factors, treatment options, and outcomes for patients dealing with post-COVID chest discomfort.

The study involved a retrospective chart review of 520 patients from the Mayo Clinic network, narrowed down to a final sample of 104. To be included, patients had to report chest discomfort 3-6 months post COVID that continued for 3-6 months after presentation, with no history of chronic chest pain before the infection.

The researchers identified no standardized method for the treatment or management of chest pain linked to long COVID. “Patients were prescribed multiple different treatments, including opioids, post-COVID treatment programs, anticoagulants, steroids, and even psychological programs,” Ms. Poole said.

The median age of the patients was around 50 years; more than 65% were female and over 90% identified as White. More than half (55%) had received one or more vaccine doses at the time of infection. The majority were classified as overweight or obese at the time of their SARS-CoV-2 infection.

Of the 104 patients analyzed, 30 were referred to one or more subspecialties within the pain medicine department, 23 were hospitalized, and 9 were admitted to the intensive care unit or critical care.

“Fifty-three of our patients visited the ER one or more times after COVID because of chest discomfort; however, only six were admitted for over 24 hours, indicating possible overuse of emergency services,” Ms. Poole noted.

Overall, chest pain was described as intermittent instead of constant, which may have been a barrier to providing adequate and timely treatment. The inconsistent presence of pain contributed to the prolonged suffering some patients experienced, Ms. Poole noted.

The study identified several comorbidities, potentially complicating the treatment and etiology of chest pain. These comorbidities – when combined with COVID-related chest pain – contributed to the wide array of prescribed treatments, including steroids, anticoagulants, beta blockers, and physical therapy. Chest pain also seldom stood alone; it was often accompanied by other long COVID–related symptoms, such as shortness of breath.

“Our current analysis indicates that chest pain continues on for years in many individuals, suggesting that COVID-related chest pain may be resistant to treatment,” Ms. Poole reported.

The observed heterogeneity in treatments and outcomes in patients experiencing long-term chest discomfort after COVID infection underscores the need for future studies to establish reliable treatment and management protocols for this population, said Dalia Elmofty, MD, an associate professor of anesthesia and critical care at the University of Chicago, who was not involved in the study. “There are things about COVID that we don’t fully understand. As we’re seeing its consequences and trying to understand its etiology, we recognize the need for further research,” Dr. Elmofty said.

“So many different disease pathologies came out of COVID, whether it’s organ pathology, myofascial pathology, or autoimmune pathology, and all of that is obviously linked to pain,” Dr. Elmofty told this news organization. “It’s an area of research that we are going to have to devote a lot of time to in order to understand, but I think we’re still in the very early phases, trying to fit the pieces of the puzzle together.”

Ms. Poole and Dr. Elmofty report no relevant financial relationships.

A version of this article appeared on Medscape.com.

As many as 87% of patients experience symptoms after COVID-19 infection that last 2 months or more, one of the most common being chest pain. And chronic chest discomfort may persist in some individuals for years after COVID, warranting future studies of reliable treatments and pain management in this population, a new study shows.

“Recent studies have shown that chest pain occurs in as many as 89% of patients who qualify as having long COVID,” said Ansley Poole, an undergraduate student at the University of South Florida, Tampa, who conducted the research under the supervision of Christine Hunt, DO, and her colleagues at Mayo Clinic, Jacksonville, Fla.

The findings, though preliminary, shed light on the prevalence, current treatments, and ongoing challenges in managing symptoms of long COVID, said Ms. Poole, who presented the research at the annual Pain Medicine Meeting sponsored by the American Society of Regional Anesthesia and Pain Medicine.

Long COVID, which affects an estimated 18 million Americans, manifests approximately 12 weeks after the initial infection and can persist for 2 months or more. Ms. Poole and her team set out to identify risk factors, treatment options, and outcomes for patients dealing with post-COVID chest discomfort.

The study involved a retrospective chart review of 520 patients from the Mayo Clinic network, narrowed down to a final sample of 104. To be included, patients had to report chest discomfort 3-6 months post COVID that continued for 3-6 months after presentation, with no history of chronic chest pain before the infection.

The researchers identified no standardized method for the treatment or management of chest pain linked to long COVID. “Patients were prescribed multiple different treatments, including opioids, post-COVID treatment programs, anticoagulants, steroids, and even psychological programs,” Ms. Poole said.

The median age of the patients was around 50 years; more than 65% were female and over 90% identified as White. More than half (55%) had received one or more vaccine doses at the time of infection. The majority were classified as overweight or obese at the time of their SARS-CoV-2 infection.

Of the 104 patients analyzed, 30 were referred to one or more subspecialties within the pain medicine department, 23 were hospitalized, and 9 were admitted to the intensive care unit or critical care.

“Fifty-three of our patients visited the ER one or more times after COVID because of chest discomfort; however, only six were admitted for over 24 hours, indicating possible overuse of emergency services,” Ms. Poole noted.

Overall, chest pain was described as intermittent instead of constant, which may have been a barrier to providing adequate and timely treatment. The inconsistent presence of pain contributed to the prolonged suffering some patients experienced, Ms. Poole noted.

The study identified several comorbidities, potentially complicating the treatment and etiology of chest pain. These comorbidities – when combined with COVID-related chest pain – contributed to the wide array of prescribed treatments, including steroids, anticoagulants, beta blockers, and physical therapy. Chest pain also seldom stood alone; it was often accompanied by other long COVID–related symptoms, such as shortness of breath.

“Our current analysis indicates that chest pain continues on for years in many individuals, suggesting that COVID-related chest pain may be resistant to treatment,” Ms. Poole reported.

The observed heterogeneity in treatments and outcomes in patients experiencing long-term chest discomfort after COVID infection underscores the need for future studies to establish reliable treatment and management protocols for this population, said Dalia Elmofty, MD, an associate professor of anesthesia and critical care at the University of Chicago, who was not involved in the study. “There are things about COVID that we don’t fully understand. As we’re seeing its consequences and trying to understand its etiology, we recognize the need for further research,” Dr. Elmofty said.

“So many different disease pathologies came out of COVID, whether it’s organ pathology, myofascial pathology, or autoimmune pathology, and all of that is obviously linked to pain,” Dr. Elmofty told this news organization. “It’s an area of research that we are going to have to devote a lot of time to in order to understand, but I think we’re still in the very early phases, trying to fit the pieces of the puzzle together.”

Ms. Poole and Dr. Elmofty report no relevant financial relationships.

A version of this article appeared on Medscape.com.

As many as 87% of patients experience symptoms after COVID-19 infection that last 2 months or more, one of the most common being chest pain. And chronic chest discomfort may persist in some individuals for years after COVID, warranting future studies of reliable treatments and pain management in this population, a new study shows.

“Recent studies have shown that chest pain occurs in as many as 89% of patients who qualify as having long COVID,” said Ansley Poole, an undergraduate student at the University of South Florida, Tampa, who conducted the research under the supervision of Christine Hunt, DO, and her colleagues at Mayo Clinic, Jacksonville, Fla.

The findings, though preliminary, shed light on the prevalence, current treatments, and ongoing challenges in managing symptoms of long COVID, said Ms. Poole, who presented the research at the annual Pain Medicine Meeting sponsored by the American Society of Regional Anesthesia and Pain Medicine.

Long COVID, which affects an estimated 18 million Americans, manifests approximately 12 weeks after the initial infection and can persist for 2 months or more. Ms. Poole and her team set out to identify risk factors, treatment options, and outcomes for patients dealing with post-COVID chest discomfort.

The study involved a retrospective chart review of 520 patients from the Mayo Clinic network, narrowed down to a final sample of 104. To be included, patients had to report chest discomfort 3-6 months post COVID that continued for 3-6 months after presentation, with no history of chronic chest pain before the infection.

The researchers identified no standardized method for the treatment or management of chest pain linked to long COVID. “Patients were prescribed multiple different treatments, including opioids, post-COVID treatment programs, anticoagulants, steroids, and even psychological programs,” Ms. Poole said.

The median age of the patients was around 50 years; more than 65% were female and over 90% identified as White. More than half (55%) had received one or more vaccine doses at the time of infection. The majority were classified as overweight or obese at the time of their SARS-CoV-2 infection.

Of the 104 patients analyzed, 30 were referred to one or more subspecialties within the pain medicine department, 23 were hospitalized, and 9 were admitted to the intensive care unit or critical care.

“Fifty-three of our patients visited the ER one or more times after COVID because of chest discomfort; however, only six were admitted for over 24 hours, indicating possible overuse of emergency services,” Ms. Poole noted.

Overall, chest pain was described as intermittent instead of constant, which may have been a barrier to providing adequate and timely treatment. The inconsistent presence of pain contributed to the prolonged suffering some patients experienced, Ms. Poole noted.

The study identified several comorbidities, potentially complicating the treatment and etiology of chest pain. These comorbidities – when combined with COVID-related chest pain – contributed to the wide array of prescribed treatments, including steroids, anticoagulants, beta blockers, and physical therapy. Chest pain also seldom stood alone; it was often accompanied by other long COVID–related symptoms, such as shortness of breath.

“Our current analysis indicates that chest pain continues on for years in many individuals, suggesting that COVID-related chest pain may be resistant to treatment,” Ms. Poole reported.

The observed heterogeneity in treatments and outcomes in patients experiencing long-term chest discomfort after COVID infection underscores the need for future studies to establish reliable treatment and management protocols for this population, said Dalia Elmofty, MD, an associate professor of anesthesia and critical care at the University of Chicago, who was not involved in the study. “There are things about COVID that we don’t fully understand. As we’re seeing its consequences and trying to understand its etiology, we recognize the need for further research,” Dr. Elmofty said.

“So many different disease pathologies came out of COVID, whether it’s organ pathology, myofascial pathology, or autoimmune pathology, and all of that is obviously linked to pain,” Dr. Elmofty told this news organization. “It’s an area of research that we are going to have to devote a lot of time to in order to understand, but I think we’re still in the very early phases, trying to fit the pieces of the puzzle together.”

Ms. Poole and Dr. Elmofty report no relevant financial relationships.

A version of this article appeared on Medscape.com.

A 49-year-old woman, previously recuperating from COVID-19, was found unconscious at her workplace, setting off a chain of events that would ultimately lead to an unexpected diagnosis.

This case report was published in the New England Journal of Medicine.

Noting the patient’s confusion and aphasia, emergency medical services were alerted, and she was taken to the emergency department of Massachusetts General Hospital. Initial examination revealed aphasia and coordination difficulties. However, imaging studies, including CT angiography, showed no signs of stroke or other neurological abnormalities.

The patient’s coworkers had observed that she appeared “unwell.” Her medical history included hypertension, which was managed with amlodipine, and there was no known family history of neurologic disorders.

During the examination, her vital signs were within normal ranges.

The patient’s potassium level of 2.5 mmol/L was noteworthy, indicating hypokalemia. Additionally, the patient presented with anemia and thrombocytopenia. Additional laboratory results unveiled thrombotic thrombocytopenic purpura (TTP), a rare blood disorder characterized by microangiopathic hemolytic anemia. The microscopic examination of a peripheral blood smear confirmed the extent of thrombocytopenia and was particularly notable for the increased number of schistocytes. The patient’s peripheral blood smear revealed five or six schistocytes per high-power field, constituting approximately 5% of the red cells. This significant number of schistocytes aligned with the severity of anemia and thrombocytopenia, confirming the diagnosis of microangiopathic hemolytic anemia.

Acquired TTP is an autoimmune condition driven by antibody-mediated clearance of the plasma enzyme ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13). Confirmatory laboratory testing for ADAMTS13 takes 1-3 days; therefore, therapeutic plasma exchange with glucocorticoid therapy and rituximab was initiated, which promptly improved her condition.

In this patient, the ADAMTS13 activity level was severely reduced (< 5%; reference value > 67%), and the inhibitor was present (1.4 inhibitor units; reference value ≤ 0.4).

Rectal cancer was diagnosed in this patient 2 months after the diagnosis of acquired TTP.

After undergoing four weekly infusions of rituximab and a 2-month tapering course of glucocorticoids, the patient experienced a relapse, approximately 6 months following the acquired TTP diagnosis. In response, therapeutic plasma exchange and glucocorticoid therapy were administered. There is a possibility that the underlying cancer played a role in the relapse. To minimize the risk for recurrence, the patient also received a second round of rituximab.

While establishing a clear cause is difficult, acquired TTP often appears to arise in connection with either an immune trigger, such as a viral infection, or immune dysregulation associated with another autoimmune disease or ongoing cancer. In this case, 4 weeks before the acquired TTP diagnosis, the patient had experienced COVID-19, which was likely to be the most probable trigger. However, rectal cancer was also identified in the patient, and whether these conditions are directly linked remains unclear.

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

A 49-year-old woman, previously recuperating from COVID-19, was found unconscious at her workplace, setting off a chain of events that would ultimately lead to an unexpected diagnosis.

This case report was published in the New England Journal of Medicine.

Noting the patient’s confusion and aphasia, emergency medical services were alerted, and she was taken to the emergency department of Massachusetts General Hospital. Initial examination revealed aphasia and coordination difficulties. However, imaging studies, including CT angiography, showed no signs of stroke or other neurological abnormalities.

The patient’s coworkers had observed that she appeared “unwell.” Her medical history included hypertension, which was managed with amlodipine, and there was no known family history of neurologic disorders.

During the examination, her vital signs were within normal ranges.

The patient’s potassium level of 2.5 mmol/L was noteworthy, indicating hypokalemia. Additionally, the patient presented with anemia and thrombocytopenia. Additional laboratory results unveiled thrombotic thrombocytopenic purpura (TTP), a rare blood disorder characterized by microangiopathic hemolytic anemia. The microscopic examination of a peripheral blood smear confirmed the extent of thrombocytopenia and was particularly notable for the increased number of schistocytes. The patient’s peripheral blood smear revealed five or six schistocytes per high-power field, constituting approximately 5% of the red cells. This significant number of schistocytes aligned with the severity of anemia and thrombocytopenia, confirming the diagnosis of microangiopathic hemolytic anemia.

Acquired TTP is an autoimmune condition driven by antibody-mediated clearance of the plasma enzyme ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13). Confirmatory laboratory testing for ADAMTS13 takes 1-3 days; therefore, therapeutic plasma exchange with glucocorticoid therapy and rituximab was initiated, which promptly improved her condition.

In this patient, the ADAMTS13 activity level was severely reduced (< 5%; reference value > 67%), and the inhibitor was present (1.4 inhibitor units; reference value ≤ 0.4).

Rectal cancer was diagnosed in this patient 2 months after the diagnosis of acquired TTP.

After undergoing four weekly infusions of rituximab and a 2-month tapering course of glucocorticoids, the patient experienced a relapse, approximately 6 months following the acquired TTP diagnosis. In response, therapeutic plasma exchange and glucocorticoid therapy were administered. There is a possibility that the underlying cancer played a role in the relapse. To minimize the risk for recurrence, the patient also received a second round of rituximab.

While establishing a clear cause is difficult, acquired TTP often appears to arise in connection with either an immune trigger, such as a viral infection, or immune dysregulation associated with another autoimmune disease or ongoing cancer. In this case, 4 weeks before the acquired TTP diagnosis, the patient had experienced COVID-19, which was likely to be the most probable trigger. However, rectal cancer was also identified in the patient, and whether these conditions are directly linked remains unclear.

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

A 49-year-old woman, previously recuperating from COVID-19, was found unconscious at her workplace, setting off a chain of events that would ultimately lead to an unexpected diagnosis.

This case report was published in the New England Journal of Medicine.

Noting the patient’s confusion and aphasia, emergency medical services were alerted, and she was taken to the emergency department of Massachusetts General Hospital. Initial examination revealed aphasia and coordination difficulties. However, imaging studies, including CT angiography, showed no signs of stroke or other neurological abnormalities.

The patient’s coworkers had observed that she appeared “unwell.” Her medical history included hypertension, which was managed with amlodipine, and there was no known family history of neurologic disorders.

During the examination, her vital signs were within normal ranges.

The patient’s potassium level of 2.5 mmol/L was noteworthy, indicating hypokalemia. Additionally, the patient presented with anemia and thrombocytopenia. Additional laboratory results unveiled thrombotic thrombocytopenic purpura (TTP), a rare blood disorder characterized by microangiopathic hemolytic anemia. The microscopic examination of a peripheral blood smear confirmed the extent of thrombocytopenia and was particularly notable for the increased number of schistocytes. The patient’s peripheral blood smear revealed five or six schistocytes per high-power field, constituting approximately 5% of the red cells. This significant number of schistocytes aligned with the severity of anemia and thrombocytopenia, confirming the diagnosis of microangiopathic hemolytic anemia.

Acquired TTP is an autoimmune condition driven by antibody-mediated clearance of the plasma enzyme ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13). Confirmatory laboratory testing for ADAMTS13 takes 1-3 days; therefore, therapeutic plasma exchange with glucocorticoid therapy and rituximab was initiated, which promptly improved her condition.

In this patient, the ADAMTS13 activity level was severely reduced (< 5%; reference value > 67%), and the inhibitor was present (1.4 inhibitor units; reference value ≤ 0.4).

Rectal cancer was diagnosed in this patient 2 months after the diagnosis of acquired TTP.

After undergoing four weekly infusions of rituximab and a 2-month tapering course of glucocorticoids, the patient experienced a relapse, approximately 6 months following the acquired TTP diagnosis. In response, therapeutic plasma exchange and glucocorticoid therapy were administered. There is a possibility that the underlying cancer played a role in the relapse. To minimize the risk for recurrence, the patient also received a second round of rituximab.

While establishing a clear cause is difficult, acquired TTP often appears to arise in connection with either an immune trigger, such as a viral infection, or immune dysregulation associated with another autoimmune disease or ongoing cancer. In this case, 4 weeks before the acquired TTP diagnosis, the patient had experienced COVID-19, which was likely to be the most probable trigger. However, rectal cancer was also identified in the patient, and whether these conditions are directly linked remains unclear.

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

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Long COVID can exacerbate existing mental health disorders or cause new-onset psychiatric symptoms, but mental illness does not cause long COVID, experts say.

The consensus guidance statement on the assessment and treatment of mental health symptoms in patients with post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID, was published online in Physical Medicine and Rehabilitation, the journal of the American Academy of Physical Medicine and Rehabilitation (AAPM&R).

The statement was developed by a task force that included experts from physical medicine, neurology, neuropsychiatry, neuropsychology, rehabilitation psychology, and primary care. It is the eighth guidance statement on long COVID published by AAPM&R).

“Many of our patients have reported experiences in which their symptoms of long COVID have been dismissed either by loved ones in the community, or also amongst health care providers, and they’ve been told their symptoms are in their head or due to a mental health condition, but that’s simply not true,” Abby L. Cheng, MD, a physiatrist at Barnes Jewish Hospital in St. Louis and a coauthor of the new guidance, said in a press briefing.

“Long COVID is real, and mental health conditions do not cause long COVID,” Dr. Cheng added.
 

Millions of Americans affected

Anxiety and depression have been reported as the second and third most common symptoms of long COVID, according to the guidance statement.

There is some evidence that the body’s inflammatory response – specifically, circulating cytokines – may contribute to the worsening of mental health symptoms or may bring on new symptoms of anxiety or depression, said Dr. Cheng. Cytokines may also affect levels of brain chemicals, such as serotonin, she said.

Researchers are also exploring whether the persistence of virus in the body, miniature blood clots in the body and brain, and changes to the gut microbiome affect the mental health of people with long COVID.

Some mental health symptoms – such as fatigue, brain fog, sleep disturbances, and tachycardia – can mimic long COVID symptoms, said Dr. Cheng.

The treatment is the same for someone with or without long COVID who has anxiety, depression, posttraumatic stress disorder, or other mental health conditions and includes treatment of coexisting medical conditions, supportive therapy and cognitive-behavioral therapy, and pharmacologic interventions, she said.

“Group therapy may have a particular role in the long COVID population because it really provides that social connection and awareness of additional resources in addition to validation of their experiences,” Dr. Cheng said.

The guidance suggests that primary care practitioners – if it’s within their comfort zone and they have the training – can be the first line for managing mental health symptoms.

But for patients whose symptoms are interfering with functioning and their ability to interact with the community, the guidance urges primary care clinicians to refer the patient to a specialist.

“It leaves the door open to them to practice within their scope but also gives guidance as to how, why, and who should be referred to the next level of care,” said Dr. Cheng.

Coauthor Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine at UT Health San Antonio, Texas, said that although fewer people are now getting long COVID, “it’s still an impactful number.”

The Centers for Disease Control and Prevention recently estimated that about 7% of American adults (18 million) and 1.3% of children had experienced long COVID.

Dr. Gutierrez said that it’s an evolving number, as some patients who have a second or third or fourth SARS-CoV-2 infection experience exacerbations of previous bouts of long COVID or develop long COVID for the first time.

“We are still getting new patients on a regular basis with long COVID,” said AAPM&R President Steven R. Flanagan, MD, a physical medicine specialist.

“This is a problem that really is not going away. It is still real and still ever-present,” said Dr. Flanagan, chair of rehabilitation medicine at NYU Langone Health.
 

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

Long COVID can exacerbate existing mental health disorders or cause new-onset psychiatric symptoms, but mental illness does not cause long COVID, experts say.

The consensus guidance statement on the assessment and treatment of mental health symptoms in patients with post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID, was published online in Physical Medicine and Rehabilitation, the journal of the American Academy of Physical Medicine and Rehabilitation (AAPM&R).

The statement was developed by a task force that included experts from physical medicine, neurology, neuropsychiatry, neuropsychology, rehabilitation psychology, and primary care. It is the eighth guidance statement on long COVID published by AAPM&R).

“Many of our patients have reported experiences in which their symptoms of long COVID have been dismissed either by loved ones in the community, or also amongst health care providers, and they’ve been told their symptoms are in their head or due to a mental health condition, but that’s simply not true,” Abby L. Cheng, MD, a physiatrist at Barnes Jewish Hospital in St. Louis and a coauthor of the new guidance, said in a press briefing.

“Long COVID is real, and mental health conditions do not cause long COVID,” Dr. Cheng added.
 

Millions of Americans affected

Anxiety and depression have been reported as the second and third most common symptoms of long COVID, according to the guidance statement.

There is some evidence that the body’s inflammatory response – specifically, circulating cytokines – may contribute to the worsening of mental health symptoms or may bring on new symptoms of anxiety or depression, said Dr. Cheng. Cytokines may also affect levels of brain chemicals, such as serotonin, she said.

Researchers are also exploring whether the persistence of virus in the body, miniature blood clots in the body and brain, and changes to the gut microbiome affect the mental health of people with long COVID.

Some mental health symptoms – such as fatigue, brain fog, sleep disturbances, and tachycardia – can mimic long COVID symptoms, said Dr. Cheng.

The treatment is the same for someone with or without long COVID who has anxiety, depression, posttraumatic stress disorder, or other mental health conditions and includes treatment of coexisting medical conditions, supportive therapy and cognitive-behavioral therapy, and pharmacologic interventions, she said.

“Group therapy may have a particular role in the long COVID population because it really provides that social connection and awareness of additional resources in addition to validation of their experiences,” Dr. Cheng said.

The guidance suggests that primary care practitioners – if it’s within their comfort zone and they have the training – can be the first line for managing mental health symptoms.

But for patients whose symptoms are interfering with functioning and their ability to interact with the community, the guidance urges primary care clinicians to refer the patient to a specialist.

“It leaves the door open to them to practice within their scope but also gives guidance as to how, why, and who should be referred to the next level of care,” said Dr. Cheng.

Coauthor Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine at UT Health San Antonio, Texas, said that although fewer people are now getting long COVID, “it’s still an impactful number.”

The Centers for Disease Control and Prevention recently estimated that about 7% of American adults (18 million) and 1.3% of children had experienced long COVID.

Dr. Gutierrez said that it’s an evolving number, as some patients who have a second or third or fourth SARS-CoV-2 infection experience exacerbations of previous bouts of long COVID or develop long COVID for the first time.

“We are still getting new patients on a regular basis with long COVID,” said AAPM&R President Steven R. Flanagan, MD, a physical medicine specialist.

“This is a problem that really is not going away. It is still real and still ever-present,” said Dr. Flanagan, chair of rehabilitation medicine at NYU Langone Health.
 

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

Long COVID can exacerbate existing mental health disorders or cause new-onset psychiatric symptoms, but mental illness does not cause long COVID, experts say.

The consensus guidance statement on the assessment and treatment of mental health symptoms in patients with post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID, was published online in Physical Medicine and Rehabilitation, the journal of the American Academy of Physical Medicine and Rehabilitation (AAPM&R).

The statement was developed by a task force that included experts from physical medicine, neurology, neuropsychiatry, neuropsychology, rehabilitation psychology, and primary care. It is the eighth guidance statement on long COVID published by AAPM&R).

“Many of our patients have reported experiences in which their symptoms of long COVID have been dismissed either by loved ones in the community, or also amongst health care providers, and they’ve been told their symptoms are in their head or due to a mental health condition, but that’s simply not true,” Abby L. Cheng, MD, a physiatrist at Barnes Jewish Hospital in St. Louis and a coauthor of the new guidance, said in a press briefing.

“Long COVID is real, and mental health conditions do not cause long COVID,” Dr. Cheng added.
 

Millions of Americans affected

Anxiety and depression have been reported as the second and third most common symptoms of long COVID, according to the guidance statement.

There is some evidence that the body’s inflammatory response – specifically, circulating cytokines – may contribute to the worsening of mental health symptoms or may bring on new symptoms of anxiety or depression, said Dr. Cheng. Cytokines may also affect levels of brain chemicals, such as serotonin, she said.

Researchers are also exploring whether the persistence of virus in the body, miniature blood clots in the body and brain, and changes to the gut microbiome affect the mental health of people with long COVID.

Some mental health symptoms – such as fatigue, brain fog, sleep disturbances, and tachycardia – can mimic long COVID symptoms, said Dr. Cheng.

The treatment is the same for someone with or without long COVID who has anxiety, depression, posttraumatic stress disorder, or other mental health conditions and includes treatment of coexisting medical conditions, supportive therapy and cognitive-behavioral therapy, and pharmacologic interventions, she said.

“Group therapy may have a particular role in the long COVID population because it really provides that social connection and awareness of additional resources in addition to validation of their experiences,” Dr. Cheng said.

The guidance suggests that primary care practitioners – if it’s within their comfort zone and they have the training – can be the first line for managing mental health symptoms.

But for patients whose symptoms are interfering with functioning and their ability to interact with the community, the guidance urges primary care clinicians to refer the patient to a specialist.

“It leaves the door open to them to practice within their scope but also gives guidance as to how, why, and who should be referred to the next level of care,” said Dr. Cheng.

Coauthor Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine at UT Health San Antonio, Texas, said that although fewer people are now getting long COVID, “it’s still an impactful number.”

The Centers for Disease Control and Prevention recently estimated that about 7% of American adults (18 million) and 1.3% of children had experienced long COVID.

Dr. Gutierrez said that it’s an evolving number, as some patients who have a second or third or fourth SARS-CoV-2 infection experience exacerbations of previous bouts of long COVID or develop long COVID for the first time.

“We are still getting new patients on a regular basis with long COVID,” said AAPM&R President Steven R. Flanagan, MD, a physical medicine specialist.

“This is a problem that really is not going away. It is still real and still ever-present,” said Dr. Flanagan, chair of rehabilitation medicine at NYU Langone Health.
 

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

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

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

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

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

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

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

Emerging treatments, psychological concerns

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Emerging treatments, psychological concerns

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Emerging treatments, psychological concerns

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Excerpts of the interview follow.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Excerpts of the interview follow.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Excerpts of the interview follow.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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