COVID-19

The passage of time felt altered for many people during the COVID-19 pandemic, ranging from difficulty keeping track of the days of the week to feeling that the hours either crawled by or sped up, new research suggests.

Results showed the sense of present focus, blurring weekdays and weekends together, and uncertainly about the future were reported by over 65% of the 5,661 survey respondents. And more than half reported the experience of feeling “time speeding up or slowing down,” report the investigators, led by E. Alison Holman, PhD, professor at the University of California, Irvine.

Significant predictors of these time distortions included being exposed to daily pandemic-related media and having a mental health diagnosis prior to the pandemic; secondary stress such as school closures and lockdown; financial stress; lifetime stress; and lifetime trauma exposure.

“Continuity between past experiences, present life, and future hopes is critical to one’s well-being, and disruption of that synergy presents mental health challenges,” Dr. Holman said in a news release.

“We were able to measure this in a nationally representative sample of Americans as they were experiencing a protracted collective trauma, which has never been done before, and this study is the first to document the prevalence and early predictors of these time distortions,” added Dr. Holman.

The findings were published online in Psychological Trauma: Theory, Research, Practice, and Policy.
 

Unique opportunity

During the pandemic, many people’s time perspective (TP), defined as “our view of time as it spans from our past into the future,” shifted as they “focused on the immediate, present danger of the COVID-19 pandemic and future plans became uncertain,” the investigators wrote.

Studies of convenience samples “suggested that many people experienced time slowing down, stopping, and/or speeding up as they coped with the challenges of the pandemic” – a phenomenon known as temporal disintegration (TD) in psychiatric literature.

Dr. Holman said in an interview that she researched TD after the Sept.11, 2001 World Trade Center attacks.

“We found that people who experienced that early sense of TD, the sense of ‘time falling apart,’ were more prone to getting stuck in the past and staying focused on the past event,” which led to feeling “more distress over time,” she said.

Research examining the prevalence of and psychosocial factors predicting TD are “quite rare” and studies examining TD “during an unfolding, protracted collective trauma are even rarer,” the researchers note. The COVID pandemic “presented a unique opportunity to conduct such a study,” the researchers wrote.

For their study, the investigators surveyed participants in the NORC AmeriSpeak online panel, a “probability-based panel” of 35,000 U.S. households selected at random from across the country.

The study was conducted in two waves: the first survey was administered March–April 2020, the second in September–October 2020.
 

Speeding up, slowing down

At wave 2, participants completed a 7-item index of TD symptoms experienced over the previous 6 months. To adjust for psychological processes that may have predisposed individuals to experience TD during the pandemic, the researchers included a Wave 1 measure of future uncertainty as a covariate.

Prepandemic health data had been collected prior to the current study.

Wave 1 participants completed a checklist reporting personal, work, and community-wide exposure to the COVID outbreak, including contracting the virus, sheltering in place, and experiencing secondary stressors. The extent and type of pandemic-related media exposure were also assessed.

At wave 2, they reported the extent of exposure to the coronavirus, financial exposures, and secondary stressors. They also completed a non–COVID-related stress/trauma exposure checklist and were asked to indicate whether the trauma, disaster, or bereavement took place prior to or during the pandemic.

The final sample consisted of 5,661 adults (52% female) who completed the wave 2 survey. Participants were divided into four age groups: 18-34, 35-49, 50-64, and 65 and older.

The most common experiences (reported by more than 65% of respondents) included being focused on the present moment, feeling that weekdays and weekends were the same, and feeling uncertain about the future.

Over half of respondents (50.4%) reported feeling as though time was speeding up, and 55.2% reported feeling as though time was slowing down. Some also reported feeling uncertain about the time of day (46.4%) and forgetting events they had just experienced (35.2%).

When the researchers controlled for feeling uncertain about the future, they found that women reported more TD than men (b = 0.11; 95% confidence interval, 0.07-0.14; P < .001).

At wave 1, associations were found between TD and COVID-related media exposure, prepandemic mental health diagnoses, and prepandemic non–COVID-related stress and trauma. At wave 2, associations were found between TD and COVID-related secondary and financial stressors (P < .001 for all).

In contrast, COVID-related work exposure at wave 1, being 45-59 years old, and living in the Midwest region were negatively associated with TD.

“The sense of the flow of the past into the present, and the present into the future is important for our mental health,” Dr. Holman said. “We need to remember who we have been, how that shaped who we are today, and where we want to go with our lives.”

Staying in the present moment is “good, when you’re doing it mindfully. But you still need to feel you can shape and work toward the future and have some sense of control,” she added.

Dr. Homan also recommended time-perspective therapy, which helps patients with PTSD to “build continuity across time – to understand and learn from the past, live in the present, and move toward the future.”
 

Widespread distortion

In an interview, Ruth Ogden, PhD, a lecturer at Liverpool (England) John Moores University, said the findings “confirm those reported in Europe, South America, and the Middle East, that widespread distortion to time was common during the pandemic and that distortions to time were greatest amongst those most negatively affected by the pandemic.”

The results also support her own recent research in the United Kingdom “suggesting that distortions to time during the pandemic extend to our memory for the length of the pandemic, with most people believing that lockdowns lasted far longer than they actually did,” said Dr. Ogden, who was not involved with Dr. Holman and colleagues’ current study.

“This type of subjective lengthening of the pandemic may reinforce trauma by making the traumatic period seem longer, further damaging health and well-being,” she noted. “As the negative fallouts of the pandemic continue, it is important to establish the long-term effects of time distortions during the pandemic on mental health and well-being.”

The study was funded by U.S. National Science Foundation and the National Institute on Minority Health and Health Disparities. The investigators reported no relevant financial relationships. Dr. Ogden receives funding from the Wellcome Trust.

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

The passage of time felt altered for many people during the COVID-19 pandemic, ranging from difficulty keeping track of the days of the week to feeling that the hours either crawled by or sped up, new research suggests.

Results showed the sense of present focus, blurring weekdays and weekends together, and uncertainly about the future were reported by over 65% of the 5,661 survey respondents. And more than half reported the experience of feeling “time speeding up or slowing down,” report the investigators, led by E. Alison Holman, PhD, professor at the University of California, Irvine.

Significant predictors of these time distortions included being exposed to daily pandemic-related media and having a mental health diagnosis prior to the pandemic; secondary stress such as school closures and lockdown; financial stress; lifetime stress; and lifetime trauma exposure.

“Continuity between past experiences, present life, and future hopes is critical to one’s well-being, and disruption of that synergy presents mental health challenges,” Dr. Holman said in a news release.

“We were able to measure this in a nationally representative sample of Americans as they were experiencing a protracted collective trauma, which has never been done before, and this study is the first to document the prevalence and early predictors of these time distortions,” added Dr. Holman.

The findings were published online in Psychological Trauma: Theory, Research, Practice, and Policy.
 

Unique opportunity

During the pandemic, many people’s time perspective (TP), defined as “our view of time as it spans from our past into the future,” shifted as they “focused on the immediate, present danger of the COVID-19 pandemic and future plans became uncertain,” the investigators wrote.

Studies of convenience samples “suggested that many people experienced time slowing down, stopping, and/or speeding up as they coped with the challenges of the pandemic” – a phenomenon known as temporal disintegration (TD) in psychiatric literature.

Dr. Holman said in an interview that she researched TD after the Sept.11, 2001 World Trade Center attacks.

“We found that people who experienced that early sense of TD, the sense of ‘time falling apart,’ were more prone to getting stuck in the past and staying focused on the past event,” which led to feeling “more distress over time,” she said.

Research examining the prevalence of and psychosocial factors predicting TD are “quite rare” and studies examining TD “during an unfolding, protracted collective trauma are even rarer,” the researchers note. The COVID pandemic “presented a unique opportunity to conduct such a study,” the researchers wrote.

For their study, the investigators surveyed participants in the NORC AmeriSpeak online panel, a “probability-based panel” of 35,000 U.S. households selected at random from across the country.

The study was conducted in two waves: the first survey was administered March–April 2020, the second in September–October 2020.
 

Speeding up, slowing down

At wave 2, participants completed a 7-item index of TD symptoms experienced over the previous 6 months. To adjust for psychological processes that may have predisposed individuals to experience TD during the pandemic, the researchers included a Wave 1 measure of future uncertainty as a covariate.

Prepandemic health data had been collected prior to the current study.

Wave 1 participants completed a checklist reporting personal, work, and community-wide exposure to the COVID outbreak, including contracting the virus, sheltering in place, and experiencing secondary stressors. The extent and type of pandemic-related media exposure were also assessed.

At wave 2, they reported the extent of exposure to the coronavirus, financial exposures, and secondary stressors. They also completed a non–COVID-related stress/trauma exposure checklist and were asked to indicate whether the trauma, disaster, or bereavement took place prior to or during the pandemic.

The final sample consisted of 5,661 adults (52% female) who completed the wave 2 survey. Participants were divided into four age groups: 18-34, 35-49, 50-64, and 65 and older.

The most common experiences (reported by more than 65% of respondents) included being focused on the present moment, feeling that weekdays and weekends were the same, and feeling uncertain about the future.

Over half of respondents (50.4%) reported feeling as though time was speeding up, and 55.2% reported feeling as though time was slowing down. Some also reported feeling uncertain about the time of day (46.4%) and forgetting events they had just experienced (35.2%).

When the researchers controlled for feeling uncertain about the future, they found that women reported more TD than men (b = 0.11; 95% confidence interval, 0.07-0.14; P < .001).

At wave 1, associations were found between TD and COVID-related media exposure, prepandemic mental health diagnoses, and prepandemic non–COVID-related stress and trauma. At wave 2, associations were found between TD and COVID-related secondary and financial stressors (P < .001 for all).

In contrast, COVID-related work exposure at wave 1, being 45-59 years old, and living in the Midwest region were negatively associated with TD.

“The sense of the flow of the past into the present, and the present into the future is important for our mental health,” Dr. Holman said. “We need to remember who we have been, how that shaped who we are today, and where we want to go with our lives.”

Staying in the present moment is “good, when you’re doing it mindfully. But you still need to feel you can shape and work toward the future and have some sense of control,” she added.

Dr. Homan also recommended time-perspective therapy, which helps patients with PTSD to “build continuity across time – to understand and learn from the past, live in the present, and move toward the future.”
 

Widespread distortion

In an interview, Ruth Ogden, PhD, a lecturer at Liverpool (England) John Moores University, said the findings “confirm those reported in Europe, South America, and the Middle East, that widespread distortion to time was common during the pandemic and that distortions to time were greatest amongst those most negatively affected by the pandemic.”

The results also support her own recent research in the United Kingdom “suggesting that distortions to time during the pandemic extend to our memory for the length of the pandemic, with most people believing that lockdowns lasted far longer than they actually did,” said Dr. Ogden, who was not involved with Dr. Holman and colleagues’ current study.

“This type of subjective lengthening of the pandemic may reinforce trauma by making the traumatic period seem longer, further damaging health and well-being,” she noted. “As the negative fallouts of the pandemic continue, it is important to establish the long-term effects of time distortions during the pandemic on mental health and well-being.”

The study was funded by U.S. National Science Foundation and the National Institute on Minority Health and Health Disparities. The investigators reported no relevant financial relationships. Dr. Ogden receives funding from the Wellcome Trust.

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

The passage of time felt altered for many people during the COVID-19 pandemic, ranging from difficulty keeping track of the days of the week to feeling that the hours either crawled by or sped up, new research suggests.

Results showed the sense of present focus, blurring weekdays and weekends together, and uncertainly about the future were reported by over 65% of the 5,661 survey respondents. And more than half reported the experience of feeling “time speeding up or slowing down,” report the investigators, led by E. Alison Holman, PhD, professor at the University of California, Irvine.

Significant predictors of these time distortions included being exposed to daily pandemic-related media and having a mental health diagnosis prior to the pandemic; secondary stress such as school closures and lockdown; financial stress; lifetime stress; and lifetime trauma exposure.

“Continuity between past experiences, present life, and future hopes is critical to one’s well-being, and disruption of that synergy presents mental health challenges,” Dr. Holman said in a news release.

“We were able to measure this in a nationally representative sample of Americans as they were experiencing a protracted collective trauma, which has never been done before, and this study is the first to document the prevalence and early predictors of these time distortions,” added Dr. Holman.

The findings were published online in Psychological Trauma: Theory, Research, Practice, and Policy.
 

Unique opportunity

During the pandemic, many people’s time perspective (TP), defined as “our view of time as it spans from our past into the future,” shifted as they “focused on the immediate, present danger of the COVID-19 pandemic and future plans became uncertain,” the investigators wrote.

Studies of convenience samples “suggested that many people experienced time slowing down, stopping, and/or speeding up as they coped with the challenges of the pandemic” – a phenomenon known as temporal disintegration (TD) in psychiatric literature.

Dr. Holman said in an interview that she researched TD after the Sept.11, 2001 World Trade Center attacks.

“We found that people who experienced that early sense of TD, the sense of ‘time falling apart,’ were more prone to getting stuck in the past and staying focused on the past event,” which led to feeling “more distress over time,” she said.

Research examining the prevalence of and psychosocial factors predicting TD are “quite rare” and studies examining TD “during an unfolding, protracted collective trauma are even rarer,” the researchers note. The COVID pandemic “presented a unique opportunity to conduct such a study,” the researchers wrote.

For their study, the investigators surveyed participants in the NORC AmeriSpeak online panel, a “probability-based panel” of 35,000 U.S. households selected at random from across the country.

The study was conducted in two waves: the first survey was administered March–April 2020, the second in September–October 2020.
 

Speeding up, slowing down

At wave 2, participants completed a 7-item index of TD symptoms experienced over the previous 6 months. To adjust for psychological processes that may have predisposed individuals to experience TD during the pandemic, the researchers included a Wave 1 measure of future uncertainty as a covariate.

Prepandemic health data had been collected prior to the current study.

Wave 1 participants completed a checklist reporting personal, work, and community-wide exposure to the COVID outbreak, including contracting the virus, sheltering in place, and experiencing secondary stressors. The extent and type of pandemic-related media exposure were also assessed.

At wave 2, they reported the extent of exposure to the coronavirus, financial exposures, and secondary stressors. They also completed a non–COVID-related stress/trauma exposure checklist and were asked to indicate whether the trauma, disaster, or bereavement took place prior to or during the pandemic.

The final sample consisted of 5,661 adults (52% female) who completed the wave 2 survey. Participants were divided into four age groups: 18-34, 35-49, 50-64, and 65 and older.

The most common experiences (reported by more than 65% of respondents) included being focused on the present moment, feeling that weekdays and weekends were the same, and feeling uncertain about the future.

Over half of respondents (50.4%) reported feeling as though time was speeding up, and 55.2% reported feeling as though time was slowing down. Some also reported feeling uncertain about the time of day (46.4%) and forgetting events they had just experienced (35.2%).

When the researchers controlled for feeling uncertain about the future, they found that women reported more TD than men (b = 0.11; 95% confidence interval, 0.07-0.14; P < .001).

At wave 1, associations were found between TD and COVID-related media exposure, prepandemic mental health diagnoses, and prepandemic non–COVID-related stress and trauma. At wave 2, associations were found between TD and COVID-related secondary and financial stressors (P < .001 for all).

In contrast, COVID-related work exposure at wave 1, being 45-59 years old, and living in the Midwest region were negatively associated with TD.

“The sense of the flow of the past into the present, and the present into the future is important for our mental health,” Dr. Holman said. “We need to remember who we have been, how that shaped who we are today, and where we want to go with our lives.”

Staying in the present moment is “good, when you’re doing it mindfully. But you still need to feel you can shape and work toward the future and have some sense of control,” she added.

Dr. Homan also recommended time-perspective therapy, which helps patients with PTSD to “build continuity across time – to understand and learn from the past, live in the present, and move toward the future.”
 

Widespread distortion

In an interview, Ruth Ogden, PhD, a lecturer at Liverpool (England) John Moores University, said the findings “confirm those reported in Europe, South America, and the Middle East, that widespread distortion to time was common during the pandemic and that distortions to time were greatest amongst those most negatively affected by the pandemic.”

The results also support her own recent research in the United Kingdom “suggesting that distortions to time during the pandemic extend to our memory for the length of the pandemic, with most people believing that lockdowns lasted far longer than they actually did,” said Dr. Ogden, who was not involved with Dr. Holman and colleagues’ current study.

“This type of subjective lengthening of the pandemic may reinforce trauma by making the traumatic period seem longer, further damaging health and well-being,” she noted. “As the negative fallouts of the pandemic continue, it is important to establish the long-term effects of time distortions during the pandemic on mental health and well-being.”

The study was funded by U.S. National Science Foundation and the National Institute on Minority Health and Health Disparities. The investigators reported no relevant financial relationships. Dr. Ogden receives funding from the Wellcome Trust.

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

Patients with COVID-19 who experience gastrointestinal symptoms have overall worse in-hospital complications but less cardiomyopathy and mortality, according to a new study.

About 20% of COVID-19 patients experience gastrointestinal symptoms, such as abdominal pain, diarrhea, nausea, and vomiting, which clinicians should consider when treating their hospitalized patients, wrote researchers led by Nikita Patil, MD, a hospitalist at Nash General Hospital–UNC Nash Healthcare in Rocky Mount, N.C., in Gastro Hep Advances.

“It’s important to know that certain complications are higher in people with GI symptoms,” she said in an interview. “Even without an increased risk of death, there are many problems that affect quality of life and lead to people not being able to do the things they were able to do before.”

Dr. Patil and colleagues analyzed the association of GI symptoms with adverse outcomes in 100,902 patients from the Cerner Real-World Data COVID-19 Database, which included hospital encounters and ED visits for COVID-19 between December 2019 to November 2020; the data were taken from EMRs at centers with which Cerner has a data use agreement. They also looked at factors associated with poor outcomes such as acute respiratory distress syndrome, sepsis, and ventilator requirement or oxygen dependence.

The average age of the patients was 52, and a higher proportion of patients with GI symptoms were 50 and older. Of those with GI symptoms, 54.5% were women. Overall, patients with GI symptoms were more likely to have higher Charlson Comorbidity Index scores and have comorbidities such as acute liver failure, gastroesophageal reflux disease, GI malignancy, and inflammatory bowel disease.

The research team found that COVID-19 patients with GI symptoms were more likely to have acute respiratory distress syndrome (odds ratio, 1.20; 95% confidence interval, 1.11-1.29), sepsis (OR, 1.19; 95% CI, 1.14-1.24), acute kidney injury (OR, 1.30; 95% CI, 1.24-1.36), venous thromboembolism (OR, 1.36; 95% CI, 1.22-1.52), and GI bleeding (OR 1.62; 95% CI, 1.47-1.79), as compared with COVID-19 patients without GI symptoms (P < .0001 for all comparisons). At the same time, those with GI symptoms were less likely to experience cardiomyopathy (OR, 0.87; 95% CI, 0.77-0.99; P = .027), respiratory failure (OR, 0.92; 95% CI, 0.88-0.95; P < .0001), or death (OR, 0.71; 95% CI, 0.67-0.75; P < .0001).

GI bleed was the most common GI complication, found among 2% of all patients, and was more likely in patients with GI symptoms than in those without (3.5% vs. 1.6%). Intestinal ischemia, pancreatitis, acute liver injury, and intestinal pseudo-obstruction weren’t associated with GI symptoms.

Among the 19,915 patients with GI symptoms, older age, higher Charlson Comorbidity Index scores, use of proton pump inhibitors, and use of H₂ receptor antagonists were associated with higher mortality, acute respiratory distress syndrome, sepsis, and ventilator or oxygen requirement. Men with GI symptoms also had a higher risk of mortality, acute respiratory distress syndrome, and sepsis.

In particular, proton pump inhibitor use was associated with more than twice the risk of acute respiratory distress syndrome (OR, 2.19; 95% CI, 1.32-1.66; P < .0001). Similarly, H₂ receptor antagonist use was associated with higher likelihood of death (OR, 1.78; 95% CI, 1.57-2.02), as well as more than three times the risk of acute respiratory distress syndrome (OR, 3.75; 95% CI, 3.29-4.28), more than twice the risk of sepsis (OR, 2.50; 95% CI, 2.28-2.73), and nearly twice the risk of ventilator or oxygen dependence (OR, 1.97; 95% CI, 1.68-2.30) (P < .0001 for all).

The findings could guide risk stratification, prognosis, and treatment decisions in COVID-19 patients with GI symptoms, as well as inform future research focused on risk mitigation and improvement of COVID-19 outcomes, Dr. Patil said.

“The protocols for COVID-19 treatment have changed over the past 2 years with blood thinners and steroids,” she said. “Although we likely can’t avoid anti-reflux medicines entirely, it’s something we need to be cognizant of and look out for in our hospitalized patients.”

One study limitation was its inclusion of only inpatient or ED encounters and, therefore, omission of those treated at home; this confers bias toward those with more aggressive disease, according to the authors.

The authors reported no grant support or funding sources for this study. One author declared grant support and consultant fees from several companies, including some medical and pharmaceutical companies, which were unrelated to this research. Dr. Patil reported no disclosures.

This article was updated Aug. 26, 2022.

Patients with COVID-19 who experience gastrointestinal symptoms have overall worse in-hospital complications but less cardiomyopathy and mortality, according to a new study.

About 20% of COVID-19 patients experience gastrointestinal symptoms, such as abdominal pain, diarrhea, nausea, and vomiting, which clinicians should consider when treating their hospitalized patients, wrote researchers led by Nikita Patil, MD, a hospitalist at Nash General Hospital–UNC Nash Healthcare in Rocky Mount, N.C., in Gastro Hep Advances.

“It’s important to know that certain complications are higher in people with GI symptoms,” she said in an interview. “Even without an increased risk of death, there are many problems that affect quality of life and lead to people not being able to do the things they were able to do before.”

Dr. Patil and colleagues analyzed the association of GI symptoms with adverse outcomes in 100,902 patients from the Cerner Real-World Data COVID-19 Database, which included hospital encounters and ED visits for COVID-19 between December 2019 to November 2020; the data were taken from EMRs at centers with which Cerner has a data use agreement. They also looked at factors associated with poor outcomes such as acute respiratory distress syndrome, sepsis, and ventilator requirement or oxygen dependence.

The average age of the patients was 52, and a higher proportion of patients with GI symptoms were 50 and older. Of those with GI symptoms, 54.5% were women. Overall, patients with GI symptoms were more likely to have higher Charlson Comorbidity Index scores and have comorbidities such as acute liver failure, gastroesophageal reflux disease, GI malignancy, and inflammatory bowel disease.

The research team found that COVID-19 patients with GI symptoms were more likely to have acute respiratory distress syndrome (odds ratio, 1.20; 95% confidence interval, 1.11-1.29), sepsis (OR, 1.19; 95% CI, 1.14-1.24), acute kidney injury (OR, 1.30; 95% CI, 1.24-1.36), venous thromboembolism (OR, 1.36; 95% CI, 1.22-1.52), and GI bleeding (OR 1.62; 95% CI, 1.47-1.79), as compared with COVID-19 patients without GI symptoms (P < .0001 for all comparisons). At the same time, those with GI symptoms were less likely to experience cardiomyopathy (OR, 0.87; 95% CI, 0.77-0.99; P = .027), respiratory failure (OR, 0.92; 95% CI, 0.88-0.95; P < .0001), or death (OR, 0.71; 95% CI, 0.67-0.75; P < .0001).

GI bleed was the most common GI complication, found among 2% of all patients, and was more likely in patients with GI symptoms than in those without (3.5% vs. 1.6%). Intestinal ischemia, pancreatitis, acute liver injury, and intestinal pseudo-obstruction weren’t associated with GI symptoms.

Among the 19,915 patients with GI symptoms, older age, higher Charlson Comorbidity Index scores, use of proton pump inhibitors, and use of H₂ receptor antagonists were associated with higher mortality, acute respiratory distress syndrome, sepsis, and ventilator or oxygen requirement. Men with GI symptoms also had a higher risk of mortality, acute respiratory distress syndrome, and sepsis.

In particular, proton pump inhibitor use was associated with more than twice the risk of acute respiratory distress syndrome (OR, 2.19; 95% CI, 1.32-1.66; P < .0001). Similarly, H₂ receptor antagonist use was associated with higher likelihood of death (OR, 1.78; 95% CI, 1.57-2.02), as well as more than three times the risk of acute respiratory distress syndrome (OR, 3.75; 95% CI, 3.29-4.28), more than twice the risk of sepsis (OR, 2.50; 95% CI, 2.28-2.73), and nearly twice the risk of ventilator or oxygen dependence (OR, 1.97; 95% CI, 1.68-2.30) (P < .0001 for all).

The findings could guide risk stratification, prognosis, and treatment decisions in COVID-19 patients with GI symptoms, as well as inform future research focused on risk mitigation and improvement of COVID-19 outcomes, Dr. Patil said.

“The protocols for COVID-19 treatment have changed over the past 2 years with blood thinners and steroids,” she said. “Although we likely can’t avoid anti-reflux medicines entirely, it’s something we need to be cognizant of and look out for in our hospitalized patients.”

One study limitation was its inclusion of only inpatient or ED encounters and, therefore, omission of those treated at home; this confers bias toward those with more aggressive disease, according to the authors.

The authors reported no grant support or funding sources for this study. One author declared grant support and consultant fees from several companies, including some medical and pharmaceutical companies, which were unrelated to this research. Dr. Patil reported no disclosures.

This article was updated Aug. 26, 2022.

Patients with COVID-19 who experience gastrointestinal symptoms have overall worse in-hospital complications but less cardiomyopathy and mortality, according to a new study.

About 20% of COVID-19 patients experience gastrointestinal symptoms, such as abdominal pain, diarrhea, nausea, and vomiting, which clinicians should consider when treating their hospitalized patients, wrote researchers led by Nikita Patil, MD, a hospitalist at Nash General Hospital–UNC Nash Healthcare in Rocky Mount, N.C., in Gastro Hep Advances.

“It’s important to know that certain complications are higher in people with GI symptoms,” she said in an interview. “Even without an increased risk of death, there are many problems that affect quality of life and lead to people not being able to do the things they were able to do before.”

Dr. Patil and colleagues analyzed the association of GI symptoms with adverse outcomes in 100,902 patients from the Cerner Real-World Data COVID-19 Database, which included hospital encounters and ED visits for COVID-19 between December 2019 to November 2020; the data were taken from EMRs at centers with which Cerner has a data use agreement. They also looked at factors associated with poor outcomes such as acute respiratory distress syndrome, sepsis, and ventilator requirement or oxygen dependence.

The average age of the patients was 52, and a higher proportion of patients with GI symptoms were 50 and older. Of those with GI symptoms, 54.5% were women. Overall, patients with GI symptoms were more likely to have higher Charlson Comorbidity Index scores and have comorbidities such as acute liver failure, gastroesophageal reflux disease, GI malignancy, and inflammatory bowel disease.

The research team found that COVID-19 patients with GI symptoms were more likely to have acute respiratory distress syndrome (odds ratio, 1.20; 95% confidence interval, 1.11-1.29), sepsis (OR, 1.19; 95% CI, 1.14-1.24), acute kidney injury (OR, 1.30; 95% CI, 1.24-1.36), venous thromboembolism (OR, 1.36; 95% CI, 1.22-1.52), and GI bleeding (OR 1.62; 95% CI, 1.47-1.79), as compared with COVID-19 patients without GI symptoms (P < .0001 for all comparisons). At the same time, those with GI symptoms were less likely to experience cardiomyopathy (OR, 0.87; 95% CI, 0.77-0.99; P = .027), respiratory failure (OR, 0.92; 95% CI, 0.88-0.95; P < .0001), or death (OR, 0.71; 95% CI, 0.67-0.75; P < .0001).

GI bleed was the most common GI complication, found among 2% of all patients, and was more likely in patients with GI symptoms than in those without (3.5% vs. 1.6%). Intestinal ischemia, pancreatitis, acute liver injury, and intestinal pseudo-obstruction weren’t associated with GI symptoms.

Among the 19,915 patients with GI symptoms, older age, higher Charlson Comorbidity Index scores, use of proton pump inhibitors, and use of H₂ receptor antagonists were associated with higher mortality, acute respiratory distress syndrome, sepsis, and ventilator or oxygen requirement. Men with GI symptoms also had a higher risk of mortality, acute respiratory distress syndrome, and sepsis.

In particular, proton pump inhibitor use was associated with more than twice the risk of acute respiratory distress syndrome (OR, 2.19; 95% CI, 1.32-1.66; P < .0001). Similarly, H₂ receptor antagonist use was associated with higher likelihood of death (OR, 1.78; 95% CI, 1.57-2.02), as well as more than three times the risk of acute respiratory distress syndrome (OR, 3.75; 95% CI, 3.29-4.28), more than twice the risk of sepsis (OR, 2.50; 95% CI, 2.28-2.73), and nearly twice the risk of ventilator or oxygen dependence (OR, 1.97; 95% CI, 1.68-2.30) (P < .0001 for all).

The findings could guide risk stratification, prognosis, and treatment decisions in COVID-19 patients with GI symptoms, as well as inform future research focused on risk mitigation and improvement of COVID-19 outcomes, Dr. Patil said.

“The protocols for COVID-19 treatment have changed over the past 2 years with blood thinners and steroids,” she said. “Although we likely can’t avoid anti-reflux medicines entirely, it’s something we need to be cognizant of and look out for in our hospitalized patients.”

One study limitation was its inclusion of only inpatient or ED encounters and, therefore, omission of those treated at home; this confers bias toward those with more aggressive disease, according to the authors.

The authors reported no grant support or funding sources for this study. One author declared grant support and consultant fees from several companies, including some medical and pharmaceutical companies, which were unrelated to this research. Dr. Patil reported no disclosures.

This article was updated Aug. 26, 2022.

The Association for the Advancement of Blood and Biotherapies has released clinical practice guidelines for using COVID-19 convalescent plasma (CCP) in hospital and outpatient settings.

In summarizing the practice statement, the authors write, “CCP is most effective when transfused with high neutralizing titers early after symptom onset.”

The five guidelines, were published in Annals of Internal Medicine. The guidelines and strength of recommendations are:

• Nonhospitalized patients at high risk for disease progression should have CCP transfusion in addition to usual standard of care. (weak)
• CCP transfusion should not be done for unselected hospitalized patients with moderate or severe disease. This does not apply to immunosuppressed patients or those who lack antibodies against SARS-CoV-2. (strong)
• CCP transfusion is suggested in addition to the usual standard of care for hospitalized patients with COVID-19 who do not have SARS-CoV-2 antibodies at admission. (weak)
• Prophylactic CCP transfusion is not recommended for uninfected people with close contact exposure to someone with COVID-19. (weak)
• The AABB suggests CCP transfusion along with standard of care for hospitalized patients with COVID-19 and preexisting immunosuppression. (weak)

Multiple guidelines for use of CCP are similar

In an accompanying editorial, Jason V. Baker, MD, MS, and H. Clifford Lane, MD, who are part of the National Institutes of Health Treatment Guidelines Panel, say guidelines from that organization around CCP generally align with those of the AABB and the Infectious Diseases Society of America.

They all note CCP’s potential for helping immunocompromised patients and they recommend against CCP in unselected, hospitalized patients.

The main difference is that the AABB also “suggests” using CCP in combination with other standard treatments for outpatients at high risk for disease progression, regardless of their immune status, write Dr. Baker, who is with Hennepin Healthcare and the department of medicine at the University of Minnesota in Minneapolis, and Dr. Lane, who is with the National Institutes of Health.

The precise circumstance for recommending CCP remains unclear, Dr. Baker and Dr. Lane write. That’s because most available evidence has come in the absence of vaccines and antiviral agents, including nirmatrelvir–ritonavir (Paxlovid), they explain.

“At this point in the pandemic, it seems that the patient most likely to benefit from passive antibody therapy is the immunocompromised host with COVID-19 who cannot mount their own antibody response to vaccine or prior infection,” they write.

“In that setting, and in the absence of other antiviral treatments or progression despite receipt of standard treatments, high-titer CCP from a recently recovered donor is a reasonable approach,” they conclude.

Eileen Barrett, MD, MPH, an assistant professor in the division of hospital medicine at the University of New Mexico in Albuquerque, said in an interview that “clinical guidelines like this really help practicing physicians as we navigate the explosion of research findings since the start of the pandemic.”

One strong recommendation

Dr. Barrett pointed out that four of the five recommendations are rated “weak.”

“The weak recommendations for convalescent plasma in most situations is very humbling,” she said, “particularly as we recall the earliest days of the pandemic when many hospitalized patients received this treatment when little was known about what could help.”

She highlighted the paper’s only strong recommendation, which was against convalescent plasma use for the vast majority of hospitalized patients with COVID.

“That clinical bottom line is what most clinicians will look for,” she said.

“Similarly,” she said, “the accompanying editorial is so helpful in reminding the reader that, despite some possible benefit to convalescent plasma in a smaller subgroup of patients, variant-appropriate monoclonal antibodies and antivirals are better options.”

The disclosures for lead author of the guidelines, Lise J. Estcourt, MB BChir, DPhil, with the National Health Service Blood and Transplant Department and Radcliffe department of medicine at the University of Oxford (England) and her colleagues are available at https://rmed.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M22-1079. The editorialists and Dr. Barrett declare no relevant financial relationships.

The Association for the Advancement of Blood and Biotherapies has released clinical practice guidelines for using COVID-19 convalescent plasma (CCP) in hospital and outpatient settings.

In summarizing the practice statement, the authors write, “CCP is most effective when transfused with high neutralizing titers early after symptom onset.”

The five guidelines, were published in Annals of Internal Medicine. The guidelines and strength of recommendations are:

• Nonhospitalized patients at high risk for disease progression should have CCP transfusion in addition to usual standard of care. (weak)
• CCP transfusion should not be done for unselected hospitalized patients with moderate or severe disease. This does not apply to immunosuppressed patients or those who lack antibodies against SARS-CoV-2. (strong)
• CCP transfusion is suggested in addition to the usual standard of care for hospitalized patients with COVID-19 who do not have SARS-CoV-2 antibodies at admission. (weak)
• Prophylactic CCP transfusion is not recommended for uninfected people with close contact exposure to someone with COVID-19. (weak)
• The AABB suggests CCP transfusion along with standard of care for hospitalized patients with COVID-19 and preexisting immunosuppression. (weak)

Multiple guidelines for use of CCP are similar

In an accompanying editorial, Jason V. Baker, MD, MS, and H. Clifford Lane, MD, who are part of the National Institutes of Health Treatment Guidelines Panel, say guidelines from that organization around CCP generally align with those of the AABB and the Infectious Diseases Society of America.

They all note CCP’s potential for helping immunocompromised patients and they recommend against CCP in unselected, hospitalized patients.

The main difference is that the AABB also “suggests” using CCP in combination with other standard treatments for outpatients at high risk for disease progression, regardless of their immune status, write Dr. Baker, who is with Hennepin Healthcare and the department of medicine at the University of Minnesota in Minneapolis, and Dr. Lane, who is with the National Institutes of Health.

The precise circumstance for recommending CCP remains unclear, Dr. Baker and Dr. Lane write. That’s because most available evidence has come in the absence of vaccines and antiviral agents, including nirmatrelvir–ritonavir (Paxlovid), they explain.

“At this point in the pandemic, it seems that the patient most likely to benefit from passive antibody therapy is the immunocompromised host with COVID-19 who cannot mount their own antibody response to vaccine or prior infection,” they write.

“In that setting, and in the absence of other antiviral treatments or progression despite receipt of standard treatments, high-titer CCP from a recently recovered donor is a reasonable approach,” they conclude.

Eileen Barrett, MD, MPH, an assistant professor in the division of hospital medicine at the University of New Mexico in Albuquerque, said in an interview that “clinical guidelines like this really help practicing physicians as we navigate the explosion of research findings since the start of the pandemic.”

One strong recommendation

Dr. Barrett pointed out that four of the five recommendations are rated “weak.”

“The weak recommendations for convalescent plasma in most situations is very humbling,” she said, “particularly as we recall the earliest days of the pandemic when many hospitalized patients received this treatment when little was known about what could help.”

She highlighted the paper’s only strong recommendation, which was against convalescent plasma use for the vast majority of hospitalized patients with COVID.

“That clinical bottom line is what most clinicians will look for,” she said.

“Similarly,” she said, “the accompanying editorial is so helpful in reminding the reader that, despite some possible benefit to convalescent plasma in a smaller subgroup of patients, variant-appropriate monoclonal antibodies and antivirals are better options.”

The disclosures for lead author of the guidelines, Lise J. Estcourt, MB BChir, DPhil, with the National Health Service Blood and Transplant Department and Radcliffe department of medicine at the University of Oxford (England) and her colleagues are available at https://rmed.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M22-1079. The editorialists and Dr. Barrett declare no relevant financial relationships.

The Association for the Advancement of Blood and Biotherapies has released clinical practice guidelines for using COVID-19 convalescent plasma (CCP) in hospital and outpatient settings.

In summarizing the practice statement, the authors write, “CCP is most effective when transfused with high neutralizing titers early after symptom onset.”

The five guidelines, were published in Annals of Internal Medicine. The guidelines and strength of recommendations are:

• Nonhospitalized patients at high risk for disease progression should have CCP transfusion in addition to usual standard of care. (weak)
• CCP transfusion should not be done for unselected hospitalized patients with moderate or severe disease. This does not apply to immunosuppressed patients or those who lack antibodies against SARS-CoV-2. (strong)
• CCP transfusion is suggested in addition to the usual standard of care for hospitalized patients with COVID-19 who do not have SARS-CoV-2 antibodies at admission. (weak)
• Prophylactic CCP transfusion is not recommended for uninfected people with close contact exposure to someone with COVID-19. (weak)
• The AABB suggests CCP transfusion along with standard of care for hospitalized patients with COVID-19 and preexisting immunosuppression. (weak)

Multiple guidelines for use of CCP are similar

In an accompanying editorial, Jason V. Baker, MD, MS, and H. Clifford Lane, MD, who are part of the National Institutes of Health Treatment Guidelines Panel, say guidelines from that organization around CCP generally align with those of the AABB and the Infectious Diseases Society of America.

They all note CCP’s potential for helping immunocompromised patients and they recommend against CCP in unselected, hospitalized patients.

The main difference is that the AABB also “suggests” using CCP in combination with other standard treatments for outpatients at high risk for disease progression, regardless of their immune status, write Dr. Baker, who is with Hennepin Healthcare and the department of medicine at the University of Minnesota in Minneapolis, and Dr. Lane, who is with the National Institutes of Health.

The precise circumstance for recommending CCP remains unclear, Dr. Baker and Dr. Lane write. That’s because most available evidence has come in the absence of vaccines and antiviral agents, including nirmatrelvir–ritonavir (Paxlovid), they explain.

“At this point in the pandemic, it seems that the patient most likely to benefit from passive antibody therapy is the immunocompromised host with COVID-19 who cannot mount their own antibody response to vaccine or prior infection,” they write.

“In that setting, and in the absence of other antiviral treatments or progression despite receipt of standard treatments, high-titer CCP from a recently recovered donor is a reasonable approach,” they conclude.

Eileen Barrett, MD, MPH, an assistant professor in the division of hospital medicine at the University of New Mexico in Albuquerque, said in an interview that “clinical guidelines like this really help practicing physicians as we navigate the explosion of research findings since the start of the pandemic.”

One strong recommendation

Dr. Barrett pointed out that four of the five recommendations are rated “weak.”

“The weak recommendations for convalescent plasma in most situations is very humbling,” she said, “particularly as we recall the earliest days of the pandemic when many hospitalized patients received this treatment when little was known about what could help.”

She highlighted the paper’s only strong recommendation, which was against convalescent plasma use for the vast majority of hospitalized patients with COVID.

“That clinical bottom line is what most clinicians will look for,” she said.

“Similarly,” she said, “the accompanying editorial is so helpful in reminding the reader that, despite some possible benefit to convalescent plasma in a smaller subgroup of patients, variant-appropriate monoclonal antibodies and antivirals are better options.”

The disclosures for lead author of the guidelines, Lise J. Estcourt, MB BChir, DPhil, with the National Health Service Blood and Transplant Department and Radcliffe department of medicine at the University of Oxford (England) and her colleagues are available at https://rmed.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M22-1079. The editorialists and Dr. Barrett declare no relevant financial relationships.

When COVID-19 emerged in March 2020, physicians were forced to evaluate the potential impacts of the pandemic on our patients and the conditions that we treat. For dermatologists, psoriasis came into particular focus, as many patients were being treated with biologic therapies. The initial concern was that these biologics might render our patients more susceptible to both COVID-19 infection and/or a more severe disease course.

In early 2020, the National Psoriasis Foundation (NPF) presented its own recommendations for treating patients with psoriatic disease during the pandemic.¹ Some highlights included the following¹:

• At the time, it was stipulated that patients with COVID-19 infection should stop taking a biologic.

• Psoriasis patients in high-risk groups (eg, concomitant systemic disease) should discuss with their dermatologist if their therapeutic regimen should be continued or altered.

• Patients taking oral immunosuppressive therapy may be at greater risk for COVID-19 infection, though there is no strong COVID-19–related evidence to provide specific guidelines or risk level.

In May 2020, the NPF COVID-19 Task Force was formed. This group—chaired by dermatologist Joel M. Gelfand, MD, MSCE (Philadelphia, Pennsylvania), and rheumatologist Christopher T. Ritchlin, MD, MPH (Rochester, New York)—was comprised of members from both the NPF Medical Board and Scientific Advisory Committee in dermatology, rheumatology, infectious disease, and critical care. The NPF COVID-19 Task Force has been critical in keeping the dermatology community apprised of the latest scientific thinking related to COVID-19 and publishing guidance statements that are updated and amended on a regular basis as new data becomes available.² Key recommendations most relevant to the daily care of patients with psoriatic disease included the following²:

• Patients with psoriasis and/or psoriatic arthritis have similar rates of SARS-CoV-2 infection and COVID-19 outcomes as the general population based on existing data, with some exceptions.

• Therapies for psoriasis and/or psoriatic arthritis do not meaningfully alter the risk for acquiring SARS-CoV-2 infection or having worse COVID-19 outcomes.

• Patients should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases, unless they become infected with SARS-CoV-2.

• Chronic systemic steroid use for psoriatic disease in the setting of acute infection with COVID-19 may be associated with worse outcomes; however, steroids may improve outcomes for COVID-19 when initiated in hospitalized patients who require oxygen therapy.

• When local restrictions or pandemic conditions limit the ability for in-person visits, offer telemedicine to manage patients.

• Patients with psoriatic disease who do not have contraindications to vaccination should receive a messenger RNA (mRNA)–based COVID-19 vaccine and boosters, based on federal, state, and local guidance. Systemic medications for psoriasis or psoriatic arthritis are not a contraindication to the mRNA-based COVID-19 vaccine. 

• Patients who are to receive an mRNA-based COVID-19 vaccine should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases.

• The use of hydroxychloroquine, chloroquine, and ivermectin is not suggested for the prevention or treatment of COVID-19 disease.

These guidelines have been critical in addressing some of the most pressing issues in psoriasis patient care, particularly the susceptibility to COVID-19, the role of psoriasis therapies in initial infection and health outcomes, and issues related to the administration of vaccines in those on systemic therapies. Based on these recommendations, we have been given a solid foundation that our current standard of care can (for the most part) continue with the continued presence of COVID-19 in our society. I encourage all providers to familiarize themselves with the NPF COVID-19 Task Force guidelines and keep abreast of updates as they become available (https://www.psoriasis.org/covid-19-task-force-guidance-statements/).

When COVID-19 emerged in March 2020, physicians were forced to evaluate the potential impacts of the pandemic on our patients and the conditions that we treat. For dermatologists, psoriasis came into particular focus, as many patients were being treated with biologic therapies. The initial concern was that these biologics might render our patients more susceptible to both COVID-19 infection and/or a more severe disease course.

In early 2020, the National Psoriasis Foundation (NPF) presented its own recommendations for treating patients with psoriatic disease during the pandemic.¹ Some highlights included the following¹:

• At the time, it was stipulated that patients with COVID-19 infection should stop taking a biologic.

• Psoriasis patients in high-risk groups (eg, concomitant systemic disease) should discuss with their dermatologist if their therapeutic regimen should be continued or altered.

• Patients taking oral immunosuppressive therapy may be at greater risk for COVID-19 infection, though there is no strong COVID-19–related evidence to provide specific guidelines or risk level.

In May 2020, the NPF COVID-19 Task Force was formed. This group—chaired by dermatologist Joel M. Gelfand, MD, MSCE (Philadelphia, Pennsylvania), and rheumatologist Christopher T. Ritchlin, MD, MPH (Rochester, New York)—was comprised of members from both the NPF Medical Board and Scientific Advisory Committee in dermatology, rheumatology, infectious disease, and critical care. The NPF COVID-19 Task Force has been critical in keeping the dermatology community apprised of the latest scientific thinking related to COVID-19 and publishing guidance statements that are updated and amended on a regular basis as new data becomes available.² Key recommendations most relevant to the daily care of patients with psoriatic disease included the following²:

• Patients with psoriasis and/or psoriatic arthritis have similar rates of SARS-CoV-2 infection and COVID-19 outcomes as the general population based on existing data, with some exceptions.

• Therapies for psoriasis and/or psoriatic arthritis do not meaningfully alter the risk for acquiring SARS-CoV-2 infection or having worse COVID-19 outcomes.

• Patients should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases, unless they become infected with SARS-CoV-2.

• Chronic systemic steroid use for psoriatic disease in the setting of acute infection with COVID-19 may be associated with worse outcomes; however, steroids may improve outcomes for COVID-19 when initiated in hospitalized patients who require oxygen therapy.

• When local restrictions or pandemic conditions limit the ability for in-person visits, offer telemedicine to manage patients.

• Patients with psoriatic disease who do not have contraindications to vaccination should receive a messenger RNA (mRNA)–based COVID-19 vaccine and boosters, based on federal, state, and local guidance. Systemic medications for psoriasis or psoriatic arthritis are not a contraindication to the mRNA-based COVID-19 vaccine. 

• Patients who are to receive an mRNA-based COVID-19 vaccine should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases.

• The use of hydroxychloroquine, chloroquine, and ivermectin is not suggested for the prevention or treatment of COVID-19 disease.

These guidelines have been critical in addressing some of the most pressing issues in psoriasis patient care, particularly the susceptibility to COVID-19, the role of psoriasis therapies in initial infection and health outcomes, and issues related to the administration of vaccines in those on systemic therapies. Based on these recommendations, we have been given a solid foundation that our current standard of care can (for the most part) continue with the continued presence of COVID-19 in our society. I encourage all providers to familiarize themselves with the NPF COVID-19 Task Force guidelines and keep abreast of updates as they become available (https://www.psoriasis.org/covid-19-task-force-guidance-statements/).

When COVID-19 emerged in March 2020, physicians were forced to evaluate the potential impacts of the pandemic on our patients and the conditions that we treat. For dermatologists, psoriasis came into particular focus, as many patients were being treated with biologic therapies. The initial concern was that these biologics might render our patients more susceptible to both COVID-19 infection and/or a more severe disease course.

In early 2020, the National Psoriasis Foundation (NPF) presented its own recommendations for treating patients with psoriatic disease during the pandemic.¹ Some highlights included the following¹:

• At the time, it was stipulated that patients with COVID-19 infection should stop taking a biologic.

• Psoriasis patients in high-risk groups (eg, concomitant systemic disease) should discuss with their dermatologist if their therapeutic regimen should be continued or altered.

• Patients taking oral immunosuppressive therapy may be at greater risk for COVID-19 infection, though there is no strong COVID-19–related evidence to provide specific guidelines or risk level.

In May 2020, the NPF COVID-19 Task Force was formed. This group—chaired by dermatologist Joel M. Gelfand, MD, MSCE (Philadelphia, Pennsylvania), and rheumatologist Christopher T. Ritchlin, MD, MPH (Rochester, New York)—was comprised of members from both the NPF Medical Board and Scientific Advisory Committee in dermatology, rheumatology, infectious disease, and critical care. The NPF COVID-19 Task Force has been critical in keeping the dermatology community apprised of the latest scientific thinking related to COVID-19 and publishing guidance statements that are updated and amended on a regular basis as new data becomes available.² Key recommendations most relevant to the daily care of patients with psoriatic disease included the following²:

• Patients with psoriasis and/or psoriatic arthritis have similar rates of SARS-CoV-2 infection and COVID-19 outcomes as the general population based on existing data, with some exceptions.

• Therapies for psoriasis and/or psoriatic arthritis do not meaningfully alter the risk for acquiring SARS-CoV-2 infection or having worse COVID-19 outcomes.

• Patients should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases, unless they become infected with SARS-CoV-2.

• Chronic systemic steroid use for psoriatic disease in the setting of acute infection with COVID-19 may be associated with worse outcomes; however, steroids may improve outcomes for COVID-19 when initiated in hospitalized patients who require oxygen therapy.

• When local restrictions or pandemic conditions limit the ability for in-person visits, offer telemedicine to manage patients.

• Patients with psoriatic disease who do not have contraindications to vaccination should receive a messenger RNA (mRNA)–based COVID-19 vaccine and boosters, based on federal, state, and local guidance. Systemic medications for psoriasis or psoriatic arthritis are not a contraindication to the mRNA-based COVID-19 vaccine. 

• Patients who are to receive an mRNA-based COVID-19 vaccine should continue their biologic or oral therapies for psoriasis and/or psoriatic arthritis in most cases.

• The use of hydroxychloroquine, chloroquine, and ivermectin is not suggested for the prevention or treatment of COVID-19 disease.

These guidelines have been critical in addressing some of the most pressing issues in psoriasis patient care, particularly the susceptibility to COVID-19, the role of psoriasis therapies in initial infection and health outcomes, and issues related to the administration of vaccines in those on systemic therapies. Based on these recommendations, we have been given a solid foundation that our current standard of care can (for the most part) continue with the continued presence of COVID-19 in our society. I encourage all providers to familiarize themselves with the NPF COVID-19 Task Force guidelines and keep abreast of updates as they become available (https://www.psoriasis.org/covid-19-task-force-guidance-statements/).

An AI-guided analysis of more than 1,000 human lung transcriptomic datasets found that COVID-19 resembles idiopathic pulmonary fibrosis (IPF) at a fundamental level, according to a study published in eBiomedicine, part of The Lancet Discovery Science.

In the aftermath of COVID-19, a significant number of patients develop a fibrotic lung disease, for which insights into pathogenesis, disease models, or treatment options are lacking, according to researchers Dr. Sinha and colleagues. This long-haul form of the disease culminates in a fibrotic type of interstitial lung disease (ILD). While the actual prevalence of post–COVID-19 ILD (PCLD) is still emerging, early analysis indicates that more than a third of COVID-19 survivors develop fibrotic abnormalities, according to the authors.

Previous research has shown that one of the important determinants for PCLD is the duration of disease. Among patients who developed fibrosis, approximately 4% of patients had a disease duration of less than 1 week; approximately 24% had a disease duration between 1 and 3 weeks; and around 61% had a disease duration longer than 3 weeks, the authors stated.

The lung transcriptomic datasets compared in their study were associated with various lung conditions. The researchers used two viral pandemic signatures (ViP and sViP) and one COVID lung-derived signature. They found that the resemblances included that COVID-19 recapitulates the gene expression patterns (ViP and IPF signatures), cytokine storm (IL15-centric), and the AT2 cytopathic changes, for example, injury, DNA damage, arrest in a transient, damage-induced progenitor state, and senescence-associated secretory phenotype (SASP).

In laboratory experiments, Dr. Sinha and colleagues were able to induce these same immunocytopathic features in preclinical COVID-19 models (human adult lung organoid and hamster) and to reverse them in the hamster model with effective anti–CoV-2 therapeutics.

PPI-network analyses pinpointed endoplasmic reticulum (ER) stress as one of the shared early triggers of both IPF and COVID-19, and immunohistochemistry studies validated the same in the lungs of deceased subjects with COVID-19 and the SARS-CoV-2–challenged hamster lungs. Additionally, lungs from transgenic mice, in which ER stress was induced specifically in the AT2 cells, faithfully recapitulated the host immune response and alveolar cytopathic changes that are induced by SARS-CoV-2.

“In this work, we found that a blood-based gene expression biomarker, which works for prognostication in COVID, also works for IPF,” stated corresponding author Pradipta Ghosh, MD, professor in the departments of medicine and cellular and molecular medicine, University of California, San Diego. “If proven in prospective studies, this biomarker could indicate who is at greatest risk for progressive fibrosis and may require lung transplantation,” she said in an interview.

Dr. Ghosh stated further, “When it comes to therapeutics in COVID lung or IPF, we also found that shared fundamental pathogenic mechanisms present excellent opportunities for developing therapeutics that can arrest the fibrogenic drivers in both diseases. One clue that emerged is a specific cytokine that is at the heart of the smoldering inflammation which is invariably associated with fibrosis. That is interleukin 15 [IL-15] and its receptor.” Dr. Ghosh observed that there are two Food and Drug Administration–approved drugs for IPF. “None are very effective in arresting this invariably fatal disease. Hence, finding better options to treat IPF is an urgent and an unmet need.”

Preclinical testing of hypotheses, Dr. Ghosh said, is next on the path to clinical trials. “We have the advantage of using human lung organoids (mini-lungs grown using stem cells) in a dish, adding additional cells to the system (like fibroblasts and immune cells), infecting them with the virus, or subjecting them to the IL-15 cytokine and monitoring lung fibrosis progression in a dish. Anti–IL-15 therapy can then be initiated to observe reversal of the fibrogenic cascade.” Hamsters have also been shown to provide appropriate models for mimicking lung fibrosis, Dr. Ghosh said. 

“The report by Sinha and colleagues describes the fascinating similarities between drivers of post-COVID lung disease and idiopathic pulmonary fibrosis,” stated David Bowton, MD, professor emeritus, section on critical care, department of anesthesiology, Wake Forest University, Winston-Salem, N.C., in an interview. He added that, “Central to the mechanisms of induction of fibrosis in both disorders appears to be endoplasmic reticulum stress in alveolar type II cells (AT2). ER stress induces the unfolded protein response (UPR) that halts protein translation and promotes the degradation of misfolded proteins. Prolonged UPR can reprogram the cell or trigger apoptosis pathways. ER stress in the lung has been reported in a variety of cell lines including AT2 in IPF, bronchial and alveolar epithelial cells in asthma and [chronic obstructive pulmonary disease], and endothelial cells in pulmonary hypertension.”

Dr. Bowton commented further, including a caution, “Sinha and colleagues suggest that the identification of these gene signatures and mechanisms will be a fruitful avenue for developing effective therapeutics for IPF and other fibrotic lung diseases. I am hopeful that these data may offer clues that expedite this process.  However, the redundancy of triggers for effector pathways in biologic systems argues that, even if successful, this will be [a] long and fraught process.”

The research study was supported by National Institutes of Health grants and funding from the Tobacco-Related Disease Research Program.

Dr. Sinha, Dr. Ghosh, and Dr. Bowton reported no relevant disclosures.

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

An AI-guided analysis of more than 1,000 human lung transcriptomic datasets found that COVID-19 resembles idiopathic pulmonary fibrosis (IPF) at a fundamental level, according to a study published in eBiomedicine, part of The Lancet Discovery Science.

In the aftermath of COVID-19, a significant number of patients develop a fibrotic lung disease, for which insights into pathogenesis, disease models, or treatment options are lacking, according to researchers Dr. Sinha and colleagues. This long-haul form of the disease culminates in a fibrotic type of interstitial lung disease (ILD). While the actual prevalence of post–COVID-19 ILD (PCLD) is still emerging, early analysis indicates that more than a third of COVID-19 survivors develop fibrotic abnormalities, according to the authors.

Previous research has shown that one of the important determinants for PCLD is the duration of disease. Among patients who developed fibrosis, approximately 4% of patients had a disease duration of less than 1 week; approximately 24% had a disease duration between 1 and 3 weeks; and around 61% had a disease duration longer than 3 weeks, the authors stated.

The lung transcriptomic datasets compared in their study were associated with various lung conditions. The researchers used two viral pandemic signatures (ViP and sViP) and one COVID lung-derived signature. They found that the resemblances included that COVID-19 recapitulates the gene expression patterns (ViP and IPF signatures), cytokine storm (IL15-centric), and the AT2 cytopathic changes, for example, injury, DNA damage, arrest in a transient, damage-induced progenitor state, and senescence-associated secretory phenotype (SASP).

In laboratory experiments, Dr. Sinha and colleagues were able to induce these same immunocytopathic features in preclinical COVID-19 models (human adult lung organoid and hamster) and to reverse them in the hamster model with effective anti–CoV-2 therapeutics.

PPI-network analyses pinpointed endoplasmic reticulum (ER) stress as one of the shared early triggers of both IPF and COVID-19, and immunohistochemistry studies validated the same in the lungs of deceased subjects with COVID-19 and the SARS-CoV-2–challenged hamster lungs. Additionally, lungs from transgenic mice, in which ER stress was induced specifically in the AT2 cells, faithfully recapitulated the host immune response and alveolar cytopathic changes that are induced by SARS-CoV-2.

“In this work, we found that a blood-based gene expression biomarker, which works for prognostication in COVID, also works for IPF,” stated corresponding author Pradipta Ghosh, MD, professor in the departments of medicine and cellular and molecular medicine, University of California, San Diego. “If proven in prospective studies, this biomarker could indicate who is at greatest risk for progressive fibrosis and may require lung transplantation,” she said in an interview.

Dr. Ghosh stated further, “When it comes to therapeutics in COVID lung or IPF, we also found that shared fundamental pathogenic mechanisms present excellent opportunities for developing therapeutics that can arrest the fibrogenic drivers in both diseases. One clue that emerged is a specific cytokine that is at the heart of the smoldering inflammation which is invariably associated with fibrosis. That is interleukin 15 [IL-15] and its receptor.” Dr. Ghosh observed that there are two Food and Drug Administration–approved drugs for IPF. “None are very effective in arresting this invariably fatal disease. Hence, finding better options to treat IPF is an urgent and an unmet need.”

Preclinical testing of hypotheses, Dr. Ghosh said, is next on the path to clinical trials. “We have the advantage of using human lung organoids (mini-lungs grown using stem cells) in a dish, adding additional cells to the system (like fibroblasts and immune cells), infecting them with the virus, or subjecting them to the IL-15 cytokine and monitoring lung fibrosis progression in a dish. Anti–IL-15 therapy can then be initiated to observe reversal of the fibrogenic cascade.” Hamsters have also been shown to provide appropriate models for mimicking lung fibrosis, Dr. Ghosh said. 

“The report by Sinha and colleagues describes the fascinating similarities between drivers of post-COVID lung disease and idiopathic pulmonary fibrosis,” stated David Bowton, MD, professor emeritus, section on critical care, department of anesthesiology, Wake Forest University, Winston-Salem, N.C., in an interview. He added that, “Central to the mechanisms of induction of fibrosis in both disorders appears to be endoplasmic reticulum stress in alveolar type II cells (AT2). ER stress induces the unfolded protein response (UPR) that halts protein translation and promotes the degradation of misfolded proteins. Prolonged UPR can reprogram the cell or trigger apoptosis pathways. ER stress in the lung has been reported in a variety of cell lines including AT2 in IPF, bronchial and alveolar epithelial cells in asthma and [chronic obstructive pulmonary disease], and endothelial cells in pulmonary hypertension.”

Dr. Bowton commented further, including a caution, “Sinha and colleagues suggest that the identification of these gene signatures and mechanisms will be a fruitful avenue for developing effective therapeutics for IPF and other fibrotic lung diseases. I am hopeful that these data may offer clues that expedite this process.  However, the redundancy of triggers for effector pathways in biologic systems argues that, even if successful, this will be [a] long and fraught process.”

The research study was supported by National Institutes of Health grants and funding from the Tobacco-Related Disease Research Program.

Dr. Sinha, Dr. Ghosh, and Dr. Bowton reported no relevant disclosures.

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

An AI-guided analysis of more than 1,000 human lung transcriptomic datasets found that COVID-19 resembles idiopathic pulmonary fibrosis (IPF) at a fundamental level, according to a study published in eBiomedicine, part of The Lancet Discovery Science.

In the aftermath of COVID-19, a significant number of patients develop a fibrotic lung disease, for which insights into pathogenesis, disease models, or treatment options are lacking, according to researchers Dr. Sinha and colleagues. This long-haul form of the disease culminates in a fibrotic type of interstitial lung disease (ILD). While the actual prevalence of post–COVID-19 ILD (PCLD) is still emerging, early analysis indicates that more than a third of COVID-19 survivors develop fibrotic abnormalities, according to the authors.

Previous research has shown that one of the important determinants for PCLD is the duration of disease. Among patients who developed fibrosis, approximately 4% of patients had a disease duration of less than 1 week; approximately 24% had a disease duration between 1 and 3 weeks; and around 61% had a disease duration longer than 3 weeks, the authors stated.

The lung transcriptomic datasets compared in their study were associated with various lung conditions. The researchers used two viral pandemic signatures (ViP and sViP) and one COVID lung-derived signature. They found that the resemblances included that COVID-19 recapitulates the gene expression patterns (ViP and IPF signatures), cytokine storm (IL15-centric), and the AT2 cytopathic changes, for example, injury, DNA damage, arrest in a transient, damage-induced progenitor state, and senescence-associated secretory phenotype (SASP).

In laboratory experiments, Dr. Sinha and colleagues were able to induce these same immunocytopathic features in preclinical COVID-19 models (human adult lung organoid and hamster) and to reverse them in the hamster model with effective anti–CoV-2 therapeutics.

PPI-network analyses pinpointed endoplasmic reticulum (ER) stress as one of the shared early triggers of both IPF and COVID-19, and immunohistochemistry studies validated the same in the lungs of deceased subjects with COVID-19 and the SARS-CoV-2–challenged hamster lungs. Additionally, lungs from transgenic mice, in which ER stress was induced specifically in the AT2 cells, faithfully recapitulated the host immune response and alveolar cytopathic changes that are induced by SARS-CoV-2.

“In this work, we found that a blood-based gene expression biomarker, which works for prognostication in COVID, also works for IPF,” stated corresponding author Pradipta Ghosh, MD, professor in the departments of medicine and cellular and molecular medicine, University of California, San Diego. “If proven in prospective studies, this biomarker could indicate who is at greatest risk for progressive fibrosis and may require lung transplantation,” she said in an interview.

Dr. Ghosh stated further, “When it comes to therapeutics in COVID lung or IPF, we also found that shared fundamental pathogenic mechanisms present excellent opportunities for developing therapeutics that can arrest the fibrogenic drivers in both diseases. One clue that emerged is a specific cytokine that is at the heart of the smoldering inflammation which is invariably associated with fibrosis. That is interleukin 15 [IL-15] and its receptor.” Dr. Ghosh observed that there are two Food and Drug Administration–approved drugs for IPF. “None are very effective in arresting this invariably fatal disease. Hence, finding better options to treat IPF is an urgent and an unmet need.”

Preclinical testing of hypotheses, Dr. Ghosh said, is next on the path to clinical trials. “We have the advantage of using human lung organoids (mini-lungs grown using stem cells) in a dish, adding additional cells to the system (like fibroblasts and immune cells), infecting them with the virus, or subjecting them to the IL-15 cytokine and monitoring lung fibrosis progression in a dish. Anti–IL-15 therapy can then be initiated to observe reversal of the fibrogenic cascade.” Hamsters have also been shown to provide appropriate models for mimicking lung fibrosis, Dr. Ghosh said. 

“The report by Sinha and colleagues describes the fascinating similarities between drivers of post-COVID lung disease and idiopathic pulmonary fibrosis,” stated David Bowton, MD, professor emeritus, section on critical care, department of anesthesiology, Wake Forest University, Winston-Salem, N.C., in an interview. He added that, “Central to the mechanisms of induction of fibrosis in both disorders appears to be endoplasmic reticulum stress in alveolar type II cells (AT2). ER stress induces the unfolded protein response (UPR) that halts protein translation and promotes the degradation of misfolded proteins. Prolonged UPR can reprogram the cell or trigger apoptosis pathways. ER stress in the lung has been reported in a variety of cell lines including AT2 in IPF, bronchial and alveolar epithelial cells in asthma and [chronic obstructive pulmonary disease], and endothelial cells in pulmonary hypertension.”

Dr. Bowton commented further, including a caution, “Sinha and colleagues suggest that the identification of these gene signatures and mechanisms will be a fruitful avenue for developing effective therapeutics for IPF and other fibrotic lung diseases. I am hopeful that these data may offer clues that expedite this process.  However, the redundancy of triggers for effector pathways in biologic systems argues that, even if successful, this will be [a] long and fraught process.”

The research study was supported by National Institutes of Health grants and funding from the Tobacco-Related Disease Research Program.

Dr. Sinha, Dr. Ghosh, and Dr. Bowton reported no relevant disclosures.

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

Pre-endoscopy viral testing may not be necessary to prevent coronavirus transmission from patients to endoscopy staff members, according to a new study published in Gut.

Instead, using personal protective equipment (PPE) and ensuring up-to-date COVID-19 vaccination among the medical team was found to be enough to substantially reduce the risk of spreading SARS-CoV-2, wrote Alexander Hann, Dr.med., gastroenterologist at University Hospital Würzburg in Germany, and colleagues.

“We suggest that pre-selection of patients using respective questionnaires, vaccination, and particularly PPE appears to be sufficient for the prevention of SARS-CoV-2 transmission in GI endoscopy,” they wrote.

Dr. Hann and colleagues analyzed 15,750 endoscopies performed by 29 staff members during the period between May 2020 and December 2021. The researchers looked at three test approaches: No testing (4,543 patients), rapid antigen testing (682 patients), and real-time PCR testing (10,465 patients). In addition, 60 endoscopies were performed in patients with known COVID-19. Overall, no staff members became infected with SARS-CoV-2 during the study period. In all three scenarios, staff used PPE, and the vaccination rate of the team was 97%.

University Hospital Würzburg, with a tertiary endoscopy unit, is located in an area that had medium COVID-19 incidence during the study period. The hospital, which is spatially divided into a center for operative medicine and a center for internal medicine, required a negative PCR test for all endoscopies in the operative medicine center. In the internal medicine center, a PCR test was required only for in-patient procedures. Starting in January 2021 a negative rapid antigen test was required for patients scheduled for complex procedures with overnight surveillance; outpatient endoscopy procedures did not require a test.

All patients were interviewed before admission for COVID-19 symptoms, close contact with infected people, and recent travel to high-risk countries. Moreover, some endoscopies were performed even if a patient had positive markers for COVID-19.

The clinical team wore recommended PPE, including a high-filter FFP2 mask, one pair of gloves, protective eyewear, and disposable gowns. For patients with known COVID-19, staff wore two pairs of gloves, a disposable hairnet, and a water-resistant disposable gown. In addition, endoscopies were performed in negative pressure intervention rooms.

Among the 29 staff members involved, 16 physicians and 13 assistants worked in the endoscopy unit for at least 2 days per week for at least 6 months. The hospital’s internal policy required medical staff to undergo PCR testing if a rapid antigen test was positive or symptoms developed. Staff were vaccinated with two doses of the Pfizer-BioNTech vaccine in January and February 2021. A single booster dose of the Pfizer or Moderna vaccine was administered in November and December 2021.

The clinical team was not tested routinely, so asymptomatic infections may have existed. Moreover, the relatively low COVID-19 incidence in the local area might have influenced the risk of transmission. “However, even at the end of 2021, when the incidence was increasing, we did not see any higher risk of transmission,” the researchers explained.

“An important limitation of our study relates to the new variant Omicron that was dominant in our local area after the analyzed time frame.” Additional studies may be needed to understand the risk of transmission with the latest Omicron variants, and given the additional costs and implications on routine activity, current testing guidelines may need to be reconsidered.

“Although our data were not part of a randomized prospective study, we were able to demonstrate on a fairly high number of patients that PPE measures in addition to a short interview for assessment of a patient’s individual risks appear to be highly effective to control transmission of SARS-CoV-2 during an endoscopy. ... Pre-procedural RT-PCR testing or RA testing did not show any additional benefit,” Dr. Hann and colleagues concluded.

The authors reported no conflicts of interest.

Pre-endoscopy viral testing may not be necessary to prevent coronavirus transmission from patients to endoscopy staff members, according to a new study published in Gut.

Instead, using personal protective equipment (PPE) and ensuring up-to-date COVID-19 vaccination among the medical team was found to be enough to substantially reduce the risk of spreading SARS-CoV-2, wrote Alexander Hann, Dr.med., gastroenterologist at University Hospital Würzburg in Germany, and colleagues.

“We suggest that pre-selection of patients using respective questionnaires, vaccination, and particularly PPE appears to be sufficient for the prevention of SARS-CoV-2 transmission in GI endoscopy,” they wrote.

Dr. Hann and colleagues analyzed 15,750 endoscopies performed by 29 staff members during the period between May 2020 and December 2021. The researchers looked at three test approaches: No testing (4,543 patients), rapid antigen testing (682 patients), and real-time PCR testing (10,465 patients). In addition, 60 endoscopies were performed in patients with known COVID-19. Overall, no staff members became infected with SARS-CoV-2 during the study period. In all three scenarios, staff used PPE, and the vaccination rate of the team was 97%.

University Hospital Würzburg, with a tertiary endoscopy unit, is located in an area that had medium COVID-19 incidence during the study period. The hospital, which is spatially divided into a center for operative medicine and a center for internal medicine, required a negative PCR test for all endoscopies in the operative medicine center. In the internal medicine center, a PCR test was required only for in-patient procedures. Starting in January 2021 a negative rapid antigen test was required for patients scheduled for complex procedures with overnight surveillance; outpatient endoscopy procedures did not require a test.

All patients were interviewed before admission for COVID-19 symptoms, close contact with infected people, and recent travel to high-risk countries. Moreover, some endoscopies were performed even if a patient had positive markers for COVID-19.

The clinical team wore recommended PPE, including a high-filter FFP2 mask, one pair of gloves, protective eyewear, and disposable gowns. For patients with known COVID-19, staff wore two pairs of gloves, a disposable hairnet, and a water-resistant disposable gown. In addition, endoscopies were performed in negative pressure intervention rooms.

Among the 29 staff members involved, 16 physicians and 13 assistants worked in the endoscopy unit for at least 2 days per week for at least 6 months. The hospital’s internal policy required medical staff to undergo PCR testing if a rapid antigen test was positive or symptoms developed. Staff were vaccinated with two doses of the Pfizer-BioNTech vaccine in January and February 2021. A single booster dose of the Pfizer or Moderna vaccine was administered in November and December 2021.

The clinical team was not tested routinely, so asymptomatic infections may have existed. Moreover, the relatively low COVID-19 incidence in the local area might have influenced the risk of transmission. “However, even at the end of 2021, when the incidence was increasing, we did not see any higher risk of transmission,” the researchers explained.

“An important limitation of our study relates to the new variant Omicron that was dominant in our local area after the analyzed time frame.” Additional studies may be needed to understand the risk of transmission with the latest Omicron variants, and given the additional costs and implications on routine activity, current testing guidelines may need to be reconsidered.

“Although our data were not part of a randomized prospective study, we were able to demonstrate on a fairly high number of patients that PPE measures in addition to a short interview for assessment of a patient’s individual risks appear to be highly effective to control transmission of SARS-CoV-2 during an endoscopy. ... Pre-procedural RT-PCR testing or RA testing did not show any additional benefit,” Dr. Hann and colleagues concluded.

The authors reported no conflicts of interest.

Pre-endoscopy viral testing may not be necessary to prevent coronavirus transmission from patients to endoscopy staff members, according to a new study published in Gut.

Instead, using personal protective equipment (PPE) and ensuring up-to-date COVID-19 vaccination among the medical team was found to be enough to substantially reduce the risk of spreading SARS-CoV-2, wrote Alexander Hann, Dr.med., gastroenterologist at University Hospital Würzburg in Germany, and colleagues.

“We suggest that pre-selection of patients using respective questionnaires, vaccination, and particularly PPE appears to be sufficient for the prevention of SARS-CoV-2 transmission in GI endoscopy,” they wrote.

Dr. Hann and colleagues analyzed 15,750 endoscopies performed by 29 staff members during the period between May 2020 and December 2021. The researchers looked at three test approaches: No testing (4,543 patients), rapid antigen testing (682 patients), and real-time PCR testing (10,465 patients). In addition, 60 endoscopies were performed in patients with known COVID-19. Overall, no staff members became infected with SARS-CoV-2 during the study period. In all three scenarios, staff used PPE, and the vaccination rate of the team was 97%.

University Hospital Würzburg, with a tertiary endoscopy unit, is located in an area that had medium COVID-19 incidence during the study period. The hospital, which is spatially divided into a center for operative medicine and a center for internal medicine, required a negative PCR test for all endoscopies in the operative medicine center. In the internal medicine center, a PCR test was required only for in-patient procedures. Starting in January 2021 a negative rapid antigen test was required for patients scheduled for complex procedures with overnight surveillance; outpatient endoscopy procedures did not require a test.

All patients were interviewed before admission for COVID-19 symptoms, close contact with infected people, and recent travel to high-risk countries. Moreover, some endoscopies were performed even if a patient had positive markers for COVID-19.

The clinical team wore recommended PPE, including a high-filter FFP2 mask, one pair of gloves, protective eyewear, and disposable gowns. For patients with known COVID-19, staff wore two pairs of gloves, a disposable hairnet, and a water-resistant disposable gown. In addition, endoscopies were performed in negative pressure intervention rooms.

Among the 29 staff members involved, 16 physicians and 13 assistants worked in the endoscopy unit for at least 2 days per week for at least 6 months. The hospital’s internal policy required medical staff to undergo PCR testing if a rapid antigen test was positive or symptoms developed. Staff were vaccinated with two doses of the Pfizer-BioNTech vaccine in January and February 2021. A single booster dose of the Pfizer or Moderna vaccine was administered in November and December 2021.

The clinical team was not tested routinely, so asymptomatic infections may have existed. Moreover, the relatively low COVID-19 incidence in the local area might have influenced the risk of transmission. “However, even at the end of 2021, when the incidence was increasing, we did not see any higher risk of transmission,” the researchers explained.

“An important limitation of our study relates to the new variant Omicron that was dominant in our local area after the analyzed time frame.” Additional studies may be needed to understand the risk of transmission with the latest Omicron variants, and given the additional costs and implications on routine activity, current testing guidelines may need to be reconsidered.

“Although our data were not part of a randomized prospective study, we were able to demonstrate on a fairly high number of patients that PPE measures in addition to a short interview for assessment of a patient’s individual risks appear to be highly effective to control transmission of SARS-CoV-2 during an endoscopy. ... Pre-procedural RT-PCR testing or RA testing did not show any additional benefit,” Dr. Hann and colleagues concluded.

The authors reported no conflicts of interest.

The picture around the BA.4 and BA.5 subvariants of Omicron has been really confusing in that the pair is driving up cases but global COVID-19 deaths remain at their lowest level since the beginning of the pandemic. I wanted to explain what is happening with these subvariants, in that the picture seems to be one of antibody evasion without the dodging of cellular immunity. Explaining the two components of the immune response – antibodies versus cellular immune responses – can help us understand where we are in the pandemic and future booster options.

These two subvariants of Omicron, as of July 5, make up more than half of the COVID-19 strains in the United States and are expected to keep increasing. One of two reasons can lead to a variant or subvariant becoming dominant strain: increased transmissibility or evasion of antibodies.

Although BA.4 and BA.5 could be more transmissible than other subvariants of Omicron (which is already very transmissible), this has not yet been established in experiments showing increased affinity for the human receptor or in animal models. What we do know is that BA.4 and BA.5 seem to evade neutralizing antibodies conferred by the vaccines or even prior BA.1 infection (an earlier subvariant of Omicron), which could be the reason we are seeing so many reinfections now. Of note, BA.1 infection conferred antibodies that protected against subsequent BA.2 infection, so we did not see the same spike in cases in the United States with BA.2 (after a large BA.1 spike over the winter) earlier this spring.

Okay, so isn’t evasion of antibodies a bad thing? Of course it is but, luckily, our immune system is “redundant” and doesn›t just rely on antibodies to protect us from infection. In fact, antibodies (such as IgA, which is the mucosal antibody most prevalent in the nose and mouth, and IgG, which is the most prevalent antibody in the bloodstream) are our first line of COVID-19 defense in the nasal mucosa. Therefore, mild upper respiratory infections will be common as BA.4/BA.5 evade our nasal antibodies. Luckily, the rate of severe disease is remaining low throughout the world, probably because of the high amounts of cellular immunity to the virus. B and T cells are our protectors from severe disease.

For instance, two-dose vaccines are still conferring high rates of protection from severe disease with the BA.4 and BA.5 variants, with 87% protection against hospitalization per South Africa data. This is probably attributable to the fact that T-cell immunity from the vaccines remains protective across variants “from Alpha to Omicron,” as described by a recent and elegant paper.

Data from Qatar show that natural infection (even occurring up to 14 months ago) remains very protective (97.3%) against severe disease with the current circulating subvariants, including BA.4 and BA.5. Again, this is probably attributable to T cells which specifically amplify in response to a piece of the virus and help recruit cells to attack the pathogen directly.

The original BA.1 subvariant of Omicron has 26-32 mutations along its spike protein that differ from the “ancestral strain,” and BA.4 and BA.5 variants have a few more. Our T-cell response, even across a mutated spike protein, is so robust that we have not seen Omicron yet able to evade the many T cells (which we produce from the vaccines or infection) that descend upon the mutated virus to fight severe disease. Antibody-producing memory B cells, generated by the vaccines (or prior infection), have been shown to actually adapt their immune response to the variant to which they are exposed.

Therefore, the story of the BA.4 and BA.5 subvariants seems to remain about antibodies vs. cellular immunity. Our immunity in the United States is growing and is from both vaccination and natural infection, with 78.3% of the population having had at least one dose of the vaccine and at least 60% of adults (and 75% of children 0-18) having been exposed to the virus by February 2022, per the Centers for Disease Control and Prevention (with exposure probably much higher now in July 2022 after subsequent Omicron subvariants waves).

So, what about Omicron-specific boosters? A booster shot will just raise antibodies temporarily, but their effectiveness wanes several months later. Moreover, a booster shot against the ancestral strain is not very effective in neutralizing BA.4 and BA.5 (with a prior BA.1 Omicron infection being more effective than a booster). Luckily, Pfizer has promised a BA.4/BA.5-specific mRNA vaccine by October, and Moderna has promised a bivalent vaccine containing BA.4/BA.5 mRNA sequences around the same time. A vaccine that specifically increases antibodies against the most prevalent circulating strain should be important as a booster for those who are predisposed to severe breakthrough infections (for example, those with immunocompromise or older individuals with multiple comorbidities). Moreover, BA.4/BA.5–specific booster vaccines may help prevent mild infections for many individuals. Finally, any booster (or exposure) should diversify and broaden T-cell responses to the virus, and a booster shot will also expand the potency of B cells, making them better able to respond to the newest subvariants as we continue to live with COVID-19.
 

Monica Gandhi, MD, MPH, is an infectious diseases doctor, professor of medicine, and associate chief in the division of HIV, infectious diseases, and global medicine at the University of California, San Francisco.

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

The picture around the BA.4 and BA.5 subvariants of Omicron has been really confusing in that the pair is driving up cases but global COVID-19 deaths remain at their lowest level since the beginning of the pandemic. I wanted to explain what is happening with these subvariants, in that the picture seems to be one of antibody evasion without the dodging of cellular immunity. Explaining the two components of the immune response – antibodies versus cellular immune responses – can help us understand where we are in the pandemic and future booster options.

These two subvariants of Omicron, as of July 5, make up more than half of the COVID-19 strains in the United States and are expected to keep increasing. One of two reasons can lead to a variant or subvariant becoming dominant strain: increased transmissibility or evasion of antibodies.

Although BA.4 and BA.5 could be more transmissible than other subvariants of Omicron (which is already very transmissible), this has not yet been established in experiments showing increased affinity for the human receptor or in animal models. What we do know is that BA.4 and BA.5 seem to evade neutralizing antibodies conferred by the vaccines or even prior BA.1 infection (an earlier subvariant of Omicron), which could be the reason we are seeing so many reinfections now. Of note, BA.1 infection conferred antibodies that protected against subsequent BA.2 infection, so we did not see the same spike in cases in the United States with BA.2 (after a large BA.1 spike over the winter) earlier this spring.

Okay, so isn’t evasion of antibodies a bad thing? Of course it is but, luckily, our immune system is “redundant” and doesn›t just rely on antibodies to protect us from infection. In fact, antibodies (such as IgA, which is the mucosal antibody most prevalent in the nose and mouth, and IgG, which is the most prevalent antibody in the bloodstream) are our first line of COVID-19 defense in the nasal mucosa. Therefore, mild upper respiratory infections will be common as BA.4/BA.5 evade our nasal antibodies. Luckily, the rate of severe disease is remaining low throughout the world, probably because of the high amounts of cellular immunity to the virus. B and T cells are our protectors from severe disease.

For instance, two-dose vaccines are still conferring high rates of protection from severe disease with the BA.4 and BA.5 variants, with 87% protection against hospitalization per South Africa data. This is probably attributable to the fact that T-cell immunity from the vaccines remains protective across variants “from Alpha to Omicron,” as described by a recent and elegant paper.

Data from Qatar show that natural infection (even occurring up to 14 months ago) remains very protective (97.3%) against severe disease with the current circulating subvariants, including BA.4 and BA.5. Again, this is probably attributable to T cells which specifically amplify in response to a piece of the virus and help recruit cells to attack the pathogen directly.

The original BA.1 subvariant of Omicron has 26-32 mutations along its spike protein that differ from the “ancestral strain,” and BA.4 and BA.5 variants have a few more. Our T-cell response, even across a mutated spike protein, is so robust that we have not seen Omicron yet able to evade the many T cells (which we produce from the vaccines or infection) that descend upon the mutated virus to fight severe disease. Antibody-producing memory B cells, generated by the vaccines (or prior infection), have been shown to actually adapt their immune response to the variant to which they are exposed.

Therefore, the story of the BA.4 and BA.5 subvariants seems to remain about antibodies vs. cellular immunity. Our immunity in the United States is growing and is from both vaccination and natural infection, with 78.3% of the population having had at least one dose of the vaccine and at least 60% of adults (and 75% of children 0-18) having been exposed to the virus by February 2022, per the Centers for Disease Control and Prevention (with exposure probably much higher now in July 2022 after subsequent Omicron subvariants waves).

So, what about Omicron-specific boosters? A booster shot will just raise antibodies temporarily, but their effectiveness wanes several months later. Moreover, a booster shot against the ancestral strain is not very effective in neutralizing BA.4 and BA.5 (with a prior BA.1 Omicron infection being more effective than a booster). Luckily, Pfizer has promised a BA.4/BA.5-specific mRNA vaccine by October, and Moderna has promised a bivalent vaccine containing BA.4/BA.5 mRNA sequences around the same time. A vaccine that specifically increases antibodies against the most prevalent circulating strain should be important as a booster for those who are predisposed to severe breakthrough infections (for example, those with immunocompromise or older individuals with multiple comorbidities). Moreover, BA.4/BA.5–specific booster vaccines may help prevent mild infections for many individuals. Finally, any booster (or exposure) should diversify and broaden T-cell responses to the virus, and a booster shot will also expand the potency of B cells, making them better able to respond to the newest subvariants as we continue to live with COVID-19.
 

Monica Gandhi, MD, MPH, is an infectious diseases doctor, professor of medicine, and associate chief in the division of HIV, infectious diseases, and global medicine at the University of California, San Francisco.

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

The picture around the BA.4 and BA.5 subvariants of Omicron has been really confusing in that the pair is driving up cases but global COVID-19 deaths remain at their lowest level since the beginning of the pandemic. I wanted to explain what is happening with these subvariants, in that the picture seems to be one of antibody evasion without the dodging of cellular immunity. Explaining the two components of the immune response – antibodies versus cellular immune responses – can help us understand where we are in the pandemic and future booster options.

These two subvariants of Omicron, as of July 5, make up more than half of the COVID-19 strains in the United States and are expected to keep increasing. One of two reasons can lead to a variant or subvariant becoming dominant strain: increased transmissibility or evasion of antibodies.

Although BA.4 and BA.5 could be more transmissible than other subvariants of Omicron (which is already very transmissible), this has not yet been established in experiments showing increased affinity for the human receptor or in animal models. What we do know is that BA.4 and BA.5 seem to evade neutralizing antibodies conferred by the vaccines or even prior BA.1 infection (an earlier subvariant of Omicron), which could be the reason we are seeing so many reinfections now. Of note, BA.1 infection conferred antibodies that protected against subsequent BA.2 infection, so we did not see the same spike in cases in the United States with BA.2 (after a large BA.1 spike over the winter) earlier this spring.

Okay, so isn’t evasion of antibodies a bad thing? Of course it is but, luckily, our immune system is “redundant” and doesn›t just rely on antibodies to protect us from infection. In fact, antibodies (such as IgA, which is the mucosal antibody most prevalent in the nose and mouth, and IgG, which is the most prevalent antibody in the bloodstream) are our first line of COVID-19 defense in the nasal mucosa. Therefore, mild upper respiratory infections will be common as BA.4/BA.5 evade our nasal antibodies. Luckily, the rate of severe disease is remaining low throughout the world, probably because of the high amounts of cellular immunity to the virus. B and T cells are our protectors from severe disease.

For instance, two-dose vaccines are still conferring high rates of protection from severe disease with the BA.4 and BA.5 variants, with 87% protection against hospitalization per South Africa data. This is probably attributable to the fact that T-cell immunity from the vaccines remains protective across variants “from Alpha to Omicron,” as described by a recent and elegant paper.

Data from Qatar show that natural infection (even occurring up to 14 months ago) remains very protective (97.3%) against severe disease with the current circulating subvariants, including BA.4 and BA.5. Again, this is probably attributable to T cells which specifically amplify in response to a piece of the virus and help recruit cells to attack the pathogen directly.

The original BA.1 subvariant of Omicron has 26-32 mutations along its spike protein that differ from the “ancestral strain,” and BA.4 and BA.5 variants have a few more. Our T-cell response, even across a mutated spike protein, is so robust that we have not seen Omicron yet able to evade the many T cells (which we produce from the vaccines or infection) that descend upon the mutated virus to fight severe disease. Antibody-producing memory B cells, generated by the vaccines (or prior infection), have been shown to actually adapt their immune response to the variant to which they are exposed.

Therefore, the story of the BA.4 and BA.5 subvariants seems to remain about antibodies vs. cellular immunity. Our immunity in the United States is growing and is from both vaccination and natural infection, with 78.3% of the population having had at least one dose of the vaccine and at least 60% of adults (and 75% of children 0-18) having been exposed to the virus by February 2022, per the Centers for Disease Control and Prevention (with exposure probably much higher now in July 2022 after subsequent Omicron subvariants waves).

So, what about Omicron-specific boosters? A booster shot will just raise antibodies temporarily, but their effectiveness wanes several months later. Moreover, a booster shot against the ancestral strain is not very effective in neutralizing BA.4 and BA.5 (with a prior BA.1 Omicron infection being more effective than a booster). Luckily, Pfizer has promised a BA.4/BA.5-specific mRNA vaccine by October, and Moderna has promised a bivalent vaccine containing BA.4/BA.5 mRNA sequences around the same time. A vaccine that specifically increases antibodies against the most prevalent circulating strain should be important as a booster for those who are predisposed to severe breakthrough infections (for example, those with immunocompromise or older individuals with multiple comorbidities). Moreover, BA.4/BA.5–specific booster vaccines may help prevent mild infections for many individuals. Finally, any booster (or exposure) should diversify and broaden T-cell responses to the virus, and a booster shot will also expand the potency of B cells, making them better able to respond to the newest subvariants as we continue to live with COVID-19.
 

Monica Gandhi, MD, MPH, is an infectious diseases doctor, professor of medicine, and associate chief in the division of HIV, infectious diseases, and global medicine at the University of California, San Francisco.

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

The American College of Cardiology and the American Heart Association have jointly issued a comprehensive set of data standards to help clarify definitions of the cardiovascular (CV) and non-CV complications of COVID-19.

It’s the work of the ACC/AHA Task Force on Clinical Data Standards and has been endorsed by the Heart Failure Society of America and Society for Cardiac Angiography and Interventions.

There is increased importance to understanding the acute and long-term impact of COVID-19 on CV health, the writing group notes. Until now, however, there has not been “clarity or consensus” on definitions of CV conditions related to COVID-19, with different diagnostic terminologies being used for overlapping conditions, such as “myocardial injury,” “myocarditis,” “type Il myocardial infarction,” “stress cardiomyopathy,” and “inflammatory cardiomyopathy,” they point out.

Floaria Bicher/iStock/Getty Images Plus

“We, as a research community, did some things right and some things wrong surrounding the COVID pandemic,” Sandeep Das, MD, MPH, vice chair of the writing group, noted in an interview with this news organization.

“The things that we really did right is that everybody responded with enthusiasm, kind of all hands on deck with a massive crisis response, and that was fantastic,” Dr. Das said.

“However, because of the need to hurry, we didn’t structure and organize in the way that we typically would for something that was sort of a slow burn kind of problem rather than an emergency. One of the consequences of that was fragmentation of how things are collected, reported, et cetera, and that leads to confusion,” he added.

The report was published simultaneously June 23 in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.
 

A necessary but not glamorous project

The new data standards for COVID-19 will help standardize definitions and set the framework to capture and better understand how COVID-19 affects CV health.

“It wasn’t exactly a glamorous-type project but, at the same time, it’s super necessary to kind of get everybody on the same page and working together,” Dr. Das said. 

Broad agreement on common vocabulary and definitions will help with efforts to pool or compare data from electronic health records, clinical registries, administrative datasets, and other databases, and determine whether these data apply to clinical practice and research endeavors, the writing group says.

They considered data elements relevant to the full range of care provided to COVID-19 patients in all care settings. Among the key items included in the document are:

• Case definitions for confirmed, probable, and suspected acute COVID-19, as well as postacute sequelae of COVID-19.
• Definitions for acute CV complications related to COVID-19, including acute myocardial injury, heart failure, shock, arrhythmia, thromboembolic complications, and .
• Data elements related to COVID-19 vaccination status, comorbidities, and preexisting CV conditions.
• Definitions for postacute CV sequelae of SARS-CoV-2 infection and long-term CV complications of COVID-19.
• Data elements for CV mortality during acute COVID-19.
• Data elements for non-CV complications to help document severity of illness and other competing diagnoses and complications that might affect CV outcomes.
• A list of symptoms and signs related to COVID-19 and CV complications.
• Data elements for diagnostic and therapeutic strategies for COVID-19 and CV conditions.
• A discussion of advanced therapies, including , extracorporeal membrane oxygenation, and end-of-life management strategies.

These data standards will be useful for researchers, registry developers, and clinicians, and they are proposed as a framework for ICD-10 code development of COVID-19–related CV conditions, the writing group says.

The standards are also of “great importance” to patients, clinicians, investigators, scientists, administrators, public health officials, policymakers, and payers, the group says.

Dr. Das said that, although there is no formal plan in place to update the document, he could see sections that might be refined.

“For example, there’s a nice long list of all the various variants, and unfortunately, I suspect that that is going to change and evolve over time,” Dr. Das told this news organization.

“We tried very hard not to include things like specifying specific treatments so we didn’t get proscriptive. We wanted to make it descriptive, so hopefully it will stand the test of time pretty well,” he added.

This research had no commercial funding. The writing group has no relevant disclosures.

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

The American College of Cardiology and the American Heart Association have jointly issued a comprehensive set of data standards to help clarify definitions of the cardiovascular (CV) and non-CV complications of COVID-19.

It’s the work of the ACC/AHA Task Force on Clinical Data Standards and has been endorsed by the Heart Failure Society of America and Society for Cardiac Angiography and Interventions.

There is increased importance to understanding the acute and long-term impact of COVID-19 on CV health, the writing group notes. Until now, however, there has not been “clarity or consensus” on definitions of CV conditions related to COVID-19, with different diagnostic terminologies being used for overlapping conditions, such as “myocardial injury,” “myocarditis,” “type Il myocardial infarction,” “stress cardiomyopathy,” and “inflammatory cardiomyopathy,” they point out.

Floaria Bicher/iStock/Getty Images Plus

“We, as a research community, did some things right and some things wrong surrounding the COVID pandemic,” Sandeep Das, MD, MPH, vice chair of the writing group, noted in an interview with this news organization.

“The things that we really did right is that everybody responded with enthusiasm, kind of all hands on deck with a massive crisis response, and that was fantastic,” Dr. Das said.

“However, because of the need to hurry, we didn’t structure and organize in the way that we typically would for something that was sort of a slow burn kind of problem rather than an emergency. One of the consequences of that was fragmentation of how things are collected, reported, et cetera, and that leads to confusion,” he added.

The report was published simultaneously June 23 in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.
 

A necessary but not glamorous project

The new data standards for COVID-19 will help standardize definitions and set the framework to capture and better understand how COVID-19 affects CV health.

“It wasn’t exactly a glamorous-type project but, at the same time, it’s super necessary to kind of get everybody on the same page and working together,” Dr. Das said. 

Broad agreement on common vocabulary and definitions will help with efforts to pool or compare data from electronic health records, clinical registries, administrative datasets, and other databases, and determine whether these data apply to clinical practice and research endeavors, the writing group says.

They considered data elements relevant to the full range of care provided to COVID-19 patients in all care settings. Among the key items included in the document are:

• Case definitions for confirmed, probable, and suspected acute COVID-19, as well as postacute sequelae of COVID-19.
• Definitions for acute CV complications related to COVID-19, including acute myocardial injury, heart failure, shock, arrhythmia, thromboembolic complications, and .
• Data elements related to COVID-19 vaccination status, comorbidities, and preexisting CV conditions.
• Definitions for postacute CV sequelae of SARS-CoV-2 infection and long-term CV complications of COVID-19.
• Data elements for CV mortality during acute COVID-19.
• Data elements for non-CV complications to help document severity of illness and other competing diagnoses and complications that might affect CV outcomes.
• A list of symptoms and signs related to COVID-19 and CV complications.
• Data elements for diagnostic and therapeutic strategies for COVID-19 and CV conditions.
• A discussion of advanced therapies, including , extracorporeal membrane oxygenation, and end-of-life management strategies.

These data standards will be useful for researchers, registry developers, and clinicians, and they are proposed as a framework for ICD-10 code development of COVID-19–related CV conditions, the writing group says.

The standards are also of “great importance” to patients, clinicians, investigators, scientists, administrators, public health officials, policymakers, and payers, the group says.

Dr. Das said that, although there is no formal plan in place to update the document, he could see sections that might be refined.

“For example, there’s a nice long list of all the various variants, and unfortunately, I suspect that that is going to change and evolve over time,” Dr. Das told this news organization.

“We tried very hard not to include things like specifying specific treatments so we didn’t get proscriptive. We wanted to make it descriptive, so hopefully it will stand the test of time pretty well,” he added.

This research had no commercial funding. The writing group has no relevant disclosures.

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

The American College of Cardiology and the American Heart Association have jointly issued a comprehensive set of data standards to help clarify definitions of the cardiovascular (CV) and non-CV complications of COVID-19.

It’s the work of the ACC/AHA Task Force on Clinical Data Standards and has been endorsed by the Heart Failure Society of America and Society for Cardiac Angiography and Interventions.

There is increased importance to understanding the acute and long-term impact of COVID-19 on CV health, the writing group notes. Until now, however, there has not been “clarity or consensus” on definitions of CV conditions related to COVID-19, with different diagnostic terminologies being used for overlapping conditions, such as “myocardial injury,” “myocarditis,” “type Il myocardial infarction,” “stress cardiomyopathy,” and “inflammatory cardiomyopathy,” they point out.

Floaria Bicher/iStock/Getty Images Plus

“We, as a research community, did some things right and some things wrong surrounding the COVID pandemic,” Sandeep Das, MD, MPH, vice chair of the writing group, noted in an interview with this news organization.

“The things that we really did right is that everybody responded with enthusiasm, kind of all hands on deck with a massive crisis response, and that was fantastic,” Dr. Das said.

“However, because of the need to hurry, we didn’t structure and organize in the way that we typically would for something that was sort of a slow burn kind of problem rather than an emergency. One of the consequences of that was fragmentation of how things are collected, reported, et cetera, and that leads to confusion,” he added.

The report was published simultaneously June 23 in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.
 

A necessary but not glamorous project

The new data standards for COVID-19 will help standardize definitions and set the framework to capture and better understand how COVID-19 affects CV health.

“It wasn’t exactly a glamorous-type project but, at the same time, it’s super necessary to kind of get everybody on the same page and working together,” Dr. Das said. 

Broad agreement on common vocabulary and definitions will help with efforts to pool or compare data from electronic health records, clinical registries, administrative datasets, and other databases, and determine whether these data apply to clinical practice and research endeavors, the writing group says.

They considered data elements relevant to the full range of care provided to COVID-19 patients in all care settings. Among the key items included in the document are:

• Case definitions for confirmed, probable, and suspected acute COVID-19, as well as postacute sequelae of COVID-19.
• Definitions for acute CV complications related to COVID-19, including acute myocardial injury, heart failure, shock, arrhythmia, thromboembolic complications, and .
• Data elements related to COVID-19 vaccination status, comorbidities, and preexisting CV conditions.
• Definitions for postacute CV sequelae of SARS-CoV-2 infection and long-term CV complications of COVID-19.
• Data elements for CV mortality during acute COVID-19.
• Data elements for non-CV complications to help document severity of illness and other competing diagnoses and complications that might affect CV outcomes.
• A list of symptoms and signs related to COVID-19 and CV complications.
• Data elements for diagnostic and therapeutic strategies for COVID-19 and CV conditions.
• A discussion of advanced therapies, including , extracorporeal membrane oxygenation, and end-of-life management strategies.

These data standards will be useful for researchers, registry developers, and clinicians, and they are proposed as a framework for ICD-10 code development of COVID-19–related CV conditions, the writing group says.

The standards are also of “great importance” to patients, clinicians, investigators, scientists, administrators, public health officials, policymakers, and payers, the group says.

Dr. Das said that, although there is no formal plan in place to update the document, he could see sections that might be refined.

“For example, there’s a nice long list of all the various variants, and unfortunately, I suspect that that is going to change and evolve over time,” Dr. Das told this news organization.

“We tried very hard not to include things like specifying specific treatments so we didn’t get proscriptive. We wanted to make it descriptive, so hopefully it will stand the test of time pretty well,” he added.

This research had no commercial funding. The writing group has no relevant disclosures.

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

ATLANTA – Disturbances in ovulation that didn’t produce any actual changes in the menstrual cycle of women were extremely common during the first year of the COVID-19 pandemic and were linked to emotional stress, according to the findings of an “experiment of nature” that allowed for comparison with women a decade earlier.

Findings from two studies of reproductive-age women, one conducted in 2006-2008 and the other in 2020-2021, were presented by Jerilynn C. Prior, MD, at the annual meeting of the Endocrine Society.

The comparison of the two time periods yielded several novel findings. “I was taught in medical school that when women don’t eat enough they lose their period. But what we now understand is there’s a graded response to various stressors, acting through the hypothalamus in a common pathway. There is a gradation of disturbances, some of which are subclinical or not obvious,” said Dr. Prior, professor of endocrinology and metabolism at the University of British Columbia, Vancouver.

Moreover, women’s menstrual cycle lengths didn’t differ across the two time periods, despite a dramatic 63% decrement in normal ovulatory function related to increased depression, anxiety, and outside stresses that the women reported in diaries.

“Assuming that regular cycles need normal ovulation is something we should just get out of our minds. It changes our concept about what’s normal if we only know about the cycle length,” she observed.

It will be critical going forward to see whether the ovulatory disturbances have resolved as the pandemic has shifted “because there’s strong evidence that ovulatory disturbances, even with normal cycle length, are related to bone loss and some evidence it’s related to early heart attacks, breast and endometrial cancers,” Dr. Prior said during a press conference.

Lisa Nainggolan/MDedge News

Asked to comment, session moderator Genevieve Neal-Perry, MD, PhD, told this news organization: “I think what we can take away is that stress itself is a modifier of the way the brain and the gonads communicate with each other, and that then has an impact on ovulatory function.”

Dr. Neal-Perry noted that the association of stress and ovulatory disruption has been reported in various ways previously, but “clearly it doesn’t affect everyone. What we don’t know is who is most susceptible. There have been some studies showing a genetic predisposition and a genetic anomaly that actually makes them more susceptible to the impact of stress on the reproductive system.”

But the lack of data on weight change in the study cohorts is a limitation. “To me one of the more important questions was what was going on with weight. Just looking at a static number doesn’t tell you whether there were changes. We know that weight gain or weight loss can stress the reproductive axis,” noted Dr. Neal-Parry of the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill.
 

‘Experiment of nature’ revealed invisible effect of pandemic stress

The women in both cohorts of the Menstruation Ovulation Study (MOS) were healthy volunteers aged 19-35 years recruited from the metropolitan Vancouver region. All were menstruating monthly and none were taking hormonal birth control. Recruitment for the second cohort had begun just prior to the March 2020 COVID-19 pandemic lockdown.

Interviewer-administered questionnaires (CaMos) covering demographics, socioeconomic status, and reproductive history, and daily diaries kept by the women (menstrual cycle diary) were identical for both cohorts.

Assessments of ovulation differed for the two studies but were cross-validated. For the earlier time period, ovulation was assessed by a threefold increase in follicular-to-luteal urinary progesterone (PdG). For the pandemic-era study, the validated quantitative basal temperature (QBT) method was used.

There were 301 women in the earlier cohort and 125 during the pandemic. Both were an average age of about 29 years and had a body mass index of about 24.3 kg/m² (within the normal range). The pandemic cohort was more racially/ethnically diverse than the earlier one and more in-line with recent census data.

More of the women were nulliparous during the pandemic than earlier (92.7% vs. 80.4%; P = .002).

The distribution of menstrual cycle lengths didn’t differ, with both cohorts averaging about 30 days (P = .893). However, while 90% of the women in the earlier cohort ovulated normally, only 37% did during the pandemic, a highly significant difference (P < .0001).

Thus, during the pandemic, 63% of women had “silent ovulatory disturbances,” either with short luteal phases after ovulation or no ovulation, compared with just 10% in the earlier cohort, “which is remarkable, unbelievable actually,” Dr. Prior remarked.  

The difference wasn’t explained by any of the demographic information collected either, including socioeconomic status, lifestyle, or reproductive history variables.

And it wasn’t because of COVID-19 vaccination, as the vaccine wasn’t available when most of the women were recruited, and of the 79 who were recruited during vaccine availability, only two received a COVID-19 vaccine during the study (and both had normal ovulation).

Employment changes, caring responsibilities, and worry likely causes

The information from the diaries was more revealing. Several diary components were far more common during the pandemic, including negative mood (feeling depressed or anxious, sleep problems, and outside stresses), self-worth, interest in sex, energy level, and appetite. All were significantly different between the two cohorts (P < .001) and between those with and without ovulatory disturbances.

“So menstrual cycle lengths and long cycles didn’t differ, but there was a much higher prevalence of silent or subclinical ovulatory disturbances, and these were related to the increased stresses that women recorded in their diaries. This means that the estrogen levels were pretty close to normal but the progesterone levels were remarkably decreased,” Dr. Prior said.

Interestingly, reported menstrual cramps were also significantly more common during the pandemic and associated with ovulatory disruption.

“That is a new observation because previously we’ve always thought that you needed to ovulate in order to even have cramps,” she commented.

Asked whether COVID-19 itself might have played a role, Dr. Prior said no woman in the study tested positive for the virus or had long COVID.

“As far as I’m aware, it was the changes in employment … and caring for elders and worry about illness in somebody you loved that was related,” she said.

Asked what she thinks the result would be if the study were conducted now, she said: “I don’t know. We’re still in a stressful time with inflation and not complete recovery, so probably the issue is still very present.”

Dr. Prior and Dr. Neal-Perry have reported no relevant financial relationships.

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

ATLANTA – Disturbances in ovulation that didn’t produce any actual changes in the menstrual cycle of women were extremely common during the first year of the COVID-19 pandemic and were linked to emotional stress, according to the findings of an “experiment of nature” that allowed for comparison with women a decade earlier.

Findings from two studies of reproductive-age women, one conducted in 2006-2008 and the other in 2020-2021, were presented by Jerilynn C. Prior, MD, at the annual meeting of the Endocrine Society.

The comparison of the two time periods yielded several novel findings. “I was taught in medical school that when women don’t eat enough they lose their period. But what we now understand is there’s a graded response to various stressors, acting through the hypothalamus in a common pathway. There is a gradation of disturbances, some of which are subclinical or not obvious,” said Dr. Prior, professor of endocrinology and metabolism at the University of British Columbia, Vancouver.

Moreover, women’s menstrual cycle lengths didn’t differ across the two time periods, despite a dramatic 63% decrement in normal ovulatory function related to increased depression, anxiety, and outside stresses that the women reported in diaries.

“Assuming that regular cycles need normal ovulation is something we should just get out of our minds. It changes our concept about what’s normal if we only know about the cycle length,” she observed.

It will be critical going forward to see whether the ovulatory disturbances have resolved as the pandemic has shifted “because there’s strong evidence that ovulatory disturbances, even with normal cycle length, are related to bone loss and some evidence it’s related to early heart attacks, breast and endometrial cancers,” Dr. Prior said during a press conference.

Lisa Nainggolan/MDedge News

Asked to comment, session moderator Genevieve Neal-Perry, MD, PhD, told this news organization: “I think what we can take away is that stress itself is a modifier of the way the brain and the gonads communicate with each other, and that then has an impact on ovulatory function.”

Dr. Neal-Perry noted that the association of stress and ovulatory disruption has been reported in various ways previously, but “clearly it doesn’t affect everyone. What we don’t know is who is most susceptible. There have been some studies showing a genetic predisposition and a genetic anomaly that actually makes them more susceptible to the impact of stress on the reproductive system.”

But the lack of data on weight change in the study cohorts is a limitation. “To me one of the more important questions was what was going on with weight. Just looking at a static number doesn’t tell you whether there were changes. We know that weight gain or weight loss can stress the reproductive axis,” noted Dr. Neal-Parry of the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill.
 

‘Experiment of nature’ revealed invisible effect of pandemic stress

The women in both cohorts of the Menstruation Ovulation Study (MOS) were healthy volunteers aged 19-35 years recruited from the metropolitan Vancouver region. All were menstruating monthly and none were taking hormonal birth control. Recruitment for the second cohort had begun just prior to the March 2020 COVID-19 pandemic lockdown.

Interviewer-administered questionnaires (CaMos) covering demographics, socioeconomic status, and reproductive history, and daily diaries kept by the women (menstrual cycle diary) were identical for both cohorts.

Assessments of ovulation differed for the two studies but were cross-validated. For the earlier time period, ovulation was assessed by a threefold increase in follicular-to-luteal urinary progesterone (PdG). For the pandemic-era study, the validated quantitative basal temperature (QBT) method was used.

There were 301 women in the earlier cohort and 125 during the pandemic. Both were an average age of about 29 years and had a body mass index of about 24.3 kg/m² (within the normal range). The pandemic cohort was more racially/ethnically diverse than the earlier one and more in-line with recent census data.

More of the women were nulliparous during the pandemic than earlier (92.7% vs. 80.4%; P = .002).

The distribution of menstrual cycle lengths didn’t differ, with both cohorts averaging about 30 days (P = .893). However, while 90% of the women in the earlier cohort ovulated normally, only 37% did during the pandemic, a highly significant difference (P < .0001).

Thus, during the pandemic, 63% of women had “silent ovulatory disturbances,” either with short luteal phases after ovulation or no ovulation, compared with just 10% in the earlier cohort, “which is remarkable, unbelievable actually,” Dr. Prior remarked.  

The difference wasn’t explained by any of the demographic information collected either, including socioeconomic status, lifestyle, or reproductive history variables.

And it wasn’t because of COVID-19 vaccination, as the vaccine wasn’t available when most of the women were recruited, and of the 79 who were recruited during vaccine availability, only two received a COVID-19 vaccine during the study (and both had normal ovulation).

Employment changes, caring responsibilities, and worry likely causes

The information from the diaries was more revealing. Several diary components were far more common during the pandemic, including negative mood (feeling depressed or anxious, sleep problems, and outside stresses), self-worth, interest in sex, energy level, and appetite. All were significantly different between the two cohorts (P < .001) and between those with and without ovulatory disturbances.

“So menstrual cycle lengths and long cycles didn’t differ, but there was a much higher prevalence of silent or subclinical ovulatory disturbances, and these were related to the increased stresses that women recorded in their diaries. This means that the estrogen levels were pretty close to normal but the progesterone levels were remarkably decreased,” Dr. Prior said.

Interestingly, reported menstrual cramps were also significantly more common during the pandemic and associated with ovulatory disruption.

“That is a new observation because previously we’ve always thought that you needed to ovulate in order to even have cramps,” she commented.

Asked whether COVID-19 itself might have played a role, Dr. Prior said no woman in the study tested positive for the virus or had long COVID.

“As far as I’m aware, it was the changes in employment … and caring for elders and worry about illness in somebody you loved that was related,” she said.

Asked what she thinks the result would be if the study were conducted now, she said: “I don’t know. We’re still in a stressful time with inflation and not complete recovery, so probably the issue is still very present.”

Dr. Prior and Dr. Neal-Perry have reported no relevant financial relationships.

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

ATLANTA – Disturbances in ovulation that didn’t produce any actual changes in the menstrual cycle of women were extremely common during the first year of the COVID-19 pandemic and were linked to emotional stress, according to the findings of an “experiment of nature” that allowed for comparison with women a decade earlier.

Findings from two studies of reproductive-age women, one conducted in 2006-2008 and the other in 2020-2021, were presented by Jerilynn C. Prior, MD, at the annual meeting of the Endocrine Society.

The comparison of the two time periods yielded several novel findings. “I was taught in medical school that when women don’t eat enough they lose their period. But what we now understand is there’s a graded response to various stressors, acting through the hypothalamus in a common pathway. There is a gradation of disturbances, some of which are subclinical or not obvious,” said Dr. Prior, professor of endocrinology and metabolism at the University of British Columbia, Vancouver.

Moreover, women’s menstrual cycle lengths didn’t differ across the two time periods, despite a dramatic 63% decrement in normal ovulatory function related to increased depression, anxiety, and outside stresses that the women reported in diaries.

“Assuming that regular cycles need normal ovulation is something we should just get out of our minds. It changes our concept about what’s normal if we only know about the cycle length,” she observed.

It will be critical going forward to see whether the ovulatory disturbances have resolved as the pandemic has shifted “because there’s strong evidence that ovulatory disturbances, even with normal cycle length, are related to bone loss and some evidence it’s related to early heart attacks, breast and endometrial cancers,” Dr. Prior said during a press conference.

Lisa Nainggolan/MDedge News

Asked to comment, session moderator Genevieve Neal-Perry, MD, PhD, told this news organization: “I think what we can take away is that stress itself is a modifier of the way the brain and the gonads communicate with each other, and that then has an impact on ovulatory function.”

Dr. Neal-Perry noted that the association of stress and ovulatory disruption has been reported in various ways previously, but “clearly it doesn’t affect everyone. What we don’t know is who is most susceptible. There have been some studies showing a genetic predisposition and a genetic anomaly that actually makes them more susceptible to the impact of stress on the reproductive system.”

But the lack of data on weight change in the study cohorts is a limitation. “To me one of the more important questions was what was going on with weight. Just looking at a static number doesn’t tell you whether there were changes. We know that weight gain or weight loss can stress the reproductive axis,” noted Dr. Neal-Parry of the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill.
 

‘Experiment of nature’ revealed invisible effect of pandemic stress

The women in both cohorts of the Menstruation Ovulation Study (MOS) were healthy volunteers aged 19-35 years recruited from the metropolitan Vancouver region. All were menstruating monthly and none were taking hormonal birth control. Recruitment for the second cohort had begun just prior to the March 2020 COVID-19 pandemic lockdown.

Interviewer-administered questionnaires (CaMos) covering demographics, socioeconomic status, and reproductive history, and daily diaries kept by the women (menstrual cycle diary) were identical for both cohorts.

Assessments of ovulation differed for the two studies but were cross-validated. For the earlier time period, ovulation was assessed by a threefold increase in follicular-to-luteal urinary progesterone (PdG). For the pandemic-era study, the validated quantitative basal temperature (QBT) method was used.

There were 301 women in the earlier cohort and 125 during the pandemic. Both were an average age of about 29 years and had a body mass index of about 24.3 kg/m² (within the normal range). The pandemic cohort was more racially/ethnically diverse than the earlier one and more in-line with recent census data.

More of the women were nulliparous during the pandemic than earlier (92.7% vs. 80.4%; P = .002).

The distribution of menstrual cycle lengths didn’t differ, with both cohorts averaging about 30 days (P = .893). However, while 90% of the women in the earlier cohort ovulated normally, only 37% did during the pandemic, a highly significant difference (P < .0001).

Thus, during the pandemic, 63% of women had “silent ovulatory disturbances,” either with short luteal phases after ovulation or no ovulation, compared with just 10% in the earlier cohort, “which is remarkable, unbelievable actually,” Dr. Prior remarked.  

The difference wasn’t explained by any of the demographic information collected either, including socioeconomic status, lifestyle, or reproductive history variables.

And it wasn’t because of COVID-19 vaccination, as the vaccine wasn’t available when most of the women were recruited, and of the 79 who were recruited during vaccine availability, only two received a COVID-19 vaccine during the study (and both had normal ovulation).

Employment changes, caring responsibilities, and worry likely causes

The information from the diaries was more revealing. Several diary components were far more common during the pandemic, including negative mood (feeling depressed or anxious, sleep problems, and outside stresses), self-worth, interest in sex, energy level, and appetite. All were significantly different between the two cohorts (P < .001) and between those with and without ovulatory disturbances.

“So menstrual cycle lengths and long cycles didn’t differ, but there was a much higher prevalence of silent or subclinical ovulatory disturbances, and these were related to the increased stresses that women recorded in their diaries. This means that the estrogen levels were pretty close to normal but the progesterone levels were remarkably decreased,” Dr. Prior said.

Interestingly, reported menstrual cramps were also significantly more common during the pandemic and associated with ovulatory disruption.

“That is a new observation because previously we’ve always thought that you needed to ovulate in order to even have cramps,” she commented.

Asked whether COVID-19 itself might have played a role, Dr. Prior said no woman in the study tested positive for the virus or had long COVID.

“As far as I’m aware, it was the changes in employment … and caring for elders and worry about illness in somebody you loved that was related,” she said.

Asked what she thinks the result would be if the study were conducted now, she said: “I don’t know. We’re still in a stressful time with inflation and not complete recovery, so probably the issue is still very present.”

Dr. Prior and Dr. Neal-Perry have reported no relevant financial relationships.

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

CHICAGO – The COVID pandemic left hospitalist Ngozi Nwankwo, MD, with the most difficult patient interactions she had ever experienced.

“At my hospital, it was such a big thing to make sure that families are called,” said Dr. Nwankwo, in an interview following a session on compassionate communication at the annual meeting of the American College of Physicians. “So you have 19 patients, and you have to call almost every family to update them. And then you call, and they say, ‘Call this person as well.’ You feel like you’re at your wit’s end a lot of times.”

Sometimes, she has had to dig deep to find the empathy for patients that she knows her patients deserve.

“You really want to care by thinking about where is this patient coming from? What’s going on in their lives? And not just label them a difficult patient,” she said.

Become curious

Auguste Fortin, MD, MPH, offered advice for handling patient interactions under these kinds of circumstances, while serving as a moderator during the session.

“When the going gets tough, turn to wonder.” Become curious about why a patient might be feeling the way they are, he said.

Dr. Fortin, professor of internal medicine at Yale University, New Haven, Conn., said using the ADOBE acronym, has helped him more effectively communicate with his patients. This tool cues him to keep the following in mind: acknowledge, discover, opportunity, boundary setting, and extend.

He went on to explain to the audience why thinking about these terms is useful when interacting with patients.

First, acknowledge the feelings of the patient. Noting that a patient is angry, perhaps counterintuitively, helps, he said. In fact, not acknowledging the anger “throws gasoline on the fire.”

Then, discover the cause of their emotion. Saying "tell me more" and "help me understand" can be powerful tools, he noted.

Next, take this as an opportunity for empathy – especially important to remember when you’re being verbally attacked.

Boundary setting is important, because it lets the patient know that the conversation won’t continue unless they show the same respect the physician is showing, he said.

Finally, physicians can extend the system of support by asking others – such as colleagues or security – for help.

Use the NURS guide to show empathy

Dr. Fortin said he uses the “NURS” guide or calling to mind “name, express, respect, and support” to show empathy:

This involves naming a patient’s emotion; expressing understanding, with phrases like "I can see how you could be …"; showing respect, acknowledging a patient is going through a lot; and offering support, by saying something like, "Let’s see what we can do together to get to the bottom of this," he explained.

“My lived experience in using [these] in this order is that by the end of it, the patient cannot stay mad at me,” Dr. Fortin said.

“It’s really quite remarkable,” he added.

Steps for nonviolent communication

Rebecca Andrews, MD, MS, another moderator for the session, offered these steps for “nonviolent communication”:

• Observing the situation without blame or judgment.
• Telling the person how this situation makes you feel.
• Connecting with a need of the other person.
• Making a request that is specific and based on action, rather than a request not to do something, such as "Would you be willing to … ?"

Dr. Andrews, who is professor of medicine at the University of Connecticut, Farmington, said this approach has worked well for her, both in interactions with patients and in her personal life.

“It is evidence based that compassion actually makes care better,” she noted.

Varun Jain, MD, a member of the audience, expressed gratitude to the session’s speakers for teaching him something that he had not learned in medical school or residency.

“Every week you will have one or two people who will be labeled as ‘difficult,’ ” and it was nice to have some proven advice on how to handle these tough interactions, said the hospitalist at St. Francis Hospital in Hartford, Conn.

“We never got any actual training on this, and we were expected to know this because we are just physicians, and physicians are expected to be compassionate,” Dr. Jain said. “No one taught us how to have compassion.”

Dr. Fortin and Dr. Andrews disclosed no relevant financial relationships.

CHICAGO – The COVID pandemic left hospitalist Ngozi Nwankwo, MD, with the most difficult patient interactions she had ever experienced.

“At my hospital, it was such a big thing to make sure that families are called,” said Dr. Nwankwo, in an interview following a session on compassionate communication at the annual meeting of the American College of Physicians. “So you have 19 patients, and you have to call almost every family to update them. And then you call, and they say, ‘Call this person as well.’ You feel like you’re at your wit’s end a lot of times.”

Sometimes, she has had to dig deep to find the empathy for patients that she knows her patients deserve.

“You really want to care by thinking about where is this patient coming from? What’s going on in their lives? And not just label them a difficult patient,” she said.

Become curious

Auguste Fortin, MD, MPH, offered advice for handling patient interactions under these kinds of circumstances, while serving as a moderator during the session.

“When the going gets tough, turn to wonder.” Become curious about why a patient might be feeling the way they are, he said.

Dr. Fortin, professor of internal medicine at Yale University, New Haven, Conn., said using the ADOBE acronym, has helped him more effectively communicate with his patients. This tool cues him to keep the following in mind: acknowledge, discover, opportunity, boundary setting, and extend.

He went on to explain to the audience why thinking about these terms is useful when interacting with patients.

First, acknowledge the feelings of the patient. Noting that a patient is angry, perhaps counterintuitively, helps, he said. In fact, not acknowledging the anger “throws gasoline on the fire.”

Then, discover the cause of their emotion. Saying "tell me more" and "help me understand" can be powerful tools, he noted.

Next, take this as an opportunity for empathy – especially important to remember when you’re being verbally attacked.

Boundary setting is important, because it lets the patient know that the conversation won’t continue unless they show the same respect the physician is showing, he said.

Finally, physicians can extend the system of support by asking others – such as colleagues or security – for help.

Use the NURS guide to show empathy

Dr. Fortin said he uses the “NURS” guide or calling to mind “name, express, respect, and support” to show empathy:

This involves naming a patient’s emotion; expressing understanding, with phrases like "I can see how you could be …"; showing respect, acknowledging a patient is going through a lot; and offering support, by saying something like, "Let’s see what we can do together to get to the bottom of this," he explained.

“My lived experience in using [these] in this order is that by the end of it, the patient cannot stay mad at me,” Dr. Fortin said.

“It’s really quite remarkable,” he added.

Steps for nonviolent communication

Rebecca Andrews, MD, MS, another moderator for the session, offered these steps for “nonviolent communication”:

• Observing the situation without blame or judgment.
• Telling the person how this situation makes you feel.
• Connecting with a need of the other person.
• Making a request that is specific and based on action, rather than a request not to do something, such as "Would you be willing to … ?"

Dr. Andrews, who is professor of medicine at the University of Connecticut, Farmington, said this approach has worked well for her, both in interactions with patients and in her personal life.

“It is evidence based that compassion actually makes care better,” she noted.

Varun Jain, MD, a member of the audience, expressed gratitude to the session’s speakers for teaching him something that he had not learned in medical school or residency.

“Every week you will have one or two people who will be labeled as ‘difficult,’ ” and it was nice to have some proven advice on how to handle these tough interactions, said the hospitalist at St. Francis Hospital in Hartford, Conn.

“We never got any actual training on this, and we were expected to know this because we are just physicians, and physicians are expected to be compassionate,” Dr. Jain said. “No one taught us how to have compassion.”

Dr. Fortin and Dr. Andrews disclosed no relevant financial relationships.

CHICAGO – The COVID pandemic left hospitalist Ngozi Nwankwo, MD, with the most difficult patient interactions she had ever experienced.

“At my hospital, it was such a big thing to make sure that families are called,” said Dr. Nwankwo, in an interview following a session on compassionate communication at the annual meeting of the American College of Physicians. “So you have 19 patients, and you have to call almost every family to update them. And then you call, and they say, ‘Call this person as well.’ You feel like you’re at your wit’s end a lot of times.”

Sometimes, she has had to dig deep to find the empathy for patients that she knows her patients deserve.

“You really want to care by thinking about where is this patient coming from? What’s going on in their lives? And not just label them a difficult patient,” she said.

Become curious

Auguste Fortin, MD, MPH, offered advice for handling patient interactions under these kinds of circumstances, while serving as a moderator during the session.

“When the going gets tough, turn to wonder.” Become curious about why a patient might be feeling the way they are, he said.

Dr. Fortin, professor of internal medicine at Yale University, New Haven, Conn., said using the ADOBE acronym, has helped him more effectively communicate with his patients. This tool cues him to keep the following in mind: acknowledge, discover, opportunity, boundary setting, and extend.

He went on to explain to the audience why thinking about these terms is useful when interacting with patients.

First, acknowledge the feelings of the patient. Noting that a patient is angry, perhaps counterintuitively, helps, he said. In fact, not acknowledging the anger “throws gasoline on the fire.”

Then, discover the cause of their emotion. Saying "tell me more" and "help me understand" can be powerful tools, he noted.

Next, take this as an opportunity for empathy – especially important to remember when you’re being verbally attacked.

Boundary setting is important, because it lets the patient know that the conversation won’t continue unless they show the same respect the physician is showing, he said.

Finally, physicians can extend the system of support by asking others – such as colleagues or security – for help.

Use the NURS guide to show empathy

Dr. Fortin said he uses the “NURS” guide or calling to mind “name, express, respect, and support” to show empathy:

This involves naming a patient’s emotion; expressing understanding, with phrases like "I can see how you could be …"; showing respect, acknowledging a patient is going through a lot; and offering support, by saying something like, "Let’s see what we can do together to get to the bottom of this," he explained.

“My lived experience in using [these] in this order is that by the end of it, the patient cannot stay mad at me,” Dr. Fortin said.

“It’s really quite remarkable,” he added.

Steps for nonviolent communication

Rebecca Andrews, MD, MS, another moderator for the session, offered these steps for “nonviolent communication”:

• Observing the situation without blame or judgment.
• Telling the person how this situation makes you feel.
• Connecting with a need of the other person.
• Making a request that is specific and based on action, rather than a request not to do something, such as "Would you be willing to … ?"

Dr. Andrews, who is professor of medicine at the University of Connecticut, Farmington, said this approach has worked well for her, both in interactions with patients and in her personal life.

“It is evidence based that compassion actually makes care better,” she noted.

Varun Jain, MD, a member of the audience, expressed gratitude to the session’s speakers for teaching him something that he had not learned in medical school or residency.

“Every week you will have one or two people who will be labeled as ‘difficult,’ ” and it was nice to have some proven advice on how to handle these tough interactions, said the hospitalist at St. Francis Hospital in Hartford, Conn.

“We never got any actual training on this, and we were expected to know this because we are just physicians, and physicians are expected to be compassionate,” Dr. Jain said. “No one taught us how to have compassion.”

Dr. Fortin and Dr. Andrews disclosed no relevant financial relationships.