Covid ICYMI

TOPLINE: 

There were few cases of SARS-CoV-2 infections among emergency department (ED) healthcare personnel and no substantial changes in the delivery of emergency medical care during the initial phase of the COVID-19 pandemic.

METHODOLOGY:

• This multicenter prospective cohort study of US ED healthcare personnel called Project COVERED was conducted from May to December 2020 to evaluate the following outcomes:
• The possibility of infected ED personnel reporting to work
• The burden of COVID-19 symptoms on an ED personnel’s work status
• The association between SARS-CoV-2 infection levels and ED staffing
• Project COVERED enrolled 1673 ED healthcare personnel with 29,825 person weeks of observational data from 25 geographically diverse EDs.
• The presence of any SARS-CoV-2 infection was determined using reverse transcription polymerase chain reaction or IgG antibody testing at baseline, week 2, week 4, and every four subsequent weeks through week 20.
• Investigators also collected weekly data on ED staffing and the incidence of SARS-CoV-2 infections in healthcare facilities.

TAKEAWAY:

• Despite the absence of widespread natural immunity or COVID-19 vaccine availability during the time of this study, only 4.5% of ED healthcare personnel tested positive for SARS-CoV-2 infections, with more than half (57.3%) not experiencing any symptoms.
• Most personnel (83%) who experienced symptoms associated with COVID-19 reported working at least one shift in the ED and nearly all of them continued to work until they received laboratory confirmation of their infection.
• The working time lost as a result of COVID-19 and related concerns was minimal, as 89 healthcare personnel reported 90 person weeks of missed work (0.3% of all weeks).
• During this study, physician-staffing levels ranged from 98.7% to 102.0% of normal staffing, with similar values noted for nursing and nonclinical staffs. Reduced staffing was rare, even during COVID-19 surges.

IN PRACTICE:

“Our findings suggest that the cumulative interaction between infected healthcare personnel and others resulted in a negligible risk of transmission on the scale of public health emergencies,” the authors wrote.

SOURCE:

This study was led by Kurt D. Weber, MD, Department of Emergency Medicine, Orlando Health, Orlando, Florida, and published online in Annals of Emergency Medicine.

LIMITATIONS:

Data regarding the Delta variant surges that occurred toward the end of December and the ED status after the advent of the COVID-19 vaccine were not recorded. There may also have been a selection bias risk in this study because the volunteer participants may have exhibited behaviors like social distancing and use of protective equipment, which may have decreased their risk for infections.

DISCLOSURES:

This study was funded by a cooperative agreement from the Centers for Disease Control and Prevention and the Institute for Clinical and Translational Science at the University of Iowa through a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE: 

There were few cases of SARS-CoV-2 infections among emergency department (ED) healthcare personnel and no substantial changes in the delivery of emergency medical care during the initial phase of the COVID-19 pandemic.

METHODOLOGY:

• This multicenter prospective cohort study of US ED healthcare personnel called Project COVERED was conducted from May to December 2020 to evaluate the following outcomes:
• The possibility of infected ED personnel reporting to work
• The burden of COVID-19 symptoms on an ED personnel’s work status
• The association between SARS-CoV-2 infection levels and ED staffing
• Project COVERED enrolled 1673 ED healthcare personnel with 29,825 person weeks of observational data from 25 geographically diverse EDs.
• The presence of any SARS-CoV-2 infection was determined using reverse transcription polymerase chain reaction or IgG antibody testing at baseline, week 2, week 4, and every four subsequent weeks through week 20.
• Investigators also collected weekly data on ED staffing and the incidence of SARS-CoV-2 infections in healthcare facilities.

TAKEAWAY:

• Despite the absence of widespread natural immunity or COVID-19 vaccine availability during the time of this study, only 4.5% of ED healthcare personnel tested positive for SARS-CoV-2 infections, with more than half (57.3%) not experiencing any symptoms.
• Most personnel (83%) who experienced symptoms associated with COVID-19 reported working at least one shift in the ED and nearly all of them continued to work until they received laboratory confirmation of their infection.
• The working time lost as a result of COVID-19 and related concerns was minimal, as 89 healthcare personnel reported 90 person weeks of missed work (0.3% of all weeks).
• During this study, physician-staffing levels ranged from 98.7% to 102.0% of normal staffing, with similar values noted for nursing and nonclinical staffs. Reduced staffing was rare, even during COVID-19 surges.

IN PRACTICE:

“Our findings suggest that the cumulative interaction between infected healthcare personnel and others resulted in a negligible risk of transmission on the scale of public health emergencies,” the authors wrote.

SOURCE:

This study was led by Kurt D. Weber, MD, Department of Emergency Medicine, Orlando Health, Orlando, Florida, and published online in Annals of Emergency Medicine.

LIMITATIONS:

Data regarding the Delta variant surges that occurred toward the end of December and the ED status after the advent of the COVID-19 vaccine were not recorded. There may also have been a selection bias risk in this study because the volunteer participants may have exhibited behaviors like social distancing and use of protective equipment, which may have decreased their risk for infections.

DISCLOSURES:

This study was funded by a cooperative agreement from the Centers for Disease Control and Prevention and the Institute for Clinical and Translational Science at the University of Iowa through a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE: 

There were few cases of SARS-CoV-2 infections among emergency department (ED) healthcare personnel and no substantial changes in the delivery of emergency medical care during the initial phase of the COVID-19 pandemic.

METHODOLOGY:

• This multicenter prospective cohort study of US ED healthcare personnel called Project COVERED was conducted from May to December 2020 to evaluate the following outcomes:
• The possibility of infected ED personnel reporting to work
• The burden of COVID-19 symptoms on an ED personnel’s work status
• The association between SARS-CoV-2 infection levels and ED staffing
• Project COVERED enrolled 1673 ED healthcare personnel with 29,825 person weeks of observational data from 25 geographically diverse EDs.
• The presence of any SARS-CoV-2 infection was determined using reverse transcription polymerase chain reaction or IgG antibody testing at baseline, week 2, week 4, and every four subsequent weeks through week 20.
• Investigators also collected weekly data on ED staffing and the incidence of SARS-CoV-2 infections in healthcare facilities.

TAKEAWAY:

• Despite the absence of widespread natural immunity or COVID-19 vaccine availability during the time of this study, only 4.5% of ED healthcare personnel tested positive for SARS-CoV-2 infections, with more than half (57.3%) not experiencing any symptoms.
• Most personnel (83%) who experienced symptoms associated with COVID-19 reported working at least one shift in the ED and nearly all of them continued to work until they received laboratory confirmation of their infection.
• The working time lost as a result of COVID-19 and related concerns was minimal, as 89 healthcare personnel reported 90 person weeks of missed work (0.3% of all weeks).
• During this study, physician-staffing levels ranged from 98.7% to 102.0% of normal staffing, with similar values noted for nursing and nonclinical staffs. Reduced staffing was rare, even during COVID-19 surges.

IN PRACTICE:

“Our findings suggest that the cumulative interaction between infected healthcare personnel and others resulted in a negligible risk of transmission on the scale of public health emergencies,” the authors wrote.

SOURCE:

This study was led by Kurt D. Weber, MD, Department of Emergency Medicine, Orlando Health, Orlando, Florida, and published online in Annals of Emergency Medicine.

LIMITATIONS:

Data regarding the Delta variant surges that occurred toward the end of December and the ED status after the advent of the COVID-19 vaccine were not recorded. There may also have been a selection bias risk in this study because the volunteer participants may have exhibited behaviors like social distancing and use of protective equipment, which may have decreased their risk for infections.

DISCLOSURES:

This study was funded by a cooperative agreement from the Centers for Disease Control and Prevention and the Institute for Clinical and Translational Science at the University of Iowa through a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

Experts worry a recent rise in long COVID cases — fueled by a spike in winter holiday infections and a decline in masking and other measures — could continue into this year.

A sudden rise in long COVID in January has persisted into a second month. About 17.6% of those surveyed by the Census Bureau in January said they have experienced long COVID. The number for February was 17.4.

Compare these new numbers to October 2023 and earlier, when long COVID numbers hovered between 14% and 15% of the US adult population as far back as June 2022.

The Census Bureau and the Centers for Disease Control and Prevention (CDC) regularly query about 70,000 people as part of its ongoing Pulse Survey.

It’s Not Just the Federal Numbers

Independently, advocates, researchers, and clinicians also reported seeing an increase in the number of people who have developed long COVID after a second or third infection.

John Baratta, MD, who runs the COVID Recovery Clinic at the University of North Carolina, said the increase is related to a higher rate of acute cases in the fall and winter of 2023.

In January, the percentage of North Carolinians reporting ever having had long COVD jumped from 12.5% to 20.2% in January and fell to 16.8% in February.

At the same time, many cases are either undetected or unreported by people who tested positive for COVID-19 at home or are not aware they have had it.

Hannah Davis, a member of the Patient-Led Research Collaborative, also linked the increase in long COVID to the wave of new infections at the end of 2023 and the start of 2024.

“It’s absolutely real,” she said via email. “There have been many new cases in the past few months, and we see those new folks in our communities as well.”

Wastewater Remains the Best Indicator

“This results in many cases of COVID flying under the radar,” Dr. Baratta said. “However, we do know from the wastewater monitoring that there was a pretty substantial rise.”

Testing wastewater for COVID levels is becoming one of the most reliable measures of estimating infection, he said. Nationally, viral measure of wastewater followed a similar path: The viral rate started creeping up in October and peaked on December 30, according to CDC measures.

RNA extracted from concentrated wastewater samples offer a good measure of SARS-CoV-2 in the community. In North Carolina and elsewhere, the state measures the virus by calculating gene copies in wastewater per capita — how many for each resident. For most of 2023, North Carolina reported fewer than 10 million viral gene copies per state resident. In late July, that number shot up to 25 million and reached 71 million per capita in March 2023 before starting to go down.

Repeat Infections, Vaccine Apathy Driving Numbers

Dr. Baratta said COVID remains a problem in rural areas. In Maine, wastewater virus counts have been much higher than the national average. There, the percentage of people who reported currently experiencing long COVID rose from 5.7% in October to 9.2% in January. The percentage reporting ever experiencing long COVID rose from 13.8% to 21% in that period.

Other factors play a role. Dr. Baratta said he is seeing patients with long COVID who have refused the vaccine or developed long COVID after a second or third infection.

He said he thinks that attitudes toward the pandemic have resulted in relaxed protection and prevention efforts.

“There is low booster vaccination rate and additional masking is utilized less that before,” he said. About 20% of the population has received the latest vaccine booster, according to the Kaiser Family Foundation.

The increase in long COVID has many causes including “infection, reinfection (eg, people getting COVID after a second, third, or fourth infection), low vaccination rates, waning immunity, and decline in the use of antivirals (such as Paxlovid),” said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, St. Louis, Missouri.

“All of these could contribute to the rise in burden of long COVID,” he said.

Not all states reported an increase. Massachusetts and Hawaii saw long COVD rates drop slightly, according to the CDC.

A version of this article appeared on Medscape.com.

Experts worry a recent rise in long COVID cases — fueled by a spike in winter holiday infections and a decline in masking and other measures — could continue into this year.

A sudden rise in long COVID in January has persisted into a second month. About 17.6% of those surveyed by the Census Bureau in January said they have experienced long COVID. The number for February was 17.4.

Compare these new numbers to October 2023 and earlier, when long COVID numbers hovered between 14% and 15% of the US adult population as far back as June 2022.

The Census Bureau and the Centers for Disease Control and Prevention (CDC) regularly query about 70,000 people as part of its ongoing Pulse Survey.

It’s Not Just the Federal Numbers

Independently, advocates, researchers, and clinicians also reported seeing an increase in the number of people who have developed long COVID after a second or third infection.

John Baratta, MD, who runs the COVID Recovery Clinic at the University of North Carolina, said the increase is related to a higher rate of acute cases in the fall and winter of 2023.

In January, the percentage of North Carolinians reporting ever having had long COVD jumped from 12.5% to 20.2% in January and fell to 16.8% in February.

At the same time, many cases are either undetected or unreported by people who tested positive for COVID-19 at home or are not aware they have had it.

Hannah Davis, a member of the Patient-Led Research Collaborative, also linked the increase in long COVID to the wave of new infections at the end of 2023 and the start of 2024.

“It’s absolutely real,” she said via email. “There have been many new cases in the past few months, and we see those new folks in our communities as well.”

Wastewater Remains the Best Indicator

“This results in many cases of COVID flying under the radar,” Dr. Baratta said. “However, we do know from the wastewater monitoring that there was a pretty substantial rise.”

Testing wastewater for COVID levels is becoming one of the most reliable measures of estimating infection, he said. Nationally, viral measure of wastewater followed a similar path: The viral rate started creeping up in October and peaked on December 30, according to CDC measures.

RNA extracted from concentrated wastewater samples offer a good measure of SARS-CoV-2 in the community. In North Carolina and elsewhere, the state measures the virus by calculating gene copies in wastewater per capita — how many for each resident. For most of 2023, North Carolina reported fewer than 10 million viral gene copies per state resident. In late July, that number shot up to 25 million and reached 71 million per capita in March 2023 before starting to go down.

Repeat Infections, Vaccine Apathy Driving Numbers

Dr. Baratta said COVID remains a problem in rural areas. In Maine, wastewater virus counts have been much higher than the national average. There, the percentage of people who reported currently experiencing long COVID rose from 5.7% in October to 9.2% in January. The percentage reporting ever experiencing long COVID rose from 13.8% to 21% in that period.

Other factors play a role. Dr. Baratta said he is seeing patients with long COVID who have refused the vaccine or developed long COVID after a second or third infection.

He said he thinks that attitudes toward the pandemic have resulted in relaxed protection and prevention efforts.

“There is low booster vaccination rate and additional masking is utilized less that before,” he said. About 20% of the population has received the latest vaccine booster, according to the Kaiser Family Foundation.

The increase in long COVID has many causes including “infection, reinfection (eg, people getting COVID after a second, third, or fourth infection), low vaccination rates, waning immunity, and decline in the use of antivirals (such as Paxlovid),” said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, St. Louis, Missouri.

“All of these could contribute to the rise in burden of long COVID,” he said.

Not all states reported an increase. Massachusetts and Hawaii saw long COVD rates drop slightly, according to the CDC.

A version of this article appeared on Medscape.com.

Experts worry a recent rise in long COVID cases — fueled by a spike in winter holiday infections and a decline in masking and other measures — could continue into this year.

A sudden rise in long COVID in January has persisted into a second month. About 17.6% of those surveyed by the Census Bureau in January said they have experienced long COVID. The number for February was 17.4.

Compare these new numbers to October 2023 and earlier, when long COVID numbers hovered between 14% and 15% of the US adult population as far back as June 2022.

The Census Bureau and the Centers for Disease Control and Prevention (CDC) regularly query about 70,000 people as part of its ongoing Pulse Survey.

It’s Not Just the Federal Numbers

Independently, advocates, researchers, and clinicians also reported seeing an increase in the number of people who have developed long COVID after a second or third infection.

John Baratta, MD, who runs the COVID Recovery Clinic at the University of North Carolina, said the increase is related to a higher rate of acute cases in the fall and winter of 2023.

In January, the percentage of North Carolinians reporting ever having had long COVD jumped from 12.5% to 20.2% in January and fell to 16.8% in February.

At the same time, many cases are either undetected or unreported by people who tested positive for COVID-19 at home or are not aware they have had it.

Hannah Davis, a member of the Patient-Led Research Collaborative, also linked the increase in long COVID to the wave of new infections at the end of 2023 and the start of 2024.

“It’s absolutely real,” she said via email. “There have been many new cases in the past few months, and we see those new folks in our communities as well.”

Wastewater Remains the Best Indicator

“This results in many cases of COVID flying under the radar,” Dr. Baratta said. “However, we do know from the wastewater monitoring that there was a pretty substantial rise.”

Testing wastewater for COVID levels is becoming one of the most reliable measures of estimating infection, he said. Nationally, viral measure of wastewater followed a similar path: The viral rate started creeping up in October and peaked on December 30, according to CDC measures.

RNA extracted from concentrated wastewater samples offer a good measure of SARS-CoV-2 in the community. In North Carolina and elsewhere, the state measures the virus by calculating gene copies in wastewater per capita — how many for each resident. For most of 2023, North Carolina reported fewer than 10 million viral gene copies per state resident. In late July, that number shot up to 25 million and reached 71 million per capita in March 2023 before starting to go down.

Repeat Infections, Vaccine Apathy Driving Numbers

Dr. Baratta said COVID remains a problem in rural areas. In Maine, wastewater virus counts have been much higher than the national average. There, the percentage of people who reported currently experiencing long COVID rose from 5.7% in October to 9.2% in January. The percentage reporting ever experiencing long COVID rose from 13.8% to 21% in that period.

Other factors play a role. Dr. Baratta said he is seeing patients with long COVID who have refused the vaccine or developed long COVID after a second or third infection.

He said he thinks that attitudes toward the pandemic have resulted in relaxed protection and prevention efforts.

“There is low booster vaccination rate and additional masking is utilized less that before,” he said. About 20% of the population has received the latest vaccine booster, according to the Kaiser Family Foundation.

The increase in long COVID has many causes including “infection, reinfection (eg, people getting COVID after a second, third, or fourth infection), low vaccination rates, waning immunity, and decline in the use of antivirals (such as Paxlovid),” said Ziyad Al-Aly, MD, chief of research at Veterans Affairs St. Louis Health Care and clinical epidemiologist at Washington University in St. Louis, St. Louis, Missouri.

“All of these could contribute to the rise in burden of long COVID,” he said.

Not all states reported an increase. Massachusetts and Hawaii saw long COVD rates drop slightly, according to the CDC.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

No matter how much we’d like to leave it in the dust, COVID-19 remains prevalent and potent. Tens of thousands of people still contract COVID per week in the United States. Hundreds die. And those who don’t may still develop long COVID.

Pleas from public health officials for people to get a COVID vaccine or booster shot have been ignored by many people. About 80% of eligible Americans haven’t taken any kind of COVID booster. Meantime, the virus continues to mutate, eroding the efficacy of the vaccine’s past versions.

How to get more people to get the jab? Vaccine hesitancy, said infectious disease specialist William Schaffner, MD, is likely rooted in a lack of trust in authority, whether it’s public health officials or politicians.

Dr. Schaffner, professor of infectious diseases at the Vanderbilt University School of Medicine, Nashville, Tennessee, and former medical director of the National Foundation for Infectious Diseases, recommended five strategies physicians can try when discussing the importance of staying up to date on COVID vaccines with patients.
 

#1: Be Patient With Your Patient

First and foremost, if doctors are feeling reluctance from their patients, they need to know “what they shouldn’t do,” Dr. Schaffner said.

When a patient initially doesn’t want the vaccine, doctors shouldn’t express surprise. “Do not scold or berate or belittle. Do not give the impression the patient is somehow wrong or has failed a test of some sort,” Dr. Schaffner said.

Step back and affirm that they understand what the patient is saying so they feel reassured, even if they don’t agree or it’s based on falsehoods about the vaccine.

He said patients need to feel “the doctor heard them; it’s okay to tell the doctor this.” When you affirm what the patient says, it puts them at ease and provides a smoother road to eventually getting them to say “yes.”

But if there’s still a roadblock, don’t bulldoze them. “You don’t want to punish the patient ... let them know you’ll continue to hear them,” Dr. Schaffner said.
 

#2: Always Acknowledge a Concern

Fear of side effects is great among some patients, even if the risks are low, Dr. Schaffner said. Patients may be hesitant because they’re afraid they’ll become one of the “two or three in a million” who suffer extremely rare side effects from the vaccine, Dr. Schaffner said.

In that case, doctors should acknowledge their concern is valid, he said. Never be dismissive. Ask the patients how they feel about the vaccine, listen to their responses, and let them know “I hear you. This is a new mRNA vaccine…you have concern about that,” Dr. Schaffner said.

Doctors can segue into how there’s little reason to wait for some elusive perfectly risk-free vaccine when they can help themselves right now.

“The adverse events that occur with vaccines occur within 2 months [and are typically mild]. I don’t know of a single vaccine that has genuinely long-term implications,” Dr. Schaffner said. “We should remember that old French philosopher Voltaire. He admonished us: Waiting for perfection is the great enemy of the current good.”
 

#3: Make a Strong Recommendation

Here’s something that may seem obvious: Don’t treat the vaccine as an afterthought. “Survey after survey tells us this ... it has everything to do with the strength of the recommendation,” Dr. Schaffner said.

Doctors typically make strong treatment recommendations such conditions as diabetes or high blood pressure, but “when it comes to vaccines, they’re often rather nonchalant,” he said.

If a patient is eligible for a vaccine, doctors should tell the patient they need to get it — not that you think they should get it. “Doctors have to make a firm recommendation: ‘You’re eligible for a vaccine ... and you need to get it ... you’ll receive it on your way out.’ It then becomes a distinct and strong recommendation,” he said.
 

#4: Appeal to Patients’ Hearts, Not Their Minds

In the opening of Charles Dickens’s novel “Hard Times,” the stern school superintendent, Mr. Gradgrind, scolds his students by beating their brow with the notion that, “Facts alone are wanted in life. Plant nothing else and root out everything else.”

The idea that facts alone can sway a vaccine-resistant patient is wrong. “It often doesn’t happen that way,” Dr. Schaffner said. “I don’t think facts do that. Psychologists tell us, yes, information is important, but it’s rarely sufficient to change behavior.”

Data and studies are foundational to medicine, but the key is to change how a patient feels about the data they’re presented with, not how they think about it. “Don’t attack their brain so much but their heart,” Dr. Schaffner said.

Dr. Schaffner has stressed with his patients that the COVID vaccine has become “the social norm,” suggesting virtually everyone he knows has received it and had no problem.

Once questions have been answered about whether the vaccine works and its various side effects, doctors could remind the patient, “You know, everyone in my office is getting the vaccine, and we’re trying to provide this protection to every patient,” he said.

You’re then delving deeper into their emotions and crossing a barrier that facts alone can’t breach.
 

#5: Make it Personal

Lead by example and personalize the fight against the virus. This allows doctors to act as if they’re building an alliance with their patients by framing the vaccine not as something that only affects them but can also confer benefits to a broader social circle.

Even after using these methods, patients may remain resistant, apprehensive, or even indifferent. In cases like these, Dr. Schaffner said it’s a good idea to let it go for the time being.

Let the patient know they “have access to you and can keep speaking with you about it” in the future, he said. “It takes more time, and you have to be cognizant of the nature of the conversation.”

Everybody is unique, but with trust, patience, and awareness of the patient’s feelings, doctors have a better shot at finding common ground with their patients and convincing them the vaccine is in their best interest, he said.

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

No matter how much we’d like to leave it in the dust, COVID-19 remains prevalent and potent. Tens of thousands of people still contract COVID per week in the United States. Hundreds die. And those who don’t may still develop long COVID.

Pleas from public health officials for people to get a COVID vaccine or booster shot have been ignored by many people. About 80% of eligible Americans haven’t taken any kind of COVID booster. Meantime, the virus continues to mutate, eroding the efficacy of the vaccine’s past versions.

How to get more people to get the jab? Vaccine hesitancy, said infectious disease specialist William Schaffner, MD, is likely rooted in a lack of trust in authority, whether it’s public health officials or politicians.

Dr. Schaffner, professor of infectious diseases at the Vanderbilt University School of Medicine, Nashville, Tennessee, and former medical director of the National Foundation for Infectious Diseases, recommended five strategies physicians can try when discussing the importance of staying up to date on COVID vaccines with patients.
 

#1: Be Patient With Your Patient

First and foremost, if doctors are feeling reluctance from their patients, they need to know “what they shouldn’t do,” Dr. Schaffner said.

When a patient initially doesn’t want the vaccine, doctors shouldn’t express surprise. “Do not scold or berate or belittle. Do not give the impression the patient is somehow wrong or has failed a test of some sort,” Dr. Schaffner said.

Step back and affirm that they understand what the patient is saying so they feel reassured, even if they don’t agree or it’s based on falsehoods about the vaccine.

He said patients need to feel “the doctor heard them; it’s okay to tell the doctor this.” When you affirm what the patient says, it puts them at ease and provides a smoother road to eventually getting them to say “yes.”

But if there’s still a roadblock, don’t bulldoze them. “You don’t want to punish the patient ... let them know you’ll continue to hear them,” Dr. Schaffner said.
 

#2: Always Acknowledge a Concern

Fear of side effects is great among some patients, even if the risks are low, Dr. Schaffner said. Patients may be hesitant because they’re afraid they’ll become one of the “two or three in a million” who suffer extremely rare side effects from the vaccine, Dr. Schaffner said.

In that case, doctors should acknowledge their concern is valid, he said. Never be dismissive. Ask the patients how they feel about the vaccine, listen to their responses, and let them know “I hear you. This is a new mRNA vaccine…you have concern about that,” Dr. Schaffner said.

Doctors can segue into how there’s little reason to wait for some elusive perfectly risk-free vaccine when they can help themselves right now.

“The adverse events that occur with vaccines occur within 2 months [and are typically mild]. I don’t know of a single vaccine that has genuinely long-term implications,” Dr. Schaffner said. “We should remember that old French philosopher Voltaire. He admonished us: Waiting for perfection is the great enemy of the current good.”
 

#3: Make a Strong Recommendation

Here’s something that may seem obvious: Don’t treat the vaccine as an afterthought. “Survey after survey tells us this ... it has everything to do with the strength of the recommendation,” Dr. Schaffner said.

Doctors typically make strong treatment recommendations such conditions as diabetes or high blood pressure, but “when it comes to vaccines, they’re often rather nonchalant,” he said.

If a patient is eligible for a vaccine, doctors should tell the patient they need to get it — not that you think they should get it. “Doctors have to make a firm recommendation: ‘You’re eligible for a vaccine ... and you need to get it ... you’ll receive it on your way out.’ It then becomes a distinct and strong recommendation,” he said.
 

#4: Appeal to Patients’ Hearts, Not Their Minds

In the opening of Charles Dickens’s novel “Hard Times,” the stern school superintendent, Mr. Gradgrind, scolds his students by beating their brow with the notion that, “Facts alone are wanted in life. Plant nothing else and root out everything else.”

The idea that facts alone can sway a vaccine-resistant patient is wrong. “It often doesn’t happen that way,” Dr. Schaffner said. “I don’t think facts do that. Psychologists tell us, yes, information is important, but it’s rarely sufficient to change behavior.”

Data and studies are foundational to medicine, but the key is to change how a patient feels about the data they’re presented with, not how they think about it. “Don’t attack their brain so much but their heart,” Dr. Schaffner said.

Dr. Schaffner has stressed with his patients that the COVID vaccine has become “the social norm,” suggesting virtually everyone he knows has received it and had no problem.

Once questions have been answered about whether the vaccine works and its various side effects, doctors could remind the patient, “You know, everyone in my office is getting the vaccine, and we’re trying to provide this protection to every patient,” he said.

You’re then delving deeper into their emotions and crossing a barrier that facts alone can’t breach.
 

#5: Make it Personal

Lead by example and personalize the fight against the virus. This allows doctors to act as if they’re building an alliance with their patients by framing the vaccine not as something that only affects them but can also confer benefits to a broader social circle.

Even after using these methods, patients may remain resistant, apprehensive, or even indifferent. In cases like these, Dr. Schaffner said it’s a good idea to let it go for the time being.

Let the patient know they “have access to you and can keep speaking with you about it” in the future, he said. “It takes more time, and you have to be cognizant of the nature of the conversation.”

Everybody is unique, but with trust, patience, and awareness of the patient’s feelings, doctors have a better shot at finding common ground with their patients and convincing them the vaccine is in their best interest, he said.

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

No matter how much we’d like to leave it in the dust, COVID-19 remains prevalent and potent. Tens of thousands of people still contract COVID per week in the United States. Hundreds die. And those who don’t may still develop long COVID.

Pleas from public health officials for people to get a COVID vaccine or booster shot have been ignored by many people. About 80% of eligible Americans haven’t taken any kind of COVID booster. Meantime, the virus continues to mutate, eroding the efficacy of the vaccine’s past versions.

How to get more people to get the jab? Vaccine hesitancy, said infectious disease specialist William Schaffner, MD, is likely rooted in a lack of trust in authority, whether it’s public health officials or politicians.

Dr. Schaffner, professor of infectious diseases at the Vanderbilt University School of Medicine, Nashville, Tennessee, and former medical director of the National Foundation for Infectious Diseases, recommended five strategies physicians can try when discussing the importance of staying up to date on COVID vaccines with patients.
 

#1: Be Patient With Your Patient

First and foremost, if doctors are feeling reluctance from their patients, they need to know “what they shouldn’t do,” Dr. Schaffner said.

When a patient initially doesn’t want the vaccine, doctors shouldn’t express surprise. “Do not scold or berate or belittle. Do not give the impression the patient is somehow wrong or has failed a test of some sort,” Dr. Schaffner said.

Step back and affirm that they understand what the patient is saying so they feel reassured, even if they don’t agree or it’s based on falsehoods about the vaccine.

He said patients need to feel “the doctor heard them; it’s okay to tell the doctor this.” When you affirm what the patient says, it puts them at ease and provides a smoother road to eventually getting them to say “yes.”

But if there’s still a roadblock, don’t bulldoze them. “You don’t want to punish the patient ... let them know you’ll continue to hear them,” Dr. Schaffner said.
 

#2: Always Acknowledge a Concern

Fear of side effects is great among some patients, even if the risks are low, Dr. Schaffner said. Patients may be hesitant because they’re afraid they’ll become one of the “two or three in a million” who suffer extremely rare side effects from the vaccine, Dr. Schaffner said.

In that case, doctors should acknowledge their concern is valid, he said. Never be dismissive. Ask the patients how they feel about the vaccine, listen to their responses, and let them know “I hear you. This is a new mRNA vaccine…you have concern about that,” Dr. Schaffner said.

Doctors can segue into how there’s little reason to wait for some elusive perfectly risk-free vaccine when they can help themselves right now.

“The adverse events that occur with vaccines occur within 2 months [and are typically mild]. I don’t know of a single vaccine that has genuinely long-term implications,” Dr. Schaffner said. “We should remember that old French philosopher Voltaire. He admonished us: Waiting for perfection is the great enemy of the current good.”
 

#3: Make a Strong Recommendation

Here’s something that may seem obvious: Don’t treat the vaccine as an afterthought. “Survey after survey tells us this ... it has everything to do with the strength of the recommendation,” Dr. Schaffner said.

Doctors typically make strong treatment recommendations such conditions as diabetes or high blood pressure, but “when it comes to vaccines, they’re often rather nonchalant,” he said.

If a patient is eligible for a vaccine, doctors should tell the patient they need to get it — not that you think they should get it. “Doctors have to make a firm recommendation: ‘You’re eligible for a vaccine ... and you need to get it ... you’ll receive it on your way out.’ It then becomes a distinct and strong recommendation,” he said.
 

#4: Appeal to Patients’ Hearts, Not Their Minds

In the opening of Charles Dickens’s novel “Hard Times,” the stern school superintendent, Mr. Gradgrind, scolds his students by beating their brow with the notion that, “Facts alone are wanted in life. Plant nothing else and root out everything else.”

The idea that facts alone can sway a vaccine-resistant patient is wrong. “It often doesn’t happen that way,” Dr. Schaffner said. “I don’t think facts do that. Psychologists tell us, yes, information is important, but it’s rarely sufficient to change behavior.”

Data and studies are foundational to medicine, but the key is to change how a patient feels about the data they’re presented with, not how they think about it. “Don’t attack their brain so much but their heart,” Dr. Schaffner said.

Dr. Schaffner has stressed with his patients that the COVID vaccine has become “the social norm,” suggesting virtually everyone he knows has received it and had no problem.

Once questions have been answered about whether the vaccine works and its various side effects, doctors could remind the patient, “You know, everyone in my office is getting the vaccine, and we’re trying to provide this protection to every patient,” he said.

You’re then delving deeper into their emotions and crossing a barrier that facts alone can’t breach.
 

#5: Make it Personal

Lead by example and personalize the fight against the virus. This allows doctors to act as if they’re building an alliance with their patients by framing the vaccine not as something that only affects them but can also confer benefits to a broader social circle.

Even after using these methods, patients may remain resistant, apprehensive, or even indifferent. In cases like these, Dr. Schaffner said it’s a good idea to let it go for the time being.

Let the patient know they “have access to you and can keep speaking with you about it” in the future, he said. “It takes more time, and you have to be cognizant of the nature of the conversation.”

Everybody is unique, but with trust, patience, and awareness of the patient’s feelings, doctors have a better shot at finding common ground with their patients and convincing them the vaccine is in their best interest, he said.

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

TOPLINE: 

The results of a recent study suggest that biologics and small molecule inhibitors (SMIs) do not impair the protective effect of COVID-19 vaccine against hospitalization in patients with psoriasis and hidradenitis suppurativa (HS).

METHODOLOGY:

• It remains unknown whether immunomodulatory therapies impair COVID-19 vaccine efficacy and increase hospitalization rates linked to COVID-19 in patients with inflammatory skin conditions such as psoriasis or HS.
• Researchers conducted a cross-sectional study using data from the Epic Cosmos database from January 2020 to October 2023, identifying 30,845 patients with psoriasis or HS.
• Overall, 22,293 patients with documented completion of their primary COVID-19 vaccine series were included in the analysis.
• Of the vaccinated patients, they compared 7046 patients with psoriasis on SMIs and 2033 with psoriasis or HS on biologics with 13,214 patients who did not receive biologics or SMIs.
• The primary outcome was the COVID-19 hospitalization rate.
• Treatment with biologics did not increase COVID-19-related hospitalization rates in vaccinated patients with psoriasis or HS (hospitalization rate, 6.0% for both those taking and those not taking a biologic; P > .99).
• Similarly, hospitalization rates did not significantly differ between vaccinated patients who received SMIs vs those who did not (7.1% vs 6.0%; P = .0596).

IN PRACTICE:

These findings “encourage dermatologists to continue treating [psoriasis]/HS confidently despite the ongoing COVID-19 pandemic,” the authors concluded.

SOURCE:

The study led by Bella R. Lee from Ohio State University Wexner Medical Center, Columbus, was published online on March 13, 2024, in the Journal of the American Academy of Dermatology. 

LIMITATIONS:

Multivariable adjustments could not be performed in this study due to unavailability of individual-level data, and hospital admissions that occurred outside the Epic system were not captured.

DISCLOSURES:

The study did not receive any funding. All authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE: 

The results of a recent study suggest that biologics and small molecule inhibitors (SMIs) do not impair the protective effect of COVID-19 vaccine against hospitalization in patients with psoriasis and hidradenitis suppurativa (HS).

METHODOLOGY:

• It remains unknown whether immunomodulatory therapies impair COVID-19 vaccine efficacy and increase hospitalization rates linked to COVID-19 in patients with inflammatory skin conditions such as psoriasis or HS.
• Researchers conducted a cross-sectional study using data from the Epic Cosmos database from January 2020 to October 2023, identifying 30,845 patients with psoriasis or HS.
• Overall, 22,293 patients with documented completion of their primary COVID-19 vaccine series were included in the analysis.
• Of the vaccinated patients, they compared 7046 patients with psoriasis on SMIs and 2033 with psoriasis or HS on biologics with 13,214 patients who did not receive biologics or SMIs.
• The primary outcome was the COVID-19 hospitalization rate.
• Treatment with biologics did not increase COVID-19-related hospitalization rates in vaccinated patients with psoriasis or HS (hospitalization rate, 6.0% for both those taking and those not taking a biologic; P > .99).
• Similarly, hospitalization rates did not significantly differ between vaccinated patients who received SMIs vs those who did not (7.1% vs 6.0%; P = .0596).

IN PRACTICE:

These findings “encourage dermatologists to continue treating [psoriasis]/HS confidently despite the ongoing COVID-19 pandemic,” the authors concluded.

SOURCE:

The study led by Bella R. Lee from Ohio State University Wexner Medical Center, Columbus, was published online on March 13, 2024, in the Journal of the American Academy of Dermatology. 

LIMITATIONS:

Multivariable adjustments could not be performed in this study due to unavailability of individual-level data, and hospital admissions that occurred outside the Epic system were not captured.

DISCLOSURES:

The study did not receive any funding. All authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE: 

The results of a recent study suggest that biologics and small molecule inhibitors (SMIs) do not impair the protective effect of COVID-19 vaccine against hospitalization in patients with psoriasis and hidradenitis suppurativa (HS).

METHODOLOGY:

• It remains unknown whether immunomodulatory therapies impair COVID-19 vaccine efficacy and increase hospitalization rates linked to COVID-19 in patients with inflammatory skin conditions such as psoriasis or HS.
• Researchers conducted a cross-sectional study using data from the Epic Cosmos database from January 2020 to October 2023, identifying 30,845 patients with psoriasis or HS.
• Overall, 22,293 patients with documented completion of their primary COVID-19 vaccine series were included in the analysis.
• Of the vaccinated patients, they compared 7046 patients with psoriasis on SMIs and 2033 with psoriasis or HS on biologics with 13,214 patients who did not receive biologics or SMIs.
• The primary outcome was the COVID-19 hospitalization rate.
• Treatment with biologics did not increase COVID-19-related hospitalization rates in vaccinated patients with psoriasis or HS (hospitalization rate, 6.0% for both those taking and those not taking a biologic; P > .99).
• Similarly, hospitalization rates did not significantly differ between vaccinated patients who received SMIs vs those who did not (7.1% vs 6.0%; P = .0596).

IN PRACTICE:

These findings “encourage dermatologists to continue treating [psoriasis]/HS confidently despite the ongoing COVID-19 pandemic,” the authors concluded.

SOURCE:

The study led by Bella R. Lee from Ohio State University Wexner Medical Center, Columbus, was published online on March 13, 2024, in the Journal of the American Academy of Dermatology. 

LIMITATIONS:

Multivariable adjustments could not be performed in this study due to unavailability of individual-level data, and hospital admissions that occurred outside the Epic system were not captured.

DISCLOSURES:

The study did not receive any funding. All authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

Stefan Bornstein, MD, PhD, professor, made it clear during a press conference at the 67th Congress of the German Society of Endocrinology (DGE) that there is more than one interaction between them. Nowadays, one can almost speak of an “endocrine virology and even of the virome as an additional, hormonally metabolically active gland,” said Dr. Bornstein, who will receive the Berthold Medal from the DGE in 2024.

Many questions remain unanswered: “We need a better understanding of the interaction of hormone systems with infectious agents — from basics to therapeutic applications,” emphasized the director of the Medical Clinic and Polyclinic III and the Center for Internal Medicine at the Carl Gustav Carus University Hospital, Dresden, Germany.

If infectious diseases could trigger diabetes and other metabolic diseases, this means that “through vaccination programs, we may be able to prevent the occurrence of common metabolic diseases such as diabetes,” said Dr. Bornstein. He highlighted that many people who experienced severe COVID-19 during the pandemic, or died from it, exhibited diabetes or a pre-metabolic syndrome.

“SARS-CoV-2 has utilized an endocrine signaling pathway to invade our cells and cause damage in the organ systems and inflammation,” said Dr. Bornstein. Conversely, it is now known that infections with coronaviruses or other infectious agents like influenza can significantly worsen metabolic status, diabetes, and other endocrine diseases.
 

SARS-CoV-2 Infects the Beta Cells

Data from the COVID-19 pandemic showed that the likelihood of developing type 1 diabetes significantly increases with a SARS-CoV-2 infection. Researchers led by Dr. Bornstein demonstrated in 2021 that SARS-CoV-2 can infect the insulin-producing cells of the organ. They examined pancreatic tissue from 20 patients who died from COVID-19 using immunofluorescence, immunohistochemistry, RNA in situ hybridization, and electron microscopy.

They found viral SARS-CoV-2 infiltration of the beta cells in all patients. In 11 patients with COVID-19, the expression of ACE2, TMPRSS, and other receptors and factors like DPP4, HMBG1, and NRP1 that can facilitate virus entry was examined. They found that even in the absence of manifest newly onset diabetes, necroptotic cell death, immune cell infiltration, and SARS-CoV-2 infection of the pancreas beta cells can contribute to varying degrees of metabolic disturbance in patients with COVID-19.

In a report published in October 2020, Tim Hollstein, MD, from the Institute for Diabetology and Clinical Metabolic Research at UKSH in Kiel, Germany, and colleagues described the case of a 19-year-old man who developed symptoms of insulin-dependent diabetes after a SARS-CoV-2 infection, without the presence of autoantibodies typical for type 1 diabetes.

The man presented to the emergency department with diabetic ketoacidosis, a C-peptide level of 0.62 µg/L, a blood glucose concentration of 30.6 mmol/L (552 mg/dL), and an A1c level of 16.8%. The patient’s history revealed a probable SARS-CoV-2 infection 5-7 weeks before admission, based on a positive antibody test against SARS-CoV-2.
 

Some Viruses Produce Insulin-Like Proteins

Recent studies have shown that some viruses can produce insulin-like proteins or hormones that interfere with the metabolism of the affected organism, reported Dr. Bornstein. In addition to metabolic regulation, these “viral hormones” also seem to influence cell turnover and cell death.

Dr. Bornstein pointed out that antiviral medications can delay the onset of type 1 diabetes by preserving the function of insulin-producing beta cells. It has also been shown that conventional medications used to treat hormonal disorders can reduce the susceptibility of the organism to infections — such as antidiabetic preparations like DPP-4 inhibitors or metformin.

In a review published in 2023, Nikolaos Perakakis, MD, professor, research group leader at the Paul Langerhans Institute Dresden, Dresden, Germany, Dr. Bornstein, and colleagues discussed scientific evidence for a close mutual dependence between various virus infections and metabolic diseases. They discussed how viruses can lead to the development or progression of metabolic diseases and vice versa and how metabolic diseases can increase the severity of a virus infection.
 

Viruses Favor Metabolic Diseases...

Viruses can favor metabolic diseases by, for example, influencing the regulation of cell survival and specific signaling pathways relevant for cell death, proliferation, or dedifferentiation in important endocrine and metabolic organs. Viruses are also capable of controlling cellular glucose metabolism by modulating glucose transporters, altering glucose uptake, regulating signaling pathways, and stimulating glycolysis in infected cells.

Due to the destruction of beta cells, enteroviruses, but also the mumps virus, parainfluenza virus, or human herpes virus 6, are associated with the development of diabetes. The timing of infection often precedes or coincides with the peak of development of islet autoantibodies. The fact that only a small proportion of patients actually develop type 1 diabetes suggests that genetic background, and likely the timing of infection, play an important role.
 

...And Metabolic Diseases Influence the Course of Infection

Infection with hepatitis C virus (HCV), on the other hand, is associated with an increased risk for type 2 diabetes, with the risk being higher for older individuals with a family history of diabetes. The negative effects of HCV on glucose balance are mainly attributed to increased insulin resistance in the liver. HCV reduces hepatic glucose uptake by downregulating the expression of glucose transporters and additionally impairs insulin signal transduction by inhibiting the PI3K/Akt signaling pathway.

People with obesity, diabetes, or insulin resistance show significant changes in the innate and adaptive functions of the immune system. Regarding the innate immune system, impaired chemotaxis and phagocytosis of neutrophils have been observed in patients with type 2 diabetes.

In the case of obesity, the number of natural killer T cells in adipose tissue decreases, whereas B cells accumulate in adipose tissue and secrete more proinflammatory cytokines. Longitudinal multiomics analyses of various biopsies from individuals with insulin resistance showed a delayed immune response to respiratory virus infections compared with individuals with normal insulin sensitivity.

This story was translated from Medscape Germany using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Stefan Bornstein, MD, PhD, professor, made it clear during a press conference at the 67th Congress of the German Society of Endocrinology (DGE) that there is more than one interaction between them. Nowadays, one can almost speak of an “endocrine virology and even of the virome as an additional, hormonally metabolically active gland,” said Dr. Bornstein, who will receive the Berthold Medal from the DGE in 2024.

Many questions remain unanswered: “We need a better understanding of the interaction of hormone systems with infectious agents — from basics to therapeutic applications,” emphasized the director of the Medical Clinic and Polyclinic III and the Center for Internal Medicine at the Carl Gustav Carus University Hospital, Dresden, Germany.

If infectious diseases could trigger diabetes and other metabolic diseases, this means that “through vaccination programs, we may be able to prevent the occurrence of common metabolic diseases such as diabetes,” said Dr. Bornstein. He highlighted that many people who experienced severe COVID-19 during the pandemic, or died from it, exhibited diabetes or a pre-metabolic syndrome.

“SARS-CoV-2 has utilized an endocrine signaling pathway to invade our cells and cause damage in the organ systems and inflammation,” said Dr. Bornstein. Conversely, it is now known that infections with coronaviruses or other infectious agents like influenza can significantly worsen metabolic status, diabetes, and other endocrine diseases.
 

SARS-CoV-2 Infects the Beta Cells

Data from the COVID-19 pandemic showed that the likelihood of developing type 1 diabetes significantly increases with a SARS-CoV-2 infection. Researchers led by Dr. Bornstein demonstrated in 2021 that SARS-CoV-2 can infect the insulin-producing cells of the organ. They examined pancreatic tissue from 20 patients who died from COVID-19 using immunofluorescence, immunohistochemistry, RNA in situ hybridization, and electron microscopy.

They found viral SARS-CoV-2 infiltration of the beta cells in all patients. In 11 patients with COVID-19, the expression of ACE2, TMPRSS, and other receptors and factors like DPP4, HMBG1, and NRP1 that can facilitate virus entry was examined. They found that even in the absence of manifest newly onset diabetes, necroptotic cell death, immune cell infiltration, and SARS-CoV-2 infection of the pancreas beta cells can contribute to varying degrees of metabolic disturbance in patients with COVID-19.

In a report published in October 2020, Tim Hollstein, MD, from the Institute for Diabetology and Clinical Metabolic Research at UKSH in Kiel, Germany, and colleagues described the case of a 19-year-old man who developed symptoms of insulin-dependent diabetes after a SARS-CoV-2 infection, without the presence of autoantibodies typical for type 1 diabetes.

The man presented to the emergency department with diabetic ketoacidosis, a C-peptide level of 0.62 µg/L, a blood glucose concentration of 30.6 mmol/L (552 mg/dL), and an A1c level of 16.8%. The patient’s history revealed a probable SARS-CoV-2 infection 5-7 weeks before admission, based on a positive antibody test against SARS-CoV-2.
 

Some Viruses Produce Insulin-Like Proteins

Recent studies have shown that some viruses can produce insulin-like proteins or hormones that interfere with the metabolism of the affected organism, reported Dr. Bornstein. In addition to metabolic regulation, these “viral hormones” also seem to influence cell turnover and cell death.

Dr. Bornstein pointed out that antiviral medications can delay the onset of type 1 diabetes by preserving the function of insulin-producing beta cells. It has also been shown that conventional medications used to treat hormonal disorders can reduce the susceptibility of the organism to infections — such as antidiabetic preparations like DPP-4 inhibitors or metformin.

In a review published in 2023, Nikolaos Perakakis, MD, professor, research group leader at the Paul Langerhans Institute Dresden, Dresden, Germany, Dr. Bornstein, and colleagues discussed scientific evidence for a close mutual dependence between various virus infections and metabolic diseases. They discussed how viruses can lead to the development or progression of metabolic diseases and vice versa and how metabolic diseases can increase the severity of a virus infection.
 

Viruses Favor Metabolic Diseases...

Viruses can favor metabolic diseases by, for example, influencing the regulation of cell survival and specific signaling pathways relevant for cell death, proliferation, or dedifferentiation in important endocrine and metabolic organs. Viruses are also capable of controlling cellular glucose metabolism by modulating glucose transporters, altering glucose uptake, regulating signaling pathways, and stimulating glycolysis in infected cells.

Due to the destruction of beta cells, enteroviruses, but also the mumps virus, parainfluenza virus, or human herpes virus 6, are associated with the development of diabetes. The timing of infection often precedes or coincides with the peak of development of islet autoantibodies. The fact that only a small proportion of patients actually develop type 1 diabetes suggests that genetic background, and likely the timing of infection, play an important role.
 

...And Metabolic Diseases Influence the Course of Infection

Infection with hepatitis C virus (HCV), on the other hand, is associated with an increased risk for type 2 diabetes, with the risk being higher for older individuals with a family history of diabetes. The negative effects of HCV on glucose balance are mainly attributed to increased insulin resistance in the liver. HCV reduces hepatic glucose uptake by downregulating the expression of glucose transporters and additionally impairs insulin signal transduction by inhibiting the PI3K/Akt signaling pathway.

People with obesity, diabetes, or insulin resistance show significant changes in the innate and adaptive functions of the immune system. Regarding the innate immune system, impaired chemotaxis and phagocytosis of neutrophils have been observed in patients with type 2 diabetes.

In the case of obesity, the number of natural killer T cells in adipose tissue decreases, whereas B cells accumulate in adipose tissue and secrete more proinflammatory cytokines. Longitudinal multiomics analyses of various biopsies from individuals with insulin resistance showed a delayed immune response to respiratory virus infections compared with individuals with normal insulin sensitivity.

This story was translated from Medscape Germany using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Stefan Bornstein, MD, PhD, professor, made it clear during a press conference at the 67th Congress of the German Society of Endocrinology (DGE) that there is more than one interaction between them. Nowadays, one can almost speak of an “endocrine virology and even of the virome as an additional, hormonally metabolically active gland,” said Dr. Bornstein, who will receive the Berthold Medal from the DGE in 2024.

Many questions remain unanswered: “We need a better understanding of the interaction of hormone systems with infectious agents — from basics to therapeutic applications,” emphasized the director of the Medical Clinic and Polyclinic III and the Center for Internal Medicine at the Carl Gustav Carus University Hospital, Dresden, Germany.

If infectious diseases could trigger diabetes and other metabolic diseases, this means that “through vaccination programs, we may be able to prevent the occurrence of common metabolic diseases such as diabetes,” said Dr. Bornstein. He highlighted that many people who experienced severe COVID-19 during the pandemic, or died from it, exhibited diabetes or a pre-metabolic syndrome.

“SARS-CoV-2 has utilized an endocrine signaling pathway to invade our cells and cause damage in the organ systems and inflammation,” said Dr. Bornstein. Conversely, it is now known that infections with coronaviruses or other infectious agents like influenza can significantly worsen metabolic status, diabetes, and other endocrine diseases.
 

SARS-CoV-2 Infects the Beta Cells

Data from the COVID-19 pandemic showed that the likelihood of developing type 1 diabetes significantly increases with a SARS-CoV-2 infection. Researchers led by Dr. Bornstein demonstrated in 2021 that SARS-CoV-2 can infect the insulin-producing cells of the organ. They examined pancreatic tissue from 20 patients who died from COVID-19 using immunofluorescence, immunohistochemistry, RNA in situ hybridization, and electron microscopy.

They found viral SARS-CoV-2 infiltration of the beta cells in all patients. In 11 patients with COVID-19, the expression of ACE2, TMPRSS, and other receptors and factors like DPP4, HMBG1, and NRP1 that can facilitate virus entry was examined. They found that even in the absence of manifest newly onset diabetes, necroptotic cell death, immune cell infiltration, and SARS-CoV-2 infection of the pancreas beta cells can contribute to varying degrees of metabolic disturbance in patients with COVID-19.

In a report published in October 2020, Tim Hollstein, MD, from the Institute for Diabetology and Clinical Metabolic Research at UKSH in Kiel, Germany, and colleagues described the case of a 19-year-old man who developed symptoms of insulin-dependent diabetes after a SARS-CoV-2 infection, without the presence of autoantibodies typical for type 1 diabetes.

The man presented to the emergency department with diabetic ketoacidosis, a C-peptide level of 0.62 µg/L, a blood glucose concentration of 30.6 mmol/L (552 mg/dL), and an A1c level of 16.8%. The patient’s history revealed a probable SARS-CoV-2 infection 5-7 weeks before admission, based on a positive antibody test against SARS-CoV-2.
 

Some Viruses Produce Insulin-Like Proteins

Recent studies have shown that some viruses can produce insulin-like proteins or hormones that interfere with the metabolism of the affected organism, reported Dr. Bornstein. In addition to metabolic regulation, these “viral hormones” also seem to influence cell turnover and cell death.

Dr. Bornstein pointed out that antiviral medications can delay the onset of type 1 diabetes by preserving the function of insulin-producing beta cells. It has also been shown that conventional medications used to treat hormonal disorders can reduce the susceptibility of the organism to infections — such as antidiabetic preparations like DPP-4 inhibitors or metformin.

In a review published in 2023, Nikolaos Perakakis, MD, professor, research group leader at the Paul Langerhans Institute Dresden, Dresden, Germany, Dr. Bornstein, and colleagues discussed scientific evidence for a close mutual dependence between various virus infections and metabolic diseases. They discussed how viruses can lead to the development or progression of metabolic diseases and vice versa and how metabolic diseases can increase the severity of a virus infection.
 

Viruses Favor Metabolic Diseases...

Viruses can favor metabolic diseases by, for example, influencing the regulation of cell survival and specific signaling pathways relevant for cell death, proliferation, or dedifferentiation in important endocrine and metabolic organs. Viruses are also capable of controlling cellular glucose metabolism by modulating glucose transporters, altering glucose uptake, regulating signaling pathways, and stimulating glycolysis in infected cells.

Due to the destruction of beta cells, enteroviruses, but also the mumps virus, parainfluenza virus, or human herpes virus 6, are associated with the development of diabetes. The timing of infection often precedes or coincides with the peak of development of islet autoantibodies. The fact that only a small proportion of patients actually develop type 1 diabetes suggests that genetic background, and likely the timing of infection, play an important role.
 

...And Metabolic Diseases Influence the Course of Infection

Infection with hepatitis C virus (HCV), on the other hand, is associated with an increased risk for type 2 diabetes, with the risk being higher for older individuals with a family history of diabetes. The negative effects of HCV on glucose balance are mainly attributed to increased insulin resistance in the liver. HCV reduces hepatic glucose uptake by downregulating the expression of glucose transporters and additionally impairs insulin signal transduction by inhibiting the PI3K/Akt signaling pathway.

People with obesity, diabetes, or insulin resistance show significant changes in the innate and adaptive functions of the immune system. Regarding the innate immune system, impaired chemotaxis and phagocytosis of neutrophils have been observed in patients with type 2 diabetes.

In the case of obesity, the number of natural killer T cells in adipose tissue decreases, whereas B cells accumulate in adipose tissue and secrete more proinflammatory cytokines. Longitudinal multiomics analyses of various biopsies from individuals with insulin resistance showed a delayed immune response to respiratory virus infections compared with individuals with normal insulin sensitivity.

This story was translated from Medscape Germany using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .

A new study from the United Kingdom provides greater clarity on how SARS-CoV-2 infection can affect cognition and memory, including novel data on how long brain fog may last after the illness resolves and which cognitive functions are most vulnerable. 

In a large community sample, researchers found that on average, people who had recovered from COVID-19 showed small cognitive deficits equivalent to a 3-point loss in IQ for up to 1 year or more after recovering from the acute illness compared with peers who never had COVID-19.

However, people who had more severe cases, requiring treatment in a hospital intensive care unit, had cognitive deficits equivalent to a 9-point drop in IQ.

“People with ongoing persistent symptoms, indicative of long COVID, had larger cognitive deficits than people whose symptoms had resolved,” first author Adam Hampshire, PhD, with Imperial College London, London, England, told this news organization. 

The largest deficits among cognitive tasks were in memory, reasoning, and executive function, he added.

“That is, people who had had COVID-19 were both slower and less accurate when performing tasks that measure those abilities,” Dr. Hampshire said. “The group with the largest cognitive deficits were patients who had been in intensive care for COVID-19.”

The study was published online in The New England Journal of Medicine. 
 

Lingering Brain Fog

Cognitive symptoms after SARS-CoV-2 infection are well recognized, but whether objectively measurable cognitive deficits exist and how long they persist remains unclear. 

To investigate, researchers invited 800,000 adults from the REACT study of SARS-CoV-2 transmission in England to complete an online assessment for cognitive function with eight domains.

Altogether, 141,583 participants started the cognitive battery by completing at least one task, and 112,964 completed all eight tasks.

The researchers estimated global cognitive scores among participants who had been previously infected with SARS-CoV-2 with symptoms that persisted for at least 12 weeks, whether or not resolved, and among uninfected participants. 

Compared with uninfected adults, those who had COVID-19 that resolved had a small cognitive deficit, corresponding to a 3-point loss in IQ, the researchers found. 

Adults with unresolved persistent COVID-19 symptoms had the equivalent of a 6-point loss in IQ, and those who had been admitted to the intensive care unit had the equivalent of a 9-point loss in IQ, in line with previous findings of cognitive deficits in patients hospitalized in a critical care unit, the researchers report. 

Larger cognitive deficits were evident in adults infected early in the pandemic by the original SARS-CoV-2 virus or the B.1.1.7 variant, whereas peers infected later in the pandemic (eg., in the Omicron period), showed smaller cognitive deficits. This finding is in line with other studies suggesting that the association between COVID-19–associated cognitive deficits attenuated as the pandemic progressed, the researchers noted. 

They also found that people who had COVID-19 after receiving two or more vaccinations showed better cognitive performance compared with those who had not been vaccinated. 

The memory, reasoning, and executive function tasks were among the most sensitive to COVID-19–related cognitive differences and performance on these tasks differed according to illness duration and hospitalization. 

Dr. Hampshire said that more research is needed to determine whether the cognitive deficits resolve with time. 

“The implications of longer-term persistence of cognitive deficits and their clinical relevance remain unclear and warrant ongoing surveillance,” he said.

 

Larger Cognitive Deficits Likely?

These results are “a concern and the broader implications require evaluation,” wrote Ziyad Al-Aly, MD, with Washington University School of Medicine in St. Louis, Missouri, and Clifford Rosen, MD, with Tufts University School of Medicine in Boston, Massachusetts, in an accompanying editorial. 

In their view, several outstanding questions remain, including what the potential functional implications of a 3-point loss in IQ may be and whether COVID-19–related cognitive deficits predispose to a higher risk for dementia later in life. 

“A deeper understanding of the biology of cognitive dysfunction after SARS-CoV-2 infection and how best to prevent and treat it are critical for addressing the needs of affected persons and preserving the cognitive health of populations,” Drs. Al-Aly and Rosen concluded. 

Commenting on the study for this news organization, Jacqueline Becker, PhD, clinical neuropsychologist and assistant professor of medicine, Icahn School of Medicine at Mount Sinai, New York City, noted that “one important caveat” is that the study used an online assessment tool for cognitive function and therefore the findings should be taken with “a grain of salt.”

“That said, this is a large sample, and the findings are generally consistent with what we’ve seen in terms of cognitive deficits post-COVID,” Dr. Becker said. 

It’s likely that this study “underestimates” the degree of cognitive deficits that would be seen on validated neuropsychological tests, she added.

In a recent study, Dr. Becker and her colleagues investigated rates of cognitive impairment in 740 COVID-19 patients who recovered and were treated in outpatient, emergency department, or inpatient hospital settings. 

Using validated neuropsychological measures, they found a relatively high frequency of cognitive impairment several months after patients contracted COVID-19. Impairments in executive functioning, processing speed, category fluency, memory encoding, and recall were predominant among hospitalized patients. 

Dr. Becker noted that in her experience, cognition typically will improve in some patients 12-18 months post COVID. 

Support for the study was provided by the National Institute for Health and Care Research and UK Research and Innovation and by the Department of Health and Social Care in England and the Huo Family Foundation. Disclosures for authors and editorial writers are available at NEJM.org. Dr. Becker has no relevant disclosures.

A version of this article appeared on Medscape.com.

A new study from the United Kingdom provides greater clarity on how SARS-CoV-2 infection can affect cognition and memory, including novel data on how long brain fog may last after the illness resolves and which cognitive functions are most vulnerable. 

In a large community sample, researchers found that on average, people who had recovered from COVID-19 showed small cognitive deficits equivalent to a 3-point loss in IQ for up to 1 year or more after recovering from the acute illness compared with peers who never had COVID-19.

However, people who had more severe cases, requiring treatment in a hospital intensive care unit, had cognitive deficits equivalent to a 9-point drop in IQ.

“People with ongoing persistent symptoms, indicative of long COVID, had larger cognitive deficits than people whose symptoms had resolved,” first author Adam Hampshire, PhD, with Imperial College London, London, England, told this news organization. 

The largest deficits among cognitive tasks were in memory, reasoning, and executive function, he added.

“That is, people who had had COVID-19 were both slower and less accurate when performing tasks that measure those abilities,” Dr. Hampshire said. “The group with the largest cognitive deficits were patients who had been in intensive care for COVID-19.”

The study was published online in The New England Journal of Medicine. 
 

Lingering Brain Fog

Cognitive symptoms after SARS-CoV-2 infection are well recognized, but whether objectively measurable cognitive deficits exist and how long they persist remains unclear. 

To investigate, researchers invited 800,000 adults from the REACT study of SARS-CoV-2 transmission in England to complete an online assessment for cognitive function with eight domains.

Altogether, 141,583 participants started the cognitive battery by completing at least one task, and 112,964 completed all eight tasks.

The researchers estimated global cognitive scores among participants who had been previously infected with SARS-CoV-2 with symptoms that persisted for at least 12 weeks, whether or not resolved, and among uninfected participants. 

Compared with uninfected adults, those who had COVID-19 that resolved had a small cognitive deficit, corresponding to a 3-point loss in IQ, the researchers found. 

Adults with unresolved persistent COVID-19 symptoms had the equivalent of a 6-point loss in IQ, and those who had been admitted to the intensive care unit had the equivalent of a 9-point loss in IQ, in line with previous findings of cognitive deficits in patients hospitalized in a critical care unit, the researchers report. 

Larger cognitive deficits were evident in adults infected early in the pandemic by the original SARS-CoV-2 virus or the B.1.1.7 variant, whereas peers infected later in the pandemic (eg., in the Omicron period), showed smaller cognitive deficits. This finding is in line with other studies suggesting that the association between COVID-19–associated cognitive deficits attenuated as the pandemic progressed, the researchers noted. 

They also found that people who had COVID-19 after receiving two or more vaccinations showed better cognitive performance compared with those who had not been vaccinated. 

The memory, reasoning, and executive function tasks were among the most sensitive to COVID-19–related cognitive differences and performance on these tasks differed according to illness duration and hospitalization. 

Dr. Hampshire said that more research is needed to determine whether the cognitive deficits resolve with time. 

“The implications of longer-term persistence of cognitive deficits and their clinical relevance remain unclear and warrant ongoing surveillance,” he said.

 

Larger Cognitive Deficits Likely?

These results are “a concern and the broader implications require evaluation,” wrote Ziyad Al-Aly, MD, with Washington University School of Medicine in St. Louis, Missouri, and Clifford Rosen, MD, with Tufts University School of Medicine in Boston, Massachusetts, in an accompanying editorial. 

In their view, several outstanding questions remain, including what the potential functional implications of a 3-point loss in IQ may be and whether COVID-19–related cognitive deficits predispose to a higher risk for dementia later in life. 

“A deeper understanding of the biology of cognitive dysfunction after SARS-CoV-2 infection and how best to prevent and treat it are critical for addressing the needs of affected persons and preserving the cognitive health of populations,” Drs. Al-Aly and Rosen concluded. 

Commenting on the study for this news organization, Jacqueline Becker, PhD, clinical neuropsychologist and assistant professor of medicine, Icahn School of Medicine at Mount Sinai, New York City, noted that “one important caveat” is that the study used an online assessment tool for cognitive function and therefore the findings should be taken with “a grain of salt.”

“That said, this is a large sample, and the findings are generally consistent with what we’ve seen in terms of cognitive deficits post-COVID,” Dr. Becker said. 

It’s likely that this study “underestimates” the degree of cognitive deficits that would be seen on validated neuropsychological tests, she added.

In a recent study, Dr. Becker and her colleagues investigated rates of cognitive impairment in 740 COVID-19 patients who recovered and were treated in outpatient, emergency department, or inpatient hospital settings. 

Using validated neuropsychological measures, they found a relatively high frequency of cognitive impairment several months after patients contracted COVID-19. Impairments in executive functioning, processing speed, category fluency, memory encoding, and recall were predominant among hospitalized patients. 

Dr. Becker noted that in her experience, cognition typically will improve in some patients 12-18 months post COVID. 

Support for the study was provided by the National Institute for Health and Care Research and UK Research and Innovation and by the Department of Health and Social Care in England and the Huo Family Foundation. Disclosures for authors and editorial writers are available at NEJM.org. Dr. Becker has no relevant disclosures.

A version of this article appeared on Medscape.com.

A new study from the United Kingdom provides greater clarity on how SARS-CoV-2 infection can affect cognition and memory, including novel data on how long brain fog may last after the illness resolves and which cognitive functions are most vulnerable. 

In a large community sample, researchers found that on average, people who had recovered from COVID-19 showed small cognitive deficits equivalent to a 3-point loss in IQ for up to 1 year or more after recovering from the acute illness compared with peers who never had COVID-19.

However, people who had more severe cases, requiring treatment in a hospital intensive care unit, had cognitive deficits equivalent to a 9-point drop in IQ.

“People with ongoing persistent symptoms, indicative of long COVID, had larger cognitive deficits than people whose symptoms had resolved,” first author Adam Hampshire, PhD, with Imperial College London, London, England, told this news organization. 

The largest deficits among cognitive tasks were in memory, reasoning, and executive function, he added.

“That is, people who had had COVID-19 were both slower and less accurate when performing tasks that measure those abilities,” Dr. Hampshire said. “The group with the largest cognitive deficits were patients who had been in intensive care for COVID-19.”

The study was published online in The New England Journal of Medicine. 
 

Lingering Brain Fog

Cognitive symptoms after SARS-CoV-2 infection are well recognized, but whether objectively measurable cognitive deficits exist and how long they persist remains unclear. 

To investigate, researchers invited 800,000 adults from the REACT study of SARS-CoV-2 transmission in England to complete an online assessment for cognitive function with eight domains.

Altogether, 141,583 participants started the cognitive battery by completing at least one task, and 112,964 completed all eight tasks.

The researchers estimated global cognitive scores among participants who had been previously infected with SARS-CoV-2 with symptoms that persisted for at least 12 weeks, whether or not resolved, and among uninfected participants. 

Compared with uninfected adults, those who had COVID-19 that resolved had a small cognitive deficit, corresponding to a 3-point loss in IQ, the researchers found. 

Adults with unresolved persistent COVID-19 symptoms had the equivalent of a 6-point loss in IQ, and those who had been admitted to the intensive care unit had the equivalent of a 9-point loss in IQ, in line with previous findings of cognitive deficits in patients hospitalized in a critical care unit, the researchers report. 

Larger cognitive deficits were evident in adults infected early in the pandemic by the original SARS-CoV-2 virus or the B.1.1.7 variant, whereas peers infected later in the pandemic (eg., in the Omicron period), showed smaller cognitive deficits. This finding is in line with other studies suggesting that the association between COVID-19–associated cognitive deficits attenuated as the pandemic progressed, the researchers noted. 

They also found that people who had COVID-19 after receiving two or more vaccinations showed better cognitive performance compared with those who had not been vaccinated. 

The memory, reasoning, and executive function tasks were among the most sensitive to COVID-19–related cognitive differences and performance on these tasks differed according to illness duration and hospitalization. 

Dr. Hampshire said that more research is needed to determine whether the cognitive deficits resolve with time. 

“The implications of longer-term persistence of cognitive deficits and their clinical relevance remain unclear and warrant ongoing surveillance,” he said.

 

Larger Cognitive Deficits Likely?

These results are “a concern and the broader implications require evaluation,” wrote Ziyad Al-Aly, MD, with Washington University School of Medicine in St. Louis, Missouri, and Clifford Rosen, MD, with Tufts University School of Medicine in Boston, Massachusetts, in an accompanying editorial. 

In their view, several outstanding questions remain, including what the potential functional implications of a 3-point loss in IQ may be and whether COVID-19–related cognitive deficits predispose to a higher risk for dementia later in life. 

“A deeper understanding of the biology of cognitive dysfunction after SARS-CoV-2 infection and how best to prevent and treat it are critical for addressing the needs of affected persons and preserving the cognitive health of populations,” Drs. Al-Aly and Rosen concluded. 

Commenting on the study for this news organization, Jacqueline Becker, PhD, clinical neuropsychologist and assistant professor of medicine, Icahn School of Medicine at Mount Sinai, New York City, noted that “one important caveat” is that the study used an online assessment tool for cognitive function and therefore the findings should be taken with “a grain of salt.”

“That said, this is a large sample, and the findings are generally consistent with what we’ve seen in terms of cognitive deficits post-COVID,” Dr. Becker said. 

It’s likely that this study “underestimates” the degree of cognitive deficits that would be seen on validated neuropsychological tests, she added.

In a recent study, Dr. Becker and her colleagues investigated rates of cognitive impairment in 740 COVID-19 patients who recovered and were treated in outpatient, emergency department, or inpatient hospital settings. 

Using validated neuropsychological measures, they found a relatively high frequency of cognitive impairment several months after patients contracted COVID-19. Impairments in executive functioning, processing speed, category fluency, memory encoding, and recall were predominant among hospitalized patients. 

Dr. Becker noted that in her experience, cognition typically will improve in some patients 12-18 months post COVID. 

Support for the study was provided by the National Institute for Health and Care Research and UK Research and Innovation and by the Department of Health and Social Care in England and the Huo Family Foundation. Disclosures for authors and editorial writers are available at NEJM.org. Dr. Becker has no relevant disclosures.

A version of this article appeared on Medscape.com.

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.