Rheumatology News

Patients who received a first prescription for medicinal cannabis for chronic pain were more likely to have new onset of arrhythmia – bradyarrhythmia, tachyarrhythmia, or a conduction disorder – within 6 months than were similar nonusers, in a new case-control study.

VladK213/Getty Images

There were no between-group differences in the incidence of heart failure or acute coronary syndrome.

The researchers identified 5,071 patients in a national Danish registry who had filled at least one prescription for medicinal cannabis for chronic pain and matched each patient with five patients of the same sex, age range, and type of chronic pain who did not receive this therapy.

The relative risk for arrhythmia was 83% higher in those who used medicinal cannabis than it was in the other patients, study author Nina Nouhravesh, MD, told this news organization in an email.

However, the absolute risks for arrhythmia were slight – a 0.86% risk (95% confidence interval, 0.61%-1.1%) in medicinal cannabis users versus a 0.47% risk (95% CI, 0.38%-0.56%) in those who did not use medicinal cannabis.

“Since medical cannabis is a relatively new drug for a large market of patients with chronic pain, it is important to investigate and report serious side effects,” said Dr. Nouhravesh, from Gentofte University Hospital, Denmark.

The study results, she said, suggest that “there may be a previously unreported risk of arrhythmias following medical cannabis use.”

“Even though the absolute risk difference is small, both patients and physicians should have as much information as possible when weighing up the pros and cons of any treatment,” Dr. Nouhravesh said, adding that “the findings of this study raise concerns for both legal and illegal [cannabis] use worldwide.”

The results will be presented at the annual European Society of Cardiology (ESC) Congress 2022.
 

Too soon to tell?

However, Brian Olshansky, MD, who was not involved with this research, cautions that it is important to consider several study limitations before drawing clinical implications.

“Other data and reports have considered the possibility of arrhythmias in relationship to marijuana use, and the data go in both directions,” Dr. Olshansky, a clinical cardiac electrophysiologist and professor emeritus at University of Iowa Hospitals, Iowa City, pointed out in an email.

“Importantly, arrhythmias, by themselves, are not necessarily consequential,” he stressed. “In any case,” he added, the risks in the current study are “extraordinarily small.”

Sinus bradycardia, sinus tachycardia, and premature atrial or ventricular contractions could be totally benign, he said. On the other hand, arrhythmias may indicate the presence of atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation, which are potentially dangerous.

There may be a specific “high risk” group who can develop potentially serious arrhythmias, Dr. Olshansky suggested.

“There is no evidence that any of these patients underwent or required any treatment for their arrhythmia or that stopping or starting the cannabinoids affected the arrhythmia one way or the other,” he said. “In addition, there is no dose/arrhythmia relationship.”

More patients in the medicinal cannabis group than in the nonuser group were also taking opioids (49% vs. 30%), nonsteroidal anti-inflammatory drugs (24% vs. 19%), antiepileptics (35% vs. 23%), or tricyclic antidepressants (11% vs. 4%), he noted.

In summary, according to Dr. Olshansky, “these data pose no obvious health concern and provide no vital knowledge for physicians prescribing cannabis.”

“My concern is that the information will be overblown,” he cautioned. “If the cannabinoid actually has benefit in terms of pain reduction, its use may be mitigated based on the fear of an arrhythmia that may occur – but the risk of an arrhythmia, in any event, is very small and undefined in terms of its seriousness.”
 

Cancer, musculoskeletal, and neurologic pain

For this analysis, the researchers identified 1.8 million patients in Denmark who were diagnosed with chronic pain between 2018 and 2021.

Of those, around 5,000 patients had claimed at least one prescription of medicinal cannabis (dronabinol 29%, cannabinoids 46%, or cannabidiol 25%).

The patients had a median age of 60 years, and 63% were women.

The cannabis users had been prescribed this therapy for musculoskeletal (35%), cancer (18%), neurological (14%), or other (33%) pain, Dr. Nouhravesh said. 

The researchers and Dr. Olshansky have no relevant financial disclosures.  

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

Patients who received a first prescription for medicinal cannabis for chronic pain were more likely to have new onset of arrhythmia – bradyarrhythmia, tachyarrhythmia, or a conduction disorder – within 6 months than were similar nonusers, in a new case-control study.

VladK213/Getty Images

There were no between-group differences in the incidence of heart failure or acute coronary syndrome.

The researchers identified 5,071 patients in a national Danish registry who had filled at least one prescription for medicinal cannabis for chronic pain and matched each patient with five patients of the same sex, age range, and type of chronic pain who did not receive this therapy.

The relative risk for arrhythmia was 83% higher in those who used medicinal cannabis than it was in the other patients, study author Nina Nouhravesh, MD, told this news organization in an email.

However, the absolute risks for arrhythmia were slight – a 0.86% risk (95% confidence interval, 0.61%-1.1%) in medicinal cannabis users versus a 0.47% risk (95% CI, 0.38%-0.56%) in those who did not use medicinal cannabis.

“Since medical cannabis is a relatively new drug for a large market of patients with chronic pain, it is important to investigate and report serious side effects,” said Dr. Nouhravesh, from Gentofte University Hospital, Denmark.

The study results, she said, suggest that “there may be a previously unreported risk of arrhythmias following medical cannabis use.”

“Even though the absolute risk difference is small, both patients and physicians should have as much information as possible when weighing up the pros and cons of any treatment,” Dr. Nouhravesh said, adding that “the findings of this study raise concerns for both legal and illegal [cannabis] use worldwide.”

The results will be presented at the annual European Society of Cardiology (ESC) Congress 2022.
 

Too soon to tell?

However, Brian Olshansky, MD, who was not involved with this research, cautions that it is important to consider several study limitations before drawing clinical implications.

“Other data and reports have considered the possibility of arrhythmias in relationship to marijuana use, and the data go in both directions,” Dr. Olshansky, a clinical cardiac electrophysiologist and professor emeritus at University of Iowa Hospitals, Iowa City, pointed out in an email.

“Importantly, arrhythmias, by themselves, are not necessarily consequential,” he stressed. “In any case,” he added, the risks in the current study are “extraordinarily small.”

Sinus bradycardia, sinus tachycardia, and premature atrial or ventricular contractions could be totally benign, he said. On the other hand, arrhythmias may indicate the presence of atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation, which are potentially dangerous.

There may be a specific “high risk” group who can develop potentially serious arrhythmias, Dr. Olshansky suggested.

“There is no evidence that any of these patients underwent or required any treatment for their arrhythmia or that stopping or starting the cannabinoids affected the arrhythmia one way or the other,” he said. “In addition, there is no dose/arrhythmia relationship.”

More patients in the medicinal cannabis group than in the nonuser group were also taking opioids (49% vs. 30%), nonsteroidal anti-inflammatory drugs (24% vs. 19%), antiepileptics (35% vs. 23%), or tricyclic antidepressants (11% vs. 4%), he noted.

In summary, according to Dr. Olshansky, “these data pose no obvious health concern and provide no vital knowledge for physicians prescribing cannabis.”

“My concern is that the information will be overblown,” he cautioned. “If the cannabinoid actually has benefit in terms of pain reduction, its use may be mitigated based on the fear of an arrhythmia that may occur – but the risk of an arrhythmia, in any event, is very small and undefined in terms of its seriousness.”
 

Cancer, musculoskeletal, and neurologic pain

For this analysis, the researchers identified 1.8 million patients in Denmark who were diagnosed with chronic pain between 2018 and 2021.

Of those, around 5,000 patients had claimed at least one prescription of medicinal cannabis (dronabinol 29%, cannabinoids 46%, or cannabidiol 25%).

The patients had a median age of 60 years, and 63% were women.

The cannabis users had been prescribed this therapy for musculoskeletal (35%), cancer (18%), neurological (14%), or other (33%) pain, Dr. Nouhravesh said. 

The researchers and Dr. Olshansky have no relevant financial disclosures.  

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

Patients who received a first prescription for medicinal cannabis for chronic pain were more likely to have new onset of arrhythmia – bradyarrhythmia, tachyarrhythmia, or a conduction disorder – within 6 months than were similar nonusers, in a new case-control study.

VladK213/Getty Images

There were no between-group differences in the incidence of heart failure or acute coronary syndrome.

The researchers identified 5,071 patients in a national Danish registry who had filled at least one prescription for medicinal cannabis for chronic pain and matched each patient with five patients of the same sex, age range, and type of chronic pain who did not receive this therapy.

The relative risk for arrhythmia was 83% higher in those who used medicinal cannabis than it was in the other patients, study author Nina Nouhravesh, MD, told this news organization in an email.

However, the absolute risks for arrhythmia were slight – a 0.86% risk (95% confidence interval, 0.61%-1.1%) in medicinal cannabis users versus a 0.47% risk (95% CI, 0.38%-0.56%) in those who did not use medicinal cannabis.

“Since medical cannabis is a relatively new drug for a large market of patients with chronic pain, it is important to investigate and report serious side effects,” said Dr. Nouhravesh, from Gentofte University Hospital, Denmark.

The study results, she said, suggest that “there may be a previously unreported risk of arrhythmias following medical cannabis use.”

“Even though the absolute risk difference is small, both patients and physicians should have as much information as possible when weighing up the pros and cons of any treatment,” Dr. Nouhravesh said, adding that “the findings of this study raise concerns for both legal and illegal [cannabis] use worldwide.”

The results will be presented at the annual European Society of Cardiology (ESC) Congress 2022.
 

Too soon to tell?

However, Brian Olshansky, MD, who was not involved with this research, cautions that it is important to consider several study limitations before drawing clinical implications.

“Other data and reports have considered the possibility of arrhythmias in relationship to marijuana use, and the data go in both directions,” Dr. Olshansky, a clinical cardiac electrophysiologist and professor emeritus at University of Iowa Hospitals, Iowa City, pointed out in an email.

“Importantly, arrhythmias, by themselves, are not necessarily consequential,” he stressed. “In any case,” he added, the risks in the current study are “extraordinarily small.”

Sinus bradycardia, sinus tachycardia, and premature atrial or ventricular contractions could be totally benign, he said. On the other hand, arrhythmias may indicate the presence of atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation, which are potentially dangerous.

There may be a specific “high risk” group who can develop potentially serious arrhythmias, Dr. Olshansky suggested.

“There is no evidence that any of these patients underwent or required any treatment for their arrhythmia or that stopping or starting the cannabinoids affected the arrhythmia one way or the other,” he said. “In addition, there is no dose/arrhythmia relationship.”

More patients in the medicinal cannabis group than in the nonuser group were also taking opioids (49% vs. 30%), nonsteroidal anti-inflammatory drugs (24% vs. 19%), antiepileptics (35% vs. 23%), or tricyclic antidepressants (11% vs. 4%), he noted.

In summary, according to Dr. Olshansky, “these data pose no obvious health concern and provide no vital knowledge for physicians prescribing cannabis.”

“My concern is that the information will be overblown,” he cautioned. “If the cannabinoid actually has benefit in terms of pain reduction, its use may be mitigated based on the fear of an arrhythmia that may occur – but the risk of an arrhythmia, in any event, is very small and undefined in terms of its seriousness.”
 

Cancer, musculoskeletal, and neurologic pain

For this analysis, the researchers identified 1.8 million patients in Denmark who were diagnosed with chronic pain between 2018 and 2021.

Of those, around 5,000 patients had claimed at least one prescription of medicinal cannabis (dronabinol 29%, cannabinoids 46%, or cannabidiol 25%).

The patients had a median age of 60 years, and 63% were women.

The cannabis users had been prescribed this therapy for musculoskeletal (35%), cancer (18%), neurological (14%), or other (33%) pain, Dr. Nouhravesh said. 

The researchers and Dr. Olshansky have no relevant financial disclosures.  

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

People with diabetes who take nonsteroidal anti-inflammatory drugs even on a short-term basis may have about a 50% greater risk of developing heart failure, according to results from a national registry study of more than 330,000 patients to be presented at the annual congress of the European Society of Cardiology.

“According to data from this study, even short-term NSAID use – within 28 days – in patients with type 2 diabetes mellitus are associated with an increased risk of first-time heart failure hospitalization,” lead author Anders Holt, MD, said in an interview.

“Further, it seems that patients above 79 years of age or with elevated hemoglobin A1c levels, along with new users of NSAIDs, are particularly susceptible.” He added that no such association was found in patients below age 65 years with normal A1c levels.

Dr. Holt has a dual appointment as a cardiologist at Copenhagen University and Herlev-Gentofte Hospital in Hellerup, Denmark, and the department of epidemiology and biostatistics at the University of Auckland (New Zealand). Jarl Emmanuel Strange, MD, PhD, a fellow at Copenhagen University, is to present the abstract on Aug. 26.

“This is quite an important observation given that, unfortunately, NSAIDs continue to be prescribed rather easily to people with diabetes and these agents do have risk,” said Rodica Busui, MD, PhD, codirector of the JDRF Center of Excellence at the University of Michigan, Ann Arbor, and president-elect for medicine and science of the American Diabetes Association. Dr. Busui is also lead author of an ADA/American College of Cardiology consensus report on heart failure in diabetes.

The study hypothesized that fluid retention “is a known but underappreciated side effect” of NSAID use and that short-term NSAID use could lead to heart failure in patients with type 2 diabetes, which has been linked to subclinical cardiomyopathy and kidney dysfunction.

“According to this study and particularly the subgroups analyses, it seems that incident heart failure associated with short-term NSAID use could be more than ‘just fluid overload,’ ” Dr. Holt said. “Further investigations into the specific mechanisms causing these associations are warranted.”

The study identified 331,189 patients with type 2 diabetes in nationwide Danish registries from 1998 to 2018. Median age was 62 years, and 23,308 (7%) were hospitalized with heart failure during follow-up, Dr. Holt said. Of them, 16% claimed at least one NSAID prescription within 2 years and 3% claimed they had at least three prescriptions.

Study follow-up started 120 days after the first-time type 2 diabetes diagnosis and focused on patients who had no previous diagnosis of heart failure or rheumatologic disease. The investigators reported on patients who had one, two, three or four prescriptions for NSAID within a year of starting follow-up.

The study used a case-crossover design, which, the abstract stated, “uses each individual as his or her own control making it suitable to study the effect of short-term exposure on immediate events while mitigating unmeasured confounding.”

Dr. Holt noted that short-term NSAID use was linked to increased risk of heart failure hospitalization (odds ratio, 1.43; 95% confidence interval, 1.27-1.63). The investigators identified even greater risks in three subgroups: age of at least 80 years (OR, 1.78; 95% CI, 1.39-2.28), elevated A1c levels treated with one or less antidiabetic medication (OR 1.68; 95% CI, 1-2.88), and patients without previous NSAID use (OR, 2.71; 95% CI, 1.78-4.23).

In the cohort, celecoxib and naproxen were rarely used (0.4 and 0.9%, respectively), while 3.3% of patients took diclofenac or 12.2% ibuprofen. The latter two NSAIDs had ORs of 1.48 and 1.46, respectively, for hospitalization for new-onset heart failure using 28-day exposure windows (95% CI for both, 1.1­-2 and 1.26-1.69). No increased risk emerged for celecoxib or naproxen.

“High age and A1c levels and being a new user were tied to the strongest associations, along with known use of RASi [renin-angiotensin system inhibitors] and diuretics,” Dr. Holt said. “On the contrary, it seemed safe – from our data – to prescribe short-term NSAIDs for patients below 65 years of age and patients with normal A1c levels.

“Interestingly,” he added, “subclinical structural heart disease among patients with type 2 diabetes could play an important role.”

The findings are noteworthy, Dr. Busui said. “Although there are some limitations with the study design in general when one looks at data extracted from registers, the very large sample size and the fact that the Danish national register captures data in a standardized fashion does make the findings very relevant, especially now that we have confirmed that heart failure is the most prevalent cardiovascular complication in people with diabetes, as we have highlighted in the most recent ADA/ACC consensus on heart failure in diabetes.”

The study received funding from the Danish Heart Foundation and a number of private foundations. Dr. Holt and colleagues have no disclosures. Dr. Busui disclosed relationships with AstraZeneca, Boehringer Ingelheim–Lilly Alliance, Novo Nordisk, Averitas Pharma, Nevro, Regenacy Pharmaceuticals and Roche Diagnostics.

 

People with diabetes who take nonsteroidal anti-inflammatory drugs even on a short-term basis may have about a 50% greater risk of developing heart failure, according to results from a national registry study of more than 330,000 patients to be presented at the annual congress of the European Society of Cardiology.

“According to data from this study, even short-term NSAID use – within 28 days – in patients with type 2 diabetes mellitus are associated with an increased risk of first-time heart failure hospitalization,” lead author Anders Holt, MD, said in an interview.

“Further, it seems that patients above 79 years of age or with elevated hemoglobin A1c levels, along with new users of NSAIDs, are particularly susceptible.” He added that no such association was found in patients below age 65 years with normal A1c levels.

Dr. Holt has a dual appointment as a cardiologist at Copenhagen University and Herlev-Gentofte Hospital in Hellerup, Denmark, and the department of epidemiology and biostatistics at the University of Auckland (New Zealand). Jarl Emmanuel Strange, MD, PhD, a fellow at Copenhagen University, is to present the abstract on Aug. 26.

“This is quite an important observation given that, unfortunately, NSAIDs continue to be prescribed rather easily to people with diabetes and these agents do have risk,” said Rodica Busui, MD, PhD, codirector of the JDRF Center of Excellence at the University of Michigan, Ann Arbor, and president-elect for medicine and science of the American Diabetes Association. Dr. Busui is also lead author of an ADA/American College of Cardiology consensus report on heart failure in diabetes.

The study hypothesized that fluid retention “is a known but underappreciated side effect” of NSAID use and that short-term NSAID use could lead to heart failure in patients with type 2 diabetes, which has been linked to subclinical cardiomyopathy and kidney dysfunction.

“According to this study and particularly the subgroups analyses, it seems that incident heart failure associated with short-term NSAID use could be more than ‘just fluid overload,’ ” Dr. Holt said. “Further investigations into the specific mechanisms causing these associations are warranted.”

The study identified 331,189 patients with type 2 diabetes in nationwide Danish registries from 1998 to 2018. Median age was 62 years, and 23,308 (7%) were hospitalized with heart failure during follow-up, Dr. Holt said. Of them, 16% claimed at least one NSAID prescription within 2 years and 3% claimed they had at least three prescriptions.

Study follow-up started 120 days after the first-time type 2 diabetes diagnosis and focused on patients who had no previous diagnosis of heart failure or rheumatologic disease. The investigators reported on patients who had one, two, three or four prescriptions for NSAID within a year of starting follow-up.

The study used a case-crossover design, which, the abstract stated, “uses each individual as his or her own control making it suitable to study the effect of short-term exposure on immediate events while mitigating unmeasured confounding.”

Dr. Holt noted that short-term NSAID use was linked to increased risk of heart failure hospitalization (odds ratio, 1.43; 95% confidence interval, 1.27-1.63). The investigators identified even greater risks in three subgroups: age of at least 80 years (OR, 1.78; 95% CI, 1.39-2.28), elevated A1c levels treated with one or less antidiabetic medication (OR 1.68; 95% CI, 1-2.88), and patients without previous NSAID use (OR, 2.71; 95% CI, 1.78-4.23).

In the cohort, celecoxib and naproxen were rarely used (0.4 and 0.9%, respectively), while 3.3% of patients took diclofenac or 12.2% ibuprofen. The latter two NSAIDs had ORs of 1.48 and 1.46, respectively, for hospitalization for new-onset heart failure using 28-day exposure windows (95% CI for both, 1.1­-2 and 1.26-1.69). No increased risk emerged for celecoxib or naproxen.

“High age and A1c levels and being a new user were tied to the strongest associations, along with known use of RASi [renin-angiotensin system inhibitors] and diuretics,” Dr. Holt said. “On the contrary, it seemed safe – from our data – to prescribe short-term NSAIDs for patients below 65 years of age and patients with normal A1c levels.

“Interestingly,” he added, “subclinical structural heart disease among patients with type 2 diabetes could play an important role.”

The findings are noteworthy, Dr. Busui said. “Although there are some limitations with the study design in general when one looks at data extracted from registers, the very large sample size and the fact that the Danish national register captures data in a standardized fashion does make the findings very relevant, especially now that we have confirmed that heart failure is the most prevalent cardiovascular complication in people with diabetes, as we have highlighted in the most recent ADA/ACC consensus on heart failure in diabetes.”

The study received funding from the Danish Heart Foundation and a number of private foundations. Dr. Holt and colleagues have no disclosures. Dr. Busui disclosed relationships with AstraZeneca, Boehringer Ingelheim–Lilly Alliance, Novo Nordisk, Averitas Pharma, Nevro, Regenacy Pharmaceuticals and Roche Diagnostics.

 

People with diabetes who take nonsteroidal anti-inflammatory drugs even on a short-term basis may have about a 50% greater risk of developing heart failure, according to results from a national registry study of more than 330,000 patients to be presented at the annual congress of the European Society of Cardiology.

“According to data from this study, even short-term NSAID use – within 28 days – in patients with type 2 diabetes mellitus are associated with an increased risk of first-time heart failure hospitalization,” lead author Anders Holt, MD, said in an interview.

“Further, it seems that patients above 79 years of age or with elevated hemoglobin A1c levels, along with new users of NSAIDs, are particularly susceptible.” He added that no such association was found in patients below age 65 years with normal A1c levels.

Dr. Holt has a dual appointment as a cardiologist at Copenhagen University and Herlev-Gentofte Hospital in Hellerup, Denmark, and the department of epidemiology and biostatistics at the University of Auckland (New Zealand). Jarl Emmanuel Strange, MD, PhD, a fellow at Copenhagen University, is to present the abstract on Aug. 26.

“This is quite an important observation given that, unfortunately, NSAIDs continue to be prescribed rather easily to people with diabetes and these agents do have risk,” said Rodica Busui, MD, PhD, codirector of the JDRF Center of Excellence at the University of Michigan, Ann Arbor, and president-elect for medicine and science of the American Diabetes Association. Dr. Busui is also lead author of an ADA/American College of Cardiology consensus report on heart failure in diabetes.

The study hypothesized that fluid retention “is a known but underappreciated side effect” of NSAID use and that short-term NSAID use could lead to heart failure in patients with type 2 diabetes, which has been linked to subclinical cardiomyopathy and kidney dysfunction.

“According to this study and particularly the subgroups analyses, it seems that incident heart failure associated with short-term NSAID use could be more than ‘just fluid overload,’ ” Dr. Holt said. “Further investigations into the specific mechanisms causing these associations are warranted.”

The study identified 331,189 patients with type 2 diabetes in nationwide Danish registries from 1998 to 2018. Median age was 62 years, and 23,308 (7%) were hospitalized with heart failure during follow-up, Dr. Holt said. Of them, 16% claimed at least one NSAID prescription within 2 years and 3% claimed they had at least three prescriptions.

Study follow-up started 120 days after the first-time type 2 diabetes diagnosis and focused on patients who had no previous diagnosis of heart failure or rheumatologic disease. The investigators reported on patients who had one, two, three or four prescriptions for NSAID within a year of starting follow-up.

The study used a case-crossover design, which, the abstract stated, “uses each individual as his or her own control making it suitable to study the effect of short-term exposure on immediate events while mitigating unmeasured confounding.”

Dr. Holt noted that short-term NSAID use was linked to increased risk of heart failure hospitalization (odds ratio, 1.43; 95% confidence interval, 1.27-1.63). The investigators identified even greater risks in three subgroups: age of at least 80 years (OR, 1.78; 95% CI, 1.39-2.28), elevated A1c levels treated with one or less antidiabetic medication (OR 1.68; 95% CI, 1-2.88), and patients without previous NSAID use (OR, 2.71; 95% CI, 1.78-4.23).

In the cohort, celecoxib and naproxen were rarely used (0.4 and 0.9%, respectively), while 3.3% of patients took diclofenac or 12.2% ibuprofen. The latter two NSAIDs had ORs of 1.48 and 1.46, respectively, for hospitalization for new-onset heart failure using 28-day exposure windows (95% CI for both, 1.1­-2 and 1.26-1.69). No increased risk emerged for celecoxib or naproxen.

“High age and A1c levels and being a new user were tied to the strongest associations, along with known use of RASi [renin-angiotensin system inhibitors] and diuretics,” Dr. Holt said. “On the contrary, it seemed safe – from our data – to prescribe short-term NSAIDs for patients below 65 years of age and patients with normal A1c levels.

“Interestingly,” he added, “subclinical structural heart disease among patients with type 2 diabetes could play an important role.”

The findings are noteworthy, Dr. Busui said. “Although there are some limitations with the study design in general when one looks at data extracted from registers, the very large sample size and the fact that the Danish national register captures data in a standardized fashion does make the findings very relevant, especially now that we have confirmed that heart failure is the most prevalent cardiovascular complication in people with diabetes, as we have highlighted in the most recent ADA/ACC consensus on heart failure in diabetes.”

The study received funding from the Danish Heart Foundation and a number of private foundations. Dr. Holt and colleagues have no disclosures. Dr. Busui disclosed relationships with AstraZeneca, Boehringer Ingelheim–Lilly Alliance, Novo Nordisk, Averitas Pharma, Nevro, Regenacy Pharmaceuticals and Roche Diagnostics.

 

Life expectancy in the United States fell by 1.8 years in 2020, the first year of the COVID-19 pandemic, new figures from the federal government show.

All 50 states and the District of Columbia saw drops in life expectancy, according to the report from the Centers for Disease Control and Prevention’s National Center for Health Statistics.

The declines were mostly because of COVID-19 and “unintentional injuries,” such as drug overdoses.

The overall drop took national life expectancy from 78.8 years in 2019 to 77 years in 2020, the first year of the pandemic, ABC News reported.

States in the West and Northwest generally had higher life expectancy, with states in the South having the lowest.

Hawaii had the highest life expectancy at 80.7 years. It was followed by Washington, Minnesota, California, and Massachusetts. Mississippi had the lowest at 71.9 years, the figures show. The others in the bottom five were West Virginia, Louisiana, Alabama, and Kentucky.

In 2020, COVID-19 was the third-highest cause of death, leading to more than 350,000, the CDC reported earlier this year. At the same time, more people are dying annually from drug overdoses. A record 83,500 fatal overdoses were reported in 2020.

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

Life expectancy in the United States fell by 1.8 years in 2020, the first year of the COVID-19 pandemic, new figures from the federal government show.

All 50 states and the District of Columbia saw drops in life expectancy, according to the report from the Centers for Disease Control and Prevention’s National Center for Health Statistics.

The declines were mostly because of COVID-19 and “unintentional injuries,” such as drug overdoses.

The overall drop took national life expectancy from 78.8 years in 2019 to 77 years in 2020, the first year of the pandemic, ABC News reported.

States in the West and Northwest generally had higher life expectancy, with states in the South having the lowest.

Hawaii had the highest life expectancy at 80.7 years. It was followed by Washington, Minnesota, California, and Massachusetts. Mississippi had the lowest at 71.9 years, the figures show. The others in the bottom five were West Virginia, Louisiana, Alabama, and Kentucky.

In 2020, COVID-19 was the third-highest cause of death, leading to more than 350,000, the CDC reported earlier this year. At the same time, more people are dying annually from drug overdoses. A record 83,500 fatal overdoses were reported in 2020.

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

Life expectancy in the United States fell by 1.8 years in 2020, the first year of the COVID-19 pandemic, new figures from the federal government show.

All 50 states and the District of Columbia saw drops in life expectancy, according to the report from the Centers for Disease Control and Prevention’s National Center for Health Statistics.

The declines were mostly because of COVID-19 and “unintentional injuries,” such as drug overdoses.

The overall drop took national life expectancy from 78.8 years in 2019 to 77 years in 2020, the first year of the pandemic, ABC News reported.

States in the West and Northwest generally had higher life expectancy, with states in the South having the lowest.

Hawaii had the highest life expectancy at 80.7 years. It was followed by Washington, Minnesota, California, and Massachusetts. Mississippi had the lowest at 71.9 years, the figures show. The others in the bottom five were West Virginia, Louisiana, Alabama, and Kentucky.

In 2020, COVID-19 was the third-highest cause of death, leading to more than 350,000, the CDC reported earlier this year. At the same time, more people are dying annually from drug overdoses. A record 83,500 fatal overdoses were reported in 2020.

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

Something about this COVID testing smells fishy

The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!

Alexander Zvir/Pexels

Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.

An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”

In the words of George Takei: “Oh my.”

Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.

“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.

Hegemony restored.
 

Not even God could save them from worms

The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.

Cambridge Archaeological Unit

So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.

This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.

Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.

Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
 

What’s a shared genotype between friends?

Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.

François Brunelle

“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”

The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.

The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.

Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
 

The secret to a good relationship? It’s a secret

Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.

bilderlounge

According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.

In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).

“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.

Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.

So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.

Something about this COVID testing smells fishy

The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!

Alexander Zvir/Pexels

Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.

An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”

In the words of George Takei: “Oh my.”

Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.

“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.

Hegemony restored.
 

Not even God could save them from worms

The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.

Cambridge Archaeological Unit

So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.

This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.

Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.

Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
 

What’s a shared genotype between friends?

Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.

François Brunelle

“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”

The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.

The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.

Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
 

The secret to a good relationship? It’s a secret

Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.

bilderlounge

According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.

In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).

“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.

Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.

So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.

Something about this COVID testing smells fishy

The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!

Alexander Zvir/Pexels

Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.

An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”

In the words of George Takei: “Oh my.”

Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.

“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.

Hegemony restored.
 

Not even God could save them from worms

The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.

Cambridge Archaeological Unit

So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.

This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.

Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.

Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
 

What’s a shared genotype between friends?

Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.

François Brunelle

“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”

The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.

The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.

Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
 

The secret to a good relationship? It’s a secret

Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.

bilderlounge

According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.

In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).

“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.

Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.

So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.

The investigational IL-6 inhibitor olokizumab fared better than placebo and was noninferior to the tumor necrosis factor inhibitor (TNFi) adalimumab (Humira) in patients with moderate to severe rheumatoid arthritis (RA) who’d had an inadequate response to methotrexate alone, according to new findings published in the New England Journal of Medicine.

The results from the phase 3, multicenter, double-blind, parallel-group, randomized, placebo- and active-comparator–controlled trial, called Clinical Rheumatoid Arthritis Development for Olokizumab (CREDO2), add to the evidence base on the drug, which was developed by R-Pharm in Russia and has been approved for use there. Last year, researchers reported results from two trials showing sustained improvements in symptoms, function, and quality of life in patients with an inadequate response to anti-TNF treatment.

“Once approved, olokizumab can be used in patients who have not responded well to either methotrexate or any biological disease-modifying antirheumatic drug or any JAK [Janus kinase] inhibitor in combination with methotrexate or alone,” said Josef Smolen, MD, chair of rheumatology at the Medical University of Vienna and the lead author on the study.

Researchers randomized 1,648 patients to 64 mg of olokizumab every 2 or 4 weeks, adalimumab every 2 weeks, or placebo. All patient groups continued to receive methotrexate. A total of 89.7% of the participants completed 24 weeks of treatment. By that point, 74.1% of those receiving olokizumab every 2 weeks had achieved an ACR 20 response, an improvement of at least 20% in American College of Rheumatology response criteria, including tender and swollen joints, and 71.4% in the group receiving olokizumab every 4 weeks; 69.0% in the adalimumab group; and 46.5% in the placebo group had achieved an ACR 20 response. Olokizumab benefits were also seen for Disease Activity Score in 28 joints, disability index scores, and ACR 50 responses, the researchers reported.

Approved IL-6 inhibitors tocilizumab (Actemra) and sarilumab (Kevzara) target the interleukin (IL)-6 receptor (IL-6R), but olokizumab targets a protein, glycoprotein 130 (GP130), to which the IL-6 and IL-6–receptor complex binds. This approach could offer an added benefit, Dr. Smolen said.

“Previously studied anti–IL-6 antibodies and anti–IL-6R antibodies prevent binding of IL-6 to the IL-6R,” he said. “Moreover, the amount of protein needed to inhibit IL-6 is lower compared to the approved antireceptor antibodies. Olokizumab has also been shown to be effective when given every 4 weeks in many patients, compared with the need for weekly or every-other-week applications with tocilizumab and sarilumab. From these perspectives, this novel mode of action may, indeed, provide an advantage.”

ACR 70 – an improvement of at least 70% in the ACR response criteria – was an exploratory endpoint in the trial. This response was seen in 28% of those receiving olokizumab, compared with 11% in the placebo group, but researchers cautioned that “no conclusions can be drawn from these results.”

Another drug, sirukumab, also targeted the IL-6 ligand rather than the receptor, but was rejected by regulators in 2017 because so many more deaths occurred in the treatment group than the placebo group.

Dr. Smolen noted that there are three binding sites for IL-6, but olokizumab is the first to target site 3, the binding site for GP130. Mortality concerns haven’t been seen for olokizumab. There were three serious adverse events leading to death in the olokizumab every-2-weeks group; two in the olokizumab every-4-weeks group; one in the adalimumab group; and one in the placebo group.

“The fact that olokizumab targets another site on the IL-6 molecule than sirukumab may be a reason for the difference,” Dr. Smolen said.

Still, researchers noted that the time horizon for this trial is not very long.

“The trial was conducted in a relatively small number of patients and over a short duration, especially for the assessment of rare events or events requiring longer durations of exposure,” they wrote. “Longer and larger trials are required to determine the efficacy and safety of olokizumab in patients with rheumatoid arthritis.”

Dr. Smolen said he expects R-Pharm will file for regulatory approval in the United States and Europe, outside of Russia, in the next year.

Paul Emery, MD, professor of rheumatology at the University of Leeds (England) who has researched IL-6 therapy in RA, said olokizumab appears to be an effective product, but its use remains a question.

“The question is where it will fit into treatment strategies,” he said. “It’ll be very interesting.”

Dr. Emery pointed out that tocilizumab, which inhibits IL-6 by blocking the IL-6 receptor, was approved in the United States at a dosage that wasn’t optimally effective after failure with TNF inhibitors (TNFi), and wondered whether olokizumab would fare differently in this regard.

While Dr. Emery said it was important that no bad safety signal has been seen, he noted that “it’s a short-term study, and you do need to see the long-term data.”

“It seems to work at both the intervals it was tested at, 2 and 4 weeks. The unknowns are whether it will be as effective as IL-6 receptor blockers in other diseases,” such as giant cell arteritis, “and early disease, and whether it will work as well post TNFi,” he said. “It could be used as first advanced therapy for people with contraindications to TNFi, but initially the majority of its use will be after TNFi, and that’s why you need to see more data on such patients.”

He added: “The final issue will be pricing. Therefore, a positive study – but much is still unknown.”

The study was supported by R-Pharm. Dr. Smolen reports financial relationships with R-Pharm, AbbVie, Janssen, Eli Lilly, Gilead, Pfizer, and other companies. Dr. Emery reports financial relationships with AbbVie, AstraZeneca, Janssen, Pfizer, Roche, and other companies, but not olokizumab manufacturer R-Pharm.

The investigational IL-6 inhibitor olokizumab fared better than placebo and was noninferior to the tumor necrosis factor inhibitor (TNFi) adalimumab (Humira) in patients with moderate to severe rheumatoid arthritis (RA) who’d had an inadequate response to methotrexate alone, according to new findings published in the New England Journal of Medicine.

The results from the phase 3, multicenter, double-blind, parallel-group, randomized, placebo- and active-comparator–controlled trial, called Clinical Rheumatoid Arthritis Development for Olokizumab (CREDO2), add to the evidence base on the drug, which was developed by R-Pharm in Russia and has been approved for use there. Last year, researchers reported results from two trials showing sustained improvements in symptoms, function, and quality of life in patients with an inadequate response to anti-TNF treatment.

“Once approved, olokizumab can be used in patients who have not responded well to either methotrexate or any biological disease-modifying antirheumatic drug or any JAK [Janus kinase] inhibitor in combination with methotrexate or alone,” said Josef Smolen, MD, chair of rheumatology at the Medical University of Vienna and the lead author on the study.

Researchers randomized 1,648 patients to 64 mg of olokizumab every 2 or 4 weeks, adalimumab every 2 weeks, or placebo. All patient groups continued to receive methotrexate. A total of 89.7% of the participants completed 24 weeks of treatment. By that point, 74.1% of those receiving olokizumab every 2 weeks had achieved an ACR 20 response, an improvement of at least 20% in American College of Rheumatology response criteria, including tender and swollen joints, and 71.4% in the group receiving olokizumab every 4 weeks; 69.0% in the adalimumab group; and 46.5% in the placebo group had achieved an ACR 20 response. Olokizumab benefits were also seen for Disease Activity Score in 28 joints, disability index scores, and ACR 50 responses, the researchers reported.

Approved IL-6 inhibitors tocilizumab (Actemra) and sarilumab (Kevzara) target the interleukin (IL)-6 receptor (IL-6R), but olokizumab targets a protein, glycoprotein 130 (GP130), to which the IL-6 and IL-6–receptor complex binds. This approach could offer an added benefit, Dr. Smolen said.

“Previously studied anti–IL-6 antibodies and anti–IL-6R antibodies prevent binding of IL-6 to the IL-6R,” he said. “Moreover, the amount of protein needed to inhibit IL-6 is lower compared to the approved antireceptor antibodies. Olokizumab has also been shown to be effective when given every 4 weeks in many patients, compared with the need for weekly or every-other-week applications with tocilizumab and sarilumab. From these perspectives, this novel mode of action may, indeed, provide an advantage.”

ACR 70 – an improvement of at least 70% in the ACR response criteria – was an exploratory endpoint in the trial. This response was seen in 28% of those receiving olokizumab, compared with 11% in the placebo group, but researchers cautioned that “no conclusions can be drawn from these results.”

Another drug, sirukumab, also targeted the IL-6 ligand rather than the receptor, but was rejected by regulators in 2017 because so many more deaths occurred in the treatment group than the placebo group.

Dr. Smolen noted that there are three binding sites for IL-6, but olokizumab is the first to target site 3, the binding site for GP130. Mortality concerns haven’t been seen for olokizumab. There were three serious adverse events leading to death in the olokizumab every-2-weeks group; two in the olokizumab every-4-weeks group; one in the adalimumab group; and one in the placebo group.

“The fact that olokizumab targets another site on the IL-6 molecule than sirukumab may be a reason for the difference,” Dr. Smolen said.

Still, researchers noted that the time horizon for this trial is not very long.

“The trial was conducted in a relatively small number of patients and over a short duration, especially for the assessment of rare events or events requiring longer durations of exposure,” they wrote. “Longer and larger trials are required to determine the efficacy and safety of olokizumab in patients with rheumatoid arthritis.”

Dr. Smolen said he expects R-Pharm will file for regulatory approval in the United States and Europe, outside of Russia, in the next year.

Paul Emery, MD, professor of rheumatology at the University of Leeds (England) who has researched IL-6 therapy in RA, said olokizumab appears to be an effective product, but its use remains a question.

“The question is where it will fit into treatment strategies,” he said. “It’ll be very interesting.”

Dr. Emery pointed out that tocilizumab, which inhibits IL-6 by blocking the IL-6 receptor, was approved in the United States at a dosage that wasn’t optimally effective after failure with TNF inhibitors (TNFi), and wondered whether olokizumab would fare differently in this regard.

While Dr. Emery said it was important that no bad safety signal has been seen, he noted that “it’s a short-term study, and you do need to see the long-term data.”

“It seems to work at both the intervals it was tested at, 2 and 4 weeks. The unknowns are whether it will be as effective as IL-6 receptor blockers in other diseases,” such as giant cell arteritis, “and early disease, and whether it will work as well post TNFi,” he said. “It could be used as first advanced therapy for people with contraindications to TNFi, but initially the majority of its use will be after TNFi, and that’s why you need to see more data on such patients.”

He added: “The final issue will be pricing. Therefore, a positive study – but much is still unknown.”

The study was supported by R-Pharm. Dr. Smolen reports financial relationships with R-Pharm, AbbVie, Janssen, Eli Lilly, Gilead, Pfizer, and other companies. Dr. Emery reports financial relationships with AbbVie, AstraZeneca, Janssen, Pfizer, Roche, and other companies, but not olokizumab manufacturer R-Pharm.

The investigational IL-6 inhibitor olokizumab fared better than placebo and was noninferior to the tumor necrosis factor inhibitor (TNFi) adalimumab (Humira) in patients with moderate to severe rheumatoid arthritis (RA) who’d had an inadequate response to methotrexate alone, according to new findings published in the New England Journal of Medicine.

The results from the phase 3, multicenter, double-blind, parallel-group, randomized, placebo- and active-comparator–controlled trial, called Clinical Rheumatoid Arthritis Development for Olokizumab (CREDO2), add to the evidence base on the drug, which was developed by R-Pharm in Russia and has been approved for use there. Last year, researchers reported results from two trials showing sustained improvements in symptoms, function, and quality of life in patients with an inadequate response to anti-TNF treatment.

“Once approved, olokizumab can be used in patients who have not responded well to either methotrexate or any biological disease-modifying antirheumatic drug or any JAK [Janus kinase] inhibitor in combination with methotrexate or alone,” said Josef Smolen, MD, chair of rheumatology at the Medical University of Vienna and the lead author on the study.

Researchers randomized 1,648 patients to 64 mg of olokizumab every 2 or 4 weeks, adalimumab every 2 weeks, or placebo. All patient groups continued to receive methotrexate. A total of 89.7% of the participants completed 24 weeks of treatment. By that point, 74.1% of those receiving olokizumab every 2 weeks had achieved an ACR 20 response, an improvement of at least 20% in American College of Rheumatology response criteria, including tender and swollen joints, and 71.4% in the group receiving olokizumab every 4 weeks; 69.0% in the adalimumab group; and 46.5% in the placebo group had achieved an ACR 20 response. Olokizumab benefits were also seen for Disease Activity Score in 28 joints, disability index scores, and ACR 50 responses, the researchers reported.

Approved IL-6 inhibitors tocilizumab (Actemra) and sarilumab (Kevzara) target the interleukin (IL)-6 receptor (IL-6R), but olokizumab targets a protein, glycoprotein 130 (GP130), to which the IL-6 and IL-6–receptor complex binds. This approach could offer an added benefit, Dr. Smolen said.

“Previously studied anti–IL-6 antibodies and anti–IL-6R antibodies prevent binding of IL-6 to the IL-6R,” he said. “Moreover, the amount of protein needed to inhibit IL-6 is lower compared to the approved antireceptor antibodies. Olokizumab has also been shown to be effective when given every 4 weeks in many patients, compared with the need for weekly or every-other-week applications with tocilizumab and sarilumab. From these perspectives, this novel mode of action may, indeed, provide an advantage.”

ACR 70 – an improvement of at least 70% in the ACR response criteria – was an exploratory endpoint in the trial. This response was seen in 28% of those receiving olokizumab, compared with 11% in the placebo group, but researchers cautioned that “no conclusions can be drawn from these results.”

Another drug, sirukumab, also targeted the IL-6 ligand rather than the receptor, but was rejected by regulators in 2017 because so many more deaths occurred in the treatment group than the placebo group.

Dr. Smolen noted that there are three binding sites for IL-6, but olokizumab is the first to target site 3, the binding site for GP130. Mortality concerns haven’t been seen for olokizumab. There were three serious adverse events leading to death in the olokizumab every-2-weeks group; two in the olokizumab every-4-weeks group; one in the adalimumab group; and one in the placebo group.

“The fact that olokizumab targets another site on the IL-6 molecule than sirukumab may be a reason for the difference,” Dr. Smolen said.

Still, researchers noted that the time horizon for this trial is not very long.

“The trial was conducted in a relatively small number of patients and over a short duration, especially for the assessment of rare events or events requiring longer durations of exposure,” they wrote. “Longer and larger trials are required to determine the efficacy and safety of olokizumab in patients with rheumatoid arthritis.”

Dr. Smolen said he expects R-Pharm will file for regulatory approval in the United States and Europe, outside of Russia, in the next year.

Paul Emery, MD, professor of rheumatology at the University of Leeds (England) who has researched IL-6 therapy in RA, said olokizumab appears to be an effective product, but its use remains a question.

“The question is where it will fit into treatment strategies,” he said. “It’ll be very interesting.”

Dr. Emery pointed out that tocilizumab, which inhibits IL-6 by blocking the IL-6 receptor, was approved in the United States at a dosage that wasn’t optimally effective after failure with TNF inhibitors (TNFi), and wondered whether olokizumab would fare differently in this regard.

While Dr. Emery said it was important that no bad safety signal has been seen, he noted that “it’s a short-term study, and you do need to see the long-term data.”

“It seems to work at both the intervals it was tested at, 2 and 4 weeks. The unknowns are whether it will be as effective as IL-6 receptor blockers in other diseases,” such as giant cell arteritis, “and early disease, and whether it will work as well post TNFi,” he said. “It could be used as first advanced therapy for people with contraindications to TNFi, but initially the majority of its use will be after TNFi, and that’s why you need to see more data on such patients.”

He added: “The final issue will be pricing. Therefore, a positive study – but much is still unknown.”

The study was supported by R-Pharm. Dr. Smolen reports financial relationships with R-Pharm, AbbVie, Janssen, Eli Lilly, Gilead, Pfizer, and other companies. Dr. Emery reports financial relationships with AbbVie, AstraZeneca, Janssen, Pfizer, Roche, and other companies, but not olokizumab manufacturer R-Pharm.

Dermatologists spent less time with Asian patients with psoriasis than patients of other races and ethnicities in a cross-sectional study using data from the National Ambulatory Medical Care Survey (NAMCS) from 2010 to 2016.

Yet the reasons for the difference are unclear and in need of further research, said the investigators and dermatologists who were asked to comment on the research.

The study covered over 4 million visits for psoriasis and found that the mean duration of visits for Asian patients was 9.2 minutes, compared with 15.7 minutes for Hispanic or Latino patients, 20.7 minutes for non-Hispanic Black patients, and 15.4 minutes for non-Hispanic White patients.

The mean duration of visits with Asian patients was 39.9% shorter, compared with visits with White patients (beta coefficient, –5,747; 95% confidence interval, –11.026 to –0.469; P = .03), and 40.6% shorter, compared with visits with non-Asian patients combined (beta coefficient, –5.908; 95% CI, –11.147 to –0.669, P = .03), April W. Armstrong, MD, MPH, professor of dermatology and director of the psoriasis program at the University of Southern California, Los Angeles, and Kevin K. Wu, MD, a dermatology resident at USC, said in a research letter published in JAMA Dermatology.

“The etiology of these differences is unclear,” they wrote. “It is possible that factors such as unconscious bias, cultural differences in communication, or residual confounding may be responsible for the observed findings.”

Their findings came from multivariable linear regression analyses that adjusted for age, sex, type of visit (new or follow-up), visit complexity based on the number of reasons for the visit, insurance status (such as private insurance or Medicaid), psoriasis severity on the basis of systemic psoriasis treatment or phototherapy, and complex topical regimens (three or more topical agents).

Commenting on the results, Deborah A. Scott, MD, codirector of the skin of color dermatology program at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, both in Boston, said in an interview that visit length “is a reasonable parameter to look at among many others” when investigating potential disparities in care.

“They’re equating [shorter visit times] with lack of time spent counseling patients,” said Dr. Scott, who was not involved in the research. But there are “many variables” that can affect visit time, such as language differences, time spent with interpreters, and differences in patient educational levels.

Clarissa Yang, MD, dermatologist-in-chief at Tufts Medical Center, Boston, agreed. “We’re worried about there being a quality of care issue. However, there could also be differences culturally in how [the patients] interact with their physicians – their styles and the questions they ask,” she said in an interview. “The study is a good first step to noting that there may be a disparity,” and there is a need to break down the differences “into more granularity.”

Previous research, the authors wrote, has found that Asian patients were less likely to receive counseling from physicians, compared with White patients. And “paradoxically,” they noted, Asian individuals tend to present with more severe psoriasis than patients of other races and ethnicities.

Dr. Scott said the tendency to present with more severe psoriasis has been documented in patients with skin of color broadly – likely because of delays in recognition and treatment.

Race and ethnicity in the study were self-reported by patients, and missing data were imputed by NAMCS researchers using a sequential regression method. Patients who did not report race and ethnicity may have different characteristics affecting visit duration than those who did report the information, Dr. Armstrong and Dr. Wu said in describing their study’s limitations.

Other differences found

In addition to visit length, they found significant differences in mean age and in the use of complex topical regimens. The mean ages of Asian, Hispanic or Latino, and non-Hispanic Black patients were 37.2, 44.7, and 33.3 years, respectively. Complex topical regimens were prescribed to 11.8% of Asian patients, compared with 1.5% of Black and 1.1% of White patients.

For practicing dermatologists, knowing for now that Asian patients have shorter visits “may bring to light some consciousness to how we practice,” Dr. Yang noted. “We may counsel differently, we may spend differing amounts of time – for reasons still unknown. But being generally aware can help us to shift any unconscious bias that may be there.”

Dermatologists, Dr. Armstrong and Dr. Wu wrote, “need to allow sufficient time to develop strong physician-patient communication regardless of patient background.”

The NAMCS – administered by the Center for Disease Control and Prevention’s National Center for Health Statistics – collects data on a sample of visits provided by non–federally employed office-based physicians.

Dr. Armstrong disclosed receiving personal fees from AbbVie and Regeneron for research funding and serving as a scientific adviser and speaker for additional pharmaceutical and therapeutic companies. Dr. Wu, Dr. Scott, and Dr. Yang did not report any disclosures.
 

Dermatologists spent less time with Asian patients with psoriasis than patients of other races and ethnicities in a cross-sectional study using data from the National Ambulatory Medical Care Survey (NAMCS) from 2010 to 2016.

Yet the reasons for the difference are unclear and in need of further research, said the investigators and dermatologists who were asked to comment on the research.

The study covered over 4 million visits for psoriasis and found that the mean duration of visits for Asian patients was 9.2 minutes, compared with 15.7 minutes for Hispanic or Latino patients, 20.7 minutes for non-Hispanic Black patients, and 15.4 minutes for non-Hispanic White patients.

The mean duration of visits with Asian patients was 39.9% shorter, compared with visits with White patients (beta coefficient, –5,747; 95% confidence interval, –11.026 to –0.469; P = .03), and 40.6% shorter, compared with visits with non-Asian patients combined (beta coefficient, –5.908; 95% CI, –11.147 to –0.669, P = .03), April W. Armstrong, MD, MPH, professor of dermatology and director of the psoriasis program at the University of Southern California, Los Angeles, and Kevin K. Wu, MD, a dermatology resident at USC, said in a research letter published in JAMA Dermatology.

“The etiology of these differences is unclear,” they wrote. “It is possible that factors such as unconscious bias, cultural differences in communication, or residual confounding may be responsible for the observed findings.”

Their findings came from multivariable linear regression analyses that adjusted for age, sex, type of visit (new or follow-up), visit complexity based on the number of reasons for the visit, insurance status (such as private insurance or Medicaid), psoriasis severity on the basis of systemic psoriasis treatment or phototherapy, and complex topical regimens (three or more topical agents).

Commenting on the results, Deborah A. Scott, MD, codirector of the skin of color dermatology program at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, both in Boston, said in an interview that visit length “is a reasonable parameter to look at among many others” when investigating potential disparities in care.

“They’re equating [shorter visit times] with lack of time spent counseling patients,” said Dr. Scott, who was not involved in the research. But there are “many variables” that can affect visit time, such as language differences, time spent with interpreters, and differences in patient educational levels.

Clarissa Yang, MD, dermatologist-in-chief at Tufts Medical Center, Boston, agreed. “We’re worried about there being a quality of care issue. However, there could also be differences culturally in how [the patients] interact with their physicians – their styles and the questions they ask,” she said in an interview. “The study is a good first step to noting that there may be a disparity,” and there is a need to break down the differences “into more granularity.”

Previous research, the authors wrote, has found that Asian patients were less likely to receive counseling from physicians, compared with White patients. And “paradoxically,” they noted, Asian individuals tend to present with more severe psoriasis than patients of other races and ethnicities.

Dr. Scott said the tendency to present with more severe psoriasis has been documented in patients with skin of color broadly – likely because of delays in recognition and treatment.

Race and ethnicity in the study were self-reported by patients, and missing data were imputed by NAMCS researchers using a sequential regression method. Patients who did not report race and ethnicity may have different characteristics affecting visit duration than those who did report the information, Dr. Armstrong and Dr. Wu said in describing their study’s limitations.

Other differences found

In addition to visit length, they found significant differences in mean age and in the use of complex topical regimens. The mean ages of Asian, Hispanic or Latino, and non-Hispanic Black patients were 37.2, 44.7, and 33.3 years, respectively. Complex topical regimens were prescribed to 11.8% of Asian patients, compared with 1.5% of Black and 1.1% of White patients.

For practicing dermatologists, knowing for now that Asian patients have shorter visits “may bring to light some consciousness to how we practice,” Dr. Yang noted. “We may counsel differently, we may spend differing amounts of time – for reasons still unknown. But being generally aware can help us to shift any unconscious bias that may be there.”

Dermatologists, Dr. Armstrong and Dr. Wu wrote, “need to allow sufficient time to develop strong physician-patient communication regardless of patient background.”

The NAMCS – administered by the Center for Disease Control and Prevention’s National Center for Health Statistics – collects data on a sample of visits provided by non–federally employed office-based physicians.

Dr. Armstrong disclosed receiving personal fees from AbbVie and Regeneron for research funding and serving as a scientific adviser and speaker for additional pharmaceutical and therapeutic companies. Dr. Wu, Dr. Scott, and Dr. Yang did not report any disclosures.
 

Dermatologists spent less time with Asian patients with psoriasis than patients of other races and ethnicities in a cross-sectional study using data from the National Ambulatory Medical Care Survey (NAMCS) from 2010 to 2016.

Yet the reasons for the difference are unclear and in need of further research, said the investigators and dermatologists who were asked to comment on the research.

The study covered over 4 million visits for psoriasis and found that the mean duration of visits for Asian patients was 9.2 minutes, compared with 15.7 minutes for Hispanic or Latino patients, 20.7 minutes for non-Hispanic Black patients, and 15.4 minutes for non-Hispanic White patients.

The mean duration of visits with Asian patients was 39.9% shorter, compared with visits with White patients (beta coefficient, –5,747; 95% confidence interval, –11.026 to –0.469; P = .03), and 40.6% shorter, compared with visits with non-Asian patients combined (beta coefficient, –5.908; 95% CI, –11.147 to –0.669, P = .03), April W. Armstrong, MD, MPH, professor of dermatology and director of the psoriasis program at the University of Southern California, Los Angeles, and Kevin K. Wu, MD, a dermatology resident at USC, said in a research letter published in JAMA Dermatology.

“The etiology of these differences is unclear,” they wrote. “It is possible that factors such as unconscious bias, cultural differences in communication, or residual confounding may be responsible for the observed findings.”

Their findings came from multivariable linear regression analyses that adjusted for age, sex, type of visit (new or follow-up), visit complexity based on the number of reasons for the visit, insurance status (such as private insurance or Medicaid), psoriasis severity on the basis of systemic psoriasis treatment or phototherapy, and complex topical regimens (three or more topical agents).

Commenting on the results, Deborah A. Scott, MD, codirector of the skin of color dermatology program at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, both in Boston, said in an interview that visit length “is a reasonable parameter to look at among many others” when investigating potential disparities in care.

“They’re equating [shorter visit times] with lack of time spent counseling patients,” said Dr. Scott, who was not involved in the research. But there are “many variables” that can affect visit time, such as language differences, time spent with interpreters, and differences in patient educational levels.

Clarissa Yang, MD, dermatologist-in-chief at Tufts Medical Center, Boston, agreed. “We’re worried about there being a quality of care issue. However, there could also be differences culturally in how [the patients] interact with their physicians – their styles and the questions they ask,” she said in an interview. “The study is a good first step to noting that there may be a disparity,” and there is a need to break down the differences “into more granularity.”

Previous research, the authors wrote, has found that Asian patients were less likely to receive counseling from physicians, compared with White patients. And “paradoxically,” they noted, Asian individuals tend to present with more severe psoriasis than patients of other races and ethnicities.

Dr. Scott said the tendency to present with more severe psoriasis has been documented in patients with skin of color broadly – likely because of delays in recognition and treatment.

Race and ethnicity in the study were self-reported by patients, and missing data were imputed by NAMCS researchers using a sequential regression method. Patients who did not report race and ethnicity may have different characteristics affecting visit duration than those who did report the information, Dr. Armstrong and Dr. Wu said in describing their study’s limitations.

Other differences found

In addition to visit length, they found significant differences in mean age and in the use of complex topical regimens. The mean ages of Asian, Hispanic or Latino, and non-Hispanic Black patients were 37.2, 44.7, and 33.3 years, respectively. Complex topical regimens were prescribed to 11.8% of Asian patients, compared with 1.5% of Black and 1.1% of White patients.

For practicing dermatologists, knowing for now that Asian patients have shorter visits “may bring to light some consciousness to how we practice,” Dr. Yang noted. “We may counsel differently, we may spend differing amounts of time – for reasons still unknown. But being generally aware can help us to shift any unconscious bias that may be there.”

Dermatologists, Dr. Armstrong and Dr. Wu wrote, “need to allow sufficient time to develop strong physician-patient communication regardless of patient background.”

The NAMCS – administered by the Center for Disease Control and Prevention’s National Center for Health Statistics – collects data on a sample of visits provided by non–federally employed office-based physicians.

Dr. Armstrong disclosed receiving personal fees from AbbVie and Regeneron for research funding and serving as a scientific adviser and speaker for additional pharmaceutical and therapeutic companies. Dr. Wu, Dr. Scott, and Dr. Yang did not report any disclosures.
 

There’s little doubt long COVID is real. The federal government recognizes long COVID as a condition and said in two reports issued in August that one in five adult COVID-19 survivors have a health condition related to their illness.

COVID-19 can damage multiple organs in the body. Sometimes this damage leads to long COVID; sometimes other reasons are at play. Doctors are beginning to sort it out.

There’s a difference between long COVID and an acute infection with lasting effects, doctors say.

“COVID itself can actually cause prolonged illness, and we don’t really call that long COVID,” said Nisha Viswanathan, MD, a doctor at UCLA Health in Los Angeles. But if symptoms extend beyond 12 weeks, that puts patients in the realm of long COVID.

Symptoms can range from mild to severe and can keep people from resuming their normal lives and jobs. Sometimes they last for months, according to the U.S. Department of Health & Human Services.
 

Multiorgan damage

Lung scarring and other lung problems are common after COVID, said Leora Horwitz, MD, an internal medicine specialist at New York University. Even after a mild case, people can have breathing issues for months, a team at Johns Hopkins Medicine, Baltimore, said in an online briefing. One study published in the journal Radiology found damage in people a full year after a COVID-19 diagnosis.

Some people have persistent heart, kidney, liver, and nervous system problems after COVID-19. A study published in 2020 in JAMA Cardiology found 60% of people who had COVID-19 had ongoing signs of heart inflammation. Nearly a third of people hospitalized for COVID-19 get kidney damage that can become chronic, and some end up needing dialysis or a transplant, said C. John Sperati, MD, a kidney specialist at Johns Hopkins Medicine.

This might be, in part, because SARS-CoV-2, the virus that causes COVID-19, directly infects the cells in many organs.

Nicole Bhave, MD, a cardiologist at University of Michigan Health, Ann Arbor is concerned that COVID-19 appears to increase the risk of heart problems in some people.

“Some of the uptick may just be recognition bias, in that people with symptoms are seeking care,” she said. “But there’s definitely a biological basis by which COVID could tip people over into a new diagnosis of heart failure.”
 

Inflammation

Inflammation is probably a key part of the long-term effects of COVID-19.

Some people have a serious immune reaction to COVID-19 called a cytokine storm, said Nitra Aggarwal Gilotra, MD, a cardiologist at Johns Hopkins Medicine. This release of inflammation-causing molecules called cytokines is meant to attack the invading virus. But it can be so severe that it wreaks havoc on healthy tissues and organs and causes lasting damage – if patients even survive it.

In some people, inflammation can affect the heart, causing myocarditis. Myocarditis symptoms include chest pain, breathlessness, and heart palpitations. Though rare, it can be serious and can raise the risk of other heart problems, including heart failure, down the line.

Long COVID may also trigger an autoimmune condition, said Eline Luning Prak, MD, PhD, a pathologist at the Hospital of the University of Pennsylvania, Philadelphia. Long COVID can share many hallmark symptoms with autoimmune diseases, including fatigue, widespread pain, memory problems, and mood disorders.
 

Blood clots

Studies have shown the overcharged inflammatory response to COVID-19 can cause blood clots. This sometimes overwhelming clotting was an early hallmark of COVID-19 infection, and when clots restrict blood flow in the brain, lungs, kidneys, or limbs, they can cause long-term damage. Some can be deadly. Researchers in Sweden found patients were at risk of deep vein thrombosis – a blood clot usually in the leg – up to 3 months after infection and at higher risk of a blood clot in the lung, called pulmonary embolism, for as long as 3 months.

Viral reservoirs

The virus itself may also linger in a patient’s body, causing continued symptoms and, potentially, new flare-ups. Zoe Swank, PhD, of Harvard Medical School, Boston, and colleagues reported in a preprint study that they found pieces of the SARS-CoV-2 virus in the blood of most patients with long COVID symptoms they tested – some as long as a year after infection. The study has not yet been peer reviewed.

Another team found evidence of the virus in stool up to 7 months later, which suggests the virus hides out in the gut. Other early studies have found bits of viral RNA in the appendix, breast tissue, heart, eyes, and brain.
 

Diabetes

Diabetes is a risk factor for getting severe COVID-19, and multiple studies have shown people can get diabetes both while battling infection and afterward. One study of veterans, published in The Lancet Diabetes and Endocrinology, found COVID-19 survivors were about 40% more likely to get diabetes over the next year.

There are a few ways this might happen. Insulin-producing cells in the pancreas have SARS-CoV-2 receptors – a type of molecular doorway the coronavirus can attach to. Damage to these cells could make the body less able to produce insulin, which in turn can lead to diabetes. The virus could also disrupt the balance in the body or cause inflammation that leads to insulin resistance, which can develop into diabetes, Ziad Al-Aly, MD, of the Veterans Affairs St. Louis Health Care System, and colleagues wrote.
 

Nervous system issues

People who get COVID-19 are also more vulnerable to postural orthostatic tachycardia syndrome (POTS). This affects what’s known as the autonomic nervous system, which regulates blood circulation, and includes those things that happen in your body without your having to think about them, like breathing, heartbeat, and digestion. POTS can cause common long COVID neurologic symptoms, including headaches, fatigue, brain fog, insomnia, and problems thinking and concentrating. “This was a known condition prior to COVID, but it was incredibly rare,” said Dr. Viswanathan. “After COVID, I’ve seen it with increasing frequency.”

Long-term outlook

Lasting issues after COVID-19 are much more likely after a moderate or severe infection. Still, plenty of people are battling them even after a mild illness. “As for why, that’s the billion-dollar question,” said Dr. Horwitz. “It’s well known that viral infections can cause long-term dysregulation. Why that is, we really just don’t know.”

Whether it’s virus hiding out in the body, long-term organ damage, or an autoimmune reaction likely differs from person to person. “I’m believing, increasingly, that it’s a combination of all of these, just based on how different patients are responding to different medications,” said Dr. Viswanathan. “One patient will respond to something beautifully, and another patient won’t at all.”

But it’s clear a significant number of people are facing long-term health struggles because of COVID-19, which has infected at least 580 million people globally and 92 million – likely many more – in the United States, according to Johns Hopkins University.

Even a small increased risk of conditions like heart disease or diabetes translates to a huge number of people, Dr. Horwitz said. “If even 1% of people getting COVID have long-term symptoms, that’s a major public health crisis, because that’s 1% of pretty much everybody in the country.”

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

There’s little doubt long COVID is real. The federal government recognizes long COVID as a condition and said in two reports issued in August that one in five adult COVID-19 survivors have a health condition related to their illness.

COVID-19 can damage multiple organs in the body. Sometimes this damage leads to long COVID; sometimes other reasons are at play. Doctors are beginning to sort it out.

There’s a difference between long COVID and an acute infection with lasting effects, doctors say.

“COVID itself can actually cause prolonged illness, and we don’t really call that long COVID,” said Nisha Viswanathan, MD, a doctor at UCLA Health in Los Angeles. But if symptoms extend beyond 12 weeks, that puts patients in the realm of long COVID.

Symptoms can range from mild to severe and can keep people from resuming their normal lives and jobs. Sometimes they last for months, according to the U.S. Department of Health & Human Services.
 

Multiorgan damage

Lung scarring and other lung problems are common after COVID, said Leora Horwitz, MD, an internal medicine specialist at New York University. Even after a mild case, people can have breathing issues for months, a team at Johns Hopkins Medicine, Baltimore, said in an online briefing. One study published in the journal Radiology found damage in people a full year after a COVID-19 diagnosis.

Some people have persistent heart, kidney, liver, and nervous system problems after COVID-19. A study published in 2020 in JAMA Cardiology found 60% of people who had COVID-19 had ongoing signs of heart inflammation. Nearly a third of people hospitalized for COVID-19 get kidney damage that can become chronic, and some end up needing dialysis or a transplant, said C. John Sperati, MD, a kidney specialist at Johns Hopkins Medicine.

This might be, in part, because SARS-CoV-2, the virus that causes COVID-19, directly infects the cells in many organs.

Nicole Bhave, MD, a cardiologist at University of Michigan Health, Ann Arbor is concerned that COVID-19 appears to increase the risk of heart problems in some people.

“Some of the uptick may just be recognition bias, in that people with symptoms are seeking care,” she said. “But there’s definitely a biological basis by which COVID could tip people over into a new diagnosis of heart failure.”
 

Inflammation

Inflammation is probably a key part of the long-term effects of COVID-19.

Some people have a serious immune reaction to COVID-19 called a cytokine storm, said Nitra Aggarwal Gilotra, MD, a cardiologist at Johns Hopkins Medicine. This release of inflammation-causing molecules called cytokines is meant to attack the invading virus. But it can be so severe that it wreaks havoc on healthy tissues and organs and causes lasting damage – if patients even survive it.

In some people, inflammation can affect the heart, causing myocarditis. Myocarditis symptoms include chest pain, breathlessness, and heart palpitations. Though rare, it can be serious and can raise the risk of other heart problems, including heart failure, down the line.

Long COVID may also trigger an autoimmune condition, said Eline Luning Prak, MD, PhD, a pathologist at the Hospital of the University of Pennsylvania, Philadelphia. Long COVID can share many hallmark symptoms with autoimmune diseases, including fatigue, widespread pain, memory problems, and mood disorders.
 

Blood clots

Studies have shown the overcharged inflammatory response to COVID-19 can cause blood clots. This sometimes overwhelming clotting was an early hallmark of COVID-19 infection, and when clots restrict blood flow in the brain, lungs, kidneys, or limbs, they can cause long-term damage. Some can be deadly. Researchers in Sweden found patients were at risk of deep vein thrombosis – a blood clot usually in the leg – up to 3 months after infection and at higher risk of a blood clot in the lung, called pulmonary embolism, for as long as 3 months.

Viral reservoirs

The virus itself may also linger in a patient’s body, causing continued symptoms and, potentially, new flare-ups. Zoe Swank, PhD, of Harvard Medical School, Boston, and colleagues reported in a preprint study that they found pieces of the SARS-CoV-2 virus in the blood of most patients with long COVID symptoms they tested – some as long as a year after infection. The study has not yet been peer reviewed.

Another team found evidence of the virus in stool up to 7 months later, which suggests the virus hides out in the gut. Other early studies have found bits of viral RNA in the appendix, breast tissue, heart, eyes, and brain.
 

Diabetes

Diabetes is a risk factor for getting severe COVID-19, and multiple studies have shown people can get diabetes both while battling infection and afterward. One study of veterans, published in The Lancet Diabetes and Endocrinology, found COVID-19 survivors were about 40% more likely to get diabetes over the next year.

There are a few ways this might happen. Insulin-producing cells in the pancreas have SARS-CoV-2 receptors – a type of molecular doorway the coronavirus can attach to. Damage to these cells could make the body less able to produce insulin, which in turn can lead to diabetes. The virus could also disrupt the balance in the body or cause inflammation that leads to insulin resistance, which can develop into diabetes, Ziad Al-Aly, MD, of the Veterans Affairs St. Louis Health Care System, and colleagues wrote.
 

Nervous system issues

People who get COVID-19 are also more vulnerable to postural orthostatic tachycardia syndrome (POTS). This affects what’s known as the autonomic nervous system, which regulates blood circulation, and includes those things that happen in your body without your having to think about them, like breathing, heartbeat, and digestion. POTS can cause common long COVID neurologic symptoms, including headaches, fatigue, brain fog, insomnia, and problems thinking and concentrating. “This was a known condition prior to COVID, but it was incredibly rare,” said Dr. Viswanathan. “After COVID, I’ve seen it with increasing frequency.”

Long-term outlook

Lasting issues after COVID-19 are much more likely after a moderate or severe infection. Still, plenty of people are battling them even after a mild illness. “As for why, that’s the billion-dollar question,” said Dr. Horwitz. “It’s well known that viral infections can cause long-term dysregulation. Why that is, we really just don’t know.”

Whether it’s virus hiding out in the body, long-term organ damage, or an autoimmune reaction likely differs from person to person. “I’m believing, increasingly, that it’s a combination of all of these, just based on how different patients are responding to different medications,” said Dr. Viswanathan. “One patient will respond to something beautifully, and another patient won’t at all.”

But it’s clear a significant number of people are facing long-term health struggles because of COVID-19, which has infected at least 580 million people globally and 92 million – likely many more – in the United States, according to Johns Hopkins University.

Even a small increased risk of conditions like heart disease or diabetes translates to a huge number of people, Dr. Horwitz said. “If even 1% of people getting COVID have long-term symptoms, that’s a major public health crisis, because that’s 1% of pretty much everybody in the country.”