Rheumatology News

Long COVID: The name says it all. It’s an illness that, for many people, has not yet stopped.

Eric Roach became ill with COVID-19 in November 2020, and he’s still sick. “I have brain fog, memory loss,” says the 67-year-old Navy veteran from Spearfish, S.D. “The fatigue has just been insane.” 

Long COVID, more formally known as post-acute sequelae of COVID (PASC), is the lay term to describe when people start to recover, or seem to recover, from a bout of COVID-19 but then continue to suffer from symptoms. For some, it’s gone on for 2 years or longer. While the governments of the United Statesand several other countries formally recognize the existence of long COVID, the National Institutes of Health (NIH) has yet to formally define it. There’s no approved treatment, and the causes are not understood.

Here’s what is known: Long COVID is a postviral condition affecting a large percentage of people who become infected with the coronavirus. It can be utterly debilitating or mildly annoying, and it is affecting enough people to cause concern for employers, health insurers, and governments.
 

First, the many symptoms

According to the Centers for Disease Control and Prvention, long COVID symptoms may include:

• Tiredness or fatigue that interferes with daily life.
• Symptoms that get worse after physical or mental effort.
• Fever.
• Difficulty breathing or shortness of breath.
• Cough.
• Chest pain.
• Heart palpitations.
• Difficulty thinking or concentrating (sometimes referred to as “brain fog”).
• Headache.
• Sleep problems.
• Dizziness when standing.
• Pins-and-needles feelings.
• Change in smell or taste.
• Depression or anxiety.
• Diarrhea.
• Stomach pain.
• Joint or muscle pain.
• Rash.
• Changes in menstrual cycles.

“People with post-COVID conditions may develop or continue to have symptoms that are hard to explain and manage,” the CDC says on its website. “Clinical evaluations and results of routine blood tests, chest x-rays, and electrocardiograms may be normal. The symptoms are similar to those reported by people with ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome) and other poorly understood chronic illnesses that may occur after other infections.” 

Doctors may not fully appreciate the subtle nature of some of the symptoms. 

“People with these unexplained symptoms may be misunderstood by their health care providers, which can result in a long time for them to get a diagnosis and receive appropriate care or treatment,” the CDC says.

Health professionals should recognize that long COVID can be disabling, the U.S. Department of Health and Human Services says. “Long COVID can substantially limit a major life activity,” HHS says in civil rights guidance. One possible example: “A person with long COVID who has lung damage that causes shortness of breath, fatigue, and related effects is substantially limited in respiratory function, among other major life activities,” the HHS notes.
 

How many people are affected?

This has been difficult to judge because not everyone who has had COVID-19 gets tested for it and there are no formal diagnostic criteria yet for long COVID. The CDC estimates that 19% of patients in the United States who have ever had COVID-19 have long COVID symptoms. 

Some estimates go higher. A University of Oxford study in September 2021 found more than a third of patients had symptoms of long COVID between 3 months and 6 months after a COVID-19 diagnosis. As many as 55% of COVID-19 patients in one Chinese study had one or more lingering symptoms 2 years later, Lixue Huang, MD, of the China-Japan Friendship Hospital in Beijing, and colleagues reported in the journal Lancet Respiratory Medicine in May.

According to the CDC, age is a factor. “Older adults are less likely to have long COVID than younger adults. Nearly three times as many adults ages 50-59 currently have long COVID than those age 80 and older,” the CDC says. Women and racial and ethnic minorities are more likely to be affected.

Many people are experiencing neurological effects, such as the so-called brain fog, according to Ziyad Al-Aly, MD, of Washington University and the VA St. Louis Health Care System, and colleagues, whose report was published in Nature Medicine in September. They estimated that 6.6 million Americans have brain impairments associated with COVID infection.

“Some of the neurologic disorders reported here are serious chronic conditions that will impact some people for a lifetime,” they wrote. “Given the colossal scale of the pandemic, and even though the absolute numbers reported in this work are small, these may translate into a large number of affected individuals around the world – and this will likely contribute to a rise in the burden of neurologic diseases.”
 

Causes

It’s not clear what the underlying causes are, but most research points to a combination of factors. Suspects include ongoing inflammation, tiny blood clots, and reactivation of latent viruses. In May, Brent Palmer, PhD, of the University of Colorado, Denver, and colleagues found people with long COVID had persistent activation of T-cells that were specific for SARS-CoV-2.

COVID-19 itself can damage organs, and long COVID might be caused by ongoing damage. In August, Alexandros Rovas, MD, of University Hospital Munster in Germany, and colleagues found patients with long COVID had evidence of damage to their capillaries. “Whether, to what extent, and when the observed damage might be reversible remains unclear,” they wrote in the journal Angiogenesis.

People with long COVID have immune responses to other viruses, such as Epstein-Barr – evidence that COVID-19 might reactivate latent viruses. “Our data suggest the involvement of persistent antigen, reactivation of latent herpesviruses, and chronic inflammation,” immunobiologist Akiko Iwasaki, PhD, of Yale University, New Haven, Conn., and colleagues wrote in a study posted in August that had not yet been peer-reviewed for publication.

This might be causing an autoimmune response. “The infection may cause the immune system to start making autoantibodies that attack a person’s own organs and tissues,” the NIH says.

There could be other factors. A study by Harvard researchers found that people who felt stressed, depressed, or lonely before catching COVID-19 were more likely to develop long COVID afterward. “Distress was more strongly associated with developing long COVID than physical health risk factors such as obesity, asthma, and hypertension,” Siwen Wang, MD, a research fellow with Harvard University’s T.H. Chan School of Public Health, Boston, said in a statement.  Plus, nearly 44% of those in the study developed COVID-19 infections after having been assessed for stress, Dr. Wang and colleagues reported in the journal JAMA Psychiatry.
 

Vaccine protection 

There’s evidence that vaccination protects against long COVID, both by preventing infection in the first place, but also even for people who have breakthrough infections.

A meta-analysis covering studies involving 17 million people found evidence vaccination might reduce the severity of COVID-19 or might help the body clear any lingering virus after an infection.

“Overall, vaccination was associated with reduced risks or odds of long COVID, with preliminary evidence suggesting that two doses are more effective than one dose,” wrote Cesar Fernandez de las Penas, PhD, of King Juan Carlos University in Madrid, and colleagues. Their report is in The Lancet’s eClinicalMedicine.

A team in Milan found that unvaccinated people in their study were nearly three times as likely to have serious symptoms for longer than 4 weeks compared to vaccinated volunteers. According to their report in JAMA, Elena Azzolini, MD, PhD, assistant professor at Humanitas Research Hospital, and colleagues found two or three doses of vaccine reduced the risk of hospitalization from COVID to 16% or 17% compared to 42% for the unvaccinated.
 

Treatments

With no diagnostic criteria and no understanding of the causes, it’s hard for doctors to determine treatments.

Most experts dealing with long COVID, even those at the specialty centers that have been set up at hospitals and health systems in the United States, recommend that patients start with their primary care doctors before moving on to specialists.

“The mainstay of management is supportive, holistic care, symptom control, and detection of treatable complications,” Trish Greenhalgh, MD, professor of primary care health sciences at the University of Oxford, England, and colleagues wrote in the journal The BMJ in September. “Patients with long COVID greatly value input from their primary care clinician. Generalist clinicians can help patients considerably by hearing the patient’s story and validating their experience … (and) making the diagnosis of long COVID (which does not have to be by exclusion) and excluding alternative diagnoses.”

Evidence is building that long COVID closely resembles other postviral conditions – something that can provide clues for treatment. For example, several studies indicate that exercise doesn’t help most patients.

But there are approaches that can work. Treatments may include pulmonary rehabilitation; autonomic conditioning therapy, which includes breathing therapy; and cognitive rehabilitation to relieve brain fog. Doctors are also trying the antidepressant amitriptyline to help with sleep disturbances and headaches; the antiseizure medication gabapentin to help with pain, numbness, and other neurological symptoms; and drugs to relieve low blood pressure in patients experiencing postural orthostatic tachycardia syndrome (POTS).

The NIH is sponsoring studies that have recruited just over 8,200 adults. And more than two dozen researchers from Harvard; Stanford; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai Hospitals; Cardiff University; and Yale announced in September they were forming the Long COVID Research Initiative to speed up studies.

The group, with funding from private enterprise, plans to conduct tissue biopsy, imaging studies, and autopsies and will search for potential biomarkers in the blood of patients.

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

Long COVID: The name says it all. It’s an illness that, for many people, has not yet stopped.

Eric Roach became ill with COVID-19 in November 2020, and he’s still sick. “I have brain fog, memory loss,” says the 67-year-old Navy veteran from Spearfish, S.D. “The fatigue has just been insane.” 

Long COVID, more formally known as post-acute sequelae of COVID (PASC), is the lay term to describe when people start to recover, or seem to recover, from a bout of COVID-19 but then continue to suffer from symptoms. For some, it’s gone on for 2 years or longer. While the governments of the United Statesand several other countries formally recognize the existence of long COVID, the National Institutes of Health (NIH) has yet to formally define it. There’s no approved treatment, and the causes are not understood.

Here’s what is known: Long COVID is a postviral condition affecting a large percentage of people who become infected with the coronavirus. It can be utterly debilitating or mildly annoying, and it is affecting enough people to cause concern for employers, health insurers, and governments.
 

First, the many symptoms

According to the Centers for Disease Control and Prvention, long COVID symptoms may include:

• Tiredness or fatigue that interferes with daily life.
• Symptoms that get worse after physical or mental effort.
• Fever.
• Difficulty breathing or shortness of breath.
• Cough.
• Chest pain.
• Heart palpitations.
• Difficulty thinking or concentrating (sometimes referred to as “brain fog”).
• Headache.
• Sleep problems.
• Dizziness when standing.
• Pins-and-needles feelings.
• Change in smell or taste.
• Depression or anxiety.
• Diarrhea.
• Stomach pain.
• Joint or muscle pain.
• Rash.
• Changes in menstrual cycles.

“People with post-COVID conditions may develop or continue to have symptoms that are hard to explain and manage,” the CDC says on its website. “Clinical evaluations and results of routine blood tests, chest x-rays, and electrocardiograms may be normal. The symptoms are similar to those reported by people with ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome) and other poorly understood chronic illnesses that may occur after other infections.” 

Doctors may not fully appreciate the subtle nature of some of the symptoms. 

“People with these unexplained symptoms may be misunderstood by their health care providers, which can result in a long time for them to get a diagnosis and receive appropriate care or treatment,” the CDC says.

Health professionals should recognize that long COVID can be disabling, the U.S. Department of Health and Human Services says. “Long COVID can substantially limit a major life activity,” HHS says in civil rights guidance. One possible example: “A person with long COVID who has lung damage that causes shortness of breath, fatigue, and related effects is substantially limited in respiratory function, among other major life activities,” the HHS notes.
 

How many people are affected?

This has been difficult to judge because not everyone who has had COVID-19 gets tested for it and there are no formal diagnostic criteria yet for long COVID. The CDC estimates that 19% of patients in the United States who have ever had COVID-19 have long COVID symptoms. 

Some estimates go higher. A University of Oxford study in September 2021 found more than a third of patients had symptoms of long COVID between 3 months and 6 months after a COVID-19 diagnosis. As many as 55% of COVID-19 patients in one Chinese study had one or more lingering symptoms 2 years later, Lixue Huang, MD, of the China-Japan Friendship Hospital in Beijing, and colleagues reported in the journal Lancet Respiratory Medicine in May.

According to the CDC, age is a factor. “Older adults are less likely to have long COVID than younger adults. Nearly three times as many adults ages 50-59 currently have long COVID than those age 80 and older,” the CDC says. Women and racial and ethnic minorities are more likely to be affected.

Many people are experiencing neurological effects, such as the so-called brain fog, according to Ziyad Al-Aly, MD, of Washington University and the VA St. Louis Health Care System, and colleagues, whose report was published in Nature Medicine in September. They estimated that 6.6 million Americans have brain impairments associated with COVID infection.

“Some of the neurologic disorders reported here are serious chronic conditions that will impact some people for a lifetime,” they wrote. “Given the colossal scale of the pandemic, and even though the absolute numbers reported in this work are small, these may translate into a large number of affected individuals around the world – and this will likely contribute to a rise in the burden of neurologic diseases.”
 

Causes

It’s not clear what the underlying causes are, but most research points to a combination of factors. Suspects include ongoing inflammation, tiny blood clots, and reactivation of latent viruses. In May, Brent Palmer, PhD, of the University of Colorado, Denver, and colleagues found people with long COVID had persistent activation of T-cells that were specific for SARS-CoV-2.

COVID-19 itself can damage organs, and long COVID might be caused by ongoing damage. In August, Alexandros Rovas, MD, of University Hospital Munster in Germany, and colleagues found patients with long COVID had evidence of damage to their capillaries. “Whether, to what extent, and when the observed damage might be reversible remains unclear,” they wrote in the journal Angiogenesis.

People with long COVID have immune responses to other viruses, such as Epstein-Barr – evidence that COVID-19 might reactivate latent viruses. “Our data suggest the involvement of persistent antigen, reactivation of latent herpesviruses, and chronic inflammation,” immunobiologist Akiko Iwasaki, PhD, of Yale University, New Haven, Conn., and colleagues wrote in a study posted in August that had not yet been peer-reviewed for publication.

This might be causing an autoimmune response. “The infection may cause the immune system to start making autoantibodies that attack a person’s own organs and tissues,” the NIH says.

There could be other factors. A study by Harvard researchers found that people who felt stressed, depressed, or lonely before catching COVID-19 were more likely to develop long COVID afterward. “Distress was more strongly associated with developing long COVID than physical health risk factors such as obesity, asthma, and hypertension,” Siwen Wang, MD, a research fellow with Harvard University’s T.H. Chan School of Public Health, Boston, said in a statement.  Plus, nearly 44% of those in the study developed COVID-19 infections after having been assessed for stress, Dr. Wang and colleagues reported in the journal JAMA Psychiatry.
 

Vaccine protection 

There’s evidence that vaccination protects against long COVID, both by preventing infection in the first place, but also even for people who have breakthrough infections.

A meta-analysis covering studies involving 17 million people found evidence vaccination might reduce the severity of COVID-19 or might help the body clear any lingering virus after an infection.

“Overall, vaccination was associated with reduced risks or odds of long COVID, with preliminary evidence suggesting that two doses are more effective than one dose,” wrote Cesar Fernandez de las Penas, PhD, of King Juan Carlos University in Madrid, and colleagues. Their report is in The Lancet’s eClinicalMedicine.

A team in Milan found that unvaccinated people in their study were nearly three times as likely to have serious symptoms for longer than 4 weeks compared to vaccinated volunteers. According to their report in JAMA, Elena Azzolini, MD, PhD, assistant professor at Humanitas Research Hospital, and colleagues found two or three doses of vaccine reduced the risk of hospitalization from COVID to 16% or 17% compared to 42% for the unvaccinated.
 

Treatments

With no diagnostic criteria and no understanding of the causes, it’s hard for doctors to determine treatments.

Most experts dealing with long COVID, even those at the specialty centers that have been set up at hospitals and health systems in the United States, recommend that patients start with their primary care doctors before moving on to specialists.

“The mainstay of management is supportive, holistic care, symptom control, and detection of treatable complications,” Trish Greenhalgh, MD, professor of primary care health sciences at the University of Oxford, England, and colleagues wrote in the journal The BMJ in September. “Patients with long COVID greatly value input from their primary care clinician. Generalist clinicians can help patients considerably by hearing the patient’s story and validating their experience … (and) making the diagnosis of long COVID (which does not have to be by exclusion) and excluding alternative diagnoses.”

Evidence is building that long COVID closely resembles other postviral conditions – something that can provide clues for treatment. For example, several studies indicate that exercise doesn’t help most patients.

But there are approaches that can work. Treatments may include pulmonary rehabilitation; autonomic conditioning therapy, which includes breathing therapy; and cognitive rehabilitation to relieve brain fog. Doctors are also trying the antidepressant amitriptyline to help with sleep disturbances and headaches; the antiseizure medication gabapentin to help with pain, numbness, and other neurological symptoms; and drugs to relieve low blood pressure in patients experiencing postural orthostatic tachycardia syndrome (POTS).

The NIH is sponsoring studies that have recruited just over 8,200 adults. And more than two dozen researchers from Harvard; Stanford; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai Hospitals; Cardiff University; and Yale announced in September they were forming the Long COVID Research Initiative to speed up studies.

The group, with funding from private enterprise, plans to conduct tissue biopsy, imaging studies, and autopsies and will search for potential biomarkers in the blood of patients.

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

Long COVID: The name says it all. It’s an illness that, for many people, has not yet stopped.

Eric Roach became ill with COVID-19 in November 2020, and he’s still sick. “I have brain fog, memory loss,” says the 67-year-old Navy veteran from Spearfish, S.D. “The fatigue has just been insane.” 

Long COVID, more formally known as post-acute sequelae of COVID (PASC), is the lay term to describe when people start to recover, or seem to recover, from a bout of COVID-19 but then continue to suffer from symptoms. For some, it’s gone on for 2 years or longer. While the governments of the United Statesand several other countries formally recognize the existence of long COVID, the National Institutes of Health (NIH) has yet to formally define it. There’s no approved treatment, and the causes are not understood.

Here’s what is known: Long COVID is a postviral condition affecting a large percentage of people who become infected with the coronavirus. It can be utterly debilitating or mildly annoying, and it is affecting enough people to cause concern for employers, health insurers, and governments.
 

First, the many symptoms

According to the Centers for Disease Control and Prvention, long COVID symptoms may include:

• Tiredness or fatigue that interferes with daily life.
• Symptoms that get worse after physical or mental effort.
• Fever.
• Difficulty breathing or shortness of breath.
• Cough.
• Chest pain.
• Heart palpitations.
• Difficulty thinking or concentrating (sometimes referred to as “brain fog”).
• Headache.
• Sleep problems.
• Dizziness when standing.
• Pins-and-needles feelings.
• Change in smell or taste.
• Depression or anxiety.
• Diarrhea.
• Stomach pain.
• Joint or muscle pain.
• Rash.
• Changes in menstrual cycles.

“People with post-COVID conditions may develop or continue to have symptoms that are hard to explain and manage,” the CDC says on its website. “Clinical evaluations and results of routine blood tests, chest x-rays, and electrocardiograms may be normal. The symptoms are similar to those reported by people with ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome) and other poorly understood chronic illnesses that may occur after other infections.” 

Doctors may not fully appreciate the subtle nature of some of the symptoms. 

“People with these unexplained symptoms may be misunderstood by their health care providers, which can result in a long time for them to get a diagnosis and receive appropriate care or treatment,” the CDC says.

Health professionals should recognize that long COVID can be disabling, the U.S. Department of Health and Human Services says. “Long COVID can substantially limit a major life activity,” HHS says in civil rights guidance. One possible example: “A person with long COVID who has lung damage that causes shortness of breath, fatigue, and related effects is substantially limited in respiratory function, among other major life activities,” the HHS notes.
 

How many people are affected?

This has been difficult to judge because not everyone who has had COVID-19 gets tested for it and there are no formal diagnostic criteria yet for long COVID. The CDC estimates that 19% of patients in the United States who have ever had COVID-19 have long COVID symptoms. 

Some estimates go higher. A University of Oxford study in September 2021 found more than a third of patients had symptoms of long COVID between 3 months and 6 months after a COVID-19 diagnosis. As many as 55% of COVID-19 patients in one Chinese study had one or more lingering symptoms 2 years later, Lixue Huang, MD, of the China-Japan Friendship Hospital in Beijing, and colleagues reported in the journal Lancet Respiratory Medicine in May.

According to the CDC, age is a factor. “Older adults are less likely to have long COVID than younger adults. Nearly three times as many adults ages 50-59 currently have long COVID than those age 80 and older,” the CDC says. Women and racial and ethnic minorities are more likely to be affected.

Many people are experiencing neurological effects, such as the so-called brain fog, according to Ziyad Al-Aly, MD, of Washington University and the VA St. Louis Health Care System, and colleagues, whose report was published in Nature Medicine in September. They estimated that 6.6 million Americans have brain impairments associated with COVID infection.

“Some of the neurologic disorders reported here are serious chronic conditions that will impact some people for a lifetime,” they wrote. “Given the colossal scale of the pandemic, and even though the absolute numbers reported in this work are small, these may translate into a large number of affected individuals around the world – and this will likely contribute to a rise in the burden of neurologic diseases.”
 

Causes

It’s not clear what the underlying causes are, but most research points to a combination of factors. Suspects include ongoing inflammation, tiny blood clots, and reactivation of latent viruses. In May, Brent Palmer, PhD, of the University of Colorado, Denver, and colleagues found people with long COVID had persistent activation of T-cells that were specific for SARS-CoV-2.

COVID-19 itself can damage organs, and long COVID might be caused by ongoing damage. In August, Alexandros Rovas, MD, of University Hospital Munster in Germany, and colleagues found patients with long COVID had evidence of damage to their capillaries. “Whether, to what extent, and when the observed damage might be reversible remains unclear,” they wrote in the journal Angiogenesis.

People with long COVID have immune responses to other viruses, such as Epstein-Barr – evidence that COVID-19 might reactivate latent viruses. “Our data suggest the involvement of persistent antigen, reactivation of latent herpesviruses, and chronic inflammation,” immunobiologist Akiko Iwasaki, PhD, of Yale University, New Haven, Conn., and colleagues wrote in a study posted in August that had not yet been peer-reviewed for publication.

This might be causing an autoimmune response. “The infection may cause the immune system to start making autoantibodies that attack a person’s own organs and tissues,” the NIH says.

There could be other factors. A study by Harvard researchers found that people who felt stressed, depressed, or lonely before catching COVID-19 were more likely to develop long COVID afterward. “Distress was more strongly associated with developing long COVID than physical health risk factors such as obesity, asthma, and hypertension,” Siwen Wang, MD, a research fellow with Harvard University’s T.H. Chan School of Public Health, Boston, said in a statement.  Plus, nearly 44% of those in the study developed COVID-19 infections after having been assessed for stress, Dr. Wang and colleagues reported in the journal JAMA Psychiatry.
 

Vaccine protection 

There’s evidence that vaccination protects against long COVID, both by preventing infection in the first place, but also even for people who have breakthrough infections.

A meta-analysis covering studies involving 17 million people found evidence vaccination might reduce the severity of COVID-19 or might help the body clear any lingering virus after an infection.

“Overall, vaccination was associated with reduced risks or odds of long COVID, with preliminary evidence suggesting that two doses are more effective than one dose,” wrote Cesar Fernandez de las Penas, PhD, of King Juan Carlos University in Madrid, and colleagues. Their report is in The Lancet’s eClinicalMedicine.

A team in Milan found that unvaccinated people in their study were nearly three times as likely to have serious symptoms for longer than 4 weeks compared to vaccinated volunteers. According to their report in JAMA, Elena Azzolini, MD, PhD, assistant professor at Humanitas Research Hospital, and colleagues found two or three doses of vaccine reduced the risk of hospitalization from COVID to 16% or 17% compared to 42% for the unvaccinated.
 

Treatments

With no diagnostic criteria and no understanding of the causes, it’s hard for doctors to determine treatments.

Most experts dealing with long COVID, even those at the specialty centers that have been set up at hospitals and health systems in the United States, recommend that patients start with their primary care doctors before moving on to specialists.

“The mainstay of management is supportive, holistic care, symptom control, and detection of treatable complications,” Trish Greenhalgh, MD, professor of primary care health sciences at the University of Oxford, England, and colleagues wrote in the journal The BMJ in September. “Patients with long COVID greatly value input from their primary care clinician. Generalist clinicians can help patients considerably by hearing the patient’s story and validating their experience … (and) making the diagnosis of long COVID (which does not have to be by exclusion) and excluding alternative diagnoses.”

Evidence is building that long COVID closely resembles other postviral conditions – something that can provide clues for treatment. For example, several studies indicate that exercise doesn’t help most patients.

But there are approaches that can work. Treatments may include pulmonary rehabilitation; autonomic conditioning therapy, which includes breathing therapy; and cognitive rehabilitation to relieve brain fog. Doctors are also trying the antidepressant amitriptyline to help with sleep disturbances and headaches; the antiseizure medication gabapentin to help with pain, numbness, and other neurological symptoms; and drugs to relieve low blood pressure in patients experiencing postural orthostatic tachycardia syndrome (POTS).

The NIH is sponsoring studies that have recruited just over 8,200 adults. And more than two dozen researchers from Harvard; Stanford; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai Hospitals; Cardiff University; and Yale announced in September they were forming the Long COVID Research Initiative to speed up studies.

The group, with funding from private enterprise, plans to conduct tissue biopsy, imaging studies, and autopsies and will search for potential biomarkers in the blood of patients.

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

Insurance coverage for specialty drugs to treat psoriasis and psoriatic arthritis varies extensively among insurance companies and often restricts coverage beyond the drug labels, according to a review of data from commercial health plans in the United States.

Although specialty medications have demonstrated effectiveness for psoriasis and psoriatic arthritis, data on insurance coverage for these indications are limited and costs are often a barrier to treatment, Christine Learned, of Tufts Medical Center, Boston, and colleagues wrote.

Catalin205/Thinkstock

In a study published in the Journal of Psoriasis and Psoriatic Arthritis, the researchers used the Tufts Medical Center Specialty Drug Evidence and Coverage database, which includes information on 158 specialty drugs covered by 17 U.S. commercial health plans, to review data on a total of 11 medications indicated for psoriasis (etanercept, adalimumab, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, guselkumab, tildrakizumab, risankizumab, and apremilast) and 11 indicated for psoriatic arthritis (etanercept, adalimumab, certolizumab pegol, golimumab, secukinumab, ixekizumab, ustekinumab, guselkumab, tofacitinib, apremilast, and abatacept) at the time of the study.

Overall, an average of 78.6% and 66.8% of insurance plans were more restrictive than the Food and Drug Association label in coverage of specialty medications for psoriasis and psoriatic arthritis, respectively.

Disease severity affected insurance coverage for psoriasis. The percentage of plans with a body surface area requirement for specialty medications ranged from 11% for apremilast to 39% for tildrakizumab, adalimumab, and certolizumab pegol. The percentage of plans with exceptions for special body locations affected by psoriasis ranged from 6% for risankizumab and brodalumab to 39% for certolizumab pegol. In addition, 6% of plans had Psoriasis Area and Severity Index requirements for etanercept and ixekizumab, and 11% had PASI requirements for adalimumab, certolizumab pegol, and tildrakizumab.

The percentage of plans with prescriber restrictions for both psoriasis and psoriatic arthritis ranged from 33% to 50%.

All 11 medications for psoriatic arthritis were approved as first-line treatments by at least one plan, compared with 3 the 11 medications with indications for psoriasis. However, medications for both psoriasis and psoriatic arthritis were approved mainly as second-line therapies.

Study designs may impact insurance coverage, as randomized, controlled trials are often used as the basis for coverage decisions for psoriasis, while coverage for psoriatic arthritis is more often based on clinical guidelines, the researchers explained.

“Our analysis confirms that variability exists for the indications of psoriasis and psoriatic arthritis,” they wrote.

The comorbidities associated with psoriasis are not always considered in insurance coverage, and coverage complications may contribute to the persistent undertreatment of many patients with psoriasis, the researchers added.

“Insurance restrictions may blunt provider and patient autonomy in selection of specialty medications and have the potential to diminish a provider’s ability to tailor regimens so as to optimize outcomes while minimizing risks,” they emphasized.

The study findings were limited by the inclusion only of publicly available policy information; therefore, some plans’ restrictions may have been missed in the analysis, the researchers said.

The results suggest that patients should review their insurance coverage of specialty drugs when choosing a health plan, and clinicians should factor in a patient’s plan a likely drug access when considering treatment options, they concluded.

The study received no outside funding. Ms. Learned had no relevant financial conflicts to disclose, but two coauthors reported financial relationships with pharmaceutical companies that manufacturer drugs for psoriasis and psoriatic arthritis.

Insurance coverage for specialty drugs to treat psoriasis and psoriatic arthritis varies extensively among insurance companies and often restricts coverage beyond the drug labels, according to a review of data from commercial health plans in the United States.

Although specialty medications have demonstrated effectiveness for psoriasis and psoriatic arthritis, data on insurance coverage for these indications are limited and costs are often a barrier to treatment, Christine Learned, of Tufts Medical Center, Boston, and colleagues wrote.

Catalin205/Thinkstock

In a study published in the Journal of Psoriasis and Psoriatic Arthritis, the researchers used the Tufts Medical Center Specialty Drug Evidence and Coverage database, which includes information on 158 specialty drugs covered by 17 U.S. commercial health plans, to review data on a total of 11 medications indicated for psoriasis (etanercept, adalimumab, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, guselkumab, tildrakizumab, risankizumab, and apremilast) and 11 indicated for psoriatic arthritis (etanercept, adalimumab, certolizumab pegol, golimumab, secukinumab, ixekizumab, ustekinumab, guselkumab, tofacitinib, apremilast, and abatacept) at the time of the study.

Overall, an average of 78.6% and 66.8% of insurance plans were more restrictive than the Food and Drug Association label in coverage of specialty medications for psoriasis and psoriatic arthritis, respectively.

Disease severity affected insurance coverage for psoriasis. The percentage of plans with a body surface area requirement for specialty medications ranged from 11% for apremilast to 39% for tildrakizumab, adalimumab, and certolizumab pegol. The percentage of plans with exceptions for special body locations affected by psoriasis ranged from 6% for risankizumab and brodalumab to 39% for certolizumab pegol. In addition, 6% of plans had Psoriasis Area and Severity Index requirements for etanercept and ixekizumab, and 11% had PASI requirements for adalimumab, certolizumab pegol, and tildrakizumab.

The percentage of plans with prescriber restrictions for both psoriasis and psoriatic arthritis ranged from 33% to 50%.

All 11 medications for psoriatic arthritis were approved as first-line treatments by at least one plan, compared with 3 the 11 medications with indications for psoriasis. However, medications for both psoriasis and psoriatic arthritis were approved mainly as second-line therapies.

Study designs may impact insurance coverage, as randomized, controlled trials are often used as the basis for coverage decisions for psoriasis, while coverage for psoriatic arthritis is more often based on clinical guidelines, the researchers explained.

“Our analysis confirms that variability exists for the indications of psoriasis and psoriatic arthritis,” they wrote.

The comorbidities associated with psoriasis are not always considered in insurance coverage, and coverage complications may contribute to the persistent undertreatment of many patients with psoriasis, the researchers added.

“Insurance restrictions may blunt provider and patient autonomy in selection of specialty medications and have the potential to diminish a provider’s ability to tailor regimens so as to optimize outcomes while minimizing risks,” they emphasized.

The study findings were limited by the inclusion only of publicly available policy information; therefore, some plans’ restrictions may have been missed in the analysis, the researchers said.

The results suggest that patients should review their insurance coverage of specialty drugs when choosing a health plan, and clinicians should factor in a patient’s plan a likely drug access when considering treatment options, they concluded.

The study received no outside funding. Ms. Learned had no relevant financial conflicts to disclose, but two coauthors reported financial relationships with pharmaceutical companies that manufacturer drugs for psoriasis and psoriatic arthritis.

Insurance coverage for specialty drugs to treat psoriasis and psoriatic arthritis varies extensively among insurance companies and often restricts coverage beyond the drug labels, according to a review of data from commercial health plans in the United States.

Although specialty medications have demonstrated effectiveness for psoriasis and psoriatic arthritis, data on insurance coverage for these indications are limited and costs are often a barrier to treatment, Christine Learned, of Tufts Medical Center, Boston, and colleagues wrote.

Catalin205/Thinkstock

In a study published in the Journal of Psoriasis and Psoriatic Arthritis, the researchers used the Tufts Medical Center Specialty Drug Evidence and Coverage database, which includes information on 158 specialty drugs covered by 17 U.S. commercial health plans, to review data on a total of 11 medications indicated for psoriasis (etanercept, adalimumab, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, guselkumab, tildrakizumab, risankizumab, and apremilast) and 11 indicated for psoriatic arthritis (etanercept, adalimumab, certolizumab pegol, golimumab, secukinumab, ixekizumab, ustekinumab, guselkumab, tofacitinib, apremilast, and abatacept) at the time of the study.

Overall, an average of 78.6% and 66.8% of insurance plans were more restrictive than the Food and Drug Association label in coverage of specialty medications for psoriasis and psoriatic arthritis, respectively.

Disease severity affected insurance coverage for psoriasis. The percentage of plans with a body surface area requirement for specialty medications ranged from 11% for apremilast to 39% for tildrakizumab, adalimumab, and certolizumab pegol. The percentage of plans with exceptions for special body locations affected by psoriasis ranged from 6% for risankizumab and brodalumab to 39% for certolizumab pegol. In addition, 6% of plans had Psoriasis Area and Severity Index requirements for etanercept and ixekizumab, and 11% had PASI requirements for adalimumab, certolizumab pegol, and tildrakizumab.

The percentage of plans with prescriber restrictions for both psoriasis and psoriatic arthritis ranged from 33% to 50%.

All 11 medications for psoriatic arthritis were approved as first-line treatments by at least one plan, compared with 3 the 11 medications with indications for psoriasis. However, medications for both psoriasis and psoriatic arthritis were approved mainly as second-line therapies.

Study designs may impact insurance coverage, as randomized, controlled trials are often used as the basis for coverage decisions for psoriasis, while coverage for psoriatic arthritis is more often based on clinical guidelines, the researchers explained.

“Our analysis confirms that variability exists for the indications of psoriasis and psoriatic arthritis,” they wrote.

The comorbidities associated with psoriasis are not always considered in insurance coverage, and coverage complications may contribute to the persistent undertreatment of many patients with psoriasis, the researchers added.

“Insurance restrictions may blunt provider and patient autonomy in selection of specialty medications and have the potential to diminish a provider’s ability to tailor regimens so as to optimize outcomes while minimizing risks,” they emphasized.

The study findings were limited by the inclusion only of publicly available policy information; therefore, some plans’ restrictions may have been missed in the analysis, the researchers said.

The results suggest that patients should review their insurance coverage of specialty drugs when choosing a health plan, and clinicians should factor in a patient’s plan a likely drug access when considering treatment options, they concluded.

The study received no outside funding. Ms. Learned had no relevant financial conflicts to disclose, but two coauthors reported financial relationships with pharmaceutical companies that manufacturer drugs for psoriasis and psoriatic arthritis.

Doctors caring for patients taking steroids now have broader flexibility for which drugs to use to prevent osteoporosis associated with the medications.

The American College of Rheumatology (ACR) has released an updated guideline that advises treatment providers on when and how long to prescribe therapies that prevent or treat glucocorticoid-induced osteoporosis (GIOP). Since the ACR last updated the guideline in 2017, the Food and Drug Administration has approved new treatments for osteoporosis, which are now included in the recommendations.

The new guideline also advises physicians that they may need to transition patients to a second treatment after concluding a first course – so-called sequential therapy – to better protect them against bone loss and fracture. It also offers detailed instructions for which drugs to use, when, and how long these medications should be administered for patients taking glucocorticoids over a long period of time.

The guideline’s inclusion of sequential therapy is significant and will be helpful to practicing clinicians, according to S.B. Tanner IV, MD, director of the Osteoporosis Clinic at Vanderbilt Health, Nashville, Tenn.

“For the first time, the ACR has offered guidance for starting and stopping treatments,” Dr. Tanner said. “This guideline supports awareness that osteoporosis is lifelong – something that will consistently need monitoring.”

An estimated 2.5 million Americans use glucocorticoids, according to a 2013 study in Arthritis Care & Research. Meanwhile, a 2019 study of residents in Denmark found 3% of people in the country were prescribed glucocorticoids annually. That study estimated 54% of glucocorticoid users were female and found the percentage of people taking glucocorticoids increased with age.

Glucocorticoids are used to treat a variety of inflammatory conditions, from multiple sclerosis to lupus, and often are prescribed to transplant patients to prevent their immune systems from rejecting new organs. When taken over time these medications can cause osteoporosis, which in turn raises the risk of fracture.

More than 10% of patients who receive long-term glucocorticoid treatment are diagnosed with clinical fractures. In addition, even low-dose glucocorticoid therapy is associated with a bone loss rate of 10% per year for a patient.

Osteoporosis prevention

After stopping some prevention therapies for GIOP, a high risk of bone loss or fracture still persists, according to Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center for the Hospital for Special Surgery, New York, and co-principal investigator of the new guideline.

“We wanted to be sure the need for sequential treatment is adequately communicated, including to patients who might not know they need to start a second medication,” Dr. Russell said.

Physicians and patients must be aware that when completing a course of one GIOP treatment, another drug for the condition should be started, as specified in the guideline.

“Early intervention can prevent glucocorticoid-induced fractures that can lead to substantial morbidity and increased mortality,” said Mary Beth Humphrey, MD, PhD, interim vice president for research at the University of Oklahoma Health Sciences Center in Oklahoma City and co-principal investigator of the ACR guideline.

Anyone can fracture

While age and other risk factors, including menopause, increase the risk of developing GIOP, bone loss can occur rapidly for a patient of any age.

Even a glucocorticoid dose as low as 2.5 mg will increase the risk of vertebral fractures, with some occurring as soon as 3 months after treatment starts, Dr. Humphrey said. For patients taking up to 7.5 mg daily, the risk of vertebral fracture doubles. Doses greater than 10 mg daily for more than 3 months raise the likelihood of a vertebral fracture by a factor of 14, and result in a 300% increase in the likelihood of hip fractures, according to Dr. Humphrey.

“When on steroids, even patients with high bone density scores can fracture,” Dr. Tanner said. “The 2017 guideline was almost too elaborate in its effort to calculate risk. The updated guideline acknowledges moderate risk and suggests that this is a group of patients who need treatment.”
 

Rank ordering adds flexibility

The updated ACR guideline no longer ranks medications based on patient fracture data, side effects, cost care, and whether the drug is provided through injection, pill, or IV.

All of the preventive treatments the panel recommends reduce the risk of steroid-induced bone loss, Dr. Humphrey said.

“We thought the 2017 guideline was too restrictive,” Dr. Russell said. “We’re giving physicians and patients more leeway to choose a medication based on their preferences.”

Patient preference of delivery mechanism – such as a desire for pills only – can now be weighed more heavily into drug treatment decisions.

“In the exam room, there are three dynamics going on: What the patient wants, what the doctor knows is most effective, and what the insurer will pay,” Dr. Tanner said. “Doing away with rank ordering opens up the conversation beyond cost to consider all those factors.”

The guideline team conducted a systematic literature review for clinical questions on nonpharmacologic and pharmacologic treatment addressed in the 2017 guideline, and for questions on new pharmacologic treatments, discontinuation of medications, and sequential and combination therapy. The voting panel consisted of two patient representatives and 13 experts representing adult and pediatric rheumatology and endocrinology, nephrology, and gastroenterology.

A full manuscript has been submitted for publication in Arthritis & Rheumatology and Arthritis Care and Research for peer review, and is expected to publish in early 2023.

Dr. Humphrey and Dr. Russell, the co-principal investigators for the guideline, and Dr. Rubin have disclosed no relevant financial relationships. Dr. Tanner reported a current research grant funded by Amgen through the University of Alabama at Birmingham and being a paid course instructor for the International Society for Clinical Densitometry bone density course, Osteoporosis Essentials.

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

Doctors caring for patients taking steroids now have broader flexibility for which drugs to use to prevent osteoporosis associated with the medications.

The American College of Rheumatology (ACR) has released an updated guideline that advises treatment providers on when and how long to prescribe therapies that prevent or treat glucocorticoid-induced osteoporosis (GIOP). Since the ACR last updated the guideline in 2017, the Food and Drug Administration has approved new treatments for osteoporosis, which are now included in the recommendations.

The new guideline also advises physicians that they may need to transition patients to a second treatment after concluding a first course – so-called sequential therapy – to better protect them against bone loss and fracture. It also offers detailed instructions for which drugs to use, when, and how long these medications should be administered for patients taking glucocorticoids over a long period of time.

The guideline’s inclusion of sequential therapy is significant and will be helpful to practicing clinicians, according to S.B. Tanner IV, MD, director of the Osteoporosis Clinic at Vanderbilt Health, Nashville, Tenn.

“For the first time, the ACR has offered guidance for starting and stopping treatments,” Dr. Tanner said. “This guideline supports awareness that osteoporosis is lifelong – something that will consistently need monitoring.”

An estimated 2.5 million Americans use glucocorticoids, according to a 2013 study in Arthritis Care & Research. Meanwhile, a 2019 study of residents in Denmark found 3% of people in the country were prescribed glucocorticoids annually. That study estimated 54% of glucocorticoid users were female and found the percentage of people taking glucocorticoids increased with age.

Glucocorticoids are used to treat a variety of inflammatory conditions, from multiple sclerosis to lupus, and often are prescribed to transplant patients to prevent their immune systems from rejecting new organs. When taken over time these medications can cause osteoporosis, which in turn raises the risk of fracture.

More than 10% of patients who receive long-term glucocorticoid treatment are diagnosed with clinical fractures. In addition, even low-dose glucocorticoid therapy is associated with a bone loss rate of 10% per year for a patient.

Osteoporosis prevention

After stopping some prevention therapies for GIOP, a high risk of bone loss or fracture still persists, according to Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center for the Hospital for Special Surgery, New York, and co-principal investigator of the new guideline.

“We wanted to be sure the need for sequential treatment is adequately communicated, including to patients who might not know they need to start a second medication,” Dr. Russell said.

Physicians and patients must be aware that when completing a course of one GIOP treatment, another drug for the condition should be started, as specified in the guideline.

“Early intervention can prevent glucocorticoid-induced fractures that can lead to substantial morbidity and increased mortality,” said Mary Beth Humphrey, MD, PhD, interim vice president for research at the University of Oklahoma Health Sciences Center in Oklahoma City and co-principal investigator of the ACR guideline.

Anyone can fracture

While age and other risk factors, including menopause, increase the risk of developing GIOP, bone loss can occur rapidly for a patient of any age.

Even a glucocorticoid dose as low as 2.5 mg will increase the risk of vertebral fractures, with some occurring as soon as 3 months after treatment starts, Dr. Humphrey said. For patients taking up to 7.5 mg daily, the risk of vertebral fracture doubles. Doses greater than 10 mg daily for more than 3 months raise the likelihood of a vertebral fracture by a factor of 14, and result in a 300% increase in the likelihood of hip fractures, according to Dr. Humphrey.

“When on steroids, even patients with high bone density scores can fracture,” Dr. Tanner said. “The 2017 guideline was almost too elaborate in its effort to calculate risk. The updated guideline acknowledges moderate risk and suggests that this is a group of patients who need treatment.”
 

Rank ordering adds flexibility

The updated ACR guideline no longer ranks medications based on patient fracture data, side effects, cost care, and whether the drug is provided through injection, pill, or IV.

All of the preventive treatments the panel recommends reduce the risk of steroid-induced bone loss, Dr. Humphrey said.

“We thought the 2017 guideline was too restrictive,” Dr. Russell said. “We’re giving physicians and patients more leeway to choose a medication based on their preferences.”

Patient preference of delivery mechanism – such as a desire for pills only – can now be weighed more heavily into drug treatment decisions.

“In the exam room, there are three dynamics going on: What the patient wants, what the doctor knows is most effective, and what the insurer will pay,” Dr. Tanner said. “Doing away with rank ordering opens up the conversation beyond cost to consider all those factors.”

The guideline team conducted a systematic literature review for clinical questions on nonpharmacologic and pharmacologic treatment addressed in the 2017 guideline, and for questions on new pharmacologic treatments, discontinuation of medications, and sequential and combination therapy. The voting panel consisted of two patient representatives and 13 experts representing adult and pediatric rheumatology and endocrinology, nephrology, and gastroenterology.

A full manuscript has been submitted for publication in Arthritis & Rheumatology and Arthritis Care and Research for peer review, and is expected to publish in early 2023.

Dr. Humphrey and Dr. Russell, the co-principal investigators for the guideline, and Dr. Rubin have disclosed no relevant financial relationships. Dr. Tanner reported a current research grant funded by Amgen through the University of Alabama at Birmingham and being a paid course instructor for the International Society for Clinical Densitometry bone density course, Osteoporosis Essentials.

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

Doctors caring for patients taking steroids now have broader flexibility for which drugs to use to prevent osteoporosis associated with the medications.

The American College of Rheumatology (ACR) has released an updated guideline that advises treatment providers on when and how long to prescribe therapies that prevent or treat glucocorticoid-induced osteoporosis (GIOP). Since the ACR last updated the guideline in 2017, the Food and Drug Administration has approved new treatments for osteoporosis, which are now included in the recommendations.

The new guideline also advises physicians that they may need to transition patients to a second treatment after concluding a first course – so-called sequential therapy – to better protect them against bone loss and fracture. It also offers detailed instructions for which drugs to use, when, and how long these medications should be administered for patients taking glucocorticoids over a long period of time.

The guideline’s inclusion of sequential therapy is significant and will be helpful to practicing clinicians, according to S.B. Tanner IV, MD, director of the Osteoporosis Clinic at Vanderbilt Health, Nashville, Tenn.

“For the first time, the ACR has offered guidance for starting and stopping treatments,” Dr. Tanner said. “This guideline supports awareness that osteoporosis is lifelong – something that will consistently need monitoring.”

An estimated 2.5 million Americans use glucocorticoids, according to a 2013 study in Arthritis Care & Research. Meanwhile, a 2019 study of residents in Denmark found 3% of people in the country were prescribed glucocorticoids annually. That study estimated 54% of glucocorticoid users were female and found the percentage of people taking glucocorticoids increased with age.

Glucocorticoids are used to treat a variety of inflammatory conditions, from multiple sclerosis to lupus, and often are prescribed to transplant patients to prevent their immune systems from rejecting new organs. When taken over time these medications can cause osteoporosis, which in turn raises the risk of fracture.

More than 10% of patients who receive long-term glucocorticoid treatment are diagnosed with clinical fractures. In addition, even low-dose glucocorticoid therapy is associated with a bone loss rate of 10% per year for a patient.

Osteoporosis prevention

After stopping some prevention therapies for GIOP, a high risk of bone loss or fracture still persists, according to Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center for the Hospital for Special Surgery, New York, and co-principal investigator of the new guideline.

“We wanted to be sure the need for sequential treatment is adequately communicated, including to patients who might not know they need to start a second medication,” Dr. Russell said.

Physicians and patients must be aware that when completing a course of one GIOP treatment, another drug for the condition should be started, as specified in the guideline.

“Early intervention can prevent glucocorticoid-induced fractures that can lead to substantial morbidity and increased mortality,” said Mary Beth Humphrey, MD, PhD, interim vice president for research at the University of Oklahoma Health Sciences Center in Oklahoma City and co-principal investigator of the ACR guideline.

Anyone can fracture

While age and other risk factors, including menopause, increase the risk of developing GIOP, bone loss can occur rapidly for a patient of any age.

Even a glucocorticoid dose as low as 2.5 mg will increase the risk of vertebral fractures, with some occurring as soon as 3 months after treatment starts, Dr. Humphrey said. For patients taking up to 7.5 mg daily, the risk of vertebral fracture doubles. Doses greater than 10 mg daily for more than 3 months raise the likelihood of a vertebral fracture by a factor of 14, and result in a 300% increase in the likelihood of hip fractures, according to Dr. Humphrey.

“When on steroids, even patients with high bone density scores can fracture,” Dr. Tanner said. “The 2017 guideline was almost too elaborate in its effort to calculate risk. The updated guideline acknowledges moderate risk and suggests that this is a group of patients who need treatment.”
 

Rank ordering adds flexibility

The updated ACR guideline no longer ranks medications based on patient fracture data, side effects, cost care, and whether the drug is provided through injection, pill, or IV.

All of the preventive treatments the panel recommends reduce the risk of steroid-induced bone loss, Dr. Humphrey said.

“We thought the 2017 guideline was too restrictive,” Dr. Russell said. “We’re giving physicians and patients more leeway to choose a medication based on their preferences.”

Patient preference of delivery mechanism – such as a desire for pills only – can now be weighed more heavily into drug treatment decisions.

“In the exam room, there are three dynamics going on: What the patient wants, what the doctor knows is most effective, and what the insurer will pay,” Dr. Tanner said. “Doing away with rank ordering opens up the conversation beyond cost to consider all those factors.”

The guideline team conducted a systematic literature review for clinical questions on nonpharmacologic and pharmacologic treatment addressed in the 2017 guideline, and for questions on new pharmacologic treatments, discontinuation of medications, and sequential and combination therapy. The voting panel consisted of two patient representatives and 13 experts representing adult and pediatric rheumatology and endocrinology, nephrology, and gastroenterology.

A full manuscript has been submitted for publication in Arthritis & Rheumatology and Arthritis Care and Research for peer review, and is expected to publish in early 2023.

Dr. Humphrey and Dr. Russell, the co-principal investigators for the guideline, and Dr. Rubin have disclosed no relevant financial relationships. Dr. Tanner reported a current research grant funded by Amgen through the University of Alabama at Birmingham and being a paid course instructor for the International Society for Clinical Densitometry bone density course, Osteoporosis Essentials.

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

Entrepreneur Maya McNulty, 49, was one of the first victims of the COVID-19 pandemic. The Schenectady, N.Y., businesswoman spent 2 months in the hospital after catching the disease in March 2020. That September, she was diagnosed with long COVID.

“Even a simple task such as unloading the dishwasher became a major challenge,” she says.

Over the next several months, Ms. McNulty saw a range of specialists, including neurologists, pulmonologists, and cardiologists. She had months of physical therapy and respiratory therapy to help regain strength and lung function. While many of the doctors she saw were sympathetic to what she was going through, not all were.

“I saw one neurologist who told me to my face that she didn’t believe in long COVID,” she recalls. “It was particularly astonishing since the hospital they were affiliated with had a long COVID clinic.”

Ms. McNulty began to connect with other patients with long COVID through a support group she created at the end of 2020 on the social media app Clubhouse. They exchanged ideas and stories about what had helped one another, which led her to try, over the next year, a plant-based diet, Chinese medicine, and vitamin C supplements, among other treatments.

She also acted on unscientific reports she found online and did her own research, which led her to discover claims that some asthma patients with chronic coughing responded well to halotherapy, or dry salt therapy, during which patients inhale micro-particles of salt into their lungs to reduce inflammation, widen airways, and thin mucus. She’s been doing this procedure at a clinic near her home for over a year and credits it with helping with her chronic cough, especially as she recovers from her second bout of COVID-19.

It’s not cheap – a single half-hour session can cost up to $50 and isn’t covered by insurance. There’s also no good research to suggest that it can help with long COVID, according to the Cleveland Clinic.

Ms. McNulty understands that but says many people who live with long COVID turn to these treatments out of a sense of desperation.

“When it comes to this condition, we kind of have to be our own advocates. People are so desperate and feel so gaslit by doctors who don’t believe in their symptoms that they play Russian roulette with their body,” she says. “Most just want some hope and a way to relieve pain.”

Across the country, 16 million Americans have long COVID, according to the Brookings Institution’s analysis of a 2022 Census Bureau report. The report also estimated that up to a quarter of them have such debilitating symptoms that they are no longer able to work. While long COVID centers may offer therapies to help relieve symptoms, “there are no evidence-based established treatments for long COVID at this point,” says Andrew Schamess, MD, a professor of internal medicine at Ohio State Wexner Medical Center, who runs its Post-COVID Recovery Program. “You can’t blame patients for looking for alternative remedies to help them. Unfortunately, there are also a lot of people out to make a buck who are selling unproven and disproven therapies.”
 

Sniffing out the snake oil

With few evidence-based treatments for long COVID, patients with debilitating symptoms can be tempted by unproven options. One that has gotten a lot of attention is hyperbaric oxygen. This therapy has traditionally been used to treat divers who have decompression sickness, or “the bends.” It’s also being touted by some clinics as an effective treatment for long COVID.

A very small trial of 73 patients with long COVID, published in the journal Scientific Reports, found that those treated in a high-pressure oxygen system 5 days a week for 2 months showed improvements in brain fog, pain, energy, sleep, anxiety, and depression, compared with similar patients who got sham treatments. But larger studies are needed to show how well it works, notes Dr. Schamess.

“It’s very expensive – roughly $120 per session – and there just isn’t the evidence there to support its use,” he says.

In addition, the therapy itself carries risks, such as ear and sinus pain, middle ear injury, temporary vision changes, and, very rarely, lung collapse, according to the U.S. Food and Drug Administration.

One “particularly troubling” treatment being offered, says Kathleen Bell, MD, chair of the department of physical medicine and rehabilitation at the University of Texas Southwestern Medical Center, is stem cell therapy. This therapy is still in its infancy, but it’s being marketed by some clinics as a way to prevent COVID-19 and also treat long-haul symptoms.

The FDA has issued advisories that there are no products approved to treat long COVID and recommends against their use, except in a clinical trial.

“There’s absolutely no regulation – you don’t know what you’re getting, and there’s no research to suggest this therapy even works,” says Dr. Bell. It’s also prohibitively expensive – one Cayman Islands–based company advertises its treatment for as much as $25,000.

Patients with long COVID are even traveling as far as Cyprus, Germany, and Switzerland for a procedure known as blood washing, in which large needles are inserted into veins to filter blood and remove lipids and inflammatory proteins, the British Medical Journal reported in July. Some patients are also prescribed blood thinners to remove microscopic blood clots that may contribute to long COVID. But this treatment is also expensive, with many people paying $10,000-$15,000 out of pocket, and there’s no published evidence to suggest it works, according to the BMJ.

It can be particularly hard to discern what may work and what’s unproven, since many primary care providers are themselves unfamiliar with even traditional long COVID treatments, Dr. Bell says.
 

Sorting through supplements

Yufang Lin, MD, an integrative specialist at the Cleveland Clinic, says many patients with long COVID enter her office with bags of supplements.

“There’s no data on them, and in large quantities, they may even be harmful,” she says.

Instead, she works closely with the Cleveland Clinic’s long COVID center to do a thorough workup of each patient, which often includes screening for certain nutritional deficiencies.

“Anecdotally, we do see many patients with long COVID who are deficient in these vitamins and minerals,” says Dr. Lin. “If someone is low, we will suggest the appropriate supplement. Otherwise, we work with them to institute some dietary changes.”

This usually involves a plant-based, anti-inflammatory eating pattern such as the Mediterranean diet, which is rich in fruits, vegetables, whole grains, nuts, fatty fish, and healthy fats such as olive oil and avocados.

Other supplements some doctors recommend for patients with long COVID are meant to treat inflammation, Dr. Bell says, although there’s not good evidence they work. One is the antioxidant coenzyme Q10.

But a small preprint study published in The Lancet, of 121 patients with long COVID who took 500 milligrams a day of coenzyme Q10 for 6 weeks saw no differences in recovery, compared with those who took a placebo. Because the study is still a preprint, it has not been peer-reviewed.

Another is probiotics. A small study, published in the journal Infectious Diseases Diagnosis & Treatment, found that a blend of five lactobacillus probiotics, along with a prebiotic called inulin, taken for 30 days, helped with long-term COVID symptoms such as coughing and fatigue. But larger studies need to be done to support their use.

One that may have more promise is omega-3 fatty acids. Like many other supplements, these may help with long COVID by easing inflammation, says Steven Flanagan, MD, a rehabilitation medicine specialist at NYU Langone who works with long COVID patients. Researchers at the Mount Sinai School of Medicine, New York, are studying whether a supplement can help patients who have lost their sense of taste or smell after an infection, but results aren’t yet available.

Among the few alternatives that have been shown to help patients are mindfulness-based therapies – in particular, mindfulness-based forms of exercise such as tai chi and qi gong may be helpful, as they combine a gentle workout with stress reduction.

“Both incorporate meditation, which helps not only to relieve some of the anxiety associated with long COVID but allows patients to redirect their thought process so that they can cope with symptoms better,” says Dr. Flanagan.

A 2022 study, published in BMJ Open, found that these two activities reduced inflammatory markers and improved respiratory muscle strength and function in patients recovering from COVID-19.

“I recommend these activities to all my long COVID patients, as it’s inexpensive and easy to find classes to do either at home or in their community,” he says. “Even if it doesn’t improve their long COVID symptoms, it has other benefits such as increased strength and flexibility that can boost their overall health.”

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

Entrepreneur Maya McNulty, 49, was one of the first victims of the COVID-19 pandemic. The Schenectady, N.Y., businesswoman spent 2 months in the hospital after catching the disease in March 2020. That September, she was diagnosed with long COVID.

“Even a simple task such as unloading the dishwasher became a major challenge,” she says.

Over the next several months, Ms. McNulty saw a range of specialists, including neurologists, pulmonologists, and cardiologists. She had months of physical therapy and respiratory therapy to help regain strength and lung function. While many of the doctors she saw were sympathetic to what she was going through, not all were.

“I saw one neurologist who told me to my face that she didn’t believe in long COVID,” she recalls. “It was particularly astonishing since the hospital they were affiliated with had a long COVID clinic.”

Ms. McNulty began to connect with other patients with long COVID through a support group she created at the end of 2020 on the social media app Clubhouse. They exchanged ideas and stories about what had helped one another, which led her to try, over the next year, a plant-based diet, Chinese medicine, and vitamin C supplements, among other treatments.

She also acted on unscientific reports she found online and did her own research, which led her to discover claims that some asthma patients with chronic coughing responded well to halotherapy, or dry salt therapy, during which patients inhale micro-particles of salt into their lungs to reduce inflammation, widen airways, and thin mucus. She’s been doing this procedure at a clinic near her home for over a year and credits it with helping with her chronic cough, especially as she recovers from her second bout of COVID-19.

It’s not cheap – a single half-hour session can cost up to $50 and isn’t covered by insurance. There’s also no good research to suggest that it can help with long COVID, according to the Cleveland Clinic.

Ms. McNulty understands that but says many people who live with long COVID turn to these treatments out of a sense of desperation.

“When it comes to this condition, we kind of have to be our own advocates. People are so desperate and feel so gaslit by doctors who don’t believe in their symptoms that they play Russian roulette with their body,” she says. “Most just want some hope and a way to relieve pain.”

Across the country, 16 million Americans have long COVID, according to the Brookings Institution’s analysis of a 2022 Census Bureau report. The report also estimated that up to a quarter of them have such debilitating symptoms that they are no longer able to work. While long COVID centers may offer therapies to help relieve symptoms, “there are no evidence-based established treatments for long COVID at this point,” says Andrew Schamess, MD, a professor of internal medicine at Ohio State Wexner Medical Center, who runs its Post-COVID Recovery Program. “You can’t blame patients for looking for alternative remedies to help them. Unfortunately, there are also a lot of people out to make a buck who are selling unproven and disproven therapies.”
 

Sniffing out the snake oil

With few evidence-based treatments for long COVID, patients with debilitating symptoms can be tempted by unproven options. One that has gotten a lot of attention is hyperbaric oxygen. This therapy has traditionally been used to treat divers who have decompression sickness, or “the bends.” It’s also being touted by some clinics as an effective treatment for long COVID.

A very small trial of 73 patients with long COVID, published in the journal Scientific Reports, found that those treated in a high-pressure oxygen system 5 days a week for 2 months showed improvements in brain fog, pain, energy, sleep, anxiety, and depression, compared with similar patients who got sham treatments. But larger studies are needed to show how well it works, notes Dr. Schamess.

“It’s very expensive – roughly $120 per session – and there just isn’t the evidence there to support its use,” he says.

In addition, the therapy itself carries risks, such as ear and sinus pain, middle ear injury, temporary vision changes, and, very rarely, lung collapse, according to the U.S. Food and Drug Administration.

One “particularly troubling” treatment being offered, says Kathleen Bell, MD, chair of the department of physical medicine and rehabilitation at the University of Texas Southwestern Medical Center, is stem cell therapy. This therapy is still in its infancy, but it’s being marketed by some clinics as a way to prevent COVID-19 and also treat long-haul symptoms.

The FDA has issued advisories that there are no products approved to treat long COVID and recommends against their use, except in a clinical trial.

“There’s absolutely no regulation – you don’t know what you’re getting, and there’s no research to suggest this therapy even works,” says Dr. Bell. It’s also prohibitively expensive – one Cayman Islands–based company advertises its treatment for as much as $25,000.

Patients with long COVID are even traveling as far as Cyprus, Germany, and Switzerland for a procedure known as blood washing, in which large needles are inserted into veins to filter blood and remove lipids and inflammatory proteins, the British Medical Journal reported in July. Some patients are also prescribed blood thinners to remove microscopic blood clots that may contribute to long COVID. But this treatment is also expensive, with many people paying $10,000-$15,000 out of pocket, and there’s no published evidence to suggest it works, according to the BMJ.

It can be particularly hard to discern what may work and what’s unproven, since many primary care providers are themselves unfamiliar with even traditional long COVID treatments, Dr. Bell says.
 

Sorting through supplements

Yufang Lin, MD, an integrative specialist at the Cleveland Clinic, says many patients with long COVID enter her office with bags of supplements.

“There’s no data on them, and in large quantities, they may even be harmful,” she says.

Instead, she works closely with the Cleveland Clinic’s long COVID center to do a thorough workup of each patient, which often includes screening for certain nutritional deficiencies.

“Anecdotally, we do see many patients with long COVID who are deficient in these vitamins and minerals,” says Dr. Lin. “If someone is low, we will suggest the appropriate supplement. Otherwise, we work with them to institute some dietary changes.”

This usually involves a plant-based, anti-inflammatory eating pattern such as the Mediterranean diet, which is rich in fruits, vegetables, whole grains, nuts, fatty fish, and healthy fats such as olive oil and avocados.

Other supplements some doctors recommend for patients with long COVID are meant to treat inflammation, Dr. Bell says, although there’s not good evidence they work. One is the antioxidant coenzyme Q10.

But a small preprint study published in The Lancet, of 121 patients with long COVID who took 500 milligrams a day of coenzyme Q10 for 6 weeks saw no differences in recovery, compared with those who took a placebo. Because the study is still a preprint, it has not been peer-reviewed.

Another is probiotics. A small study, published in the journal Infectious Diseases Diagnosis & Treatment, found that a blend of five lactobacillus probiotics, along with a prebiotic called inulin, taken for 30 days, helped with long-term COVID symptoms such as coughing and fatigue. But larger studies need to be done to support their use.

One that may have more promise is omega-3 fatty acids. Like many other supplements, these may help with long COVID by easing inflammation, says Steven Flanagan, MD, a rehabilitation medicine specialist at NYU Langone who works with long COVID patients. Researchers at the Mount Sinai School of Medicine, New York, are studying whether a supplement can help patients who have lost their sense of taste or smell after an infection, but results aren’t yet available.

Among the few alternatives that have been shown to help patients are mindfulness-based therapies – in particular, mindfulness-based forms of exercise such as tai chi and qi gong may be helpful, as they combine a gentle workout with stress reduction.

“Both incorporate meditation, which helps not only to relieve some of the anxiety associated with long COVID but allows patients to redirect their thought process so that they can cope with symptoms better,” says Dr. Flanagan.

A 2022 study, published in BMJ Open, found that these two activities reduced inflammatory markers and improved respiratory muscle strength and function in patients recovering from COVID-19.

“I recommend these activities to all my long COVID patients, as it’s inexpensive and easy to find classes to do either at home or in their community,” he says. “Even if it doesn’t improve their long COVID symptoms, it has other benefits such as increased strength and flexibility that can boost their overall health.”

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

Entrepreneur Maya McNulty, 49, was one of the first victims of the COVID-19 pandemic. The Schenectady, N.Y., businesswoman spent 2 months in the hospital after catching the disease in March 2020. That September, she was diagnosed with long COVID.

“Even a simple task such as unloading the dishwasher became a major challenge,” she says.

Over the next several months, Ms. McNulty saw a range of specialists, including neurologists, pulmonologists, and cardiologists. She had months of physical therapy and respiratory therapy to help regain strength and lung function. While many of the doctors she saw were sympathetic to what she was going through, not all were.

“I saw one neurologist who told me to my face that she didn’t believe in long COVID,” she recalls. “It was particularly astonishing since the hospital they were affiliated with had a long COVID clinic.”

Ms. McNulty began to connect with other patients with long COVID through a support group she created at the end of 2020 on the social media app Clubhouse. They exchanged ideas and stories about what had helped one another, which led her to try, over the next year, a plant-based diet, Chinese medicine, and vitamin C supplements, among other treatments.

She also acted on unscientific reports she found online and did her own research, which led her to discover claims that some asthma patients with chronic coughing responded well to halotherapy, or dry salt therapy, during which patients inhale micro-particles of salt into their lungs to reduce inflammation, widen airways, and thin mucus. She’s been doing this procedure at a clinic near her home for over a year and credits it with helping with her chronic cough, especially as she recovers from her second bout of COVID-19.

It’s not cheap – a single half-hour session can cost up to $50 and isn’t covered by insurance. There’s also no good research to suggest that it can help with long COVID, according to the Cleveland Clinic.

Ms. McNulty understands that but says many people who live with long COVID turn to these treatments out of a sense of desperation.

“When it comes to this condition, we kind of have to be our own advocates. People are so desperate and feel so gaslit by doctors who don’t believe in their symptoms that they play Russian roulette with their body,” she says. “Most just want some hope and a way to relieve pain.”

Across the country, 16 million Americans have long COVID, according to the Brookings Institution’s analysis of a 2022 Census Bureau report. The report also estimated that up to a quarter of them have such debilitating symptoms that they are no longer able to work. While long COVID centers may offer therapies to help relieve symptoms, “there are no evidence-based established treatments for long COVID at this point,” says Andrew Schamess, MD, a professor of internal medicine at Ohio State Wexner Medical Center, who runs its Post-COVID Recovery Program. “You can’t blame patients for looking for alternative remedies to help them. Unfortunately, there are also a lot of people out to make a buck who are selling unproven and disproven therapies.”
 

Sniffing out the snake oil

With few evidence-based treatments for long COVID, patients with debilitating symptoms can be tempted by unproven options. One that has gotten a lot of attention is hyperbaric oxygen. This therapy has traditionally been used to treat divers who have decompression sickness, or “the bends.” It’s also being touted by some clinics as an effective treatment for long COVID.

A very small trial of 73 patients with long COVID, published in the journal Scientific Reports, found that those treated in a high-pressure oxygen system 5 days a week for 2 months showed improvements in brain fog, pain, energy, sleep, anxiety, and depression, compared with similar patients who got sham treatments. But larger studies are needed to show how well it works, notes Dr. Schamess.

“It’s very expensive – roughly $120 per session – and there just isn’t the evidence there to support its use,” he says.

In addition, the therapy itself carries risks, such as ear and sinus pain, middle ear injury, temporary vision changes, and, very rarely, lung collapse, according to the U.S. Food and Drug Administration.

One “particularly troubling” treatment being offered, says Kathleen Bell, MD, chair of the department of physical medicine and rehabilitation at the University of Texas Southwestern Medical Center, is stem cell therapy. This therapy is still in its infancy, but it’s being marketed by some clinics as a way to prevent COVID-19 and also treat long-haul symptoms.

The FDA has issued advisories that there are no products approved to treat long COVID and recommends against their use, except in a clinical trial.

“There’s absolutely no regulation – you don’t know what you’re getting, and there’s no research to suggest this therapy even works,” says Dr. Bell. It’s also prohibitively expensive – one Cayman Islands–based company advertises its treatment for as much as $25,000.

Patients with long COVID are even traveling as far as Cyprus, Germany, and Switzerland for a procedure known as blood washing, in which large needles are inserted into veins to filter blood and remove lipids and inflammatory proteins, the British Medical Journal reported in July. Some patients are also prescribed blood thinners to remove microscopic blood clots that may contribute to long COVID. But this treatment is also expensive, with many people paying $10,000-$15,000 out of pocket, and there’s no published evidence to suggest it works, according to the BMJ.

It can be particularly hard to discern what may work and what’s unproven, since many primary care providers are themselves unfamiliar with even traditional long COVID treatments, Dr. Bell says.
 

Sorting through supplements

Yufang Lin, MD, an integrative specialist at the Cleveland Clinic, says many patients with long COVID enter her office with bags of supplements.

“There’s no data on them, and in large quantities, they may even be harmful,” she says.

Instead, she works closely with the Cleveland Clinic’s long COVID center to do a thorough workup of each patient, which often includes screening for certain nutritional deficiencies.

“Anecdotally, we do see many patients with long COVID who are deficient in these vitamins and minerals,” says Dr. Lin. “If someone is low, we will suggest the appropriate supplement. Otherwise, we work with them to institute some dietary changes.”

This usually involves a plant-based, anti-inflammatory eating pattern such as the Mediterranean diet, which is rich in fruits, vegetables, whole grains, nuts, fatty fish, and healthy fats such as olive oil and avocados.

Other supplements some doctors recommend for patients with long COVID are meant to treat inflammation, Dr. Bell says, although there’s not good evidence they work. One is the antioxidant coenzyme Q10.

But a small preprint study published in The Lancet, of 121 patients with long COVID who took 500 milligrams a day of coenzyme Q10 for 6 weeks saw no differences in recovery, compared with those who took a placebo. Because the study is still a preprint, it has not been peer-reviewed.

Another is probiotics. A small study, published in the journal Infectious Diseases Diagnosis & Treatment, found that a blend of five lactobacillus probiotics, along with a prebiotic called inulin, taken for 30 days, helped with long-term COVID symptoms such as coughing and fatigue. But larger studies need to be done to support their use.

One that may have more promise is omega-3 fatty acids. Like many other supplements, these may help with long COVID by easing inflammation, says Steven Flanagan, MD, a rehabilitation medicine specialist at NYU Langone who works with long COVID patients. Researchers at the Mount Sinai School of Medicine, New York, are studying whether a supplement can help patients who have lost their sense of taste or smell after an infection, but results aren’t yet available.

Among the few alternatives that have been shown to help patients are mindfulness-based therapies – in particular, mindfulness-based forms of exercise such as tai chi and qi gong may be helpful, as they combine a gentle workout with stress reduction.

“Both incorporate meditation, which helps not only to relieve some of the anxiety associated with long COVID but allows patients to redirect their thought process so that they can cope with symptoms better,” says Dr. Flanagan.

A 2022 study, published in BMJ Open, found that these two activities reduced inflammatory markers and improved respiratory muscle strength and function in patients recovering from COVID-19.

“I recommend these activities to all my long COVID patients, as it’s inexpensive and easy to find classes to do either at home or in their community,” he says. “Even if it doesn’t improve their long COVID symptoms, it has other benefits such as increased strength and flexibility that can boost their overall health.”

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

A statement by the Society for Healthcare Epidemiology of America, published online in Infection Control & Hospital Epidemiology, offers health care providers guidelines on how to prevent inappropriate antibiotic use in future pandemics and to avoid some of the negative scenarios that have been seen with COVID-19.

According to the U.S. Centers of Disease Control and Prevention, the COVID-19 pandemic brought an alarming increase in antimicrobial resistance in hospitals, with infections and deaths caused by resistant bacteria and fungi going up by 15%. For some pathogens, such as the Carbapenem-resistant Acinetobacter, that number is now as high as 78%.

The culprit might be the widespread antibiotic overprescription during the current pandemic. A 2022 meta-analysis revealed that in high-income countries, 58% of patients with COVID-19 were given antibiotics, whereas in lower- and middle-income countries, 89% of patients were put on such drugs. Some hospitals in Europe and the United States reported similarly elevated numbers, sometimes approaching 100%.

“We’ve lost control,” Natasha Pettit, PharmD, pharmacy director at University of Chicago Medicine, told this news organization. Dr. Pettit was not involved in the SHEA study. “Even if CDC didn’t come out with that data, I can tell you right now more of my time is spent trying to figure out how to manage these multi-drug–resistant infections, and we are running out of options for these patients,”

“Dealing with uncertainty, exhaustion, [and] critical illness in often young, otherwise healthy patients meant doctors wanted to do something for their patients,” said Tamar Barlam, MD, an infectious diseases expert at the Boston Medical Center who led the development of the SHEA white paper, in an interview.

That something often was a prescription for antibiotics, even without a clear indication that they were actually needed. A British study revealed that in times of pandemic uncertainty, clinicians often reached for antibiotics “just in case” and referred to conservative prescribing as “bravery.”

Studies have shown, however, that bacterial co-infections in COVID-19 are rare. A 2020 meta-analysis of 24 studies concluded that only 3.5% of patients had a bacterial co-infection on presentation, and 14.3% had a secondary infection. Similar patterns had previously been observed in other viral outbreaks. Research on MERS-CoV, for example, documented only 1% of patients with a bacterial co-infection on admission. During the 2009 H1N1 influenza pandemic, that number was 12% of non–ICU hospitalized patients.

Yet, according to Dr. Pettit, even when such data became available, it didn’t necessarily change prescribing patterns. “Information was coming at us so quickly, I think the providers didn’t have a moment to see the data, to understand what it meant for their prescribing. Having external guidance earlier on would have been hugely helpful,” she told this news organization.

That’s where the newly published SHEA statement comes in: It outlines recommendations on when to prescribe antibiotics during a respiratory viral pandemic, what tests to order, and when to de-escalate or discontinue the treatment. These recommendations include, for instance, advice to not trust inflammatory markers as reliable indicators of bacterial or fungal infection and to not use procalcitonin routinely to aid in the decision to initiate antibiotics.

According to Dr. Barlam, one of the crucial lessons here is that if clinicians see patients with symptoms that are consistent with the current pandemic, they should trust their own impressions and avoid reaching for antimicrobials “just in case.”

Another important lesson is that antibiotic stewardship programs have a huge role to play during pandemics. They should not only monitor prescribing but also compile new information on bacterial co-infections as it gets released and make sure it reaches the clinicians in a clear form.

Evidence suggests that such programs and guidelines do work to limit unnecessary antibiotic use. In one medical center in Chicago, for example, before recommendations on when to initiate and discontinue antimicrobials were released, over 74% of COVID-19 patients received antibiotics. After guidelines were put in place, the use of such drugs fell to 42%.

Dr. Pettit believes, however, that it’s important not to leave each medical center to its own devices. “Hindsight is always twenty-twenty,” she said, “but I think it would be great that, if we start hearing about a pathogen that might lead to another pandemic, we should have a mechanism in place to call together an expert body to get guidance for how antimicrobial stewardship programs should get involved.”

One of the authors of the SHEA statement, Susan Seo, reports an investigator-initiated Merck grant on cost-effectiveness of letermovir in hematopoietic stem cell transplant patients. Another author, Graeme Forrest, reports a clinical study grant from Regeneron for inpatient monoclonals against SARS-CoV-2. All other authors report no conflicts of interest. The study was independently supported.

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

A statement by the Society for Healthcare Epidemiology of America, published online in Infection Control & Hospital Epidemiology, offers health care providers guidelines on how to prevent inappropriate antibiotic use in future pandemics and to avoid some of the negative scenarios that have been seen with COVID-19.

According to the U.S. Centers of Disease Control and Prevention, the COVID-19 pandemic brought an alarming increase in antimicrobial resistance in hospitals, with infections and deaths caused by resistant bacteria and fungi going up by 15%. For some pathogens, such as the Carbapenem-resistant Acinetobacter, that number is now as high as 78%.

The culprit might be the widespread antibiotic overprescription during the current pandemic. A 2022 meta-analysis revealed that in high-income countries, 58% of patients with COVID-19 were given antibiotics, whereas in lower- and middle-income countries, 89% of patients were put on such drugs. Some hospitals in Europe and the United States reported similarly elevated numbers, sometimes approaching 100%.

“We’ve lost control,” Natasha Pettit, PharmD, pharmacy director at University of Chicago Medicine, told this news organization. Dr. Pettit was not involved in the SHEA study. “Even if CDC didn’t come out with that data, I can tell you right now more of my time is spent trying to figure out how to manage these multi-drug–resistant infections, and we are running out of options for these patients,”

“Dealing with uncertainty, exhaustion, [and] critical illness in often young, otherwise healthy patients meant doctors wanted to do something for their patients,” said Tamar Barlam, MD, an infectious diseases expert at the Boston Medical Center who led the development of the SHEA white paper, in an interview.

That something often was a prescription for antibiotics, even without a clear indication that they were actually needed. A British study revealed that in times of pandemic uncertainty, clinicians often reached for antibiotics “just in case” and referred to conservative prescribing as “bravery.”

Studies have shown, however, that bacterial co-infections in COVID-19 are rare. A 2020 meta-analysis of 24 studies concluded that only 3.5% of patients had a bacterial co-infection on presentation, and 14.3% had a secondary infection. Similar patterns had previously been observed in other viral outbreaks. Research on MERS-CoV, for example, documented only 1% of patients with a bacterial co-infection on admission. During the 2009 H1N1 influenza pandemic, that number was 12% of non–ICU hospitalized patients.

Yet, according to Dr. Pettit, even when such data became available, it didn’t necessarily change prescribing patterns. “Information was coming at us so quickly, I think the providers didn’t have a moment to see the data, to understand what it meant for their prescribing. Having external guidance earlier on would have been hugely helpful,” she told this news organization.

That’s where the newly published SHEA statement comes in: It outlines recommendations on when to prescribe antibiotics during a respiratory viral pandemic, what tests to order, and when to de-escalate or discontinue the treatment. These recommendations include, for instance, advice to not trust inflammatory markers as reliable indicators of bacterial or fungal infection and to not use procalcitonin routinely to aid in the decision to initiate antibiotics.

According to Dr. Barlam, one of the crucial lessons here is that if clinicians see patients with symptoms that are consistent with the current pandemic, they should trust their own impressions and avoid reaching for antimicrobials “just in case.”

Another important lesson is that antibiotic stewardship programs have a huge role to play during pandemics. They should not only monitor prescribing but also compile new information on bacterial co-infections as it gets released and make sure it reaches the clinicians in a clear form.

Evidence suggests that such programs and guidelines do work to limit unnecessary antibiotic use. In one medical center in Chicago, for example, before recommendations on when to initiate and discontinue antimicrobials were released, over 74% of COVID-19 patients received antibiotics. After guidelines were put in place, the use of such drugs fell to 42%.

Dr. Pettit believes, however, that it’s important not to leave each medical center to its own devices. “Hindsight is always twenty-twenty,” she said, “but I think it would be great that, if we start hearing about a pathogen that might lead to another pandemic, we should have a mechanism in place to call together an expert body to get guidance for how antimicrobial stewardship programs should get involved.”

One of the authors of the SHEA statement, Susan Seo, reports an investigator-initiated Merck grant on cost-effectiveness of letermovir in hematopoietic stem cell transplant patients. Another author, Graeme Forrest, reports a clinical study grant from Regeneron for inpatient monoclonals against SARS-CoV-2. All other authors report no conflicts of interest. The study was independently supported.

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

A statement by the Society for Healthcare Epidemiology of America, published online in Infection Control & Hospital Epidemiology, offers health care providers guidelines on how to prevent inappropriate antibiotic use in future pandemics and to avoid some of the negative scenarios that have been seen with COVID-19.

According to the U.S. Centers of Disease Control and Prevention, the COVID-19 pandemic brought an alarming increase in antimicrobial resistance in hospitals, with infections and deaths caused by resistant bacteria and fungi going up by 15%. For some pathogens, such as the Carbapenem-resistant Acinetobacter, that number is now as high as 78%.

The culprit might be the widespread antibiotic overprescription during the current pandemic. A 2022 meta-analysis revealed that in high-income countries, 58% of patients with COVID-19 were given antibiotics, whereas in lower- and middle-income countries, 89% of patients were put on such drugs. Some hospitals in Europe and the United States reported similarly elevated numbers, sometimes approaching 100%.

“We’ve lost control,” Natasha Pettit, PharmD, pharmacy director at University of Chicago Medicine, told this news organization. Dr. Pettit was not involved in the SHEA study. “Even if CDC didn’t come out with that data, I can tell you right now more of my time is spent trying to figure out how to manage these multi-drug–resistant infections, and we are running out of options for these patients,”

“Dealing with uncertainty, exhaustion, [and] critical illness in often young, otherwise healthy patients meant doctors wanted to do something for their patients,” said Tamar Barlam, MD, an infectious diseases expert at the Boston Medical Center who led the development of the SHEA white paper, in an interview.

That something often was a prescription for antibiotics, even without a clear indication that they were actually needed. A British study revealed that in times of pandemic uncertainty, clinicians often reached for antibiotics “just in case” and referred to conservative prescribing as “bravery.”

Studies have shown, however, that bacterial co-infections in COVID-19 are rare. A 2020 meta-analysis of 24 studies concluded that only 3.5% of patients had a bacterial co-infection on presentation, and 14.3% had a secondary infection. Similar patterns had previously been observed in other viral outbreaks. Research on MERS-CoV, for example, documented only 1% of patients with a bacterial co-infection on admission. During the 2009 H1N1 influenza pandemic, that number was 12% of non–ICU hospitalized patients.

Yet, according to Dr. Pettit, even when such data became available, it didn’t necessarily change prescribing patterns. “Information was coming at us so quickly, I think the providers didn’t have a moment to see the data, to understand what it meant for their prescribing. Having external guidance earlier on would have been hugely helpful,” she told this news organization.

That’s where the newly published SHEA statement comes in: It outlines recommendations on when to prescribe antibiotics during a respiratory viral pandemic, what tests to order, and when to de-escalate or discontinue the treatment. These recommendations include, for instance, advice to not trust inflammatory markers as reliable indicators of bacterial or fungal infection and to not use procalcitonin routinely to aid in the decision to initiate antibiotics.

According to Dr. Barlam, one of the crucial lessons here is that if clinicians see patients with symptoms that are consistent with the current pandemic, they should trust their own impressions and avoid reaching for antimicrobials “just in case.”

Another important lesson is that antibiotic stewardship programs have a huge role to play during pandemics. They should not only monitor prescribing but also compile new information on bacterial co-infections as it gets released and make sure it reaches the clinicians in a clear form.

Evidence suggests that such programs and guidelines do work to limit unnecessary antibiotic use. In one medical center in Chicago, for example, before recommendations on when to initiate and discontinue antimicrobials were released, over 74% of COVID-19 patients received antibiotics. After guidelines were put in place, the use of such drugs fell to 42%.

Dr. Pettit believes, however, that it’s important not to leave each medical center to its own devices. “Hindsight is always twenty-twenty,” she said, “but I think it would be great that, if we start hearing about a pathogen that might lead to another pandemic, we should have a mechanism in place to call together an expert body to get guidance for how antimicrobial stewardship programs should get involved.”

One of the authors of the SHEA statement, Susan Seo, reports an investigator-initiated Merck grant on cost-effectiveness of letermovir in hematopoietic stem cell transplant patients. Another author, Graeme Forrest, reports a clinical study grant from Regeneron for inpatient monoclonals against SARS-CoV-2. All other authors report no conflicts of interest. The study was independently supported.

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

In a first-of-its-kind clinical trial, researchers in Germany used a cancer-killing cell therapy to successfully treat lupus in a small number of patients.

Their study, published online in Nature Medicine, included five patients with systemic lupus erythematosus (SLE). All of the patients were treated with chimeric antigen receptor (CAR) T-cell therapy, a treatment regularly used to kill cancer cells. Researchers harvested the patients’ immune cells and engineered them to destroy dysfunctional cells when infused back into the body.

The five patients – all of whom had an aggressive form of the autoimmune disease – underwent a single infusion of the experimental treatment. All five patients were able to stop their standard treatments for as long as 17 months following the therapy, the study found. The patients also stopped experiencing severe symptoms such as lung inflammation, fibrosis of the heart valves, arthritis, and fatigue. The patients have not relapsed.

“Our data reveal unexpected insights for a role of CAR T cells in nonmalignant diseases that could provide new opportunities for the treatment of autoimmune disease,” the study authors wrote.

Lupus is a chronic inflammatory disease in which the immune system attacks the body’s own cells. Both antibody-producing B and T cells in individuals with lupus become overactive, which can lead to a flare of symptoms that range from mild pain and fatigue to life-threatening inflammation and tissue damage. They are often treated with medications that deplete their B cells or change the way they function to help wipe out infected cells.

The approach used by the study researchers is similar to monoclonal antibody therapies that destroy dysfunctional B cells, such as rituximab (Rituxan and biosimilars) and obinutuzumab (Gazyva), according to Michael Belmont, MD, codirector of New York University’s Lupus Center and medical director of Bellevue Hospital Lupus Clinic, also in New York.

“Previously, this has been accomplished with monoclonal antibodies that target surface markers on B cells and results in their removal,” said Dr. Belmont, who was not connected to the study. “The report describes a novel approach that harnesses a patient’s own T cells, another type of white blood cell, to eliminate that patient’s own B cells.”

Preclinical studies involving mice previously showed that CAR T-cell therapy could help to reset the immune system. However, this latest study also found that patients did not need to continue any of their previous therapies, even after they regained their B cells about 4 months after the therapy.

“A deep depletion of CD19+ B cells and plasmablasts in the tissues could trigger an immune reset in SLE that could allow the cessation of immunosuppressive treatment,” said Mehrnaz Hojjati, MD, a rheumatologist and director of rheumatology operations at Loma Linda (Calif.) University Health. Dr. Hojjati was not affiliated with the study.

While the single-treatment therapy is promising, transfused T cells do carry risks. Some of the patients in the study experienced fever and muscle pain following the procedure, the authors noted. Dr. Belmont said more serious risks for this kind of therapy may include organ injury.

“This treatment can [also] increase incidence, for example, of pneumonia or shingles,” he said.

The study authors initially documented their work in a correspondence published in August 2021 in the New England Journal of Medicine. At that time, they reported that a 20-year-old woman with a severe refractory SLE went into remission following the treatment.

The five patients in the current study – four women and one man – were aged 18-24 years. All of the patients had previously been treated with several immunosuppressive medications, the study authors noted.

“This is an exciting approach, but many more patients need to be treated to really understand the efficacy and safety,” Dr. Belmont said.

Experts, including Dr. Belmont, also said the procedure is also costly and requires access to labs that can engineer a patient’s own T cells after they’ve been donated.

“The entire process must maintain sterility to avoid contamination, which would be harmful when reinfused into the patient,” he said.

According to Arthur Kavanaugh, MD, professor of medicine at UC San Diego Health, this form of therapy may be an option for severe refractory patients who have not responded well to other more established therapies.

“[It’s] exciting data, but very intense and so not likely to be something for an average patient in the near future,” said Dr. Kavanaugh, who was not affiliated with the study.

The study authors say they intend to create a larger trial to further explore which type of patient may benefit the most from this treatment, and for how long.

The study was supported by the German Research Foundation, the German Federal Ministry of Education and Research, the European Union, and the Innovative Medicines Initiative–funded project, Rheuma Tolerance for Cure. The study received no commercial funding, and the authors said they had no competing interests related to the study. None of the experts interviewed reported relevant financial relationships.

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

In a first-of-its-kind clinical trial, researchers in Germany used a cancer-killing cell therapy to successfully treat lupus in a small number of patients.

Their study, published online in Nature Medicine, included five patients with systemic lupus erythematosus (SLE). All of the patients were treated with chimeric antigen receptor (CAR) T-cell therapy, a treatment regularly used to kill cancer cells. Researchers harvested the patients’ immune cells and engineered them to destroy dysfunctional cells when infused back into the body.

The five patients – all of whom had an aggressive form of the autoimmune disease – underwent a single infusion of the experimental treatment. All five patients were able to stop their standard treatments for as long as 17 months following the therapy, the study found. The patients also stopped experiencing severe symptoms such as lung inflammation, fibrosis of the heart valves, arthritis, and fatigue. The patients have not relapsed.

“Our data reveal unexpected insights for a role of CAR T cells in nonmalignant diseases that could provide new opportunities for the treatment of autoimmune disease,” the study authors wrote.

Lupus is a chronic inflammatory disease in which the immune system attacks the body’s own cells. Both antibody-producing B and T cells in individuals with lupus become overactive, which can lead to a flare of symptoms that range from mild pain and fatigue to life-threatening inflammation and tissue damage. They are often treated with medications that deplete their B cells or change the way they function to help wipe out infected cells.

The approach used by the study researchers is similar to monoclonal antibody therapies that destroy dysfunctional B cells, such as rituximab (Rituxan and biosimilars) and obinutuzumab (Gazyva), according to Michael Belmont, MD, codirector of New York University’s Lupus Center and medical director of Bellevue Hospital Lupus Clinic, also in New York.

“Previously, this has been accomplished with monoclonal antibodies that target surface markers on B cells and results in their removal,” said Dr. Belmont, who was not connected to the study. “The report describes a novel approach that harnesses a patient’s own T cells, another type of white blood cell, to eliminate that patient’s own B cells.”

Preclinical studies involving mice previously showed that CAR T-cell therapy could help to reset the immune system. However, this latest study also found that patients did not need to continue any of their previous therapies, even after they regained their B cells about 4 months after the therapy.

“A deep depletion of CD19+ B cells and plasmablasts in the tissues could trigger an immune reset in SLE that could allow the cessation of immunosuppressive treatment,” said Mehrnaz Hojjati, MD, a rheumatologist and director of rheumatology operations at Loma Linda (Calif.) University Health. Dr. Hojjati was not affiliated with the study.

While the single-treatment therapy is promising, transfused T cells do carry risks. Some of the patients in the study experienced fever and muscle pain following the procedure, the authors noted. Dr. Belmont said more serious risks for this kind of therapy may include organ injury.

“This treatment can [also] increase incidence, for example, of pneumonia or shingles,” he said.

The study authors initially documented their work in a correspondence published in August 2021 in the New England Journal of Medicine. At that time, they reported that a 20-year-old woman with a severe refractory SLE went into remission following the treatment.

The five patients in the current study – four women and one man – were aged 18-24 years. All of the patients had previously been treated with several immunosuppressive medications, the study authors noted.

“This is an exciting approach, but many more patients need to be treated to really understand the efficacy and safety,” Dr. Belmont said.

Experts, including Dr. Belmont, also said the procedure is also costly and requires access to labs that can engineer a patient’s own T cells after they’ve been donated.

“The entire process must maintain sterility to avoid contamination, which would be harmful when reinfused into the patient,” he said.

According to Arthur Kavanaugh, MD, professor of medicine at UC San Diego Health, this form of therapy may be an option for severe refractory patients who have not responded well to other more established therapies.

“[It’s] exciting data, but very intense and so not likely to be something for an average patient in the near future,” said Dr. Kavanaugh, who was not affiliated with the study.

The study authors say they intend to create a larger trial to further explore which type of patient may benefit the most from this treatment, and for how long.

The study was supported by the German Research Foundation, the German Federal Ministry of Education and Research, the European Union, and the Innovative Medicines Initiative–funded project, Rheuma Tolerance for Cure. The study received no commercial funding, and the authors said they had no competing interests related to the study. None of the experts interviewed reported relevant financial relationships.

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

In a first-of-its-kind clinical trial, researchers in Germany used a cancer-killing cell therapy to successfully treat lupus in a small number of patients.

Their study, published online in Nature Medicine, included five patients with systemic lupus erythematosus (SLE). All of the patients were treated with chimeric antigen receptor (CAR) T-cell therapy, a treatment regularly used to kill cancer cells. Researchers harvested the patients’ immune cells and engineered them to destroy dysfunctional cells when infused back into the body.

The five patients – all of whom had an aggressive form of the autoimmune disease – underwent a single infusion of the experimental treatment. All five patients were able to stop their standard treatments for as long as 17 months following the therapy, the study found. The patients also stopped experiencing severe symptoms such as lung inflammation, fibrosis of the heart valves, arthritis, and fatigue. The patients have not relapsed.

“Our data reveal unexpected insights for a role of CAR T cells in nonmalignant diseases that could provide new opportunities for the treatment of autoimmune disease,” the study authors wrote.

Lupus is a chronic inflammatory disease in which the immune system attacks the body’s own cells. Both antibody-producing B and T cells in individuals with lupus become overactive, which can lead to a flare of symptoms that range from mild pain and fatigue to life-threatening inflammation and tissue damage. They are often treated with medications that deplete their B cells or change the way they function to help wipe out infected cells.

The approach used by the study researchers is similar to monoclonal antibody therapies that destroy dysfunctional B cells, such as rituximab (Rituxan and biosimilars) and obinutuzumab (Gazyva), according to Michael Belmont, MD, codirector of New York University’s Lupus Center and medical director of Bellevue Hospital Lupus Clinic, also in New York.

“Previously, this has been accomplished with monoclonal antibodies that target surface markers on B cells and results in their removal,” said Dr. Belmont, who was not connected to the study. “The report describes a novel approach that harnesses a patient’s own T cells, another type of white blood cell, to eliminate that patient’s own B cells.”

Preclinical studies involving mice previously showed that CAR T-cell therapy could help to reset the immune system. However, this latest study also found that patients did not need to continue any of their previous therapies, even after they regained their B cells about 4 months after the therapy.

“A deep depletion of CD19+ B cells and plasmablasts in the tissues could trigger an immune reset in SLE that could allow the cessation of immunosuppressive treatment,” said Mehrnaz Hojjati, MD, a rheumatologist and director of rheumatology operations at Loma Linda (Calif.) University Health. Dr. Hojjati was not affiliated with the study.

While the single-treatment therapy is promising, transfused T cells do carry risks. Some of the patients in the study experienced fever and muscle pain following the procedure, the authors noted. Dr. Belmont said more serious risks for this kind of therapy may include organ injury.

“This treatment can [also] increase incidence, for example, of pneumonia or shingles,” he said.

The study authors initially documented their work in a correspondence published in August 2021 in the New England Journal of Medicine. At that time, they reported that a 20-year-old woman with a severe refractory SLE went into remission following the treatment.

The five patients in the current study – four women and one man – were aged 18-24 years. All of the patients had previously been treated with several immunosuppressive medications, the study authors noted.

“This is an exciting approach, but many more patients need to be treated to really understand the efficacy and safety,” Dr. Belmont said.

Experts, including Dr. Belmont, also said the procedure is also costly and requires access to labs that can engineer a patient’s own T cells after they’ve been donated.

“The entire process must maintain sterility to avoid contamination, which would be harmful when reinfused into the patient,” he said.

According to Arthur Kavanaugh, MD, professor of medicine at UC San Diego Health, this form of therapy may be an option for severe refractory patients who have not responded well to other more established therapies.

“[It’s] exciting data, but very intense and so not likely to be something for an average patient in the near future,” said Dr. Kavanaugh, who was not affiliated with the study.

The study authors say they intend to create a larger trial to further explore which type of patient may benefit the most from this treatment, and for how long.

The study was supported by the German Research Foundation, the German Federal Ministry of Education and Research, the European Union, and the Innovative Medicines Initiative–funded project, Rheuma Tolerance for Cure. The study received no commercial funding, and the authors said they had no competing interests related to the study. None of the experts interviewed reported relevant financial relationships.

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

Metabolism a player in circadian rhythm section

Are you an early bird, or do you wake up and stare at your phone, wondering why you were up watching “The Crown” until 3 a.m.? Recent research suggests that people who wake up earlier tend to be more active during the day and burn more fat than those who sleep in. Fat builds up in the night owls, putting them at higher risk of type 2 diabetes and heart disease.

The study gives physicians something to think about when assessing a patient’s risk factors. “This could help medical professionals consider another behavioral factor contributing to disease risk,” Steven Malin, PhD, lead author of the study and expert in metabolism at Rutgers University in New Brunswick, N.J., said in The Guardian.

Geber86/E+

For the research, 51 participants were divided into night owls and early birds, depending on their answers to a questionnaire. They were examined, monitored for a week, and assessed while doing various activities. Those who woke up early tended to be more sensitive to insulin and burned off fat faster than those who woke up late, the researchers explained.

“Night owls are reported to have a higher risk of obesity, type 2 diabetes, and cardiovascular disease when compared with early birds,” Dr. Malin said. “A potential explanation is they become misaligned with their circadian rhythm for various reasons, but most notably among adults would be work.”

We all know that we may not be at our best when we throw off our internal clocks by going to sleep late and waking up early. Think about that next time you start another episode on Netflix at 2:57 a.m.
 

Mosquitoes, chemical cocktails, and glass sock beads

We all know that mosquitoes are annoying little disease vectors with a taste for human blood. One of the less-known things about mosquitoes is what attracts them to humans in the first place. It’s so less known that, until now, it was unknown. Oh sure, we knew that odor was involved, and that lactic acid was part of the odor equation, but what are the specific chemicals? Well, there’s carbon dioxide … and ammonia. Those were already known.

Ring Cardé, PhD, an entomologist at the University of California, Riverside, wasn’t convinced. “I suspected there was something undiscovered about the chemistry of odors luring the yellow fever mosquito. I wanted to nail down the exact blend,” he said in a statement from the university.

Dr. Cardé and his associates eventually figured out that the exact chemical cocktail attracting female Aedes aegypti mosquitoes was a combination of carbon dioxide plus two chemicals, 2-ketoglutaric acid and lactic acid. The odor from these chemicals enables mosquitoes to locate and land on their victim and “also encourages probing, the use of piercing mouthparts to find blood,” the university said.

This amazing destination of science is important, but we have to acknowledge the journey as well. To do that we turn to one of Dr. Cardé’s associates, Jan Bello, PhD, formerly of Cal-Riverside and now with insect pest control company Provivi. Turns out that 2-ketoglutaric acid is tricky stuff because the methods typically used to identify chemicals don’t work on it.

Dr. Bello employed a somewhat unorthodox chemical extraction method: He filled his socks with glass beads and walked around with the beads in his socks.

Jan Bello/UCR

“Wearing the beads felt almost like a massage, like squeezing stress balls full of sand, but with your feet,” Dr. Bello said. “The most frustrating part of doing it for a long time is that they would get stuck in between your toes, so it would be uncomfortable after a while.”

We hate when science gets stuck between our toes, but we love it when scientists write their own punchlines.
 

The MS drugs are better down where it’s wetter, take it from me

The myth of the mermaid is one with hundreds, if not thousands, of years of history. The ancient Greeks had the mythological siren, while the Babylonians depicted kulullû (which were mermen – never let the Babylonians be known as noninclusive) in artwork as far back as 1600 BC. Cultures as far flung as Japan, southern Africa, and New Zealand have folkloric figures similar to the mermaid. It is most decidedly not a creation of western Europe, Hans Christian Andersen, or Disney.

AG Kostenis-Gomeza / University of Bonn

With that mild rant out of the way, let’s move to Germany and a group of researchers from the University of Bonn, who have not created a mermaid. They did, however, add human genes to a zebrafish for research purposes, which feels uncomfortably close. Nothing better than unholy animal-human hybrids, right?

Stick with us here, because the researchers did have a good reason for their gene splicing. Zebrafish and humans both have the GPR17 receptor, which is highly active in nerve tissue. When GPR17 is overactivated, diseases such as multiple sclerosis can develop. Because the zebrafish has this receptor, which performs the same function in its body as in ours, it’s a prime candidate for replacement. Also, zebrafish larvae are transparent, which makes it very easy to observe a drug working.

That said, fish and humans are very far apart, genetically speaking. Big shock right there. But by replacing their GPR17 receptor with ours, the scientists have created a fish that we could test drug candidates on and be assured that they would also work on humans. Actually testing drugs for MS on these humanized zebrafish was beyond the scope of the study, but the researchers said that the new genes function normally in the fish larvae, making them a promising new avenue for MS drug development.

Can we all promise not to tell Disney that human DNA can be spliced into a fish without consequence? Otherwise, we’re just going to have to sit through another “Little Mermaid” adaptation in 30 years, this one in super live-action featuring actual, real-life mermaids. And we’re not ready for that level of man-made horror just yet.
 

Beware of the fly vomit

Picture this: You’re outside at a picnic or barbecue, loading a plate with food. In a brief moment of conversation a fly lands right on top of your sandwich. You shoo it away and think nothing more of it, eating the sandwich anyway. We’ve all been there.

A recent study is making us think again.

John Stoffolano, an entomology professor at the University of Massachusetts, Amherst, claims that too much attention has been focused on pathogen transmission by the biting, blood-feeding flies when really we should be taking note of the nonbiting, or synanthropic, flies we live with, which may have a greater impact on the transmission of pathogens right in our own homes.

arian.suresh/PxHere

Metabolism a player in circadian rhythm section

Are you an early bird, or do you wake up and stare at your phone, wondering why you were up watching “The Crown” until 3 a.m.? Recent research suggests that people who wake up earlier tend to be more active during the day and burn more fat than those who sleep in. Fat builds up in the night owls, putting them at higher risk of type 2 diabetes and heart disease.

The study gives physicians something to think about when assessing a patient’s risk factors. “This could help medical professionals consider another behavioral factor contributing to disease risk,” Steven Malin, PhD, lead author of the study and expert in metabolism at Rutgers University in New Brunswick, N.J., said in The Guardian.

Geber86/E+

For the research, 51 participants were divided into night owls and early birds, depending on their answers to a questionnaire. They were examined, monitored for a week, and assessed while doing various activities. Those who woke up early tended to be more sensitive to insulin and burned off fat faster than those who woke up late, the researchers explained.

“Night owls are reported to have a higher risk of obesity, type 2 diabetes, and cardiovascular disease when compared with early birds,” Dr. Malin said. “A potential explanation is they become misaligned with their circadian rhythm for various reasons, but most notably among adults would be work.”

We all know that we may not be at our best when we throw off our internal clocks by going to sleep late and waking up early. Think about that next time you start another episode on Netflix at 2:57 a.m.
 

Mosquitoes, chemical cocktails, and glass sock beads

We all know that mosquitoes are annoying little disease vectors with a taste for human blood. One of the less-known things about mosquitoes is what attracts them to humans in the first place. It’s so less known that, until now, it was unknown. Oh sure, we knew that odor was involved, and that lactic acid was part of the odor equation, but what are the specific chemicals? Well, there’s carbon dioxide … and ammonia. Those were already known.

Ring Cardé, PhD, an entomologist at the University of California, Riverside, wasn’t convinced. “I suspected there was something undiscovered about the chemistry of odors luring the yellow fever mosquito. I wanted to nail down the exact blend,” he said in a statement from the university.

Dr. Cardé and his associates eventually figured out that the exact chemical cocktail attracting female Aedes aegypti mosquitoes was a combination of carbon dioxide plus two chemicals, 2-ketoglutaric acid and lactic acid. The odor from these chemicals enables mosquitoes to locate and land on their victim and “also encourages probing, the use of piercing mouthparts to find blood,” the university said.

This amazing destination of science is important, but we have to acknowledge the journey as well. To do that we turn to one of Dr. Cardé’s associates, Jan Bello, PhD, formerly of Cal-Riverside and now with insect pest control company Provivi. Turns out that 2-ketoglutaric acid is tricky stuff because the methods typically used to identify chemicals don’t work on it.

Dr. Bello employed a somewhat unorthodox chemical extraction method: He filled his socks with glass beads and walked around with the beads in his socks.

Jan Bello/UCR

“Wearing the beads felt almost like a massage, like squeezing stress balls full of sand, but with your feet,” Dr. Bello said. “The most frustrating part of doing it for a long time is that they would get stuck in between your toes, so it would be uncomfortable after a while.”

We hate when science gets stuck between our toes, but we love it when scientists write their own punchlines.
 

The MS drugs are better down where it’s wetter, take it from me

The myth of the mermaid is one with hundreds, if not thousands, of years of history. The ancient Greeks had the mythological siren, while the Babylonians depicted kulullû (which were mermen – never let the Babylonians be known as noninclusive) in artwork as far back as 1600 BC. Cultures as far flung as Japan, southern Africa, and New Zealand have folkloric figures similar to the mermaid. It is most decidedly not a creation of western Europe, Hans Christian Andersen, or Disney.

AG Kostenis-Gomeza / University of Bonn

With that mild rant out of the way, let’s move to Germany and a group of researchers from the University of Bonn, who have not created a mermaid. They did, however, add human genes to a zebrafish for research purposes, which feels uncomfortably close. Nothing better than unholy animal-human hybrids, right?

Stick with us here, because the researchers did have a good reason for their gene splicing. Zebrafish and humans both have the GPR17 receptor, which is highly active in nerve tissue. When GPR17 is overactivated, diseases such as multiple sclerosis can develop. Because the zebrafish has this receptor, which performs the same function in its body as in ours, it’s a prime candidate for replacement. Also, zebrafish larvae are transparent, which makes it very easy to observe a drug working.

That said, fish and humans are very far apart, genetically speaking. Big shock right there. But by replacing their GPR17 receptor with ours, the scientists have created a fish that we could test drug candidates on and be assured that they would also work on humans. Actually testing drugs for MS on these humanized zebrafish was beyond the scope of the study, but the researchers said that the new genes function normally in the fish larvae, making them a promising new avenue for MS drug development.

Can we all promise not to tell Disney that human DNA can be spliced into a fish without consequence? Otherwise, we’re just going to have to sit through another “Little Mermaid” adaptation in 30 years, this one in super live-action featuring actual, real-life mermaids. And we’re not ready for that level of man-made horror just yet.
 

Beware of the fly vomit

Picture this: You’re outside at a picnic or barbecue, loading a plate with food. In a brief moment of conversation a fly lands right on top of your sandwich. You shoo it away and think nothing more of it, eating the sandwich anyway. We’ve all been there.

A recent study is making us think again.

John Stoffolano, an entomology professor at the University of Massachusetts, Amherst, claims that too much attention has been focused on pathogen transmission by the biting, blood-feeding flies when really we should be taking note of the nonbiting, or synanthropic, flies we live with, which may have a greater impact on the transmission of pathogens right in our own homes.

arian.suresh/PxHere

Metabolism a player in circadian rhythm section

Are you an early bird, or do you wake up and stare at your phone, wondering why you were up watching “The Crown” until 3 a.m.? Recent research suggests that people who wake up earlier tend to be more active during the day and burn more fat than those who sleep in. Fat builds up in the night owls, putting them at higher risk of type 2 diabetes and heart disease.

The study gives physicians something to think about when assessing a patient’s risk factors. “This could help medical professionals consider another behavioral factor contributing to disease risk,” Steven Malin, PhD, lead author of the study and expert in metabolism at Rutgers University in New Brunswick, N.J., said in The Guardian.

Geber86/E+

For the research, 51 participants were divided into night owls and early birds, depending on their answers to a questionnaire. They were examined, monitored for a week, and assessed while doing various activities. Those who woke up early tended to be more sensitive to insulin and burned off fat faster than those who woke up late, the researchers explained.

“Night owls are reported to have a higher risk of obesity, type 2 diabetes, and cardiovascular disease when compared with early birds,” Dr. Malin said. “A potential explanation is they become misaligned with their circadian rhythm for various reasons, but most notably among adults would be work.”

We all know that we may not be at our best when we throw off our internal clocks by going to sleep late and waking up early. Think about that next time you start another episode on Netflix at 2:57 a.m.
 

Mosquitoes, chemical cocktails, and glass sock beads

We all know that mosquitoes are annoying little disease vectors with a taste for human blood. One of the less-known things about mosquitoes is what attracts them to humans in the first place. It’s so less known that, until now, it was unknown. Oh sure, we knew that odor was involved, and that lactic acid was part of the odor equation, but what are the specific chemicals? Well, there’s carbon dioxide … and ammonia. Those were already known.

Ring Cardé, PhD, an entomologist at the University of California, Riverside, wasn’t convinced. “I suspected there was something undiscovered about the chemistry of odors luring the yellow fever mosquito. I wanted to nail down the exact blend,” he said in a statement from the university.

Dr. Cardé and his associates eventually figured out that the exact chemical cocktail attracting female Aedes aegypti mosquitoes was a combination of carbon dioxide plus two chemicals, 2-ketoglutaric acid and lactic acid. The odor from these chemicals enables mosquitoes to locate and land on their victim and “also encourages probing, the use of piercing mouthparts to find blood,” the university said.

This amazing destination of science is important, but we have to acknowledge the journey as well. To do that we turn to one of Dr. Cardé’s associates, Jan Bello, PhD, formerly of Cal-Riverside and now with insect pest control company Provivi. Turns out that 2-ketoglutaric acid is tricky stuff because the methods typically used to identify chemicals don’t work on it.

Dr. Bello employed a somewhat unorthodox chemical extraction method: He filled his socks with glass beads and walked around with the beads in his socks.

Jan Bello/UCR

“Wearing the beads felt almost like a massage, like squeezing stress balls full of sand, but with your feet,” Dr. Bello said. “The most frustrating part of doing it for a long time is that they would get stuck in between your toes, so it would be uncomfortable after a while.”

We hate when science gets stuck between our toes, but we love it when scientists write their own punchlines.
 

The MS drugs are better down where it’s wetter, take it from me

The myth of the mermaid is one with hundreds, if not thousands, of years of history. The ancient Greeks had the mythological siren, while the Babylonians depicted kulullû (which were mermen – never let the Babylonians be known as noninclusive) in artwork as far back as 1600 BC. Cultures as far flung as Japan, southern Africa, and New Zealand have folkloric figures similar to the mermaid. It is most decidedly not a creation of western Europe, Hans Christian Andersen, or Disney.

AG Kostenis-Gomeza / University of Bonn

With that mild rant out of the way, let’s move to Germany and a group of researchers from the University of Bonn, who have not created a mermaid. They did, however, add human genes to a zebrafish for research purposes, which feels uncomfortably close. Nothing better than unholy animal-human hybrids, right?

Stick with us here, because the researchers did have a good reason for their gene splicing. Zebrafish and humans both have the GPR17 receptor, which is highly active in nerve tissue. When GPR17 is overactivated, diseases such as multiple sclerosis can develop. Because the zebrafish has this receptor, which performs the same function in its body as in ours, it’s a prime candidate for replacement. Also, zebrafish larvae are transparent, which makes it very easy to observe a drug working.

That said, fish and humans are very far apart, genetically speaking. Big shock right there. But by replacing their GPR17 receptor with ours, the scientists have created a fish that we could test drug candidates on and be assured that they would also work on humans. Actually testing drugs for MS on these humanized zebrafish was beyond the scope of the study, but the researchers said that the new genes function normally in the fish larvae, making them a promising new avenue for MS drug development.

Can we all promise not to tell Disney that human DNA can be spliced into a fish without consequence? Otherwise, we’re just going to have to sit through another “Little Mermaid” adaptation in 30 years, this one in super live-action featuring actual, real-life mermaids. And we’re not ready for that level of man-made horror just yet.
 

Beware of the fly vomit

Picture this: You’re outside at a picnic or barbecue, loading a plate with food. In a brief moment of conversation a fly lands right on top of your sandwich. You shoo it away and think nothing more of it, eating the sandwich anyway. We’ve all been there.

A recent study is making us think again.

John Stoffolano, an entomology professor at the University of Massachusetts, Amherst, claims that too much attention has been focused on pathogen transmission by the biting, blood-feeding flies when really we should be taking note of the nonbiting, or synanthropic, flies we live with, which may have a greater impact on the transmission of pathogens right in our own homes.

arian.suresh/PxHere

Patients with iron overload – serum ferritin greater than 1,000 mcg/L or a diagnosis of hemochromatosis or thalassemia – were 60% more likely to have an osteoporotic fracture during an up to 10-year follow-up than matched control patients, in a large study.

Compared with control patients, those with iron overload had a roughly twofold increased risk of a vertebral fracture, as well as an increased risk of a hip or humerus fracture, but not a forearm fracture.

The increased risk of fracture in men with iron overload (compared with other matched men) was greater than the increased risk of fracture in women with iron overload (compared with other matched women).

Andrea Burden, PhD, presented the findings during a late-breaking clinical science session at the annual meeting of the American Society of Bone and Mineral Research.
 

‘We should worry about the bones as well as the liver’

Based on these results, clinicians should probably do earlier bone mineral density (BMD) determinations to screen for osteoporosis and perhaps consider prophylaxis with vitamin D and calcium, said Dr. Burden, assistant professor, Institute of Pharmaceutical Sciences, ETH Zürich.

“However, I say that with a bunch of caution,” she added, “because we actually don’t have much evidence of the impact of these treatment differences on fracture risk.”

“This is the first large population study on this topic,” although there have been a few case reports, Dr. Burden explained in an interview.

However, “the high iron overload of greater than 1,000 mcg/L is not common, and hereditary hemochromatosis or thalassemia also are very rare,” she noted.

“The study shows that, once patients have an iron overload of more than 1,000 mcg/L, we need to be doing regular checks for their BMD and figuring how to best minimize their fracture risk,” she said.

“A twofold risk for a vertebral fracture” in patients with iron overload “is really high,” she noted. It is known that men with iron overload have loss of testosterone, but it may be less well known that they have an increased fracture risk.

“We worry about the liver,” she said, “not so much about the bones, and this shows us that we really should.”

Session comoderator Michael J. Econs, MD, who was not involved with the research, agreed. “Iron overload does occur, and it is a clinically important problem and can lead to hemochromatosis, which can lead to a whole host of diseases, but the most common is liver disease,” he told this news organization.

“So, it is a clinically important problem, not only in people who are genetically predisposed but in people who get frequent transfusion,” said Dr. Econs, distinguished professor of medicine and medical and molecular genetics at Indiana University, Indianapolis.

Now this new study has found an increase in fractures in such people, he noted.
 

Large case-control study used U.K. database

Using data from the IQVIA Medical Research Database, researchers identified 21,166 iron overload patients aged 18 years and older who saw a general practitioner in the United Kingdom between 2010 and 2020 and had a serum ferritin level above 1,000 mcg/L or a diagnostic code for hemochromatosis or nonanemic thalassemia.

They matched each iron overload patient with up to 10 control patients based on age, sex, year, and general practitioner, for a total of 198,037 control patients.

Patients were a mean age of 59 years and 59% were men.

During follow-up there were 777 fractures in the iron-overload patients (9.61 fractures per 1,000 patient-years) and 4,344 fractures in the control group (4.68 fractures per 1,000 patient-years).

In adjusted hazard ratio models, researchers adjusted for age, sex, body mass index, alcohol, smoking, history of fractures earlier than 365 days prior to study entry, hypogonadism, osteoporosis, medications, and comorbidities.

Overall, patients in the iron overload group had a 60% higher risk of an osteoporotic fracture (aHR, 1.60).

Among women, the incidence of osteoporotic fracture was 12.63 per 1,000 patient-years in the iron overload group and 7.09 per 1,000 patient-years in the control group.

Women with iron overload had a 48% higher risk of osteoporotic fracture, compared with other women (aHR, 1.48).

Among men, the incidence of osteoporotic fracture was 6.71 per 1,000 patient-years in the iron overload group and 3.01 per 1,000 patient-years in the control group.

Men with iron overload therefore had an 82% higher risk of osteoporotic fracture, compared with other men (aHR, 1.82).

Compared with patients without iron overload, patients with iron overload had an increased risk of a vertebral (aHR, 2.18), hip (aHR, 1.60), and humerus (aHR, 1.82) fracture but not a forearm fracture.

The researchers acknowledge that study limitations include they did not look at phlebotomy or changes in ferritin levels, and they excluded patients with hereditary hemochromatosis diagnosed before age 18.

The work was funded by the German Research Foundation. One of the researchers has reported receiving an independent grant from Pharmacosmos. The other researchers as well as Dr. Econs have reported no relevant financial relationships.