Rheumatology News

At the center of the emerging science on the unintended consequences of daily long-term use of marijuana lies a paradox.

For years, medical marijuana has been used to ease nausea from cancer chemotherapy and GI conditions. Now, with greater legalization comes growing awareness that chronic use of marijuana – also known as cannabis – can trigger a condition where, ironically, a person has hard-to-control vomiting and nausea.

Doug Menuez/thinkstock

Some people with the disorder, known as “cannabinoid hyperemesis syndrome,” also report crippling belly pain.

Linda can relate. The 33-year-old Oregon resident, who asked to remain anonymous to protect her privacy, refers to a medieval spiky metal ball on a chain when describing the pain.

“Picture a mace inside your stomach, pushing up inside your chest and, at the same time, exploding out,” she said.

To seek relief, she gets down on her knees, adopts a child’s yoga pose, and runs hot water in the bathroom for hours on end, a trick many with the disorder says has provided relief. She also occasionally goes outside and tries walking it off.

“I would just wander around my neighborhood, a lot of times at like 4 or 5 in the morning,” she said. “The fresh air helps a little bit. I just keep walking down the street, take about 10 steps, stop, vomit – walk a little bit more, stop, vomit.”

Her first experience with the disorder began in the middle of one night in 2017 while she was at a conference in Las Vegas.

“We went out to eat the night before, and I woke up about 4 in the morning with just the most intense pain I’ve ever had,” she said. “I found myself in a really hot shower in between throwing up everything and trying to say get some water down. I was sharing an Airbnb with my colleagues, so it was less than ideal.”

Many people with cannabinoid hyperemesis syndrome find relief from hot baths or showers. Researchers believe that hot water helps because temperature sensors in the skin send signals to the brain that can help ease the symptoms, at least for a while.

The problem is that people with this syndrome “can’t live in the water,” said emergency doctor and medical cannabis expert Leigh Vinocur, MD.

Fast-forward 6 months to another event in Boulder, Colo. Again, Linda woke up and could not stop vomiting.

“I was not feeling any better. Showering wasn’t helping. I ended up in the hospital,” she said.

She received opioids for her pain. But neither she nor the ED staff were quite sure what was happening. Her discharge paperwork read “cannabis allergy.”

Cannabinoid hyperemesis syndrome “shatters that image of cannabis only being a good thing. It’s a bold statement, but, you know, once you start to think about it, it’s like a little too much of anything isn’t good,” Linda said.

Experts suggest greater awareness is needed to identify this syndrome earlier, by both cannabinoid users and doctors. The bouts of vomiting, in particular, can get so severe that people can end up hospitalized with dehydration, electrolyte disorders, and weight loss.

The severe electrolyte imbalances “can really be life-threatening,” said David Johnson, MD, a professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk.

“By the time they come into emergency care, they’re in bad shape,” Dr. Vinocur agreed. “Many try to ignore it, but they continue to vomit.”
 

Genetic risk factors?

One mystery is why some regular marijuana users get this syndrome while others do not.

“I can say that not everybody gets this, thank goodness,” said Ethan Russo, MD. “But there has to be a reason that certain people are susceptible and others are not.”

Interestingly, a new study from Dr. Russo and colleagues suggests that genes play a role. They identified five genetic changes that could make a chronic marijuana user more likely to have cannabinoid hyperemesis syndrome in a study published July 5, 2021, in the journal Cannabis and Cannabinoid Research.

They compared 28 people with the disorder with 12 other high-frequency marijuana users without these symptoms.

The results are not final but could help guide future research, Dr. Russo said.

“What we’ve discovered – and it was far more than we expected – is that there’s a lot more to this than a hypersensitivity to cannabis,” said Dr. Russo, a neurologist and founder/CEO of CReDO Science, a firm that promotes cannabis research and develops commercial products.

Also, he said, those affected by cannabinoid hyperemesis syndrome could be at higher risk for other conditions, such as addiction to alcohol or other substances, dementia, diabetes, and heart disease.

“Most people with [cannabinoid hyperemesis syndrome] are going to be younger,” he said. “What we’ve demonstrated is there is a risk for more serious problems for decades to come. So someone who has these symptoms really deserves a look at this genetic screening.”
 

Battling disbelief

Getting back to the paradox, many users don’t believe marijuana can trigger serious vomiting and nausea because of its reputation for doing the opposite.

“Folks that have this are just uniquely resistant to the concept that cannabis is actually the problem and not the solution,” Dr. Russo said.

“It’s kind of counterintuitive because people think: ‘Oh, cannabis helps with nausea,’ so they use more of it,” said Dr. Vinocur, who is also a spokesperson for the American College of Emergency Physicians and runs a medical cannabis practice.

Most kinds of marijuana act in this way – doing opposite things at different doses. Once a certain threshold is passed, people with cannabinoid hyperemesis syndrome are “just uniquely susceptible and really can’t tolerate any significant amount of THC,” Dr. Russo said, referring to tetrahydrocannabinol, the substance that gets marijuana users high.

Once diagnosed, quitting is the most effective strategy. But it can be tough to persuade someone to stop using marijuana.

“You do have to try and convince them ... to try abstinence and to watch and see what happens,” Dr. Vinocur said.

People should “realize the root cause of this is its cannabinoid ingestion, and the treatment is really best directed at absolute avoidance,” Dr. Johnson said.

Unfortunately, evidence also shows that once a person stops using marijuana and gets relief, going back to marijuana or other forms of cannabinoids can cause the syndrome to start all over again.

“We’ve had people that quit for a month, a year, 2 years and upon resumption, almost invariably, they’re back into bouts of the hyperemesis along with all the other [symptoms],” Dr. Russo said.

Marijuana and cannabinoids can cause digestive problems, Dr. Johnson said, which may cause more problems.
 

What recent research reveals

Cannabinoid hyperemesis syndrome is a relatively young disorder – first described in 2004 – and early reports and case studies are giving way now to studies looking into potential treatments.

So far, the strongest evidence suggests a role for an over-the-counter cream called capsaicin to help manage symptoms, but more studies are needed.

Similar to hot showers, this ingredient from chili peppers can warm the skin and trigger the temperature-sensitive skin sensors to lessen the symptoms, Dr. Johnson said.

An October 2021 study in Spain looked at 54 ED visits among 29 people with cannabinoid hyperemesis syndrome. For the 75% treated with capsaicin, vomiting stopped after an average of 18 minutes.

Lead author Guillermo Burillo-Putze, MD, PhD, said he is most surprised by the growing number of new cases of the disorder.

“This should be of concern given the increase in cannabis use due to its legalization and permissiveness,” said Dr. Burillo-Putze, an emergency doctor at Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain.

Cannabinoid hyperemesis syndrome appears not to discriminate across racial and ethic groups. Although most studies to date include White participants, a July 2021 study of 29 people, 90% of whom were Black, found repeat visits to the ED were common.

The study found that 16 people returned 42 times to the ED and accounted for 10 hospital admissions, for example.
 

Cannabis conspiracy theories

“Unfortunately, this condition has become the subject of great speculation hinging on conspiracy theories as its true cause,” Dr. Russo noted in a September 2021 letter to the editor in the American Journal of Emergency Medicine.

Some “myth busting” is in order, he said.

For example, cannabinoid hyperemesis syndrome does not happen because of exposure to products from a tree called neem or from pesticides applied to marijuana plants during cultivation, Dr. Russo said. It can also occur with high-dose synthetic cannabinoids.
 

The state of recreational and medical marijuana

Recreational marijuana is legal in 18 states, Washington, D.C., and Guam as of January 2022, according to a report in U.S. News. More states permit medical marijuana use – 37 in total, plus Washington, D.C., according to Britannica ProCon.

One of the states where only medicinal use is legal is Maryland, which is where Dr. Vinocur practices.

“We are seeing increasing numbers of cases” of cannabinoid hyperemesis syndrome, she said.

In addition to chronic use or higher doses, it’s likely that the higher potency levels of THC in the legal marijuana industry trigger the syndrome in some people as well.

Linda estimates she ended up in emergency rooms at least a half-dozen times in the last 5 years. In April 2021, she had a “pretty serious event.” She blames it on traveling a lot for work, not eating right, and not getting enough sleep. She broke her 2-year abstinence with alcohol.

“I basically didn’t listen to my body and paid a pretty significant price for it,” she said.

Linda did not stop altogether but said she “drastically changed the types and form of the cannabis I was using.”

“I can tell you on the record that I would be a hundred percent dead without this plant,” she said.

“The prospect of living without it was more detrimental to me than all of those things I just described to you, because addiction runs in my family and I had opiate problems myself that I overcame with cannabis.”

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

At the center of the emerging science on the unintended consequences of daily long-term use of marijuana lies a paradox.

For years, medical marijuana has been used to ease nausea from cancer chemotherapy and GI conditions. Now, with greater legalization comes growing awareness that chronic use of marijuana – also known as cannabis – can trigger a condition where, ironically, a person has hard-to-control vomiting and nausea.

Doug Menuez/thinkstock

Some people with the disorder, known as “cannabinoid hyperemesis syndrome,” also report crippling belly pain.

Linda can relate. The 33-year-old Oregon resident, who asked to remain anonymous to protect her privacy, refers to a medieval spiky metal ball on a chain when describing the pain.

“Picture a mace inside your stomach, pushing up inside your chest and, at the same time, exploding out,” she said.

To seek relief, she gets down on her knees, adopts a child’s yoga pose, and runs hot water in the bathroom for hours on end, a trick many with the disorder says has provided relief. She also occasionally goes outside and tries walking it off.

“I would just wander around my neighborhood, a lot of times at like 4 or 5 in the morning,” she said. “The fresh air helps a little bit. I just keep walking down the street, take about 10 steps, stop, vomit – walk a little bit more, stop, vomit.”

Her first experience with the disorder began in the middle of one night in 2017 while she was at a conference in Las Vegas.

“We went out to eat the night before, and I woke up about 4 in the morning with just the most intense pain I’ve ever had,” she said. “I found myself in a really hot shower in between throwing up everything and trying to say get some water down. I was sharing an Airbnb with my colleagues, so it was less than ideal.”

Many people with cannabinoid hyperemesis syndrome find relief from hot baths or showers. Researchers believe that hot water helps because temperature sensors in the skin send signals to the brain that can help ease the symptoms, at least for a while.

The problem is that people with this syndrome “can’t live in the water,” said emergency doctor and medical cannabis expert Leigh Vinocur, MD.

Fast-forward 6 months to another event in Boulder, Colo. Again, Linda woke up and could not stop vomiting.

“I was not feeling any better. Showering wasn’t helping. I ended up in the hospital,” she said.

She received opioids for her pain. But neither she nor the ED staff were quite sure what was happening. Her discharge paperwork read “cannabis allergy.”

Cannabinoid hyperemesis syndrome “shatters that image of cannabis only being a good thing. It’s a bold statement, but, you know, once you start to think about it, it’s like a little too much of anything isn’t good,” Linda said.

Experts suggest greater awareness is needed to identify this syndrome earlier, by both cannabinoid users and doctors. The bouts of vomiting, in particular, can get so severe that people can end up hospitalized with dehydration, electrolyte disorders, and weight loss.

The severe electrolyte imbalances “can really be life-threatening,” said David Johnson, MD, a professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk.

“By the time they come into emergency care, they’re in bad shape,” Dr. Vinocur agreed. “Many try to ignore it, but they continue to vomit.”
 

Genetic risk factors?

One mystery is why some regular marijuana users get this syndrome while others do not.

“I can say that not everybody gets this, thank goodness,” said Ethan Russo, MD. “But there has to be a reason that certain people are susceptible and others are not.”

Interestingly, a new study from Dr. Russo and colleagues suggests that genes play a role. They identified five genetic changes that could make a chronic marijuana user more likely to have cannabinoid hyperemesis syndrome in a study published July 5, 2021, in the journal Cannabis and Cannabinoid Research.

They compared 28 people with the disorder with 12 other high-frequency marijuana users without these symptoms.

The results are not final but could help guide future research, Dr. Russo said.

“What we’ve discovered – and it was far more than we expected – is that there’s a lot more to this than a hypersensitivity to cannabis,” said Dr. Russo, a neurologist and founder/CEO of CReDO Science, a firm that promotes cannabis research and develops commercial products.

Also, he said, those affected by cannabinoid hyperemesis syndrome could be at higher risk for other conditions, such as addiction to alcohol or other substances, dementia, diabetes, and heart disease.

“Most people with [cannabinoid hyperemesis syndrome] are going to be younger,” he said. “What we’ve demonstrated is there is a risk for more serious problems for decades to come. So someone who has these symptoms really deserves a look at this genetic screening.”
 

Battling disbelief

Getting back to the paradox, many users don’t believe marijuana can trigger serious vomiting and nausea because of its reputation for doing the opposite.

“Folks that have this are just uniquely resistant to the concept that cannabis is actually the problem and not the solution,” Dr. Russo said.

“It’s kind of counterintuitive because people think: ‘Oh, cannabis helps with nausea,’ so they use more of it,” said Dr. Vinocur, who is also a spokesperson for the American College of Emergency Physicians and runs a medical cannabis practice.

Most kinds of marijuana act in this way – doing opposite things at different doses. Once a certain threshold is passed, people with cannabinoid hyperemesis syndrome are “just uniquely susceptible and really can’t tolerate any significant amount of THC,” Dr. Russo said, referring to tetrahydrocannabinol, the substance that gets marijuana users high.

Once diagnosed, quitting is the most effective strategy. But it can be tough to persuade someone to stop using marijuana.

“You do have to try and convince them ... to try abstinence and to watch and see what happens,” Dr. Vinocur said.

People should “realize the root cause of this is its cannabinoid ingestion, and the treatment is really best directed at absolute avoidance,” Dr. Johnson said.

Unfortunately, evidence also shows that once a person stops using marijuana and gets relief, going back to marijuana or other forms of cannabinoids can cause the syndrome to start all over again.

“We’ve had people that quit for a month, a year, 2 years and upon resumption, almost invariably, they’re back into bouts of the hyperemesis along with all the other [symptoms],” Dr. Russo said.

Marijuana and cannabinoids can cause digestive problems, Dr. Johnson said, which may cause more problems.
 

What recent research reveals

Cannabinoid hyperemesis syndrome is a relatively young disorder – first described in 2004 – and early reports and case studies are giving way now to studies looking into potential treatments.

So far, the strongest evidence suggests a role for an over-the-counter cream called capsaicin to help manage symptoms, but more studies are needed.

Similar to hot showers, this ingredient from chili peppers can warm the skin and trigger the temperature-sensitive skin sensors to lessen the symptoms, Dr. Johnson said.

An October 2021 study in Spain looked at 54 ED visits among 29 people with cannabinoid hyperemesis syndrome. For the 75% treated with capsaicin, vomiting stopped after an average of 18 minutes.

Lead author Guillermo Burillo-Putze, MD, PhD, said he is most surprised by the growing number of new cases of the disorder.

“This should be of concern given the increase in cannabis use due to its legalization and permissiveness,” said Dr. Burillo-Putze, an emergency doctor at Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain.

Cannabinoid hyperemesis syndrome appears not to discriminate across racial and ethic groups. Although most studies to date include White participants, a July 2021 study of 29 people, 90% of whom were Black, found repeat visits to the ED were common.

The study found that 16 people returned 42 times to the ED and accounted for 10 hospital admissions, for example.
 

Cannabis conspiracy theories

“Unfortunately, this condition has become the subject of great speculation hinging on conspiracy theories as its true cause,” Dr. Russo noted in a September 2021 letter to the editor in the American Journal of Emergency Medicine.

Some “myth busting” is in order, he said.

For example, cannabinoid hyperemesis syndrome does not happen because of exposure to products from a tree called neem or from pesticides applied to marijuana plants during cultivation, Dr. Russo said. It can also occur with high-dose synthetic cannabinoids.
 

The state of recreational and medical marijuana

Recreational marijuana is legal in 18 states, Washington, D.C., and Guam as of January 2022, according to a report in U.S. News. More states permit medical marijuana use – 37 in total, plus Washington, D.C., according to Britannica ProCon.

One of the states where only medicinal use is legal is Maryland, which is where Dr. Vinocur practices.

“We are seeing increasing numbers of cases” of cannabinoid hyperemesis syndrome, she said.

In addition to chronic use or higher doses, it’s likely that the higher potency levels of THC in the legal marijuana industry trigger the syndrome in some people as well.

Linda estimates she ended up in emergency rooms at least a half-dozen times in the last 5 years. In April 2021, she had a “pretty serious event.” She blames it on traveling a lot for work, not eating right, and not getting enough sleep. She broke her 2-year abstinence with alcohol.

“I basically didn’t listen to my body and paid a pretty significant price for it,” she said.

Linda did not stop altogether but said she “drastically changed the types and form of the cannabis I was using.”

“I can tell you on the record that I would be a hundred percent dead without this plant,” she said.

“The prospect of living without it was more detrimental to me than all of those things I just described to you, because addiction runs in my family and I had opiate problems myself that I overcame with cannabis.”

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

At the center of the emerging science on the unintended consequences of daily long-term use of marijuana lies a paradox.

For years, medical marijuana has been used to ease nausea from cancer chemotherapy and GI conditions. Now, with greater legalization comes growing awareness that chronic use of marijuana – also known as cannabis – can trigger a condition where, ironically, a person has hard-to-control vomiting and nausea.

Doug Menuez/thinkstock

Some people with the disorder, known as “cannabinoid hyperemesis syndrome,” also report crippling belly pain.

Linda can relate. The 33-year-old Oregon resident, who asked to remain anonymous to protect her privacy, refers to a medieval spiky metal ball on a chain when describing the pain.

“Picture a mace inside your stomach, pushing up inside your chest and, at the same time, exploding out,” she said.

To seek relief, she gets down on her knees, adopts a child’s yoga pose, and runs hot water in the bathroom for hours on end, a trick many with the disorder says has provided relief. She also occasionally goes outside and tries walking it off.

“I would just wander around my neighborhood, a lot of times at like 4 or 5 in the morning,” she said. “The fresh air helps a little bit. I just keep walking down the street, take about 10 steps, stop, vomit – walk a little bit more, stop, vomit.”

Her first experience with the disorder began in the middle of one night in 2017 while she was at a conference in Las Vegas.

“We went out to eat the night before, and I woke up about 4 in the morning with just the most intense pain I’ve ever had,” she said. “I found myself in a really hot shower in between throwing up everything and trying to say get some water down. I was sharing an Airbnb with my colleagues, so it was less than ideal.”

Many people with cannabinoid hyperemesis syndrome find relief from hot baths or showers. Researchers believe that hot water helps because temperature sensors in the skin send signals to the brain that can help ease the symptoms, at least for a while.

The problem is that people with this syndrome “can’t live in the water,” said emergency doctor and medical cannabis expert Leigh Vinocur, MD.

Fast-forward 6 months to another event in Boulder, Colo. Again, Linda woke up and could not stop vomiting.

“I was not feeling any better. Showering wasn’t helping. I ended up in the hospital,” she said.

She received opioids for her pain. But neither she nor the ED staff were quite sure what was happening. Her discharge paperwork read “cannabis allergy.”

Cannabinoid hyperemesis syndrome “shatters that image of cannabis only being a good thing. It’s a bold statement, but, you know, once you start to think about it, it’s like a little too much of anything isn’t good,” Linda said.

Experts suggest greater awareness is needed to identify this syndrome earlier, by both cannabinoid users and doctors. The bouts of vomiting, in particular, can get so severe that people can end up hospitalized with dehydration, electrolyte disorders, and weight loss.

The severe electrolyte imbalances “can really be life-threatening,” said David Johnson, MD, a professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk.

“By the time they come into emergency care, they’re in bad shape,” Dr. Vinocur agreed. “Many try to ignore it, but they continue to vomit.”
 

Genetic risk factors?

One mystery is why some regular marijuana users get this syndrome while others do not.

“I can say that not everybody gets this, thank goodness,” said Ethan Russo, MD. “But there has to be a reason that certain people are susceptible and others are not.”

Interestingly, a new study from Dr. Russo and colleagues suggests that genes play a role. They identified five genetic changes that could make a chronic marijuana user more likely to have cannabinoid hyperemesis syndrome in a study published July 5, 2021, in the journal Cannabis and Cannabinoid Research.

They compared 28 people with the disorder with 12 other high-frequency marijuana users without these symptoms.

The results are not final but could help guide future research, Dr. Russo said.

“What we’ve discovered – and it was far more than we expected – is that there’s a lot more to this than a hypersensitivity to cannabis,” said Dr. Russo, a neurologist and founder/CEO of CReDO Science, a firm that promotes cannabis research and develops commercial products.

Also, he said, those affected by cannabinoid hyperemesis syndrome could be at higher risk for other conditions, such as addiction to alcohol or other substances, dementia, diabetes, and heart disease.

“Most people with [cannabinoid hyperemesis syndrome] are going to be younger,” he said. “What we’ve demonstrated is there is a risk for more serious problems for decades to come. So someone who has these symptoms really deserves a look at this genetic screening.”
 

Battling disbelief

Getting back to the paradox, many users don’t believe marijuana can trigger serious vomiting and nausea because of its reputation for doing the opposite.

“Folks that have this are just uniquely resistant to the concept that cannabis is actually the problem and not the solution,” Dr. Russo said.

“It’s kind of counterintuitive because people think: ‘Oh, cannabis helps with nausea,’ so they use more of it,” said Dr. Vinocur, who is also a spokesperson for the American College of Emergency Physicians and runs a medical cannabis practice.

Most kinds of marijuana act in this way – doing opposite things at different doses. Once a certain threshold is passed, people with cannabinoid hyperemesis syndrome are “just uniquely susceptible and really can’t tolerate any significant amount of THC,” Dr. Russo said, referring to tetrahydrocannabinol, the substance that gets marijuana users high.

Once diagnosed, quitting is the most effective strategy. But it can be tough to persuade someone to stop using marijuana.

“You do have to try and convince them ... to try abstinence and to watch and see what happens,” Dr. Vinocur said.

People should “realize the root cause of this is its cannabinoid ingestion, and the treatment is really best directed at absolute avoidance,” Dr. Johnson said.

Unfortunately, evidence also shows that once a person stops using marijuana and gets relief, going back to marijuana or other forms of cannabinoids can cause the syndrome to start all over again.

“We’ve had people that quit for a month, a year, 2 years and upon resumption, almost invariably, they’re back into bouts of the hyperemesis along with all the other [symptoms],” Dr. Russo said.

Marijuana and cannabinoids can cause digestive problems, Dr. Johnson said, which may cause more problems.
 

What recent research reveals

Cannabinoid hyperemesis syndrome is a relatively young disorder – first described in 2004 – and early reports and case studies are giving way now to studies looking into potential treatments.

So far, the strongest evidence suggests a role for an over-the-counter cream called capsaicin to help manage symptoms, but more studies are needed.

Similar to hot showers, this ingredient from chili peppers can warm the skin and trigger the temperature-sensitive skin sensors to lessen the symptoms, Dr. Johnson said.

An October 2021 study in Spain looked at 54 ED visits among 29 people with cannabinoid hyperemesis syndrome. For the 75% treated with capsaicin, vomiting stopped after an average of 18 minutes.

Lead author Guillermo Burillo-Putze, MD, PhD, said he is most surprised by the growing number of new cases of the disorder.

“This should be of concern given the increase in cannabis use due to its legalization and permissiveness,” said Dr. Burillo-Putze, an emergency doctor at Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain.

Cannabinoid hyperemesis syndrome appears not to discriminate across racial and ethic groups. Although most studies to date include White participants, a July 2021 study of 29 people, 90% of whom were Black, found repeat visits to the ED were common.

The study found that 16 people returned 42 times to the ED and accounted for 10 hospital admissions, for example.
 

Cannabis conspiracy theories

“Unfortunately, this condition has become the subject of great speculation hinging on conspiracy theories as its true cause,” Dr. Russo noted in a September 2021 letter to the editor in the American Journal of Emergency Medicine.

Some “myth busting” is in order, he said.

For example, cannabinoid hyperemesis syndrome does not happen because of exposure to products from a tree called neem or from pesticides applied to marijuana plants during cultivation, Dr. Russo said. It can also occur with high-dose synthetic cannabinoids.
 

The state of recreational and medical marijuana

Recreational marijuana is legal in 18 states, Washington, D.C., and Guam as of January 2022, according to a report in U.S. News. More states permit medical marijuana use – 37 in total, plus Washington, D.C., according to Britannica ProCon.

One of the states where only medicinal use is legal is Maryland, which is where Dr. Vinocur practices.

“We are seeing increasing numbers of cases” of cannabinoid hyperemesis syndrome, she said.

In addition to chronic use or higher doses, it’s likely that the higher potency levels of THC in the legal marijuana industry trigger the syndrome in some people as well.

Linda estimates she ended up in emergency rooms at least a half-dozen times in the last 5 years. In April 2021, she had a “pretty serious event.” She blames it on traveling a lot for work, not eating right, and not getting enough sleep. She broke her 2-year abstinence with alcohol.

“I basically didn’t listen to my body and paid a pretty significant price for it,” she said.

Linda did not stop altogether but said she “drastically changed the types and form of the cannabis I was using.”

“I can tell you on the record that I would be a hundred percent dead without this plant,” she said.

“The prospect of living without it was more detrimental to me than all of those things I just described to you, because addiction runs in my family and I had opiate problems myself that I overcame with cannabis.”

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

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

Motionless, every Olympic skater starts off perfectly. Once the music starts, it’s up to them whether they will continue on perfectly or not. In this way, you’re just like an Olympic skater. Each day, a skating program. The music starts the moment your foot touches the floor in the morning. It’s up to you if the rest of the day will continue on flawlessly or not. To this point, I’ve yet to have a perfect day.

If I’m honest, my “perfect day” streak typically ends once I’ve made coffee. By then, I’ll have spilled a few grains of grounds or clinked mugs together when taking one from the cupboard. (D’oh!) Hardly ever can I make it to backing out of the driveway, let alone through a patient encounter. I’ve had a few procedures that when complete I’ve thought, “well, that looks great.” I can remember encounters that went brilliantly despite a high technical difficulty. I’ve also tagged a 7-iron shot 160 downwind yards to within inches of the cup. But I’ve hardly ever done anything in my life perfectly.

What does it mean to be perfect? Well, there have been 23 perfect baseball games. In 1972, the Miami Dolphins had the only perfect NFL season, 14-0 (although my 2007 Patriots went 18-0 before losing to the – ugh – Giants). Every year, several hundred students score a perfect 1600 on the SAT. In an underground vault somewhere in France is a perfect sphere, a perfectly spherical 1-kg mass of pure silicon. There are at least 51 perfect numbers. And model Bella Hadid’s exactly 1.62-ratioed face is said to be perfectly beautiful. But yet, U.S. skater Nathan Chen’s seemingly flawless 113.97-point short program in Beijing, still imperfect.

Attempting a perfect day or perfect surgery or a perfect pour over coffee is a fun game, but perfectionism has an insidious side. Having perfectionistic concerns significantly increases the risk for burnout, depression, and eating disorders. Some of us feel this way every day: We must do it exactly right, every time. Even an insignificant imperfection or error feels like failure. A 3.90 GPA is a fail. 515 on the MCAT, not nearly good enough. For them, the burden of perfection is crushing. It is hard for some to recognize that even if your performance could not be improved, the outcome can still be flawed. A chip in the ice, a patient showing up late, an interviewer with an agenda, a missed referee call can all flub up an otherwise flawless day. It isn’t necessary to abandon hope, all ye who live in the real world. Although achieving perfection is usually impossible, reward comes from the pursuit of perfection, not from holding it. It is called perfectionistic striving and in contrast to perfectionistic concerns, it is associated with resilience and positive mood. To do so you must combine giving your all with acceptance of whatever the outcome.

Keith Jarrett is one of the greatest jazz pianists of all time. He is a true perfectionist, precise in his standards and exacting in expectations. In 1975 in Cologne, Germany, he agreed to play at the behest of a teenage girl who arranged to have him perform at the opera house. Except, there was a miscommunication and only a small, broken rehearsal piano was available. As the story goes, she approached him as he waited to be taken back to his hotel, the concert was canceled and she somehow convinced him to play on the nearly unplayable instrument. The result is the Köln Concert, one of the greatest jazz performances in history. It was perfectly imperfect.

Yes, even the 1-kg sphere has femtogram quantities of other elements mixed in – the universal standard for perfect is itself, imperfect. It doesn’t matter. It’s the pursuit of such that makes life worthwhile. There’s always tomorrow. Have your coffee grinders ready.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

“Children are not little adults” is a common refrain in pediatric medicine, but when it comes to a condition like juvenile idiopathic arthritis (JIA), rheumatologists might be better off treating pediatric and adult rheumatic disease more similarly.

A recent study published in Arthritis Care & Research followed children diagnosed with JIA for 18 years. Although not the first long-term study to examine children with JIA, it is unique in that it took place “during a time where biologic DMARDs [disease-modifying antirheumatic drugs] were emerging as a fundamental therapy in the management of children with JIA,” said Dawn M. Wahezi, MD, chief of the division of pediatric rheumatology at the Children’s Hospital at Montefiore in New York, who was not involved with the study.

SrdjanPav/E+/Getty Images

Additionally, the study highlights the International League of Associations for Rheumatology (ILAR) consensus-based classification criteria as an imperfect method to categorize patients with JIA.

Mia Glerup, MD, PhD, of the department of pediatrics at Aarhus (Denmark) University Hospital and colleagues prospectively analyzed 373 patients from Denmark, Norway, Sweden, and Finland with new-onset JIA between 1997 and 2000 and evaluated them at baseline, 8 years, and 18 years. At each visit, the researchers collected data on demographics, disease activity, ILAR category, treatment, and blood samples.

Patients in the cohort were mostly girls (66.7%) with a median age of 5.9 years at onset. Approximately one-third (34.8%) of patients were antinuclear antibody (ANA) positive and 21.6% were HLA-B27 positive. The most common JIA categories at baseline were persistent oligoarthritis (53.9%), polyarticular rheumatoid factor (RF) negative (21.1%), and undifferentiated arthritis (10.2%).

Dr. Glerup and colleagues found that the proportion of patients not receiving DMARDs declined from 73.2% at baseline to 59.7% at 8 years, and then rose again to 70% at 18 years (risk ratio, 1.3; P = .003). The group of 103 patients who used conventional DMARDs (cDMARDs) either as monotherapy or in combination with a biologic DMARD (bDMARD) at 8 years dwindled to 44 (42.7%) at 18 years (RR, 0.4; P < .001), whereas 32 of 52 patients (61.5%) using bDMARDs at 8 years were still taking them at 18 years (RR, 0.6; P = .02). Across the whole study, 14.7% of patients never received any JIA treatment, and 33 of 85 patients (38.8%) on continuous DMARDs developed uveitis during the study period.

Overall, 62.7% of patients received DMARDs at least once, including 89.7% with polyarticular RF negative, 77.3% with oligoarticular extended, 76.9% with systemic, 75.7% with juvenile enthesitis-related arthritis (ERA), 66.7% with polyarticular RF-positive, 65.2% with juvenile psoriatic arthritis (JPsA), 58.9% with undifferentiated JIA, and 27.6% of patients with persistent oligoarticular disease.

The median number of active joints dropped from 3 (range, 1-30) at baseline to 0 at 8 years (range, 0-13), whereas the median cumulative number of affected joints rose from 3 at baseline (range, 1-30) to 6 at 8 years (range, 1-41). At last follow-up, the median number of active joints was 0 (range, 0-5) and median cumulative number of affected joints was 7 (range, 1-47). The percentage of patients in remission barely changed from 52% at 8 years to 51% at 18.

Some patients also changed ILAR categories during the study period, with 7% shifting between baseline and 8 years, and 11% shifting between 8-year and 18-year follow-up. Compared with baseline, by the 18-year follow-up time point there was a significant decrease in the number of patients categorized as oligoarticular (230 vs. 197 patients; P = .02), a significant increase in patients in the psoriatic ILAR category (8 vs. 28 patients; P < .001), and a nonsignificant increase in the number of patients in the undifferentiated category (45 vs. 63 patients; P = .06).

“Almost half of the changes in the distribution between the ILAR categories were caused by updated information on heredity in a first-degree relative obtained at the follow-up visits,” Dr. Glerup and colleagues write.

“That kind of weaves its way through the whole study, because then they show a lot of patients have come off their medication. Patients who had more severe disease in more joints would be less likely, I think, to just stop their medication and stop going to doctors,” Dr. Imundo explained.

Although the study is valuable for its long-term follow-up, there is also a question of generalizability across a more diverse ethnic and racial group. The authors do not elaborate on the racial breakdown of their patients, Dr. Imundo said, “so we’re going to have to assume that the vast majority are going to [have] Caucasian Nordic ethnic background, and that goes along with them having this high percentage of HLA-B27 positivity, which is a gene that’s more prevalent in northern European populations.”

Jonathan Hausmann, MD, a pediatric and adult rheumatologist at Boston Children’s Hospital, Boston,, told this news organization that he believes the overall conclusions from the study – that JIA persists over time and that ILAR classification is a somewhat imprecise measure of assessing JIA types in children – would be generalizable to other groups.

However, long-term registries evaluating JIA in more diverse populations, such as the Childhood Arthritis and Rheumatology Research Alliance (CARRA) registry, could confirm these results, said Dr. Hausmann, who is a registry informatics associate with CARRA and was not associated with the research.
 

Long-term management of JIA

In an accompanying editorial, Jaime Guzman, MD, MSc, and Ross E. Petty, MD, PhD, of British Columbia Children’s Hospital and the University of British Columbia, Vancouver, said a rheumatologist’s interpretation of the study would be tied to what they learned about children with arthritis in medical school. They would see the glass as “half full” if children who achieved remission stayed in remission if they learned that a child might end up outgrowing JIA but potentially develop lifelong disability, whereas others may focus on the outcome of approximately half of patients not achieving remission.

“When I was going through medical school, I remember learning that JIA is a disease of children, and typically, they outgrow it as they become adults,” Dr. Hausmann said. “I think this study and many other studies have shown that that’s actually not the case – that, in fact, it may be a majority of kids continue having active disease even through adulthood.”

If a rheumatologist knows JIA is likely to continue into adulthood, “that’s huge,” Dr. Hausmann said. “That means when we first diagnose patients with JIA as kids, we need to set expectations with the families that this may not just go away; this may be something that could be more lifelong.”

Education on the part of the patient, their parents, and their clinician on the expected trajectory of the disease is critical so that children can continue their own care as they transition to adulthood, Dr. Hausmann explained. “The earlier the kids develop the skills to discuss their medicines, their side effects, the better they’ll be able to transition to adult medicine,” he said.

For the patients who go into remission and stay in remission, the message is also important. “To have the reassurance that a lot of those kids won’t be having active joint symptoms or need to be on medication, that’s a huge positive message that can get out there, so I think that’s great,” Dr. Imundo said.
 

Time to move on from ILAR classification?

Another big takeaway from the study was how patients’ ILAR classification changed across the 18-year follow-up. First proposed in 1995, the JIA ILAR classification has been revised several times for clarification purposes. In its current form, the ILAR classification considers a patient’s history when categorizing JIA types but also includes factors such as immediate family history. This system of assessing JIA has been criticized and there are initiatives to create a new JIA classification system to replace it.

“The ILAR criteria were designed to classify patients 6 months after disease onset in an attempt to find some commonality in clinical phenotypes, prognosis, and suggested management,” Dr. Wahezi said. “While there continues to be debate as to whether we can improve our classification of JIA patients, it is not surprising that phenotypes may evolve over time as new clinical features develop. As pediatric rheumatologists, we are well accustomed to having to modify management plans as children manifest with new clinical features over time.”

Although the percentage of patients who switched ILAR classifications over the study period was “much higher” than she would have thought, Dr. Imundo said it was the reasons provided in the study that seemed odd to her. “The classification scheme relies on your family history, like someone else in your family now has psoriasis, so your arthritis classification changes,” she explained.

“We want to head toward a much more unified classification scheme, a simpler one. We now understand that some of the diseases that we see in pediatrics are really the equivalent or same disease in adults,” she said.

“Most of the pediatric categories of JIA have distinct adult correlates,” Dr. Hausmann agreed. RF-positive polyarthritis in children and rheumatoid arthritis in adults are correlated, as are systemic JIA and adult-onset Still’s disease, he explained. “That has been borne out also by genetic susceptibility studies that the genetic predispositions to systemic arthritis in children is the same as the genetic predisposition to adult-onset Still’s disease in adults. By and large, there are a lot of similarities between the two.

“I think we need to incorporate some of that knowledge in better classifying kids with JIA so that we can find the best treatments and the best outcomes, and we can provide information to families about the expected course of the disease over time so that can inform our discussions.”

Some pediatric rheumatologists accept the classification system is flawed, but not all concur with the degree to which these problems impact patient care. “While the ILAR classification criteria may be subject to criticism, it does provide general context and prognostic implications for patients and families,” Dr. Wahezi said.

“The medicines certainly are very similar across the JIA categories, so the implications are not as broad” when classification changes,” Dr. Hausmann said. “But it certainly shows that there are things that we still don’t know. I think classification is actually pretty important because it might give you a sense of how persistent the disease will be.”

Dr. Imundo said the ILAR classification’s “time is limited,” and rheumatologists may soon need to adopt a new way of classifying children with rheumatic disease – “a more data-driven, genetics-driven scheme.”

“These categories are so imperfect, and the patients are changing. I feel like that says to me, let’s find something that’s more predictive that really helps us a little better than what we have now,” she said.

The study had no specific funding. The authors of the study and the editorial have disclosed no relevant financial relationships. Dr. Hausmann reports receiving salary support from CARRA. Dr. Imundo and Dr. Wahezi have disclosed no relevant financial relationships.

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

“Children are not little adults” is a common refrain in pediatric medicine, but when it comes to a condition like juvenile idiopathic arthritis (JIA), rheumatologists might be better off treating pediatric and adult rheumatic disease more similarly.

A recent study published in Arthritis Care & Research followed children diagnosed with JIA for 18 years. Although not the first long-term study to examine children with JIA, it is unique in that it took place “during a time where biologic DMARDs [disease-modifying antirheumatic drugs] were emerging as a fundamental therapy in the management of children with JIA,” said Dawn M. Wahezi, MD, chief of the division of pediatric rheumatology at the Children’s Hospital at Montefiore in New York, who was not involved with the study.

SrdjanPav/E+/Getty Images

Additionally, the study highlights the International League of Associations for Rheumatology (ILAR) consensus-based classification criteria as an imperfect method to categorize patients with JIA.

Mia Glerup, MD, PhD, of the department of pediatrics at Aarhus (Denmark) University Hospital and colleagues prospectively analyzed 373 patients from Denmark, Norway, Sweden, and Finland with new-onset JIA between 1997 and 2000 and evaluated them at baseline, 8 years, and 18 years. At each visit, the researchers collected data on demographics, disease activity, ILAR category, treatment, and blood samples.

Patients in the cohort were mostly girls (66.7%) with a median age of 5.9 years at onset. Approximately one-third (34.8%) of patients were antinuclear antibody (ANA) positive and 21.6% were HLA-B27 positive. The most common JIA categories at baseline were persistent oligoarthritis (53.9%), polyarticular rheumatoid factor (RF) negative (21.1%), and undifferentiated arthritis (10.2%).

Dr. Glerup and colleagues found that the proportion of patients not receiving DMARDs declined from 73.2% at baseline to 59.7% at 8 years, and then rose again to 70% at 18 years (risk ratio, 1.3; P = .003). The group of 103 patients who used conventional DMARDs (cDMARDs) either as monotherapy or in combination with a biologic DMARD (bDMARD) at 8 years dwindled to 44 (42.7%) at 18 years (RR, 0.4; P < .001), whereas 32 of 52 patients (61.5%) using bDMARDs at 8 years were still taking them at 18 years (RR, 0.6; P = .02). Across the whole study, 14.7% of patients never received any JIA treatment, and 33 of 85 patients (38.8%) on continuous DMARDs developed uveitis during the study period.

Overall, 62.7% of patients received DMARDs at least once, including 89.7% with polyarticular RF negative, 77.3% with oligoarticular extended, 76.9% with systemic, 75.7% with juvenile enthesitis-related arthritis (ERA), 66.7% with polyarticular RF-positive, 65.2% with juvenile psoriatic arthritis (JPsA), 58.9% with undifferentiated JIA, and 27.6% of patients with persistent oligoarticular disease.

The median number of active joints dropped from 3 (range, 1-30) at baseline to 0 at 8 years (range, 0-13), whereas the median cumulative number of affected joints rose from 3 at baseline (range, 1-30) to 6 at 8 years (range, 1-41). At last follow-up, the median number of active joints was 0 (range, 0-5) and median cumulative number of affected joints was 7 (range, 1-47). The percentage of patients in remission barely changed from 52% at 8 years to 51% at 18.

Some patients also changed ILAR categories during the study period, with 7% shifting between baseline and 8 years, and 11% shifting between 8-year and 18-year follow-up. Compared with baseline, by the 18-year follow-up time point there was a significant decrease in the number of patients categorized as oligoarticular (230 vs. 197 patients; P = .02), a significant increase in patients in the psoriatic ILAR category (8 vs. 28 patients; P < .001), and a nonsignificant increase in the number of patients in the undifferentiated category (45 vs. 63 patients; P = .06).

“Almost half of the changes in the distribution between the ILAR categories were caused by updated information on heredity in a first-degree relative obtained at the follow-up visits,” Dr. Glerup and colleagues write.

“That kind of weaves its way through the whole study, because then they show a lot of patients have come off their medication. Patients who had more severe disease in more joints would be less likely, I think, to just stop their medication and stop going to doctors,” Dr. Imundo explained.

Although the study is valuable for its long-term follow-up, there is also a question of generalizability across a more diverse ethnic and racial group. The authors do not elaborate on the racial breakdown of their patients, Dr. Imundo said, “so we’re going to have to assume that the vast majority are going to [have] Caucasian Nordic ethnic background, and that goes along with them having this high percentage of HLA-B27 positivity, which is a gene that’s more prevalent in northern European populations.”

Jonathan Hausmann, MD, a pediatric and adult rheumatologist at Boston Children’s Hospital, Boston,, told this news organization that he believes the overall conclusions from the study – that JIA persists over time and that ILAR classification is a somewhat imprecise measure of assessing JIA types in children – would be generalizable to other groups.

However, long-term registries evaluating JIA in more diverse populations, such as the Childhood Arthritis and Rheumatology Research Alliance (CARRA) registry, could confirm these results, said Dr. Hausmann, who is a registry informatics associate with CARRA and was not associated with the research.
 

Long-term management of JIA

In an accompanying editorial, Jaime Guzman, MD, MSc, and Ross E. Petty, MD, PhD, of British Columbia Children’s Hospital and the University of British Columbia, Vancouver, said a rheumatologist’s interpretation of the study would be tied to what they learned about children with arthritis in medical school. They would see the glass as “half full” if children who achieved remission stayed in remission if they learned that a child might end up outgrowing JIA but potentially develop lifelong disability, whereas others may focus on the outcome of approximately half of patients not achieving remission.

“When I was going through medical school, I remember learning that JIA is a disease of children, and typically, they outgrow it as they become adults,” Dr. Hausmann said. “I think this study and many other studies have shown that that’s actually not the case – that, in fact, it may be a majority of kids continue having active disease even through adulthood.”

If a rheumatologist knows JIA is likely to continue into adulthood, “that’s huge,” Dr. Hausmann said. “That means when we first diagnose patients with JIA as kids, we need to set expectations with the families that this may not just go away; this may be something that could be more lifelong.”

Education on the part of the patient, their parents, and their clinician on the expected trajectory of the disease is critical so that children can continue their own care as they transition to adulthood, Dr. Hausmann explained. “The earlier the kids develop the skills to discuss their medicines, their side effects, the better they’ll be able to transition to adult medicine,” he said.

For the patients who go into remission and stay in remission, the message is also important. “To have the reassurance that a lot of those kids won’t be having active joint symptoms or need to be on medication, that’s a huge positive message that can get out there, so I think that’s great,” Dr. Imundo said.
 

Time to move on from ILAR classification?

Another big takeaway from the study was how patients’ ILAR classification changed across the 18-year follow-up. First proposed in 1995, the JIA ILAR classification has been revised several times for clarification purposes. In its current form, the ILAR classification considers a patient’s history when categorizing JIA types but also includes factors such as immediate family history. This system of assessing JIA has been criticized and there are initiatives to create a new JIA classification system to replace it.

“The ILAR criteria were designed to classify patients 6 months after disease onset in an attempt to find some commonality in clinical phenotypes, prognosis, and suggested management,” Dr. Wahezi said. “While there continues to be debate as to whether we can improve our classification of JIA patients, it is not surprising that phenotypes may evolve over time as new clinical features develop. As pediatric rheumatologists, we are well accustomed to having to modify management plans as children manifest with new clinical features over time.”

Although the percentage of patients who switched ILAR classifications over the study period was “much higher” than she would have thought, Dr. Imundo said it was the reasons provided in the study that seemed odd to her. “The classification scheme relies on your family history, like someone else in your family now has psoriasis, so your arthritis classification changes,” she explained.

“We want to head toward a much more unified classification scheme, a simpler one. We now understand that some of the diseases that we see in pediatrics are really the equivalent or same disease in adults,” she said.

“Most of the pediatric categories of JIA have distinct adult correlates,” Dr. Hausmann agreed. RF-positive polyarthritis in children and rheumatoid arthritis in adults are correlated, as are systemic JIA and adult-onset Still’s disease, he explained. “That has been borne out also by genetic susceptibility studies that the genetic predispositions to systemic arthritis in children is the same as the genetic predisposition to adult-onset Still’s disease in adults. By and large, there are a lot of similarities between the two.

“I think we need to incorporate some of that knowledge in better classifying kids with JIA so that we can find the best treatments and the best outcomes, and we can provide information to families about the expected course of the disease over time so that can inform our discussions.”

Some pediatric rheumatologists accept the classification system is flawed, but not all concur with the degree to which these problems impact patient care. “While the ILAR classification criteria may be subject to criticism, it does provide general context and prognostic implications for patients and families,” Dr. Wahezi said.

“The medicines certainly are very similar across the JIA categories, so the implications are not as broad” when classification changes,” Dr. Hausmann said. “But it certainly shows that there are things that we still don’t know. I think classification is actually pretty important because it might give you a sense of how persistent the disease will be.”

Dr. Imundo said the ILAR classification’s “time is limited,” and rheumatologists may soon need to adopt a new way of classifying children with rheumatic disease – “a more data-driven, genetics-driven scheme.”

“These categories are so imperfect, and the patients are changing. I feel like that says to me, let’s find something that’s more predictive that really helps us a little better than what we have now,” she said.

The study had no specific funding. The authors of the study and the editorial have disclosed no relevant financial relationships. Dr. Hausmann reports receiving salary support from CARRA. Dr. Imundo and Dr. Wahezi have disclosed no relevant financial relationships.

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

“Children are not little adults” is a common refrain in pediatric medicine, but when it comes to a condition like juvenile idiopathic arthritis (JIA), rheumatologists might be better off treating pediatric and adult rheumatic disease more similarly.

A recent study published in Arthritis Care & Research followed children diagnosed with JIA for 18 years. Although not the first long-term study to examine children with JIA, it is unique in that it took place “during a time where biologic DMARDs [disease-modifying antirheumatic drugs] were emerging as a fundamental therapy in the management of children with JIA,” said Dawn M. Wahezi, MD, chief of the division of pediatric rheumatology at the Children’s Hospital at Montefiore in New York, who was not involved with the study.

SrdjanPav/E+/Getty Images

Additionally, the study highlights the International League of Associations for Rheumatology (ILAR) consensus-based classification criteria as an imperfect method to categorize patients with JIA.

Mia Glerup, MD, PhD, of the department of pediatrics at Aarhus (Denmark) University Hospital and colleagues prospectively analyzed 373 patients from Denmark, Norway, Sweden, and Finland with new-onset JIA between 1997 and 2000 and evaluated them at baseline, 8 years, and 18 years. At each visit, the researchers collected data on demographics, disease activity, ILAR category, treatment, and blood samples.

Patients in the cohort were mostly girls (66.7%) with a median age of 5.9 years at onset. Approximately one-third (34.8%) of patients were antinuclear antibody (ANA) positive and 21.6% were HLA-B27 positive. The most common JIA categories at baseline were persistent oligoarthritis (53.9%), polyarticular rheumatoid factor (RF) negative (21.1%), and undifferentiated arthritis (10.2%).

Dr. Glerup and colleagues found that the proportion of patients not receiving DMARDs declined from 73.2% at baseline to 59.7% at 8 years, and then rose again to 70% at 18 years (risk ratio, 1.3; P = .003). The group of 103 patients who used conventional DMARDs (cDMARDs) either as monotherapy or in combination with a biologic DMARD (bDMARD) at 8 years dwindled to 44 (42.7%) at 18 years (RR, 0.4; P < .001), whereas 32 of 52 patients (61.5%) using bDMARDs at 8 years were still taking them at 18 years (RR, 0.6; P = .02). Across the whole study, 14.7% of patients never received any JIA treatment, and 33 of 85 patients (38.8%) on continuous DMARDs developed uveitis during the study period.

Overall, 62.7% of patients received DMARDs at least once, including 89.7% with polyarticular RF negative, 77.3% with oligoarticular extended, 76.9% with systemic, 75.7% with juvenile enthesitis-related arthritis (ERA), 66.7% with polyarticular RF-positive, 65.2% with juvenile psoriatic arthritis (JPsA), 58.9% with undifferentiated JIA, and 27.6% of patients with persistent oligoarticular disease.

The median number of active joints dropped from 3 (range, 1-30) at baseline to 0 at 8 years (range, 0-13), whereas the median cumulative number of affected joints rose from 3 at baseline (range, 1-30) to 6 at 8 years (range, 1-41). At last follow-up, the median number of active joints was 0 (range, 0-5) and median cumulative number of affected joints was 7 (range, 1-47). The percentage of patients in remission barely changed from 52% at 8 years to 51% at 18.

Some patients also changed ILAR categories during the study period, with 7% shifting between baseline and 8 years, and 11% shifting between 8-year and 18-year follow-up. Compared with baseline, by the 18-year follow-up time point there was a significant decrease in the number of patients categorized as oligoarticular (230 vs. 197 patients; P = .02), a significant increase in patients in the psoriatic ILAR category (8 vs. 28 patients; P < .001), and a nonsignificant increase in the number of patients in the undifferentiated category (45 vs. 63 patients; P = .06).

“Almost half of the changes in the distribution between the ILAR categories were caused by updated information on heredity in a first-degree relative obtained at the follow-up visits,” Dr. Glerup and colleagues write.

“That kind of weaves its way through the whole study, because then they show a lot of patients have come off their medication. Patients who had more severe disease in more joints would be less likely, I think, to just stop their medication and stop going to doctors,” Dr. Imundo explained.

Although the study is valuable for its long-term follow-up, there is also a question of generalizability across a more diverse ethnic and racial group. The authors do not elaborate on the racial breakdown of their patients, Dr. Imundo said, “so we’re going to have to assume that the vast majority are going to [have] Caucasian Nordic ethnic background, and that goes along with them having this high percentage of HLA-B27 positivity, which is a gene that’s more prevalent in northern European populations.”

Jonathan Hausmann, MD, a pediatric and adult rheumatologist at Boston Children’s Hospital, Boston,, told this news organization that he believes the overall conclusions from the study – that JIA persists over time and that ILAR classification is a somewhat imprecise measure of assessing JIA types in children – would be generalizable to other groups.

However, long-term registries evaluating JIA in more diverse populations, such as the Childhood Arthritis and Rheumatology Research Alliance (CARRA) registry, could confirm these results, said Dr. Hausmann, who is a registry informatics associate with CARRA and was not associated with the research.
 

Long-term management of JIA

In an accompanying editorial, Jaime Guzman, MD, MSc, and Ross E. Petty, MD, PhD, of British Columbia Children’s Hospital and the University of British Columbia, Vancouver, said a rheumatologist’s interpretation of the study would be tied to what they learned about children with arthritis in medical school. They would see the glass as “half full” if children who achieved remission stayed in remission if they learned that a child might end up outgrowing JIA but potentially develop lifelong disability, whereas others may focus on the outcome of approximately half of patients not achieving remission.

“When I was going through medical school, I remember learning that JIA is a disease of children, and typically, they outgrow it as they become adults,” Dr. Hausmann said. “I think this study and many other studies have shown that that’s actually not the case – that, in fact, it may be a majority of kids continue having active disease even through adulthood.”

If a rheumatologist knows JIA is likely to continue into adulthood, “that’s huge,” Dr. Hausmann said. “That means when we first diagnose patients with JIA as kids, we need to set expectations with the families that this may not just go away; this may be something that could be more lifelong.”

Education on the part of the patient, their parents, and their clinician on the expected trajectory of the disease is critical so that children can continue their own care as they transition to adulthood, Dr. Hausmann explained. “The earlier the kids develop the skills to discuss their medicines, their side effects, the better they’ll be able to transition to adult medicine,” he said.

For the patients who go into remission and stay in remission, the message is also important. “To have the reassurance that a lot of those kids won’t be having active joint symptoms or need to be on medication, that’s a huge positive message that can get out there, so I think that’s great,” Dr. Imundo said.
 

Time to move on from ILAR classification?

Another big takeaway from the study was how patients’ ILAR classification changed across the 18-year follow-up. First proposed in 1995, the JIA ILAR classification has been revised several times for clarification purposes. In its current form, the ILAR classification considers a patient’s history when categorizing JIA types but also includes factors such as immediate family history. This system of assessing JIA has been criticized and there are initiatives to create a new JIA classification system to replace it.

“The ILAR criteria were designed to classify patients 6 months after disease onset in an attempt to find some commonality in clinical phenotypes, prognosis, and suggested management,” Dr. Wahezi said. “While there continues to be debate as to whether we can improve our classification of JIA patients, it is not surprising that phenotypes may evolve over time as new clinical features develop. As pediatric rheumatologists, we are well accustomed to having to modify management plans as children manifest with new clinical features over time.”

Although the percentage of patients who switched ILAR classifications over the study period was “much higher” than she would have thought, Dr. Imundo said it was the reasons provided in the study that seemed odd to her. “The classification scheme relies on your family history, like someone else in your family now has psoriasis, so your arthritis classification changes,” she explained.

“We want to head toward a much more unified classification scheme, a simpler one. We now understand that some of the diseases that we see in pediatrics are really the equivalent or same disease in adults,” she said.

“Most of the pediatric categories of JIA have distinct adult correlates,” Dr. Hausmann agreed. RF-positive polyarthritis in children and rheumatoid arthritis in adults are correlated, as are systemic JIA and adult-onset Still’s disease, he explained. “That has been borne out also by genetic susceptibility studies that the genetic predispositions to systemic arthritis in children is the same as the genetic predisposition to adult-onset Still’s disease in adults. By and large, there are a lot of similarities between the two.

“I think we need to incorporate some of that knowledge in better classifying kids with JIA so that we can find the best treatments and the best outcomes, and we can provide information to families about the expected course of the disease over time so that can inform our discussions.”

Some pediatric rheumatologists accept the classification system is flawed, but not all concur with the degree to which these problems impact patient care. “While the ILAR classification criteria may be subject to criticism, it does provide general context and prognostic implications for patients and families,” Dr. Wahezi said.

“The medicines certainly are very similar across the JIA categories, so the implications are not as broad” when classification changes,” Dr. Hausmann said. “But it certainly shows that there are things that we still don’t know. I think classification is actually pretty important because it might give you a sense of how persistent the disease will be.”

Dr. Imundo said the ILAR classification’s “time is limited,” and rheumatologists may soon need to adopt a new way of classifying children with rheumatic disease – “a more data-driven, genetics-driven scheme.”

“These categories are so imperfect, and the patients are changing. I feel like that says to me, let’s find something that’s more predictive that really helps us a little better than what we have now,” she said.

The study had no specific funding. The authors of the study and the editorial have disclosed no relevant financial relationships. Dr. Hausmann reports receiving salary support from CARRA. Dr. Imundo and Dr. Wahezi have disclosed no relevant financial relationships.

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

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.

What are ways that we can connect well with our patients so that both the patient and the physician are lifted up by the relationship?

Be curious

When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.

Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
 

Limit use of EHRs when possible

Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.

Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.¹

Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
 

Consider teaching medical students

When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.

By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.

In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.²
 

Use healing words

Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.

I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.

As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
 

Explain as you examine

People love to hear the term normal. When you are examining a patient, let them know when findings are normal.

I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.

When patients feel their physicians are thorough, they have more confidence in them.
 

In summary

• Be curious.
• Do not overly focus on the EHR.
• Consider teaching a medical student.
• Be careful of word choice.
• “Overexplain” the physical exam.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.

2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.

Several long COVID symptoms could be linked to the effects of the coronavirus on a vital central nerve, according to new research being released in the spring.

The vagus nerve, which runs from the brain into the body, connects to the heart, lungs, intestines, and several muscles involved with swallowing. It plays a role in several body functions that control heart rate, speech, the gag reflex, sweating, and digestion.

Those with long COVID and vagus nerve problems could face long-term issues with their voice, a hard time swallowing, dizziness, a high heart rate, low blood pressure, and diarrhea, the study authors found.

Their findings will be presented at the 2022 European Congress of Clinical Microbiology and Infectious Diseases in late April.

“Most long COVID subjects with vagus nerve dysfunction symptoms had a range of significant, clinically relevant, structural and/or functional alterations in their vagus nerve, including nerve thickening, trouble swallowing, and symptoms of impaired breathing,” the study authors wrote. “Our findings so far thus point at vagus nerve dysfunction as a central pathophysiological feature of long COVID.”

Researchers from the University Hospital Germans Trias i Pujol in Barcelona performed a study to look at vagus nerve functioning in long COVID patients. Among 348 patients, about 66% had at least one symptom that suggested vagus nerve dysfunction. The researchers did a broad evaluation with imaging and functional tests for 22 patients in the university’s Long COVID Clinic from March to June 2021.

Of the 22 patients, 20 were women, and the median age was 44. The most frequent symptoms related to vagus nerve dysfunction were diarrhea (73%), high heart rates (59%), dizziness (45%), swallowing problems (45%), voice problems (45%), and low blood pressure (14%).

Almost all (19 of 22 patients) had three or more symptoms related to vagus nerve dysfunction. The average length of symptoms was 14 months.

Of 22 patients, 6 had a change in the vagus nerve in the neck, which the researchers observed by ultrasound. They had a thickening of the vagus nerve and increased “echogenicity,” which suggests inflammation.

What’s more, 10 of 22 patients had flattened “diaphragmatic curves” during a thoracic ultrasound, which means the diaphragm doesn’t move as well as it should during breathing, and abnormal breathing. In another assessment, 10 of 16 patients had lower maximum inspiration pressures, suggesting a weakness in breathing muscles.

Eating and digestion were also impaired in some patients, with 13 reporting trouble with swallowing. During a gastric and bowel function assessment, eight patients couldn’t move food from the esophagus to the stomach as well as they should, while nine patients had acid reflux. Three patients had a hiatal hernia, which happens when the upper part of the stomach bulges through the diaphragm into the chest cavity.

The voices of some patients changed as well. Eight patients had an abnormal voice handicap index 30 test, which is a standard way to measure voice function. Among those, seven patients had dysphonia, or persistent voice problems.

The study is ongoing, and the research team is continuing to recruit patients to study the links between long COVID and the vagus nerve. The full paper isn’t yet available, and the research hasn’t yet been peer reviewed.

“The study appears to add to a growing collection of data suggesting at least some of the symptoms of long COVID is mediated through a direct impact on the nervous system,” David Strain, MD, a clinical senior lecturer at the University of Exeter (England), told the Science Media Centre.

“Establishing vagal nerve damage is useful information, as there are recognized, albeit not perfect, treatments for other causes of vagal nerve dysfunction that may be extrapolated to be beneficial for people with this type of long COVID,” he said.

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

Several long COVID symptoms could be linked to the effects of the coronavirus on a vital central nerve, according to new research being released in the spring.

The vagus nerve, which runs from the brain into the body, connects to the heart, lungs, intestines, and several muscles involved with swallowing. It plays a role in several body functions that control heart rate, speech, the gag reflex, sweating, and digestion.

Those with long COVID and vagus nerve problems could face long-term issues with their voice, a hard time swallowing, dizziness, a high heart rate, low blood pressure, and diarrhea, the study authors found.

Their findings will be presented at the 2022 European Congress of Clinical Microbiology and Infectious Diseases in late April.

“Most long COVID subjects with vagus nerve dysfunction symptoms had a range of significant, clinically relevant, structural and/or functional alterations in their vagus nerve, including nerve thickening, trouble swallowing, and symptoms of impaired breathing,” the study authors wrote. “Our findings so far thus point at vagus nerve dysfunction as a central pathophysiological feature of long COVID.”

Researchers from the University Hospital Germans Trias i Pujol in Barcelona performed a study to look at vagus nerve functioning in long COVID patients. Among 348 patients, about 66% had at least one symptom that suggested vagus nerve dysfunction. The researchers did a broad evaluation with imaging and functional tests for 22 patients in the university’s Long COVID Clinic from March to June 2021.

Of the 22 patients, 20 were women, and the median age was 44. The most frequent symptoms related to vagus nerve dysfunction were diarrhea (73%), high heart rates (59%), dizziness (45%), swallowing problems (45%), voice problems (45%), and low blood pressure (14%).

Almost all (19 of 22 patients) had three or more symptoms related to vagus nerve dysfunction. The average length of symptoms was 14 months.

Of 22 patients, 6 had a change in the vagus nerve in the neck, which the researchers observed by ultrasound. They had a thickening of the vagus nerve and increased “echogenicity,” which suggests inflammation.

What’s more, 10 of 22 patients had flattened “diaphragmatic curves” during a thoracic ultrasound, which means the diaphragm doesn’t move as well as it should during breathing, and abnormal breathing. In another assessment, 10 of 16 patients had lower maximum inspiration pressures, suggesting a weakness in breathing muscles.

Eating and digestion were also impaired in some patients, with 13 reporting trouble with swallowing. During a gastric and bowel function assessment, eight patients couldn’t move food from the esophagus to the stomach as well as they should, while nine patients had acid reflux. Three patients had a hiatal hernia, which happens when the upper part of the stomach bulges through the diaphragm into the chest cavity.

The voices of some patients changed as well. Eight patients had an abnormal voice handicap index 30 test, which is a standard way to measure voice function. Among those, seven patients had dysphonia, or persistent voice problems.

The study is ongoing, and the research team is continuing to recruit patients to study the links between long COVID and the vagus nerve. The full paper isn’t yet available, and the research hasn’t yet been peer reviewed.

“The study appears to add to a growing collection of data suggesting at least some of the symptoms of long COVID is mediated through a direct impact on the nervous system,” David Strain, MD, a clinical senior lecturer at the University of Exeter (England), told the Science Media Centre.

“Establishing vagal nerve damage is useful information, as there are recognized, albeit not perfect, treatments for other causes of vagal nerve dysfunction that may be extrapolated to be beneficial for people with this type of long COVID,” he said.

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

Several long COVID symptoms could be linked to the effects of the coronavirus on a vital central nerve, according to new research being released in the spring.

The vagus nerve, which runs from the brain into the body, connects to the heart, lungs, intestines, and several muscles involved with swallowing. It plays a role in several body functions that control heart rate, speech, the gag reflex, sweating, and digestion.

Those with long COVID and vagus nerve problems could face long-term issues with their voice, a hard time swallowing, dizziness, a high heart rate, low blood pressure, and diarrhea, the study authors found.

Their findings will be presented at the 2022 European Congress of Clinical Microbiology and Infectious Diseases in late April.

“Most long COVID subjects with vagus nerve dysfunction symptoms had a range of significant, clinically relevant, structural and/or functional alterations in their vagus nerve, including nerve thickening, trouble swallowing, and symptoms of impaired breathing,” the study authors wrote. “Our findings so far thus point at vagus nerve dysfunction as a central pathophysiological feature of long COVID.”

Researchers from the University Hospital Germans Trias i Pujol in Barcelona performed a study to look at vagus nerve functioning in long COVID patients. Among 348 patients, about 66% had at least one symptom that suggested vagus nerve dysfunction. The researchers did a broad evaluation with imaging and functional tests for 22 patients in the university’s Long COVID Clinic from March to June 2021.

Of the 22 patients, 20 were women, and the median age was 44. The most frequent symptoms related to vagus nerve dysfunction were diarrhea (73%), high heart rates (59%), dizziness (45%), swallowing problems (45%), voice problems (45%), and low blood pressure (14%).

Almost all (19 of 22 patients) had three or more symptoms related to vagus nerve dysfunction. The average length of symptoms was 14 months.

Of 22 patients, 6 had a change in the vagus nerve in the neck, which the researchers observed by ultrasound. They had a thickening of the vagus nerve and increased “echogenicity,” which suggests inflammation.

What’s more, 10 of 22 patients had flattened “diaphragmatic curves” during a thoracic ultrasound, which means the diaphragm doesn’t move as well as it should during breathing, and abnormal breathing. In another assessment, 10 of 16 patients had lower maximum inspiration pressures, suggesting a weakness in breathing muscles.

Eating and digestion were also impaired in some patients, with 13 reporting trouble with swallowing. During a gastric and bowel function assessment, eight patients couldn’t move food from the esophagus to the stomach as well as they should, while nine patients had acid reflux. Three patients had a hiatal hernia, which happens when the upper part of the stomach bulges through the diaphragm into the chest cavity.

The voices of some patients changed as well. Eight patients had an abnormal voice handicap index 30 test, which is a standard way to measure voice function. Among those, seven patients had dysphonia, or persistent voice problems.

The study is ongoing, and the research team is continuing to recruit patients to study the links between long COVID and the vagus nerve. The full paper isn’t yet available, and the research hasn’t yet been peer reviewed.

“The study appears to add to a growing collection of data suggesting at least some of the symptoms of long COVID is mediated through a direct impact on the nervous system,” David Strain, MD, a clinical senior lecturer at the University of Exeter (England), told the Science Media Centre.

“Establishing vagal nerve damage is useful information, as there are recognized, albeit not perfect, treatments for other causes of vagal nerve dysfunction that may be extrapolated to be beneficial for people with this type of long COVID,” he said.

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

Contrary to conventional clinical wisdom, greater body fat is associated with lower bone mineral density (BMD), particularly in men, an analysis of data from a large, nationally representative sample has found.  

Much previous research has suggested that obesity protects against fractures and loss of BMD for a variety of reasons, including the beneficial effects of weight-bearing on the skeleton and hormonal factors linked to body fat. But the new findings should prompt a reconsideration of the relationship between obesity and fracture risk, according to the investigators, whose study appears in the Journal of Clinical Endocrinology & Metabolism.

“While higher BMI [body mass index] is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, of the University of Chicago said in an interview.

Dr. Jain and a colleague, Tamara Vokes, MD, used multivariant modeling to examine the relationship between BMD and body composition of 10,814 men and women aged 20-59 years from the National Health and Nutrition Examination Survey (NHANES) 2011-2018. All underwent total body dual-energy x-ray absorptiometry scans.

Participants were stratified into sex-specific quartiles based on lean mass index (LMI; lean mass divided by height squared) and fat mass index (FMI; fat mass divided by height squared). Lean mass had a strong positive association with bone density, whereas fat mass had a moderate negative effect, the researchers found.

An additional kg/m² of FMI was associated with a 0.10 lower T score, the number of standard deviations from the expected bone density of a young adult (P < .001). The negative effect was greater in men, who had a 0.13 lower T score per additional 1 kg/m² of FMI, compared with 0.08 lower in women (P < .001). The effect was most pronounced in people in the highest FMI quartile.

Body composition is not a routine clinical measurement, Dr. Jain and Dr. Vokes noted. Prior studies of the effect of body composition on bone density have been limited by small patient numbers, referral bias, lack of racial or ethnic diversity, and the use of estimates rather than true measures of fat and lean tissue. NHANES is designed to mirror the U.S. population.

The researchers say when it comes to patients with obesity, the findings “should not dissuade clinicians from assessing bone density, particularly if other risk factors are present.”
 

Useful clinical proxies for body composition

Clinicians have no routine way to measure body composition in an office setting. As a result, Dr. Jain advised clinicians to look at factors that correlate with high body fat, such as the presence of diabetes, or with low lean mass, such as poor performance on physical activity measures like grip strength, when deciding whether to consider osteoporosis screening. Patients with obesity should undergo recommended bone density screening, especially if they have other risk factors such as older age, previous fracture, steroid use, or a family history of fracture.

Although some extra weight may have a beneficial loading effect, too much extra weight can lead to metabolic problems and restrict movement, according to Rodrigo J. Valderrábano, MD, medical director of clinical research for the Research Program in Men’s Health: Aging and Metabolism, Brigham and Women’s Hospital in Boston. “There’s a general sense that the extra weight is only good for your bones if you can carry it around,” said Dr. Valderrábano, who was not involved in the study.

More research is needed to understand why fat affects men and women differently, Dr. Jain noted. The researchers found that testosterone and estradiol values did not fully explain the variation.

Adipokines released by fat cells may be important in driving bone loss but were not measured in the study, Peter R. Ebeling, MD, president of the American Society of Bone and Mineral Research, said in an interview. Distribution of fractures in obesity suggests that a high FMI may preferentially affect cortical bone instead of trabecular bone, but further studies using high-resolution peripheral quantitative CT are required to confirm the difference.

Dr. Ebeling, who was not involved in the new study, agreed that the positive relationship between BMI and BMD has led to false reassurance that people with obesity may be protected from fragility fractures. “The take-home message for clinicians is that we should not neglect bone health in our patients with obesity, both male and female.”

Dr. Jain has reported receiving grant support from the Amgen Foundation and being a consultant for Radius Health. Dr. Vokes has reported being an investigator, consultant, and speaker for Radius Health, investigator and consultant for Takeda Pharmaceutical, and investigator for Ascendis Pharma. Dr. Valderrábano and Dr. Ebeling reported no relevant financial relationships.

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

Contrary to conventional clinical wisdom, greater body fat is associated with lower bone mineral density (BMD), particularly in men, an analysis of data from a large, nationally representative sample has found.  

Much previous research has suggested that obesity protects against fractures and loss of BMD for a variety of reasons, including the beneficial effects of weight-bearing on the skeleton and hormonal factors linked to body fat. But the new findings should prompt a reconsideration of the relationship between obesity and fracture risk, according to the investigators, whose study appears in the Journal of Clinical Endocrinology & Metabolism.

“While higher BMI [body mass index] is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, of the University of Chicago said in an interview.

Dr. Jain and a colleague, Tamara Vokes, MD, used multivariant modeling to examine the relationship between BMD and body composition of 10,814 men and women aged 20-59 years from the National Health and Nutrition Examination Survey (NHANES) 2011-2018. All underwent total body dual-energy x-ray absorptiometry scans.

Participants were stratified into sex-specific quartiles based on lean mass index (LMI; lean mass divided by height squared) and fat mass index (FMI; fat mass divided by height squared). Lean mass had a strong positive association with bone density, whereas fat mass had a moderate negative effect, the researchers found.

An additional kg/m² of FMI was associated with a 0.10 lower T score, the number of standard deviations from the expected bone density of a young adult (P < .001). The negative effect was greater in men, who had a 0.13 lower T score per additional 1 kg/m² of FMI, compared with 0.08 lower in women (P < .001). The effect was most pronounced in people in the highest FMI quartile.

Body composition is not a routine clinical measurement, Dr. Jain and Dr. Vokes noted. Prior studies of the effect of body composition on bone density have been limited by small patient numbers, referral bias, lack of racial or ethnic diversity, and the use of estimates rather than true measures of fat and lean tissue. NHANES is designed to mirror the U.S. population.

The researchers say when it comes to patients with obesity, the findings “should not dissuade clinicians from assessing bone density, particularly if other risk factors are present.”
 

Useful clinical proxies for body composition

Clinicians have no routine way to measure body composition in an office setting. As a result, Dr. Jain advised clinicians to look at factors that correlate with high body fat, such as the presence of diabetes, or with low lean mass, such as poor performance on physical activity measures like grip strength, when deciding whether to consider osteoporosis screening. Patients with obesity should undergo recommended bone density screening, especially if they have other risk factors such as older age, previous fracture, steroid use, or a family history of fracture.

Although some extra weight may have a beneficial loading effect, too much extra weight can lead to metabolic problems and restrict movement, according to Rodrigo J. Valderrábano, MD, medical director of clinical research for the Research Program in Men’s Health: Aging and Metabolism, Brigham and Women’s Hospital in Boston. “There’s a general sense that the extra weight is only good for your bones if you can carry it around,” said Dr. Valderrábano, who was not involved in the study.

More research is needed to understand why fat affects men and women differently, Dr. Jain noted. The researchers found that testosterone and estradiol values did not fully explain the variation.

Adipokines released by fat cells may be important in driving bone loss but were not measured in the study, Peter R. Ebeling, MD, president of the American Society of Bone and Mineral Research, said in an interview. Distribution of fractures in obesity suggests that a high FMI may preferentially affect cortical bone instead of trabecular bone, but further studies using high-resolution peripheral quantitative CT are required to confirm the difference.

Dr. Ebeling, who was not involved in the new study, agreed that the positive relationship between BMI and BMD has led to false reassurance that people with obesity may be protected from fragility fractures. “The take-home message for clinicians is that we should not neglect bone health in our patients with obesity, both male and female.”

Dr. Jain has reported receiving grant support from the Amgen Foundation and being a consultant for Radius Health. Dr. Vokes has reported being an investigator, consultant, and speaker for Radius Health, investigator and consultant for Takeda Pharmaceutical, and investigator for Ascendis Pharma. Dr. Valderrábano and Dr. Ebeling reported no relevant financial relationships.

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

Contrary to conventional clinical wisdom, greater body fat is associated with lower bone mineral density (BMD), particularly in men, an analysis of data from a large, nationally representative sample has found.  

Much previous research has suggested that obesity protects against fractures and loss of BMD for a variety of reasons, including the beneficial effects of weight-bearing on the skeleton and hormonal factors linked to body fat. But the new findings should prompt a reconsideration of the relationship between obesity and fracture risk, according to the investigators, whose study appears in the Journal of Clinical Endocrinology & Metabolism.

“While higher BMI [body mass index] is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, of the University of Chicago said in an interview.

Dr. Jain and a colleague, Tamara Vokes, MD, used multivariant modeling to examine the relationship between BMD and body composition of 10,814 men and women aged 20-59 years from the National Health and Nutrition Examination Survey (NHANES) 2011-2018. All underwent total body dual-energy x-ray absorptiometry scans.

Participants were stratified into sex-specific quartiles based on lean mass index (LMI; lean mass divided by height squared) and fat mass index (FMI; fat mass divided by height squared). Lean mass had a strong positive association with bone density, whereas fat mass had a moderate negative effect, the researchers found.

An additional kg/m² of FMI was associated with a 0.10 lower T score, the number of standard deviations from the expected bone density of a young adult (P < .001). The negative effect was greater in men, who had a 0.13 lower T score per additional 1 kg/m² of FMI, compared with 0.08 lower in women (P < .001). The effect was most pronounced in people in the highest FMI quartile.

Body composition is not a routine clinical measurement, Dr. Jain and Dr. Vokes noted. Prior studies of the effect of body composition on bone density have been limited by small patient numbers, referral bias, lack of racial or ethnic diversity, and the use of estimates rather than true measures of fat and lean tissue. NHANES is designed to mirror the U.S. population.

The researchers say when it comes to patients with obesity, the findings “should not dissuade clinicians from assessing bone density, particularly if other risk factors are present.”
 

Useful clinical proxies for body composition

Clinicians have no routine way to measure body composition in an office setting. As a result, Dr. Jain advised clinicians to look at factors that correlate with high body fat, such as the presence of diabetes, or with low lean mass, such as poor performance on physical activity measures like grip strength, when deciding whether to consider osteoporosis screening. Patients with obesity should undergo recommended bone density screening, especially if they have other risk factors such as older age, previous fracture, steroid use, or a family history of fracture.

Although some extra weight may have a beneficial loading effect, too much extra weight can lead to metabolic problems and restrict movement, according to Rodrigo J. Valderrábano, MD, medical director of clinical research for the Research Program in Men’s Health: Aging and Metabolism, Brigham and Women’s Hospital in Boston. “There’s a general sense that the extra weight is only good for your bones if you can carry it around,” said Dr. Valderrábano, who was not involved in the study.

More research is needed to understand why fat affects men and women differently, Dr. Jain noted. The researchers found that testosterone and estradiol values did not fully explain the variation.

Adipokines released by fat cells may be important in driving bone loss but were not measured in the study, Peter R. Ebeling, MD, president of the American Society of Bone and Mineral Research, said in an interview. Distribution of fractures in obesity suggests that a high FMI may preferentially affect cortical bone instead of trabecular bone, but further studies using high-resolution peripheral quantitative CT are required to confirm the difference.

Dr. Ebeling, who was not involved in the new study, agreed that the positive relationship between BMI and BMD has led to false reassurance that people with obesity may be protected from fragility fractures. “The take-home message for clinicians is that we should not neglect bone health in our patients with obesity, both male and female.”

Dr. Jain has reported receiving grant support from the Amgen Foundation and being a consultant for Radius Health. Dr. Vokes has reported being an investigator, consultant, and speaker for Radius Health, investigator and consultant for Takeda Pharmaceutical, and investigator for Ascendis Pharma. Dr. Valderrábano and Dr. Ebeling reported no relevant financial relationships.

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

Sepsis is an alarmingly common cause behind ICU admissions in patients with multiple sclerosis (MS), a retrospective, population-based cohort study indicates.

Furthermore, it contributes to a disproportionately high percentage of the short-term mortality risk among patients with MS admitted to the ICU, findings also show. Short-term mortality risk was defined in the study as a combination of in-hospital death or discharge to hospice.

“We found that the risk of short-term mortality in critically ill patients with MS is four times higher among those with sepsis ... so sepsis appears to be comparatively more lethal among patients with MS than in the general population,” Lavi Oud, MD, professor of medicine, Texas Tech University HSC at the Permian Basin, Odessa, said in an email.

“[Although] the specific mechanisms underlying the markedly higher risk of sepsis among patients with MS compared to the general population remain to be fully elucidated ... it’s thought that the risk may stem from the dysfunction of the immune system in these patients related to MS itself and to the potentially adverse effect of the immunomodulating therapy we use in these patients,” he added.

The study was published online Jan. 11 in the Journal of Critical Care.
 

Sepsis rates

The Texas Inpatient Public Use Data File was used to identify adults with a diagnosis of MS admitted to the hospital between 2010 and 2017. Among the 19,837 patients with MS admitted to the ICU during the study interval, almost one-third (31.5%) had sepsis, investigators report. “The rate of sepsis among ICU admissions increased with age, ranging from 20.8% among those aged 18-44 to 39.4% among those aged 65 years or older,” investigators note.

The most common site of infection among MS patients admitted to the ICU were urinary in nature (65.2%), followed by respiratory (36.1%). A smaller proportion of infections (7.6%) involved the skin and soft tissues, researchers note. A full one-quarter of patients developed septic shock in response to their infection while the length of stay among patients with sepsis (mean of 10.9 days) was substantially longer than it was for those without sepsis (mean of 5.6 days), they observe.

At a mean total hospital cost of $121,797 for each ICU patient with sepsis, the cost of caring for each patient was nearly twofold higher than the mean total cost of taking care of ICU patients without sepsis (mean total cost, $65,179). On adjusted analysis, sepsis was associated with a 42.7% (95% confidence interval, 38.9-46.5; P < .0001) longer length of hospital stay and a 26.2% (95% CI, 23.1-29.1; P < .0001) higher total hospital cost compared with patients without sepsis, the authors point out.

Indeed, ICU admissions with sepsis accounted for 47.3% of all hospital days and for 46.1% of the aggregate hospital charges among all MS patients admitted to the ICU.

“The adjusted probability of short-term mortality was 13.4% (95% CI, 13.0-13.7) among ICU admissions with sepsis and 3.3% (95% CI, 3.2-3.4) among ICU admissions without sepsis,” the authors report.

This translated into a 44% higher risk of short-term mortality at an adjusted odds ratio of 1.44 (95% CI, 1.23-1.69; P < .0001) for those with sepsis, compared with those without, they add. Among all ICU admissions, sepsis was reported in over two-thirds of documented short-term mortality events. The risk of short-term mortality was also almost threefold higher among patients with sepsis who were age 65 years and older compared with patients aged 18-44. 

As Dr. Oud noted, there is no specific test for sepsis, and it can initially present in an atypical manner, especially in older, frailer, chronically ill patients as well as in patients with immune dysfunction. “Thus, considering sepsis as a possible cause of new deterioration in a patient’s condition is essential, along with the timely start of sepsis-related care,” Dr. Oud observed.

A limitation of the study was that the dataset did not include information on the type of MS a patient had, the duration of their illness, the treatment received, the level of disease activity, or the level of disability.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

Sepsis is an alarmingly common cause behind ICU admissions in patients with multiple sclerosis (MS), a retrospective, population-based cohort study indicates.

Furthermore, it contributes to a disproportionately high percentage of the short-term mortality risk among patients with MS admitted to the ICU, findings also show. Short-term mortality risk was defined in the study as a combination of in-hospital death or discharge to hospice.

“We found that the risk of short-term mortality in critically ill patients with MS is four times higher among those with sepsis ... so sepsis appears to be comparatively more lethal among patients with MS than in the general population,” Lavi Oud, MD, professor of medicine, Texas Tech University HSC at the Permian Basin, Odessa, said in an email.

“[Although] the specific mechanisms underlying the markedly higher risk of sepsis among patients with MS compared to the general population remain to be fully elucidated ... it’s thought that the risk may stem from the dysfunction of the immune system in these patients related to MS itself and to the potentially adverse effect of the immunomodulating therapy we use in these patients,” he added.

The study was published online Jan. 11 in the Journal of Critical Care.
 

Sepsis rates

The Texas Inpatient Public Use Data File was used to identify adults with a diagnosis of MS admitted to the hospital between 2010 and 2017. Among the 19,837 patients with MS admitted to the ICU during the study interval, almost one-third (31.5%) had sepsis, investigators report. “The rate of sepsis among ICU admissions increased with age, ranging from 20.8% among those aged 18-44 to 39.4% among those aged 65 years or older,” investigators note.

The most common site of infection among MS patients admitted to the ICU were urinary in nature (65.2%), followed by respiratory (36.1%). A smaller proportion of infections (7.6%) involved the skin and soft tissues, researchers note. A full one-quarter of patients developed septic shock in response to their infection while the length of stay among patients with sepsis (mean of 10.9 days) was substantially longer than it was for those without sepsis (mean of 5.6 days), they observe.

At a mean total hospital cost of $121,797 for each ICU patient with sepsis, the cost of caring for each patient was nearly twofold higher than the mean total cost of taking care of ICU patients without sepsis (mean total cost, $65,179). On adjusted analysis, sepsis was associated with a 42.7% (95% confidence interval, 38.9-46.5; P < .0001) longer length of hospital stay and a 26.2% (95% CI, 23.1-29.1; P < .0001) higher total hospital cost compared with patients without sepsis, the authors point out.

Indeed, ICU admissions with sepsis accounted for 47.3% of all hospital days and for 46.1% of the aggregate hospital charges among all MS patients admitted to the ICU.

“The adjusted probability of short-term mortality was 13.4% (95% CI, 13.0-13.7) among ICU admissions with sepsis and 3.3% (95% CI, 3.2-3.4) among ICU admissions without sepsis,” the authors report.

This translated into a 44% higher risk of short-term mortality at an adjusted odds ratio of 1.44 (95% CI, 1.23-1.69; P < .0001) for those with sepsis, compared with those without, they add. Among all ICU admissions, sepsis was reported in over two-thirds of documented short-term mortality events. The risk of short-term mortality was also almost threefold higher among patients with sepsis who were age 65 years and older compared with patients aged 18-44. 

As Dr. Oud noted, there is no specific test for sepsis, and it can initially present in an atypical manner, especially in older, frailer, chronically ill patients as well as in patients with immune dysfunction. “Thus, considering sepsis as a possible cause of new deterioration in a patient’s condition is essential, along with the timely start of sepsis-related care,” Dr. Oud observed.

A limitation of the study was that the dataset did not include information on the type of MS a patient had, the duration of their illness, the treatment received, the level of disease activity, or the level of disability.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

Sepsis is an alarmingly common cause behind ICU admissions in patients with multiple sclerosis (MS), a retrospective, population-based cohort study indicates.

Furthermore, it contributes to a disproportionately high percentage of the short-term mortality risk among patients with MS admitted to the ICU, findings also show. Short-term mortality risk was defined in the study as a combination of in-hospital death or discharge to hospice.

“We found that the risk of short-term mortality in critically ill patients with MS is four times higher among those with sepsis ... so sepsis appears to be comparatively more lethal among patients with MS than in the general population,” Lavi Oud, MD, professor of medicine, Texas Tech University HSC at the Permian Basin, Odessa, said in an email.

“[Although] the specific mechanisms underlying the markedly higher risk of sepsis among patients with MS compared to the general population remain to be fully elucidated ... it’s thought that the risk may stem from the dysfunction of the immune system in these patients related to MS itself and to the potentially adverse effect of the immunomodulating therapy we use in these patients,” he added.

The study was published online Jan. 11 in the Journal of Critical Care.
 

Sepsis rates

The Texas Inpatient Public Use Data File was used to identify adults with a diagnosis of MS admitted to the hospital between 2010 and 2017. Among the 19,837 patients with MS admitted to the ICU during the study interval, almost one-third (31.5%) had sepsis, investigators report. “The rate of sepsis among ICU admissions increased with age, ranging from 20.8% among those aged 18-44 to 39.4% among those aged 65 years or older,” investigators note.

The most common site of infection among MS patients admitted to the ICU were urinary in nature (65.2%), followed by respiratory (36.1%). A smaller proportion of infections (7.6%) involved the skin and soft tissues, researchers note. A full one-quarter of patients developed septic shock in response to their infection while the length of stay among patients with sepsis (mean of 10.9 days) was substantially longer than it was for those without sepsis (mean of 5.6 days), they observe.

At a mean total hospital cost of $121,797 for each ICU patient with sepsis, the cost of caring for each patient was nearly twofold higher than the mean total cost of taking care of ICU patients without sepsis (mean total cost, $65,179). On adjusted analysis, sepsis was associated with a 42.7% (95% confidence interval, 38.9-46.5; P < .0001) longer length of hospital stay and a 26.2% (95% CI, 23.1-29.1; P < .0001) higher total hospital cost compared with patients without sepsis, the authors point out.

Indeed, ICU admissions with sepsis accounted for 47.3% of all hospital days and for 46.1% of the aggregate hospital charges among all MS patients admitted to the ICU.

“The adjusted probability of short-term mortality was 13.4% (95% CI, 13.0-13.7) among ICU admissions with sepsis and 3.3% (95% CI, 3.2-3.4) among ICU admissions without sepsis,” the authors report.

This translated into a 44% higher risk of short-term mortality at an adjusted odds ratio of 1.44 (95% CI, 1.23-1.69; P < .0001) for those with sepsis, compared with those without, they add. Among all ICU admissions, sepsis was reported in over two-thirds of documented short-term mortality events. The risk of short-term mortality was also almost threefold higher among patients with sepsis who were age 65 years and older compared with patients aged 18-44. 

As Dr. Oud noted, there is no specific test for sepsis, and it can initially present in an atypical manner, especially in older, frailer, chronically ill patients as well as in patients with immune dysfunction. “Thus, considering sepsis as a possible cause of new deterioration in a patient’s condition is essential, along with the timely start of sepsis-related care,” Dr. Oud observed.

A limitation of the study was that the dataset did not include information on the type of MS a patient had, the duration of their illness, the treatment received, the level of disease activity, or the level of disability.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

Researchers have developed a quick and easy scoring system to predict which hospitalized COVID-19 patients are more at risk for stroke.

“The system is simple. You can calculate the points in 5 seconds and then predict the chances the patient will have a stroke,” Alexander E. Merkler, MD, assistant professor of neurology at Weill Cornell Medical College/NewYork-Presbyterian Hospital, and lead author of a study of the system, told this news organization.

The new system will allow clinicians to stratify patients and lead to closer monitoring of those at highest risk for stroke, said Dr. Merkler.

The study was presented during the International Stroke Conference, presented by the American Stroke Association, a division of the American Heart Association.

Some, but not all, studies suggest COVID-19 increases the risk of stroke and worsens stroke outcomes, and the association isn’t clear, investigators note.

Researchers used the American Heart Association Get With the Guidelines COVID-19 cardiovascular disease registry for this analysis. They evaluated 21,420 adult patients (mean age 61 years, 54% men), who were hospitalized with COVID-19 at 122 centers from March 2020 to March 2021.

Investigators tapped into the vast amounts of data in this registry on different variables, including demographics, comorbidities, and lab values.

The outcome was a cerebrovascular event, defined as any ischemic or hemorrhagic stroke, transient ischemic attack (TIA), or cerebral vein thrombosis. Of the total hospitalized COVID-19 population, 312 (1.5%) had a cerebrovascular event.

Researchers first used standard statistical models to determine which risk factors are most associated with the development of stroke. They identified six such factors:

• history of stroke
• no fever at the time of hospital admission
• no history of pulmonary disease
• high white blood cell count
• history of hypertension
• high systolic blood pressure at the time of hospital admission

That the list of risk factors included absence of fever and no history of pulmonary disease was somewhat surprising, said Dr. Merkler, but there may be possible explanations, he added.

A high fever is an inflammatory response, and perhaps patients who aren’t responding appropriately “could be sicker in general and have a poor immune system, and thereby be at increased risk for stroke,” said Dr. Merkler.

In the case of pulmonary disease, patients without a history who are admitted for COVID “may have an extremely high burden of COVID, or are extremely sick, and that’s why they’re at higher risk for stroke.”

The scoring system assigns points for each variable, with more points conferring a higher risk of stroke. For example, someone who has 0-1 points has 0.2% risk of having a stroke, and someone with 4-6 points has 2% to 3% risk, said Dr. Merkler.

“So, we’re talking about a 10- to 15-fold increased risk of having a stroke with 4 to 6 versus 0 to 1 variables.”

The accuracy of the risk stratification score (C-statistic of 0.66; 95% confidence interval, 0.60-0.72) is “fairly good or modestly good,” said Dr. Merkler.

A patient with a score of 5 or 6 may need more vigilant monitoring to make sure symptoms are caught early and therapies such as thrombolytics and thrombectomy are readily available, he added.

Researchers also used a sophisticated machine-learning approach where a computer takes all the variables and identifies the best algorithm to predict stroke.

“The machine-learning algorithm was basically just as good as our standard model; it was almost identical,” said Dr. Merkler.

Outside of COVID, other scoring systems are used to predict stroke. For example, the ABCD2 score uses various factors to predict risk of recurrent stroke.

Philip B. Gorelick, MD, adjunct professor, Northwestern University Feinberg School of Medicine, Chicago, said the results are promising, as they may lead to identifying modifiable factors to prevent stroke.

Dr. Gorelick noted that the authors identified risk factors to predict risk of stroke “after an extensive analysis of baseline factors that included an internal validation process.”

The finding that no fever and no history of pulmonary disease were included in those risk factors was “unexpected,” said Dr. Gorelick, who is also medical director of the Hauenstein Neuroscience Center in Grand Rapids, Michigan. “This may reflect the baseline timing of data collection.”

He added further validation of the results in other data sets “will be useful to determine the consistency of the predictive model and its potential value in general practice.”

Louise D. McCullough, MD, PhD, professor and chair of neurology, McGovern Medical School, The University of Texas Health Science Center, Houston, said the association between stroke risk and COVID exposure “has been very unclear.”

“Some people find a very strong association between stroke and COVID, some do not,” said Dr. McCullough, who served as the chair of the ISC 2022 meeting.

This new study looking at a risk stratification model for COVID patients was “very nicely done,” she added.

“They used the American Heart Association Get With The Guidelines COVID registry, which was an amazing feat that was done very quickly by the AHA to establish COVID reporting in the Get With The Guidelines data, allowing us to really look at other factors related to stroke that are in this unique database.”

The study received funding support from the American Stroke Association. Dr. Merkler has received funding from the American Heart Association and the Leon Levy Foundation. Dr. Gorelick was not involved in the study and has disclosed no relevant financial relationships.

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

Researchers have developed a quick and easy scoring system to predict which hospitalized COVID-19 patients are more at risk for stroke.

“The system is simple. You can calculate the points in 5 seconds and then predict the chances the patient will have a stroke,” Alexander E. Merkler, MD, assistant professor of neurology at Weill Cornell Medical College/NewYork-Presbyterian Hospital, and lead author of a study of the system, told this news organization.

The new system will allow clinicians to stratify patients and lead to closer monitoring of those at highest risk for stroke, said Dr. Merkler.

The study was presented during the International Stroke Conference, presented by the American Stroke Association, a division of the American Heart Association.

Some, but not all, studies suggest COVID-19 increases the risk of stroke and worsens stroke outcomes, and the association isn’t clear, investigators note.

Researchers used the American Heart Association Get With the Guidelines COVID-19 cardiovascular disease registry for this analysis. They evaluated 21,420 adult patients (mean age 61 years, 54% men), who were hospitalized with COVID-19 at 122 centers from March 2020 to March 2021.

Investigators tapped into the vast amounts of data in this registry on different variables, including demographics, comorbidities, and lab values.

The outcome was a cerebrovascular event, defined as any ischemic or hemorrhagic stroke, transient ischemic attack (TIA), or cerebral vein thrombosis. Of the total hospitalized COVID-19 population, 312 (1.5%) had a cerebrovascular event.

Researchers first used standard statistical models to determine which risk factors are most associated with the development of stroke. They identified six such factors: