MDedge Rheumatology

Doctors or AI? Lukewarm vote of confidence goes to …

Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.

Alexandra_Koch/Pixabay

And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.

They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?

And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.

How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
 

Explaining the joke makes it funnier, right?

Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”

Amy/Pixabay

This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.

Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.

In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.

During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.

The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
 

Hot take: Humans aren’t that special

We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.

jacoblund/iStock/Getty Images

Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.

This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.

“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.

The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.

Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.

So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.

Doctors or AI? Lukewarm vote of confidence goes to …

Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.

Alexandra_Koch/Pixabay

And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.

They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?

And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.

How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
 

Explaining the joke makes it funnier, right?

Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”

Amy/Pixabay

This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.

Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.

In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.

During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.

The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
 

Hot take: Humans aren’t that special

We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.

jacoblund/iStock/Getty Images

Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.

This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.

“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.

The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.

Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.

So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.

Doctors or AI? Lukewarm vote of confidence goes to …

Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.

Alexandra_Koch/Pixabay

And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.

They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?

And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.

How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
 

Explaining the joke makes it funnier, right?

Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”

Amy/Pixabay

This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.

Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.

In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.

During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.

The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
 

Hot take: Humans aren’t that special

We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.

jacoblund/iStock/Getty Images

Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.

This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.

“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.

The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.

Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.

So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.

CLEVELAND – About half (52%) of patients living with both axial spondyloarthritis and inflammatory bowel disease (IBD) reached clinical remission of axSpA at 12 months after starting a tumor necrosis factor inhibitor (TNFi), researchers have found.

The disease course for axSpA among patients with IBD who start anti-TNF agents is not well understood.

Rahul S. Dalal, MD, an advanced fellow in IBD with the division of gastroenterology, hepatology, and endoscopy at Brigham and Women’s Hospital, Boston, and colleagues studied whether certain clinical factors were associated with remission of axSpA after patients with axSpA, who also had Crohn’s disease (CD) or ulcerative colitis (UC), started anti-TNF therapy.
 

Short IBD duration, adalimumab linked with higher remission odds

They found that those who had IBD for less than 5 years and those taking the TNFi adalimumab (Humira and biosimilars), as opposed to another TNFi, had a higher likelihood of reaching axSpA remission at 1 year. The odds ratios calculated for those factors were statistically significant.

Dr. Dalal said that most of the patients in the study (70%) were prescribed adalimumab, and because the study didn’t compare TNFis head to head, it’s hard to say whether adalimumab should be the preferred treatment for these patients.

“But it’s an interesting question that should be addressed in a bigger study,” he said.

Other TNFis included infliximab (Remicade and biosimilars) in 27%, golimumab (Simponi) in 2%, and certolizumab pegol (Cimzia) in 1%.

He presented the results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

Study details

Included in the retrospective cohort study were 82 adults with IBD and either ankylosing spondylitis or sacroiliitis who started anti-TNF agents approved for IBD between January 2012 and October 2021 at a large academic center.

Clinical remission of axSpA was the primary outcome, defined as the absence or adequate control of pain and/or stiffness related to axSpA as documented in the rheumatology note 1 year (+/– 2 months) after starting anti-TNF agents.

The secondary outcome was clinical remission of IBD, defined as 2 or less on the simple clinical colitis activity index, a score of less than 5 on the Harvey-Bradshaw Index, or provider assessment with no use of oral or intravenous glucocorticoids for 30 days. Dr. Dalal said 74% in the study reached that endpoint in the study period.

“Some patients had good response to anti-TNF treatments for their IBD but not necessarily for their spondyloarthritis,” he explained.

There were insufficient observations to calculate odds ratios for the variables, including Hispanic ethnicity, endoscopic inflammation, and prior history of using vedolizumab (Entyvio), secukinumab (Cosentyx), and ustekinumab (Stelara), the authors noted.

Dr. Dalal said it’s important to study this population because patients with IBD and axSpA take some of the same medications, but it’s not known how each medication acts in patients.

“We don’t have much data to tell us who’s going to respond to treatments from both diseases simultaneously,” he said.
 

Conclusions called ‘reassuring’

Jean Liew, MD, a spondyloarthritis specialist at Boston University, who was not part of the study, noted that the team reported univariate associations of clinical factors with achievement of clinical axSpA remission, but no multivariable analyses with adjustment for potential confounders.

She said the finding of half the patients achieving clinical remission is “reassuring, as anecdotally we may find that patients with IBD-associated spondyloarthritis tend to have more difficult-to-treat symptoms as well as more limited treatment options. For example, they cannot use [interleukin]-17 inhibitors.”

She noted the study is small and descriptive and further analyses are limited by the small number of patients.

“I think if a study of the same type could be performed at a larger scale with larger numbers, it could generate more data on which type of patient with IBD-associated spondyloarthritis is more likely to have a good response after starting a TNF inhibitor,” she said. “Of course, the other question is how long those patients would have good disease control while on the TNF inhibitor. What is the persistence of the medication? This study doesn’t ask or answer that question.”

Dr. Dalal added that in future research it will be important to look at response to medications beyond TNFis, especially Janus kinase inhibitors.

That will help show “whether there is a treatment algorithm that can be tailored to this population in terms of what agents to choose first,” he said. “I think we need multicenter studies to do this.”

Dr. Dalal has received grant funding from Pfizer and Janssen and has served as a consultant for Centaur Labs and Janssen. Dr. Liew has no relevant financial relationships.

CLEVELAND – About half (52%) of patients living with both axial spondyloarthritis and inflammatory bowel disease (IBD) reached clinical remission of axSpA at 12 months after starting a tumor necrosis factor inhibitor (TNFi), researchers have found.

The disease course for axSpA among patients with IBD who start anti-TNF agents is not well understood.

Rahul S. Dalal, MD, an advanced fellow in IBD with the division of gastroenterology, hepatology, and endoscopy at Brigham and Women’s Hospital, Boston, and colleagues studied whether certain clinical factors were associated with remission of axSpA after patients with axSpA, who also had Crohn’s disease (CD) or ulcerative colitis (UC), started anti-TNF therapy.
 

Short IBD duration, adalimumab linked with higher remission odds

They found that those who had IBD for less than 5 years and those taking the TNFi adalimumab (Humira and biosimilars), as opposed to another TNFi, had a higher likelihood of reaching axSpA remission at 1 year. The odds ratios calculated for those factors were statistically significant.

Dr. Dalal said that most of the patients in the study (70%) were prescribed adalimumab, and because the study didn’t compare TNFis head to head, it’s hard to say whether adalimumab should be the preferred treatment for these patients.

“But it’s an interesting question that should be addressed in a bigger study,” he said.

Other TNFis included infliximab (Remicade and biosimilars) in 27%, golimumab (Simponi) in 2%, and certolizumab pegol (Cimzia) in 1%.

He presented the results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

Study details

Included in the retrospective cohort study were 82 adults with IBD and either ankylosing spondylitis or sacroiliitis who started anti-TNF agents approved for IBD between January 2012 and October 2021 at a large academic center.

Clinical remission of axSpA was the primary outcome, defined as the absence or adequate control of pain and/or stiffness related to axSpA as documented in the rheumatology note 1 year (+/– 2 months) after starting anti-TNF agents.

The secondary outcome was clinical remission of IBD, defined as 2 or less on the simple clinical colitis activity index, a score of less than 5 on the Harvey-Bradshaw Index, or provider assessment with no use of oral or intravenous glucocorticoids for 30 days. Dr. Dalal said 74% in the study reached that endpoint in the study period.

“Some patients had good response to anti-TNF treatments for their IBD but not necessarily for their spondyloarthritis,” he explained.

There were insufficient observations to calculate odds ratios for the variables, including Hispanic ethnicity, endoscopic inflammation, and prior history of using vedolizumab (Entyvio), secukinumab (Cosentyx), and ustekinumab (Stelara), the authors noted.

Dr. Dalal said it’s important to study this population because patients with IBD and axSpA take some of the same medications, but it’s not known how each medication acts in patients.

“We don’t have much data to tell us who’s going to respond to treatments from both diseases simultaneously,” he said.
 

Conclusions called ‘reassuring’

Jean Liew, MD, a spondyloarthritis specialist at Boston University, who was not part of the study, noted that the team reported univariate associations of clinical factors with achievement of clinical axSpA remission, but no multivariable analyses with adjustment for potential confounders.

She said the finding of half the patients achieving clinical remission is “reassuring, as anecdotally we may find that patients with IBD-associated spondyloarthritis tend to have more difficult-to-treat symptoms as well as more limited treatment options. For example, they cannot use [interleukin]-17 inhibitors.”

She noted the study is small and descriptive and further analyses are limited by the small number of patients.

“I think if a study of the same type could be performed at a larger scale with larger numbers, it could generate more data on which type of patient with IBD-associated spondyloarthritis is more likely to have a good response after starting a TNF inhibitor,” she said. “Of course, the other question is how long those patients would have good disease control while on the TNF inhibitor. What is the persistence of the medication? This study doesn’t ask or answer that question.”

Dr. Dalal added that in future research it will be important to look at response to medications beyond TNFis, especially Janus kinase inhibitors.

That will help show “whether there is a treatment algorithm that can be tailored to this population in terms of what agents to choose first,” he said. “I think we need multicenter studies to do this.”

Dr. Dalal has received grant funding from Pfizer and Janssen and has served as a consultant for Centaur Labs and Janssen. Dr. Liew has no relevant financial relationships.

CLEVELAND – About half (52%) of patients living with both axial spondyloarthritis and inflammatory bowel disease (IBD) reached clinical remission of axSpA at 12 months after starting a tumor necrosis factor inhibitor (TNFi), researchers have found.

The disease course for axSpA among patients with IBD who start anti-TNF agents is not well understood.

Rahul S. Dalal, MD, an advanced fellow in IBD with the division of gastroenterology, hepatology, and endoscopy at Brigham and Women’s Hospital, Boston, and colleagues studied whether certain clinical factors were associated with remission of axSpA after patients with axSpA, who also had Crohn’s disease (CD) or ulcerative colitis (UC), started anti-TNF therapy.
 

Short IBD duration, adalimumab linked with higher remission odds

They found that those who had IBD for less than 5 years and those taking the TNFi adalimumab (Humira and biosimilars), as opposed to another TNFi, had a higher likelihood of reaching axSpA remission at 1 year. The odds ratios calculated for those factors were statistically significant.

Dr. Dalal said that most of the patients in the study (70%) were prescribed adalimumab, and because the study didn’t compare TNFis head to head, it’s hard to say whether adalimumab should be the preferred treatment for these patients.

“But it’s an interesting question that should be addressed in a bigger study,” he said.

Other TNFis included infliximab (Remicade and biosimilars) in 27%, golimumab (Simponi) in 2%, and certolizumab pegol (Cimzia) in 1%.

He presented the results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

Study details

Included in the retrospective cohort study were 82 adults with IBD and either ankylosing spondylitis or sacroiliitis who started anti-TNF agents approved for IBD between January 2012 and October 2021 at a large academic center.

Clinical remission of axSpA was the primary outcome, defined as the absence or adequate control of pain and/or stiffness related to axSpA as documented in the rheumatology note 1 year (+/– 2 months) after starting anti-TNF agents.

The secondary outcome was clinical remission of IBD, defined as 2 or less on the simple clinical colitis activity index, a score of less than 5 on the Harvey-Bradshaw Index, or provider assessment with no use of oral or intravenous glucocorticoids for 30 days. Dr. Dalal said 74% in the study reached that endpoint in the study period.

“Some patients had good response to anti-TNF treatments for their IBD but not necessarily for their spondyloarthritis,” he explained.

There were insufficient observations to calculate odds ratios for the variables, including Hispanic ethnicity, endoscopic inflammation, and prior history of using vedolizumab (Entyvio), secukinumab (Cosentyx), and ustekinumab (Stelara), the authors noted.

Dr. Dalal said it’s important to study this population because patients with IBD and axSpA take some of the same medications, but it’s not known how each medication acts in patients.

“We don’t have much data to tell us who’s going to respond to treatments from both diseases simultaneously,” he said.
 

Conclusions called ‘reassuring’

Jean Liew, MD, a spondyloarthritis specialist at Boston University, who was not part of the study, noted that the team reported univariate associations of clinical factors with achievement of clinical axSpA remission, but no multivariable analyses with adjustment for potential confounders.

She said the finding of half the patients achieving clinical remission is “reassuring, as anecdotally we may find that patients with IBD-associated spondyloarthritis tend to have more difficult-to-treat symptoms as well as more limited treatment options. For example, they cannot use [interleukin]-17 inhibitors.”

She noted the study is small and descriptive and further analyses are limited by the small number of patients.

“I think if a study of the same type could be performed at a larger scale with larger numbers, it could generate more data on which type of patient with IBD-associated spondyloarthritis is more likely to have a good response after starting a TNF inhibitor,” she said. “Of course, the other question is how long those patients would have good disease control while on the TNF inhibitor. What is the persistence of the medication? This study doesn’t ask or answer that question.”

Dr. Dalal added that in future research it will be important to look at response to medications beyond TNFis, especially Janus kinase inhibitors.

That will help show “whether there is a treatment algorithm that can be tailored to this population in terms of what agents to choose first,” he said. “I think we need multicenter studies to do this.”

Dr. Dalal has received grant funding from Pfizer and Janssen and has served as a consultant for Centaur Labs and Janssen. Dr. Liew has no relevant financial relationships.

The U.S. Food and Drug Administration has approved the biosimilar adalimumab-aaty (Yuflyma) in a citrate-free, high-concentration formulation, the manufacturer, Celltrion USA, announced today. It is the ninth biosimilar of adalimumab (Humira) to be approved in the United States.
 

Yuflyma is approved for the treatment of adult patients with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis, plaque psoriasis, and hidradenitis suppurativa. It is also approved for polyarticular juvenile idiopathic arthritis for patients aged 2 years or older, as well as for Crohn’s disease in adults and in pediatric patients aged 6 years or older.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The formulation was approved on the basis of a comprehensive data package of analytic, preclinical, and clinical studies, according to Celltrion USA, “demonstrating that Yuflyma is comparable to the reference product Humira in terms of efficacy, safety, pharmacokinetics, and immunogenicity up to 24 weeks and 1 year following treatment.”

The company conducted a double-blind, randomized phase 3 trial that compared switching from reference adalimumab to Yuflyma with continuing either reference adalimumab or Yuflyma for patients with active rheumatoid arthritis. In that trial, the efficacy, pharmacokinetics, safety, and immunogenicity of Yuflyma and reference adalimumab were comparable after 1 year of treatment, including after switching from reference adalimumab to Yuflyma.

“Currently, more than 80% of patients treated with Humira in the United States rely on a high-concentration and citrate-free formulation of this medication. The availability of a high-concentration and citrate-free formulation adalimumab biosimilar provides an important treatment option for patients with inflammatory diseases who benefit from this effective therapy,” said Jonathan Kay, MD, of the University of Massachusetts, Worcester, in the press release.

The citrate-free formulation is thought to lead to less pain on injection.

Yuflyma will be available in prefilled syringe and autoinjector administration options.

Celltrion USA plans to market the drug in the United States in July 2023. Following the initial launch of 40 mg/0.4 mL, the company plans to launch dose forms of 80 mg/0.8 mL and 20 mg/0.2 mL.

Celltrion USA is also seeking an interchangeability designation from the FDA following the completion of an interchangeability trial of 366 patients with chronic plaque psoriasis. The interchangeability designation would mean that patients successfully switched from Humira to Yuflyma multiple times in the trial. The interchangeability designation would allow pharmacists to autosubstitute Humira with Yuflyma. In these cases, individual state laws control how and whether physicians will be notified of this switch.

If interchangeability is approved for Yuflyma, which the company tentatively expects in the fourth quarter of 2024, it would be just the third interchangeable biosimilar approved by the FDA overall and the second adalimumab biosimilar to be designated as such, after adalimumab-adbm (Cyltezo) in October 2021.

Yuflyma was approved in Canada in December 2021 for 10 indications: rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, adult Crohn’s disease, adult ulcerative colitis, hidradenitis suppurativa, plaque psoriasis, adult uveitis, and pediatric uveitis.

In February 2022, the European Commission granted marketing authorization for Yuflyma across those 10 indications, as well as for nonradiographic axial spondyloarthritis, pediatric plaque psoriasis, and pediatric Crohn’s disease.

In April 2022, Celltrion USA signed a licensing agreement with AbbVie, the manufacturer of Humira. Under that agreement, Celltrion will pay royalties to AbbVie on sales of their individual biosimilars, and AbbVie agreed to drop all patent litigation.

The full prescribing information for Yuflyma is available here.

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

The U.S. Food and Drug Administration has approved the biosimilar adalimumab-aaty (Yuflyma) in a citrate-free, high-concentration formulation, the manufacturer, Celltrion USA, announced today. It is the ninth biosimilar of adalimumab (Humira) to be approved in the United States.
 

Yuflyma is approved for the treatment of adult patients with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis, plaque psoriasis, and hidradenitis suppurativa. It is also approved for polyarticular juvenile idiopathic arthritis for patients aged 2 years or older, as well as for Crohn’s disease in adults and in pediatric patients aged 6 years or older.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The formulation was approved on the basis of a comprehensive data package of analytic, preclinical, and clinical studies, according to Celltrion USA, “demonstrating that Yuflyma is comparable to the reference product Humira in terms of efficacy, safety, pharmacokinetics, and immunogenicity up to 24 weeks and 1 year following treatment.”

The company conducted a double-blind, randomized phase 3 trial that compared switching from reference adalimumab to Yuflyma with continuing either reference adalimumab or Yuflyma for patients with active rheumatoid arthritis. In that trial, the efficacy, pharmacokinetics, safety, and immunogenicity of Yuflyma and reference adalimumab were comparable after 1 year of treatment, including after switching from reference adalimumab to Yuflyma.

“Currently, more than 80% of patients treated with Humira in the United States rely on a high-concentration and citrate-free formulation of this medication. The availability of a high-concentration and citrate-free formulation adalimumab biosimilar provides an important treatment option for patients with inflammatory diseases who benefit from this effective therapy,” said Jonathan Kay, MD, of the University of Massachusetts, Worcester, in the press release.

The citrate-free formulation is thought to lead to less pain on injection.

Yuflyma will be available in prefilled syringe and autoinjector administration options.

Celltrion USA plans to market the drug in the United States in July 2023. Following the initial launch of 40 mg/0.4 mL, the company plans to launch dose forms of 80 mg/0.8 mL and 20 mg/0.2 mL.

Celltrion USA is also seeking an interchangeability designation from the FDA following the completion of an interchangeability trial of 366 patients with chronic plaque psoriasis. The interchangeability designation would mean that patients successfully switched from Humira to Yuflyma multiple times in the trial. The interchangeability designation would allow pharmacists to autosubstitute Humira with Yuflyma. In these cases, individual state laws control how and whether physicians will be notified of this switch.

If interchangeability is approved for Yuflyma, which the company tentatively expects in the fourth quarter of 2024, it would be just the third interchangeable biosimilar approved by the FDA overall and the second adalimumab biosimilar to be designated as such, after adalimumab-adbm (Cyltezo) in October 2021.

Yuflyma was approved in Canada in December 2021 for 10 indications: rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, adult Crohn’s disease, adult ulcerative colitis, hidradenitis suppurativa, plaque psoriasis, adult uveitis, and pediatric uveitis.

In February 2022, the European Commission granted marketing authorization for Yuflyma across those 10 indications, as well as for nonradiographic axial spondyloarthritis, pediatric plaque psoriasis, and pediatric Crohn’s disease.

In April 2022, Celltrion USA signed a licensing agreement with AbbVie, the manufacturer of Humira. Under that agreement, Celltrion will pay royalties to AbbVie on sales of their individual biosimilars, and AbbVie agreed to drop all patent litigation.

The full prescribing information for Yuflyma is available here.

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

The U.S. Food and Drug Administration has approved the biosimilar adalimumab-aaty (Yuflyma) in a citrate-free, high-concentration formulation, the manufacturer, Celltrion USA, announced today. It is the ninth biosimilar of adalimumab (Humira) to be approved in the United States.
 

Yuflyma is approved for the treatment of adult patients with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis, plaque psoriasis, and hidradenitis suppurativa. It is also approved for polyarticular juvenile idiopathic arthritis for patients aged 2 years or older, as well as for Crohn’s disease in adults and in pediatric patients aged 6 years or older.

Wikimedia Commons/FitzColinGerald/Creative Commons License

The formulation was approved on the basis of a comprehensive data package of analytic, preclinical, and clinical studies, according to Celltrion USA, “demonstrating that Yuflyma is comparable to the reference product Humira in terms of efficacy, safety, pharmacokinetics, and immunogenicity up to 24 weeks and 1 year following treatment.”

The company conducted a double-blind, randomized phase 3 trial that compared switching from reference adalimumab to Yuflyma with continuing either reference adalimumab or Yuflyma for patients with active rheumatoid arthritis. In that trial, the efficacy, pharmacokinetics, safety, and immunogenicity of Yuflyma and reference adalimumab were comparable after 1 year of treatment, including after switching from reference adalimumab to Yuflyma.

“Currently, more than 80% of patients treated with Humira in the United States rely on a high-concentration and citrate-free formulation of this medication. The availability of a high-concentration and citrate-free formulation adalimumab biosimilar provides an important treatment option for patients with inflammatory diseases who benefit from this effective therapy,” said Jonathan Kay, MD, of the University of Massachusetts, Worcester, in the press release.

The citrate-free formulation is thought to lead to less pain on injection.

Yuflyma will be available in prefilled syringe and autoinjector administration options.

Celltrion USA plans to market the drug in the United States in July 2023. Following the initial launch of 40 mg/0.4 mL, the company plans to launch dose forms of 80 mg/0.8 mL and 20 mg/0.2 mL.

Celltrion USA is also seeking an interchangeability designation from the FDA following the completion of an interchangeability trial of 366 patients with chronic plaque psoriasis. The interchangeability designation would mean that patients successfully switched from Humira to Yuflyma multiple times in the trial. The interchangeability designation would allow pharmacists to autosubstitute Humira with Yuflyma. In these cases, individual state laws control how and whether physicians will be notified of this switch.

If interchangeability is approved for Yuflyma, which the company tentatively expects in the fourth quarter of 2024, it would be just the third interchangeable biosimilar approved by the FDA overall and the second adalimumab biosimilar to be designated as such, after adalimumab-adbm (Cyltezo) in October 2021.

Yuflyma was approved in Canada in December 2021 for 10 indications: rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, adult Crohn’s disease, adult ulcerative colitis, hidradenitis suppurativa, plaque psoriasis, adult uveitis, and pediatric uveitis.

In February 2022, the European Commission granted marketing authorization for Yuflyma across those 10 indications, as well as for nonradiographic axial spondyloarthritis, pediatric plaque psoriasis, and pediatric Crohn’s disease.

In April 2022, Celltrion USA signed a licensing agreement with AbbVie, the manufacturer of Humira. Under that agreement, Celltrion will pay royalties to AbbVie on sales of their individual biosimilars, and AbbVie agreed to drop all patent litigation.

The full prescribing information for Yuflyma is available here.

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

A new prospective, observational study from the Lupus Research Alliance (LRA) aims to enroll 3,500 patients in an effort to accelerate the development of personalized treatments for individuals living with systemic lupus erythematosus (SLE).

The LRA on May 23 announced the launch of the Lupus Landmark Study (LLS). The study will be conducted in partnership with Lupus Therapeutics, the clinical research affiliate of the LRA.

The study will be a key feature of the Lupus Nexus, a unique combination of lupus patient registry, biorepository, and portal for data sharing and analysis.

“The aim of the Lupus Nexus is to transform lupus research and drug development through unprecedented information exchange capabilities,” according to the LRA press release.

“SLE is a debilitating autoimmune disease that disproportionately impacts women and people from minority groups, but the cause of lupus is unknown, and no single laboratory test can definitively identify lupus,” lead investigator S. Sam Lim, MD, of Emory University, Atlanta, told this news organization.

“Nevertheless, early detection and treatment can often lessen the progression and severity of the disease. Although there are numerous contributing factors to the lag in research discoveries and new treatments for patients with lupus, limited access to standardized, high-quality biological samples and natural history data provides a significant roadblock to advancing lupus research,” Dr. Lim said.

“Existing registry and biorepository resources in the lupus field are largely siloed, mostly limited to relatively small or discrete patient populations, and frequently not designed for broad sharing across all stakeholders of the research community,” Dr. Lim said. The LRA and its affiliate Lupus Therapeutics are committed to developing Lupus Nexus, a first-of-its-kind registry and biorepository, to serve as a collaborative research platform for lupus and a leading source of prospective, longitudinal patient data and biological samples for the research community, Dr. Lim added.

“The Lupus Landmark Study will form the foundation of this registry and biorepository and will provide a critical resource to enable the understanding of lupus heterogeneity at the molecular level,” Dr. Lim said. The molecular data can be linked to clinical phenotypes, he explained, “while providing an opportunity to better understand the holistic experience of patients with lupus, thus helping patients address the daily life challenges they face.”

The Lupus Accelerating Breakthroughs Consortium (Lupus ABC) was announced earlier this spring by the LRA. It represents a collaboration between the U.S. Food and Drug Administration and the lupus community to improve and accelerate the development of safer and more effective treatments for people with lupus, Dr. Lim said. “Data and other results from the LLS will inform this collaboration,” he said.

“The LLS will provide greater insight into the pathogenesis and evolution of the condition, providing much needed information and guidance to clinicians so that the disease can be detected and treated earlier and with better precision,” Dr. Lim said. “The partnership with patients will ensure that advances will not only be meaningful to clinicians but their patients and caregivers as well,” he added.

Individuals living with lupus were essential to the development of the Lupus Nexus, and patients will continue to be engaged through participation in the LLS, which will not only generate data to promote patient-centered treatments but will also give participants more insight into their health data, according to the LRA press release.

The clinical coordinating center and biorepository elements of the Lupus Nexus will be managed by Embleema and Azenta Life Sciences, respectively, according the LRA.

Biomarker analysis will be conducted by DxTerity Diagnostics via the company’s proprietary DxCollection MicroCollection Device and Modular Immune Profile platform.

The LLS is scheduled to begin enrolling patients through select academic medical centers in the Lupus Therapeutics Lupus Clinical Investigators Network later in 2023, with an expanded roll-out in 2024, according to the press release. More information about the Lupus Landmark Study is available from Lupus Nexus at [email protected].

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

A new prospective, observational study from the Lupus Research Alliance (LRA) aims to enroll 3,500 patients in an effort to accelerate the development of personalized treatments for individuals living with systemic lupus erythematosus (SLE).

The LRA on May 23 announced the launch of the Lupus Landmark Study (LLS). The study will be conducted in partnership with Lupus Therapeutics, the clinical research affiliate of the LRA.

The study will be a key feature of the Lupus Nexus, a unique combination of lupus patient registry, biorepository, and portal for data sharing and analysis.

“The aim of the Lupus Nexus is to transform lupus research and drug development through unprecedented information exchange capabilities,” according to the LRA press release.

“SLE is a debilitating autoimmune disease that disproportionately impacts women and people from minority groups, but the cause of lupus is unknown, and no single laboratory test can definitively identify lupus,” lead investigator S. Sam Lim, MD, of Emory University, Atlanta, told this news organization.

“Nevertheless, early detection and treatment can often lessen the progression and severity of the disease. Although there are numerous contributing factors to the lag in research discoveries and new treatments for patients with lupus, limited access to standardized, high-quality biological samples and natural history data provides a significant roadblock to advancing lupus research,” Dr. Lim said.

“Existing registry and biorepository resources in the lupus field are largely siloed, mostly limited to relatively small or discrete patient populations, and frequently not designed for broad sharing across all stakeholders of the research community,” Dr. Lim said. The LRA and its affiliate Lupus Therapeutics are committed to developing Lupus Nexus, a first-of-its-kind registry and biorepository, to serve as a collaborative research platform for lupus and a leading source of prospective, longitudinal patient data and biological samples for the research community, Dr. Lim added.

“The Lupus Landmark Study will form the foundation of this registry and biorepository and will provide a critical resource to enable the understanding of lupus heterogeneity at the molecular level,” Dr. Lim said. The molecular data can be linked to clinical phenotypes, he explained, “while providing an opportunity to better understand the holistic experience of patients with lupus, thus helping patients address the daily life challenges they face.”

The Lupus Accelerating Breakthroughs Consortium (Lupus ABC) was announced earlier this spring by the LRA. It represents a collaboration between the U.S. Food and Drug Administration and the lupus community to improve and accelerate the development of safer and more effective treatments for people with lupus, Dr. Lim said. “Data and other results from the LLS will inform this collaboration,” he said.

“The LLS will provide greater insight into the pathogenesis and evolution of the condition, providing much needed information and guidance to clinicians so that the disease can be detected and treated earlier and with better precision,” Dr. Lim said. “The partnership with patients will ensure that advances will not only be meaningful to clinicians but their patients and caregivers as well,” he added.

Individuals living with lupus were essential to the development of the Lupus Nexus, and patients will continue to be engaged through participation in the LLS, which will not only generate data to promote patient-centered treatments but will also give participants more insight into their health data, according to the LRA press release.

The clinical coordinating center and biorepository elements of the Lupus Nexus will be managed by Embleema and Azenta Life Sciences, respectively, according the LRA.

Biomarker analysis will be conducted by DxTerity Diagnostics via the company’s proprietary DxCollection MicroCollection Device and Modular Immune Profile platform.

The LLS is scheduled to begin enrolling patients through select academic medical centers in the Lupus Therapeutics Lupus Clinical Investigators Network later in 2023, with an expanded roll-out in 2024, according to the press release. More information about the Lupus Landmark Study is available from Lupus Nexus at [email protected].

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

A new prospective, observational study from the Lupus Research Alliance (LRA) aims to enroll 3,500 patients in an effort to accelerate the development of personalized treatments for individuals living with systemic lupus erythematosus (SLE).

The LRA on May 23 announced the launch of the Lupus Landmark Study (LLS). The study will be conducted in partnership with Lupus Therapeutics, the clinical research affiliate of the LRA.

The study will be a key feature of the Lupus Nexus, a unique combination of lupus patient registry, biorepository, and portal for data sharing and analysis.

“The aim of the Lupus Nexus is to transform lupus research and drug development through unprecedented information exchange capabilities,” according to the LRA press release.

“SLE is a debilitating autoimmune disease that disproportionately impacts women and people from minority groups, but the cause of lupus is unknown, and no single laboratory test can definitively identify lupus,” lead investigator S. Sam Lim, MD, of Emory University, Atlanta, told this news organization.

“Nevertheless, early detection and treatment can often lessen the progression and severity of the disease. Although there are numerous contributing factors to the lag in research discoveries and new treatments for patients with lupus, limited access to standardized, high-quality biological samples and natural history data provides a significant roadblock to advancing lupus research,” Dr. Lim said.

“Existing registry and biorepository resources in the lupus field are largely siloed, mostly limited to relatively small or discrete patient populations, and frequently not designed for broad sharing across all stakeholders of the research community,” Dr. Lim said. The LRA and its affiliate Lupus Therapeutics are committed to developing Lupus Nexus, a first-of-its-kind registry and biorepository, to serve as a collaborative research platform for lupus and a leading source of prospective, longitudinal patient data and biological samples for the research community, Dr. Lim added.

“The Lupus Landmark Study will form the foundation of this registry and biorepository and will provide a critical resource to enable the understanding of lupus heterogeneity at the molecular level,” Dr. Lim said. The molecular data can be linked to clinical phenotypes, he explained, “while providing an opportunity to better understand the holistic experience of patients with lupus, thus helping patients address the daily life challenges they face.”

The Lupus Accelerating Breakthroughs Consortium (Lupus ABC) was announced earlier this spring by the LRA. It represents a collaboration between the U.S. Food and Drug Administration and the lupus community to improve and accelerate the development of safer and more effective treatments for people with lupus, Dr. Lim said. “Data and other results from the LLS will inform this collaboration,” he said.

“The LLS will provide greater insight into the pathogenesis and evolution of the condition, providing much needed information and guidance to clinicians so that the disease can be detected and treated earlier and with better precision,” Dr. Lim said. “The partnership with patients will ensure that advances will not only be meaningful to clinicians but their patients and caregivers as well,” he added.

Individuals living with lupus were essential to the development of the Lupus Nexus, and patients will continue to be engaged through participation in the LLS, which will not only generate data to promote patient-centered treatments but will also give participants more insight into their health data, according to the LRA press release.

The clinical coordinating center and biorepository elements of the Lupus Nexus will be managed by Embleema and Azenta Life Sciences, respectively, according the LRA.

Biomarker analysis will be conducted by DxTerity Diagnostics via the company’s proprietary DxCollection MicroCollection Device and Modular Immune Profile platform.

The LLS is scheduled to begin enrolling patients through select academic medical centers in the Lupus Therapeutics Lupus Clinical Investigators Network later in 2023, with an expanded roll-out in 2024, according to the press release. More information about the Lupus Landmark Study is available from Lupus Nexus at [email protected].

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

The relationship between enthesitis and synovitis is of considerable interest to both clinicians and researchers. This relationship is best evaluated using imaging, particularly ultrasonography, and could provide pathophysiologic insights. Balulu and colleagues recruited 158 patients with PsA who underwent sonographic assessment of 52 joints, 40 tendons, and 14 entheses as well as clinical evaluation. Overall, total sonographic enthesitis scores were significantly associated with total sonographic synovitis and sonographic tenosynovitis scores and also with older age, male sex, swollen joint count, C-reactive protein, physical occupation, and patient-reported outcomes. The association between enthesitis and synovitis was also demonstrated at the elbows, knees, and ankles. This study demonstrates that psoriatic enthesitis and synovitis are closely related and thus may share pathophysiologic mechanisms. Longitudinal studies in very early PsA using ultrasound might provide clues to confirm the hypothesis that psoriatic synovitis is secondary to enthesitis.

Another important domain that is increasingly studied is axial PsA. Currently, the evidence for treatment of axial PsA is extrapolated from that for axial spondyloarthritis (SpA), in the belief that the two diseases are pathophysiologically similar. However, there is increasing evidence for differences between axial PsA and axial SpA that might influence the choice of treatment. In a recent study, de Hooge and colleagues demonstrated that patients with axial PsA have lower severity of damage to the spine compared with those with axial SpA. Using data from 312 patients with PsA and 213 patients with SpA who underwent radiographic imaging assessment in the Belgian Epidemiological Psoriatic Arthritis Study (BEPAS) and the Ghent and Belgian Inflammatory Arthritis and Spondylitis (Be-GIANT) study, respectively, they show that the proportion of patients with PsA vs SpA having spinal damage was comparable. Patients with SpA and spinal damage had higher modified Stoke Ankylosing Spondylitis Spine Scores, indicating more severe damage. These results are consistent with other published studies and indicate that patients with PsA have less severe spinal disease compared with other patients with axial SpA. Randomized controlled trials (RCTs) specifically investigating the treatment of axial PsA are currently underway. Nevertheless, post hoc analyses of data from PsA RCTs indicate that most drugs efficacious for PsA overall also provide benefit in axial disease.

In a recent report, Baraliakos and colleagues analyzed data from the SELECT-PsA 1 and SELECT-PsA 2 trials that evaluated the efficacy of upadacitinib in PsA. They show that, compared with placebo, 15 mg upadacitinib led to a greater improvement in axial symptoms. The improvement in overall Bath Ankylosing Spondylitis Disease Activity Index score at week 24 was significantly higher with 15 mg upadacitinib compared with placebo in both trials. However, these results are not definitive because there is yet no consensus on the definition of and outcome measures for axial PsA.

The relationship between enthesitis and synovitis is of considerable interest to both clinicians and researchers. This relationship is best evaluated using imaging, particularly ultrasonography, and could provide pathophysiologic insights. Balulu and colleagues recruited 158 patients with PsA who underwent sonographic assessment of 52 joints, 40 tendons, and 14 entheses as well as clinical evaluation. Overall, total sonographic enthesitis scores were significantly associated with total sonographic synovitis and sonographic tenosynovitis scores and also with older age, male sex, swollen joint count, C-reactive protein, physical occupation, and patient-reported outcomes. The association between enthesitis and synovitis was also demonstrated at the elbows, knees, and ankles. This study demonstrates that psoriatic enthesitis and synovitis are closely related and thus may share pathophysiologic mechanisms. Longitudinal studies in very early PsA using ultrasound might provide clues to confirm the hypothesis that psoriatic synovitis is secondary to enthesitis.

Another important domain that is increasingly studied is axial PsA. Currently, the evidence for treatment of axial PsA is extrapolated from that for axial spondyloarthritis (SpA), in the belief that the two diseases are pathophysiologically similar. However, there is increasing evidence for differences between axial PsA and axial SpA that might influence the choice of treatment. In a recent study, de Hooge and colleagues demonstrated that patients with axial PsA have lower severity of damage to the spine compared with those with axial SpA. Using data from 312 patients with PsA and 213 patients with SpA who underwent radiographic imaging assessment in the Belgian Epidemiological Psoriatic Arthritis Study (BEPAS) and the Ghent and Belgian Inflammatory Arthritis and Spondylitis (Be-GIANT) study, respectively, they show that the proportion of patients with PsA vs SpA having spinal damage was comparable. Patients with SpA and spinal damage had higher modified Stoke Ankylosing Spondylitis Spine Scores, indicating more severe damage. These results are consistent with other published studies and indicate that patients with PsA have less severe spinal disease compared with other patients with axial SpA. Randomized controlled trials (RCTs) specifically investigating the treatment of axial PsA are currently underway. Nevertheless, post hoc analyses of data from PsA RCTs indicate that most drugs efficacious for PsA overall also provide benefit in axial disease.

In a recent report, Baraliakos and colleagues analyzed data from the SELECT-PsA 1 and SELECT-PsA 2 trials that evaluated the efficacy of upadacitinib in PsA. They show that, compared with placebo, 15 mg upadacitinib led to a greater improvement in axial symptoms. The improvement in overall Bath Ankylosing Spondylitis Disease Activity Index score at week 24 was significantly higher with 15 mg upadacitinib compared with placebo in both trials. However, these results are not definitive because there is yet no consensus on the definition of and outcome measures for axial PsA.

The relationship between enthesitis and synovitis is of considerable interest to both clinicians and researchers. This relationship is best evaluated using imaging, particularly ultrasonography, and could provide pathophysiologic insights. Balulu and colleagues recruited 158 patients with PsA who underwent sonographic assessment of 52 joints, 40 tendons, and 14 entheses as well as clinical evaluation. Overall, total sonographic enthesitis scores were significantly associated with total sonographic synovitis and sonographic tenosynovitis scores and also with older age, male sex, swollen joint count, C-reactive protein, physical occupation, and patient-reported outcomes. The association between enthesitis and synovitis was also demonstrated at the elbows, knees, and ankles. This study demonstrates that psoriatic enthesitis and synovitis are closely related and thus may share pathophysiologic mechanisms. Longitudinal studies in very early PsA using ultrasound might provide clues to confirm the hypothesis that psoriatic synovitis is secondary to enthesitis.

Another important domain that is increasingly studied is axial PsA. Currently, the evidence for treatment of axial PsA is extrapolated from that for axial spondyloarthritis (SpA), in the belief that the two diseases are pathophysiologically similar. However, there is increasing evidence for differences between axial PsA and axial SpA that might influence the choice of treatment. In a recent study, de Hooge and colleagues demonstrated that patients with axial PsA have lower severity of damage to the spine compared with those with axial SpA. Using data from 312 patients with PsA and 213 patients with SpA who underwent radiographic imaging assessment in the Belgian Epidemiological Psoriatic Arthritis Study (BEPAS) and the Ghent and Belgian Inflammatory Arthritis and Spondylitis (Be-GIANT) study, respectively, they show that the proportion of patients with PsA vs SpA having spinal damage was comparable. Patients with SpA and spinal damage had higher modified Stoke Ankylosing Spondylitis Spine Scores, indicating more severe damage. These results are consistent with other published studies and indicate that patients with PsA have less severe spinal disease compared with other patients with axial SpA. Randomized controlled trials (RCTs) specifically investigating the treatment of axial PsA are currently underway. Nevertheless, post hoc analyses of data from PsA RCTs indicate that most drugs efficacious for PsA overall also provide benefit in axial disease.

In a recent report, Baraliakos and colleagues analyzed data from the SELECT-PsA 1 and SELECT-PsA 2 trials that evaluated the efficacy of upadacitinib in PsA. They show that, compared with placebo, 15 mg upadacitinib led to a greater improvement in axial symptoms. The improvement in overall Bath Ankylosing Spondylitis Disease Activity Index score at week 24 was significantly higher with 15 mg upadacitinib compared with placebo in both trials. However, these results are not definitive because there is yet no consensus on the definition of and outcome measures for axial PsA.

CLEVELAND – Documenting the prevalence of axial spondyloarthritis (axSpA) among Black Americans has been difficult because of little published data, but new research suggests that when Black Americans do have the disease, it seems to be more severe.

Iman Abutineh, MD, of the University of Tennessee, Memphis, discussed her team’s work at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

A total of 244 patients with axSpA were identified, including 168 (69%) males, 78 (32%) Black patients, and 143 (59%) White patients.

Average age of onset for patients overall was 27.7 years, and age at diagnosis was 36.1 years with a 7-year delay in diagnosis. Sixty-six (27%) patients had nonradiographic axSpA, 83% were on tumor necrosis factor inhibitors, and 38% were prescribed glucocorticoids.

The researchers found several differences by race.

White patients were more likely to be HLA-B27 positive (77% vs. 59%; P = .010). White patients also had higher prevalence of psoriasis, coronary artery disease, and family history of SpA. White females had a higher prevalence of inflammatory bowel disease, fibromyalgia, depression, and lower grades of sacroiliitis.
 

Black patients had more hip involvement

A higher percentage of Black patients had elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and hip involvement. In comparing hip involvement, the researchers found that 39 (39%) White males had hip involvement as did 9 (21%) White females. In comparison, 22 (45%) Black men in the study and 14 (54%) Black women showed hip involvement (P = .035).

After adjustment for age, sex, HLA-B27, and insurance status, Black patients had higher grades of sacroiliitis with an odds ratio of 2.32 (95% confidence interval, 1.23-4.44). Black patients had a numerically longer delay in diagnosis, compared with Whites (7.93 vs. 6.64 years), but this did not achieve statistical significance (P = .454), the researchers wrote.
 

Study addresses racial disparities

“Traditionally we think of axial spondyloarthritis largely in Caucasian males who are HLA-B27 positive,” Dr. Abutineh said, “and we found that there is still a significant portion of patients who don’t meet the criteria that do have disease that is very significant.”

Although actual prevalence was not clear from this study, Dr. Abutineh said their data suggest a 3-to-1 ratio of White-to-Black patients with spondyloarthritis, “but of the Black patients who are diagnosed, their disease is almost always more severe. That points to why it’s important to have a high index of suspicion for this disease in that patient population because if you miss it, it could be detrimental to the patients.”

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who was not part of the study, said in an interview, “It is an excellent and timely study addressing the racial disparities and inequities surrounding axSpA diagnosis. It highlights the delay in diagnosis and increased burden of disease among Black Americans.”

She said the study may prompt a further look into barriers to care for Black Americans and their beliefs regarding seeking health care for their pain.
 

Higher rates of nonradiographic axSpA among Black patients

The rate of nonradiographic axSpA among Black Americans was more than twice that of their White counterparts, which, Dr. Alexander noted, could make it more difficult to diagnose axSpA in that population.

The odds ratio for Black patients having nonradiographic axSpA, compared with Whites, was 2.265 (95% CI, 1.082-4.999; P = .035), after adjustment for age, sex, and HLA-B27 status.

Adult patients with axSpA were identified from rheumatology clinics at four major hospital systems and one private clinic in Shelby County, Tenn., between 2011 and 2021. Patients met modified New York (mNY) or Assessment of Spondyloarthritis International Society (ASAS) criteria as assessed by reviewers.

The authors and Dr. Alexander reported no relevant financial relationships.

CLEVELAND – Documenting the prevalence of axial spondyloarthritis (axSpA) among Black Americans has been difficult because of little published data, but new research suggests that when Black Americans do have the disease, it seems to be more severe.

Iman Abutineh, MD, of the University of Tennessee, Memphis, discussed her team’s work at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

A total of 244 patients with axSpA were identified, including 168 (69%) males, 78 (32%) Black patients, and 143 (59%) White patients.

Average age of onset for patients overall was 27.7 years, and age at diagnosis was 36.1 years with a 7-year delay in diagnosis. Sixty-six (27%) patients had nonradiographic axSpA, 83% were on tumor necrosis factor inhibitors, and 38% were prescribed glucocorticoids.

The researchers found several differences by race.

White patients were more likely to be HLA-B27 positive (77% vs. 59%; P = .010). White patients also had higher prevalence of psoriasis, coronary artery disease, and family history of SpA. White females had a higher prevalence of inflammatory bowel disease, fibromyalgia, depression, and lower grades of sacroiliitis.
 

Black patients had more hip involvement

A higher percentage of Black patients had elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and hip involvement. In comparing hip involvement, the researchers found that 39 (39%) White males had hip involvement as did 9 (21%) White females. In comparison, 22 (45%) Black men in the study and 14 (54%) Black women showed hip involvement (P = .035).

After adjustment for age, sex, HLA-B27, and insurance status, Black patients had higher grades of sacroiliitis with an odds ratio of 2.32 (95% confidence interval, 1.23-4.44). Black patients had a numerically longer delay in diagnosis, compared with Whites (7.93 vs. 6.64 years), but this did not achieve statistical significance (P = .454), the researchers wrote.
 

Study addresses racial disparities

“Traditionally we think of axial spondyloarthritis largely in Caucasian males who are HLA-B27 positive,” Dr. Abutineh said, “and we found that there is still a significant portion of patients who don’t meet the criteria that do have disease that is very significant.”

Although actual prevalence was not clear from this study, Dr. Abutineh said their data suggest a 3-to-1 ratio of White-to-Black patients with spondyloarthritis, “but of the Black patients who are diagnosed, their disease is almost always more severe. That points to why it’s important to have a high index of suspicion for this disease in that patient population because if you miss it, it could be detrimental to the patients.”

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who was not part of the study, said in an interview, “It is an excellent and timely study addressing the racial disparities and inequities surrounding axSpA diagnosis. It highlights the delay in diagnosis and increased burden of disease among Black Americans.”

She said the study may prompt a further look into barriers to care for Black Americans and their beliefs regarding seeking health care for their pain.
 

Higher rates of nonradiographic axSpA among Black patients

The rate of nonradiographic axSpA among Black Americans was more than twice that of their White counterparts, which, Dr. Alexander noted, could make it more difficult to diagnose axSpA in that population.

The odds ratio for Black patients having nonradiographic axSpA, compared with Whites, was 2.265 (95% CI, 1.082-4.999; P = .035), after adjustment for age, sex, and HLA-B27 status.

Adult patients with axSpA were identified from rheumatology clinics at four major hospital systems and one private clinic in Shelby County, Tenn., between 2011 and 2021. Patients met modified New York (mNY) or Assessment of Spondyloarthritis International Society (ASAS) criteria as assessed by reviewers.

The authors and Dr. Alexander reported no relevant financial relationships.

CLEVELAND – Documenting the prevalence of axial spondyloarthritis (axSpA) among Black Americans has been difficult because of little published data, but new research suggests that when Black Americans do have the disease, it seems to be more severe.

Iman Abutineh, MD, of the University of Tennessee, Memphis, discussed her team’s work at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN).

A total of 244 patients with axSpA were identified, including 168 (69%) males, 78 (32%) Black patients, and 143 (59%) White patients.

Average age of onset for patients overall was 27.7 years, and age at diagnosis was 36.1 years with a 7-year delay in diagnosis. Sixty-six (27%) patients had nonradiographic axSpA, 83% were on tumor necrosis factor inhibitors, and 38% were prescribed glucocorticoids.

The researchers found several differences by race.

White patients were more likely to be HLA-B27 positive (77% vs. 59%; P = .010). White patients also had higher prevalence of psoriasis, coronary artery disease, and family history of SpA. White females had a higher prevalence of inflammatory bowel disease, fibromyalgia, depression, and lower grades of sacroiliitis.
 

Black patients had more hip involvement

A higher percentage of Black patients had elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and hip involvement. In comparing hip involvement, the researchers found that 39 (39%) White males had hip involvement as did 9 (21%) White females. In comparison, 22 (45%) Black men in the study and 14 (54%) Black women showed hip involvement (P = .035).

After adjustment for age, sex, HLA-B27, and insurance status, Black patients had higher grades of sacroiliitis with an odds ratio of 2.32 (95% confidence interval, 1.23-4.44). Black patients had a numerically longer delay in diagnosis, compared with Whites (7.93 vs. 6.64 years), but this did not achieve statistical significance (P = .454), the researchers wrote.
 

Study addresses racial disparities

“Traditionally we think of axial spondyloarthritis largely in Caucasian males who are HLA-B27 positive,” Dr. Abutineh said, “and we found that there is still a significant portion of patients who don’t meet the criteria that do have disease that is very significant.”

Although actual prevalence was not clear from this study, Dr. Abutineh said their data suggest a 3-to-1 ratio of White-to-Black patients with spondyloarthritis, “but of the Black patients who are diagnosed, their disease is almost always more severe. That points to why it’s important to have a high index of suspicion for this disease in that patient population because if you miss it, it could be detrimental to the patients.”

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who was not part of the study, said in an interview, “It is an excellent and timely study addressing the racial disparities and inequities surrounding axSpA diagnosis. It highlights the delay in diagnosis and increased burden of disease among Black Americans.”

She said the study may prompt a further look into barriers to care for Black Americans and their beliefs regarding seeking health care for their pain.
 

Higher rates of nonradiographic axSpA among Black patients

The rate of nonradiographic axSpA among Black Americans was more than twice that of their White counterparts, which, Dr. Alexander noted, could make it more difficult to diagnose axSpA in that population.

The odds ratio for Black patients having nonradiographic axSpA, compared with Whites, was 2.265 (95% CI, 1.082-4.999; P = .035), after adjustment for age, sex, and HLA-B27 status.

Adult patients with axSpA were identified from rheumatology clinics at four major hospital systems and one private clinic in Shelby County, Tenn., between 2011 and 2021. Patients met modified New York (mNY) or Assessment of Spondyloarthritis International Society (ASAS) criteria as assessed by reviewers.

The authors and Dr. Alexander reported no relevant financial relationships.

The U.S. Food and Drug Administration on May 22 approved a new autoinjection option for adalimumab-adbm (Cyltezo), a biosimilar to AbbVie’s adalimumab (Humira), ahead of Cyltezo’s commercial launch on July 1, 2023.

Cyltezo was approved by the FDA in 2017 as a prefilled syringe and was the first biosimilar deemed to be interchangeable with Humira in 2021. It is indicated to treat multiple chronic inflammatory conditions, including rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and hidradenitis suppurativa. This new design, which features one-button, three-step activation, has been certified as an “Ease of Use” product by the Arthritis Foundation, Boehringer Ingelheim said in a press release. The 40-mg, prefilled Cyltezo Pen will be available in two-, four-, and six-pack options.

“The FDA approval of the Cyltezo Pen is great news for patients living with chronic inflammatory diseases who may prefer administering the medication needed to manage their conditions via an autoinjector,” said Stephen Pagnotta, the executive director and biosimilar commercial lead at Boehringer Ingelheim in a statement; “we’re excited to be able to offer the Cyltezo Pen as an additional option to patients at Cyltezo’s launch on July 1.”

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

The U.S. Food and Drug Administration on May 22 approved a new autoinjection option for adalimumab-adbm (Cyltezo), a biosimilar to AbbVie’s adalimumab (Humira), ahead of Cyltezo’s commercial launch on July 1, 2023.

Cyltezo was approved by the FDA in 2017 as a prefilled syringe and was the first biosimilar deemed to be interchangeable with Humira in 2021. It is indicated to treat multiple chronic inflammatory conditions, including rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and hidradenitis suppurativa. This new design, which features one-button, three-step activation, has been certified as an “Ease of Use” product by the Arthritis Foundation, Boehringer Ingelheim said in a press release. The 40-mg, prefilled Cyltezo Pen will be available in two-, four-, and six-pack options.

“The FDA approval of the Cyltezo Pen is great news for patients living with chronic inflammatory diseases who may prefer administering the medication needed to manage their conditions via an autoinjector,” said Stephen Pagnotta, the executive director and biosimilar commercial lead at Boehringer Ingelheim in a statement; “we’re excited to be able to offer the Cyltezo Pen as an additional option to patients at Cyltezo’s launch on July 1.”

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

The U.S. Food and Drug Administration on May 22 approved a new autoinjection option for adalimumab-adbm (Cyltezo), a biosimilar to AbbVie’s adalimumab (Humira), ahead of Cyltezo’s commercial launch on July 1, 2023.

Cyltezo was approved by the FDA in 2017 as a prefilled syringe and was the first biosimilar deemed to be interchangeable with Humira in 2021. It is indicated to treat multiple chronic inflammatory conditions, including rheumatoid arthritis, polyarticular juvenile idiopathic arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and hidradenitis suppurativa. This new design, which features one-button, three-step activation, has been certified as an “Ease of Use” product by the Arthritis Foundation, Boehringer Ingelheim said in a press release. The 40-mg, prefilled Cyltezo Pen will be available in two-, four-, and six-pack options.

“The FDA approval of the Cyltezo Pen is great news for patients living with chronic inflammatory diseases who may prefer administering the medication needed to manage their conditions via an autoinjector,” said Stephen Pagnotta, the executive director and biosimilar commercial lead at Boehringer Ingelheim in a statement; “we’re excited to be able to offer the Cyltezo Pen as an additional option to patients at Cyltezo’s launch on July 1.”

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

SEOUL, SOUTH KOREA – Nearly 8% of people with lupus nephritis who achieve complete remission of disease within 1 year of starting treatment will still go on to develop advanced chronic kidney disease (CKD), according to a presentation at an international congress on systemic lupus erythematosus.

Rheumatologist Dafna Gladman, MD, professor of medicine at the University of Toronto and codirector of the Lupus Clinic at Toronto Western Hospital, showed data from the Lupus Clinic’s prospective longitudinal cohort study in 273 patients with confirmed lupus nephritis who achieved complete remission within 12 months of baseline.

Bianca Nogrady/MDedge News

Remission was defined as less than 0.5 g proteinuria over 24 hours, inactive urinary sediment, and serum creatinine less than 120% of baseline.

Of this group, 21 (7.7%) progressed to advanced CKD during follow-up, which ranged from 0.7 to 31.7 years with a median of 5.8 years, after enrollment.

Patients who had experienced at least one flare during their first 5 years were around 4.5 times more likely to progress to advanced CKD than were those who did not experience a flare.

While the study excluded patients who already had advanced CKD, the analysis found those with evidence of impaired kidney function at baseline also had more than a fourfold higher risk of developing advanced CKD.

Other significant risk factors for progression were having low complement C3 levels at baseline and having had a longer duration of disease before enrollment.

“Those patients already have abnormal renal function, so the message is that patients who are already in trouble, you’ve got to watch them very carefully,” Dr. Gladman said in an interview.

The study also looked at whether there was a difference between patients who developed advanced CKD earlier – before the median of 5.8 years – or later. While the numbers were small, Dr. Gladman said patients who progressed earlier tended to be older and were more likely to be on antihypertensive treatment and have lower estimated glomerular filtration rate and a lower Systemic Lupus Erythematosus Disease Activity Index–2K, compared with those who progressed later. Some patients also were noncompliant and/or experienced concomitant infections; four had moderate to severe interstitial fibrosis and tubular atrophy.

“We conclude that such patients should be monitored closely despite early remission, and we also highlight the importance of maintenance therapy, which should be communicated to the patients to prevent noncompliance and subsequent flare,” Dr. Gladman told the conference.

Dr. Gladman said her clinic told patients from the very beginning of their treatment that they would need to be seen at 2- to 6-month intervals, regardless of how well their disease was doing.

Commenting on the presentation, rheumatologist Mandana Nikpour MD, PhD, of St. Vincent’s Hospital in Melbourne, said the findings showed the importance of keeping a close eye on patients with lupus nephritis, even if their disease appears to be in remission.

“If you’ve had nephritis, and you go into remission, you may already have a degree of damage in your kidneys,” said Dr. Nikpour, also from the University of Melbourne. “If there’s a degree of uncontrolled hypertension, or if a patient is noncompliant with their treatment, and there’s a degree of grumbling disease activity, that can all conspire and add up to result in long-term kidney damage and loss of renal function.”

Dr. Gladman has received grants or research support from, or has consulted for, Amgen, AbbVie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Bristol-Myers Squibb, Galapagos, and Gilead.

SEOUL, SOUTH KOREA – Nearly 8% of people with lupus nephritis who achieve complete remission of disease within 1 year of starting treatment will still go on to develop advanced chronic kidney disease (CKD), according to a presentation at an international congress on systemic lupus erythematosus.

Rheumatologist Dafna Gladman, MD, professor of medicine at the University of Toronto and codirector of the Lupus Clinic at Toronto Western Hospital, showed data from the Lupus Clinic’s prospective longitudinal cohort study in 273 patients with confirmed lupus nephritis who achieved complete remission within 12 months of baseline.

Bianca Nogrady/MDedge News

Remission was defined as less than 0.5 g proteinuria over 24 hours, inactive urinary sediment, and serum creatinine less than 120% of baseline.

Of this group, 21 (7.7%) progressed to advanced CKD during follow-up, which ranged from 0.7 to 31.7 years with a median of 5.8 years, after enrollment.

Patients who had experienced at least one flare during their first 5 years were around 4.5 times more likely to progress to advanced CKD than were those who did not experience a flare.

While the study excluded patients who already had advanced CKD, the analysis found those with evidence of impaired kidney function at baseline also had more than a fourfold higher risk of developing advanced CKD.

Other significant risk factors for progression were having low complement C3 levels at baseline and having had a longer duration of disease before enrollment.

“Those patients already have abnormal renal function, so the message is that patients who are already in trouble, you’ve got to watch them very carefully,” Dr. Gladman said in an interview.

The study also looked at whether there was a difference between patients who developed advanced CKD earlier – before the median of 5.8 years – or later. While the numbers were small, Dr. Gladman said patients who progressed earlier tended to be older and were more likely to be on antihypertensive treatment and have lower estimated glomerular filtration rate and a lower Systemic Lupus Erythematosus Disease Activity Index–2K, compared with those who progressed later. Some patients also were noncompliant and/or experienced concomitant infections; four had moderate to severe interstitial fibrosis and tubular atrophy.

“We conclude that such patients should be monitored closely despite early remission, and we also highlight the importance of maintenance therapy, which should be communicated to the patients to prevent noncompliance and subsequent flare,” Dr. Gladman told the conference.

Dr. Gladman said her clinic told patients from the very beginning of their treatment that they would need to be seen at 2- to 6-month intervals, regardless of how well their disease was doing.

Commenting on the presentation, rheumatologist Mandana Nikpour MD, PhD, of St. Vincent’s Hospital in Melbourne, said the findings showed the importance of keeping a close eye on patients with lupus nephritis, even if their disease appears to be in remission.

“If you’ve had nephritis, and you go into remission, you may already have a degree of damage in your kidneys,” said Dr. Nikpour, also from the University of Melbourne. “If there’s a degree of uncontrolled hypertension, or if a patient is noncompliant with their treatment, and there’s a degree of grumbling disease activity, that can all conspire and add up to result in long-term kidney damage and loss of renal function.”

Dr. Gladman has received grants or research support from, or has consulted for, Amgen, AbbVie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Bristol-Myers Squibb, Galapagos, and Gilead.

SEOUL, SOUTH KOREA – Nearly 8% of people with lupus nephritis who achieve complete remission of disease within 1 year of starting treatment will still go on to develop advanced chronic kidney disease (CKD), according to a presentation at an international congress on systemic lupus erythematosus.

Rheumatologist Dafna Gladman, MD, professor of medicine at the University of Toronto and codirector of the Lupus Clinic at Toronto Western Hospital, showed data from the Lupus Clinic’s prospective longitudinal cohort study in 273 patients with confirmed lupus nephritis who achieved complete remission within 12 months of baseline.

Bianca Nogrady/MDedge News

Remission was defined as less than 0.5 g proteinuria over 24 hours, inactive urinary sediment, and serum creatinine less than 120% of baseline.

Of this group, 21 (7.7%) progressed to advanced CKD during follow-up, which ranged from 0.7 to 31.7 years with a median of 5.8 years, after enrollment.

Patients who had experienced at least one flare during their first 5 years were around 4.5 times more likely to progress to advanced CKD than were those who did not experience a flare.

While the study excluded patients who already had advanced CKD, the analysis found those with evidence of impaired kidney function at baseline also had more than a fourfold higher risk of developing advanced CKD.

Other significant risk factors for progression were having low complement C3 levels at baseline and having had a longer duration of disease before enrollment.

“Those patients already have abnormal renal function, so the message is that patients who are already in trouble, you’ve got to watch them very carefully,” Dr. Gladman said in an interview.

The study also looked at whether there was a difference between patients who developed advanced CKD earlier – before the median of 5.8 years – or later. While the numbers were small, Dr. Gladman said patients who progressed earlier tended to be older and were more likely to be on antihypertensive treatment and have lower estimated glomerular filtration rate and a lower Systemic Lupus Erythematosus Disease Activity Index–2K, compared with those who progressed later. Some patients also were noncompliant and/or experienced concomitant infections; four had moderate to severe interstitial fibrosis and tubular atrophy.

“We conclude that such patients should be monitored closely despite early remission, and we also highlight the importance of maintenance therapy, which should be communicated to the patients to prevent noncompliance and subsequent flare,” Dr. Gladman told the conference.

Dr. Gladman said her clinic told patients from the very beginning of their treatment that they would need to be seen at 2- to 6-month intervals, regardless of how well their disease was doing.

Commenting on the presentation, rheumatologist Mandana Nikpour MD, PhD, of St. Vincent’s Hospital in Melbourne, said the findings showed the importance of keeping a close eye on patients with lupus nephritis, even if their disease appears to be in remission.

“If you’ve had nephritis, and you go into remission, you may already have a degree of damage in your kidneys,” said Dr. Nikpour, also from the University of Melbourne. “If there’s a degree of uncontrolled hypertension, or if a patient is noncompliant with their treatment, and there’s a degree of grumbling disease activity, that can all conspire and add up to result in long-term kidney damage and loss of renal function.”

Dr. Gladman has received grants or research support from, or has consulted for, Amgen, AbbVie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Bristol-Myers Squibb, Galapagos, and Gilead.

CLEVELAND – With early diagnosis an ongoing complex target for axial spondyloarthritis (axSpA), new research may help to answer where the biggest delays lie.

Gregory McDermott, MD, a research fellow at Brigham and Women’s Hospital in Boston, led a pilot study with data from Mass General Brigham electronic health records. He shared top results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN) , where addressing delay in diagnosis was a major theme.

Included in the cohort were 554 patients who had three ICD-9 or ICD-10 codes and an imaging report of sacroiliitis, ankylosis, or syndesmophytes, and were screened via manual chart review for modified New York and Assessment of Spondyloarthritis International Society criteria.

The average diagnostic delay for axSpA was 6.8 years in this study (median, 3.8 years), relatively consistent with findings in previous studies globally, and the average age of onset was 29.5.

The researchers also factored in history of specialty care for back pain (orthopedics, physical medicine and rehabilitation, pain medicine) or extra-articular manifestations (ophthalmology, dermatology, gastroenterology) before axSpA diagnosis. Other factors included smoking and insurance status, along with age, sex, race, and other demographic data.

The results showed shorter delays in diagnosing axSpA were associated with older age at symptom onset and peripheral arthritis, whereas longer delays (more than 4 years) were associated with a history of uveitis, ankylosing spondylitis at diagnosis, and being among those in the 80-99th percentile on the social vulnerability index (SVI). The SVI includes U.S. census data on factors including housing type, household composition and disability status, employment status, minority status, non-English speaking, educational attainment, transportation, and mean income level.
 

Notable uveitis finding

Dr. McDermott said the team was surprised by the association between having had uveitis and delayed axSpA diagnosis.

Among patients with uveitis, 12% had a short delay from symptom onset to axSpA diagnosis of 0-1 years, but more than twice that percentage (27%) had a delay of more than 4 years (P < .001).

“We thought the finding related to uveitis was interesting and potentially clinically meaningful as 27% of axSpA patients in our cohort with more than 4 years of diagnostic delay sought ophthalmology care prior to their diagnosis, [compared with 13% of patients with a diagnosis within 1 year],” Dr. McDermott said. “This practice setting in particular may be a place where we can intervene with simple screening or increased education in order to get people appropriately referred to rheumatology care.”

Longer delays can lead to more functional impairment, radiographic progression, and work disability, as well as poorer quality of life, increased depression, and higher unemployment and health care costs, Dr. McDermott said.
 

Patients may miss key treatment window

Maureen Dubreuil, MD, MSc, assistant professor at Boston University and a rheumatologist with the VA Boston Healthcare System, who was not part of the study, said: “This study addressed a critically important problem in the field – that diagnosis of axSpA is delayed by 7 years, which is much longer than the average time to diagnosis for other forms of arthritis, such as rheumatoid arthritis, which is under 6 months.

“It is critical that diagnostic delay is reduced in axSpA because undiagnosed individuals may miss an important window of opportunity to receive treatment that prevents permanent structural damage and functional declines. This work, if confirmed in other data, would allow development of interventions to improve timely evaluation of individuals with chronic back pain who may have axSpA, particularly among those with within lower socioeconomic strata, and those who are older or have uveitis.”
 

Study tests screening tool

Among the ideas proposed for reducing the delay was a referral strategy with a screening tool.

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who presented her team’s poster, noted that, in the United States, patients with chronic back pain often come first to a primary care doctor or another specialty and not to a rheumatologist.

As an internal medicine resident at Yale University, New Haven, Conn., Dr. Alexander and colleagues there conducted the Finding Axial Spondyloarthritis (FaxSpA) study to test whether patient self-referral or referral by other physicians, guided by answers to a screening tool, could help to speed the process of getting patients more likely to have axSpA to a rheumatologist.

Dr. Alexander said they found that using the screening tool was better than having no referral strategy, explaining that screening helped diagnose about 34% of the study population with axSpA, whereas if a patient came in with chronic back pain to a primary care physician without any screening and ultimately to a rheumatologist, “you’re only capturing about 20%,” she said, citing estimates in the literature.
 

Questions may need rewording

However, the researchers found that patient interpretation of the screening questions was different depending on whether they were answering online or directly from a rheumatologist’s in-person questions. For more success, Dr. Alexander said, the questions may need to be reworded or more education may be needed for both patients and physicians to get more valid information.

For instance, she said, when the screening tool asks about inflammation, the patient may assume the physician is asking about pain and answer one way, but when a rheumatologist asks the question a slightly different way in the clinic, the patient may give a different answer.
 

First questions in portal, on social media

In the screening intervention (called A-tool) patients first answered three questions via the MyChart portal or Facebook. If they answered all three questions positively, they would move on to another round of questions and the answers would decide whether they would be eligible to come into the rheumatologist to get evaluated for axSpA.

At the study visit, rheumatologists asked the same questions as the online A-tool, which focus on SpA features with reasonable sensitivity and specificity for axSpA (no labs or imaging included). Clinicians’ judgment was considered the gold standard for diagnosis of axSpA.

The authors reported that 1,274 patients answered questions with the screening tool via Facebook (50%) and MyChart (50%) from April 2019 to February 2022. Among the responders, 507 (40%) were eligible for a rheumatologist visit.

As of May 2022, 100 patients were enrolled. Of the enrolled patients, 86 patients completed all the study procedures, including study visit, labs, and imaging (x-ray and MRI of the pelvis). Of the 86 patients, 29 (34%) were diagnosed with axSpA.

The tool appears to help narrow the chronic back pain patients who need to be seen by a rheumatologist for potential axSpA, Dr. Alexander said, which may help to speed diagnosis and also save time and resources.

Dr. McDermott, Dr. Dubreuil, and Dr. Alexander reported no relevant financial relationships. The FaxSpA study was supported with funding from Novartis and the Spondylitis Association of America.

CLEVELAND – With early diagnosis an ongoing complex target for axial spondyloarthritis (axSpA), new research may help to answer where the biggest delays lie.

Gregory McDermott, MD, a research fellow at Brigham and Women’s Hospital in Boston, led a pilot study with data from Mass General Brigham electronic health records. He shared top results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN) , where addressing delay in diagnosis was a major theme.

Included in the cohort were 554 patients who had three ICD-9 or ICD-10 codes and an imaging report of sacroiliitis, ankylosis, or syndesmophytes, and were screened via manual chart review for modified New York and Assessment of Spondyloarthritis International Society criteria.

The average diagnostic delay for axSpA was 6.8 years in this study (median, 3.8 years), relatively consistent with findings in previous studies globally, and the average age of onset was 29.5.

The researchers also factored in history of specialty care for back pain (orthopedics, physical medicine and rehabilitation, pain medicine) or extra-articular manifestations (ophthalmology, dermatology, gastroenterology) before axSpA diagnosis. Other factors included smoking and insurance status, along with age, sex, race, and other demographic data.

The results showed shorter delays in diagnosing axSpA were associated with older age at symptom onset and peripheral arthritis, whereas longer delays (more than 4 years) were associated with a history of uveitis, ankylosing spondylitis at diagnosis, and being among those in the 80-99th percentile on the social vulnerability index (SVI). The SVI includes U.S. census data on factors including housing type, household composition and disability status, employment status, minority status, non-English speaking, educational attainment, transportation, and mean income level.
 

Notable uveitis finding

Dr. McDermott said the team was surprised by the association between having had uveitis and delayed axSpA diagnosis.

Among patients with uveitis, 12% had a short delay from symptom onset to axSpA diagnosis of 0-1 years, but more than twice that percentage (27%) had a delay of more than 4 years (P < .001).

“We thought the finding related to uveitis was interesting and potentially clinically meaningful as 27% of axSpA patients in our cohort with more than 4 years of diagnostic delay sought ophthalmology care prior to their diagnosis, [compared with 13% of patients with a diagnosis within 1 year],” Dr. McDermott said. “This practice setting in particular may be a place where we can intervene with simple screening or increased education in order to get people appropriately referred to rheumatology care.”

Longer delays can lead to more functional impairment, radiographic progression, and work disability, as well as poorer quality of life, increased depression, and higher unemployment and health care costs, Dr. McDermott said.
 

Patients may miss key treatment window

Maureen Dubreuil, MD, MSc, assistant professor at Boston University and a rheumatologist with the VA Boston Healthcare System, who was not part of the study, said: “This study addressed a critically important problem in the field – that diagnosis of axSpA is delayed by 7 years, which is much longer than the average time to diagnosis for other forms of arthritis, such as rheumatoid arthritis, which is under 6 months.

“It is critical that diagnostic delay is reduced in axSpA because undiagnosed individuals may miss an important window of opportunity to receive treatment that prevents permanent structural damage and functional declines. This work, if confirmed in other data, would allow development of interventions to improve timely evaluation of individuals with chronic back pain who may have axSpA, particularly among those with within lower socioeconomic strata, and those who are older or have uveitis.”
 

Study tests screening tool

Among the ideas proposed for reducing the delay was a referral strategy with a screening tool.

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who presented her team’s poster, noted that, in the United States, patients with chronic back pain often come first to a primary care doctor or another specialty and not to a rheumatologist.

As an internal medicine resident at Yale University, New Haven, Conn., Dr. Alexander and colleagues there conducted the Finding Axial Spondyloarthritis (FaxSpA) study to test whether patient self-referral or referral by other physicians, guided by answers to a screening tool, could help to speed the process of getting patients more likely to have axSpA to a rheumatologist.

Dr. Alexander said they found that using the screening tool was better than having no referral strategy, explaining that screening helped diagnose about 34% of the study population with axSpA, whereas if a patient came in with chronic back pain to a primary care physician without any screening and ultimately to a rheumatologist, “you’re only capturing about 20%,” she said, citing estimates in the literature.
 

Questions may need rewording

However, the researchers found that patient interpretation of the screening questions was different depending on whether they were answering online or directly from a rheumatologist’s in-person questions. For more success, Dr. Alexander said, the questions may need to be reworded or more education may be needed for both patients and physicians to get more valid information.

For instance, she said, when the screening tool asks about inflammation, the patient may assume the physician is asking about pain and answer one way, but when a rheumatologist asks the question a slightly different way in the clinic, the patient may give a different answer.
 

First questions in portal, on social media

In the screening intervention (called A-tool) patients first answered three questions via the MyChart portal or Facebook. If they answered all three questions positively, they would move on to another round of questions and the answers would decide whether they would be eligible to come into the rheumatologist to get evaluated for axSpA.

At the study visit, rheumatologists asked the same questions as the online A-tool, which focus on SpA features with reasonable sensitivity and specificity for axSpA (no labs or imaging included). Clinicians’ judgment was considered the gold standard for diagnosis of axSpA.

The authors reported that 1,274 patients answered questions with the screening tool via Facebook (50%) and MyChart (50%) from April 2019 to February 2022. Among the responders, 507 (40%) were eligible for a rheumatologist visit.

As of May 2022, 100 patients were enrolled. Of the enrolled patients, 86 patients completed all the study procedures, including study visit, labs, and imaging (x-ray and MRI of the pelvis). Of the 86 patients, 29 (34%) were diagnosed with axSpA.

The tool appears to help narrow the chronic back pain patients who need to be seen by a rheumatologist for potential axSpA, Dr. Alexander said, which may help to speed diagnosis and also save time and resources.

Dr. McDermott, Dr. Dubreuil, and Dr. Alexander reported no relevant financial relationships. The FaxSpA study was supported with funding from Novartis and the Spondylitis Association of America.

CLEVELAND – With early diagnosis an ongoing complex target for axial spondyloarthritis (axSpA), new research may help to answer where the biggest delays lie.

Gregory McDermott, MD, a research fellow at Brigham and Women’s Hospital in Boston, led a pilot study with data from Mass General Brigham electronic health records. He shared top results at the annual meeting of the Spondyloarthritis Research and Treatment Network (SPARTAN) , where addressing delay in diagnosis was a major theme.

Included in the cohort were 554 patients who had three ICD-9 or ICD-10 codes and an imaging report of sacroiliitis, ankylosis, or syndesmophytes, and were screened via manual chart review for modified New York and Assessment of Spondyloarthritis International Society criteria.

The average diagnostic delay for axSpA was 6.8 years in this study (median, 3.8 years), relatively consistent with findings in previous studies globally, and the average age of onset was 29.5.

The researchers also factored in history of specialty care for back pain (orthopedics, physical medicine and rehabilitation, pain medicine) or extra-articular manifestations (ophthalmology, dermatology, gastroenterology) before axSpA diagnosis. Other factors included smoking and insurance status, along with age, sex, race, and other demographic data.

The results showed shorter delays in diagnosing axSpA were associated with older age at symptom onset and peripheral arthritis, whereas longer delays (more than 4 years) were associated with a history of uveitis, ankylosing spondylitis at diagnosis, and being among those in the 80-99th percentile on the social vulnerability index (SVI). The SVI includes U.S. census data on factors including housing type, household composition and disability status, employment status, minority status, non-English speaking, educational attainment, transportation, and mean income level.
 

Notable uveitis finding

Dr. McDermott said the team was surprised by the association between having had uveitis and delayed axSpA diagnosis.

Among patients with uveitis, 12% had a short delay from symptom onset to axSpA diagnosis of 0-1 years, but more than twice that percentage (27%) had a delay of more than 4 years (P < .001).

“We thought the finding related to uveitis was interesting and potentially clinically meaningful as 27% of axSpA patients in our cohort with more than 4 years of diagnostic delay sought ophthalmology care prior to their diagnosis, [compared with 13% of patients with a diagnosis within 1 year],” Dr. McDermott said. “This practice setting in particular may be a place where we can intervene with simple screening or increased education in order to get people appropriately referred to rheumatology care.”

Longer delays can lead to more functional impairment, radiographic progression, and work disability, as well as poorer quality of life, increased depression, and higher unemployment and health care costs, Dr. McDermott said.
 

Patients may miss key treatment window

Maureen Dubreuil, MD, MSc, assistant professor at Boston University and a rheumatologist with the VA Boston Healthcare System, who was not part of the study, said: “This study addressed a critically important problem in the field – that diagnosis of axSpA is delayed by 7 years, which is much longer than the average time to diagnosis for other forms of arthritis, such as rheumatoid arthritis, which is under 6 months.

“It is critical that diagnostic delay is reduced in axSpA because undiagnosed individuals may miss an important window of opportunity to receive treatment that prevents permanent structural damage and functional declines. This work, if confirmed in other data, would allow development of interventions to improve timely evaluation of individuals with chronic back pain who may have axSpA, particularly among those with within lower socioeconomic strata, and those who are older or have uveitis.”
 

Study tests screening tool

Among the ideas proposed for reducing the delay was a referral strategy with a screening tool.

Swetha Alexander, MD, a rheumatology fellow at the University of Utah, Salt Lake City, who presented her team’s poster, noted that, in the United States, patients with chronic back pain often come first to a primary care doctor or another specialty and not to a rheumatologist.

As an internal medicine resident at Yale University, New Haven, Conn., Dr. Alexander and colleagues there conducted the Finding Axial Spondyloarthritis (FaxSpA) study to test whether patient self-referral or referral by other physicians, guided by answers to a screening tool, could help to speed the process of getting patients more likely to have axSpA to a rheumatologist.

Dr. Alexander said they found that using the screening tool was better than having no referral strategy, explaining that screening helped diagnose about 34% of the study population with axSpA, whereas if a patient came in with chronic back pain to a primary care physician without any screening and ultimately to a rheumatologist, “you’re only capturing about 20%,” she said, citing estimates in the literature.
 

Questions may need rewording

However, the researchers found that patient interpretation of the screening questions was different depending on whether they were answering online or directly from a rheumatologist’s in-person questions. For more success, Dr. Alexander said, the questions may need to be reworded or more education may be needed for both patients and physicians to get more valid information.

For instance, she said, when the screening tool asks about inflammation, the patient may assume the physician is asking about pain and answer one way, but when a rheumatologist asks the question a slightly different way in the clinic, the patient may give a different answer.
 

First questions in portal, on social media

In the screening intervention (called A-tool) patients first answered three questions via the MyChart portal or Facebook. If they answered all three questions positively, they would move on to another round of questions and the answers would decide whether they would be eligible to come into the rheumatologist to get evaluated for axSpA.

At the study visit, rheumatologists asked the same questions as the online A-tool, which focus on SpA features with reasonable sensitivity and specificity for axSpA (no labs or imaging included). Clinicians’ judgment was considered the gold standard for diagnosis of axSpA.

The authors reported that 1,274 patients answered questions with the screening tool via Facebook (50%) and MyChart (50%) from April 2019 to February 2022. Among the responders, 507 (40%) were eligible for a rheumatologist visit.

As of May 2022, 100 patients were enrolled. Of the enrolled patients, 86 patients completed all the study procedures, including study visit, labs, and imaging (x-ray and MRI of the pelvis). Of the 86 patients, 29 (34%) were diagnosed with axSpA.

The tool appears to help narrow the chronic back pain patients who need to be seen by a rheumatologist for potential axSpA, Dr. Alexander said, which may help to speed diagnosis and also save time and resources.

Dr. McDermott, Dr. Dubreuil, and Dr. Alexander reported no relevant financial relationships. The FaxSpA study was supported with funding from Novartis and the Spondylitis Association of America.

SEOUL, SOUTH KOREA – A panel of urinary biomarkers may do better than measuring proteinuria in predicting which patients with lupus nephritis are going to respond to treatment, according to a presentation at an international congress on systemic lupus erythematosus.

Physician-scientist Andrea Fava, MD, of the division of rheumatology at Johns Hopkins University, Baltimore, presented data from a study using urine proteomics to identify biomarkers present in the urine of patients with lupus nephritis at 3 months after starting treatment that were linked to better outcomes from that treatment at 1 year.

While proteinuria is the standard measure used to guide decisions about whether to do a kidney biopsy and how to treat lupus nephritis, it doesn’t always correlate with what’s actually going on inside the kidney in terms of histology and inflammation, Dr. Fava said.

Bianca Nogrady/MDedge News

He pointed to an earlier study in which researchers did kidney biopsies 6 months after patients with lupus nephritis started treatment with mycophenolate. This suggested that around half of patients who showed a clinical response to treatment – defined as proteinuria below 500 mg/day – still had significant histologic disease activity. Another study suggested that this elevated histologic disease activity is associated with a risk of flare, which can result in significant nephron loss. On the flip side, nearly two-thirds of patients in complete histologic remission still had elevated proteinuria.

Unfortunately, it’s not possible or practical to biopsy patients on a regular basis, Dr. Fava said. “So we need better biomarkers, and to do so, we need better knowledge of the pathophysiology because if we have biomarkers that reflect tissue biology in real-time, that may surely guide personalized treatments,” he said at the congress.

Dr. Fava and colleagues enrolled 225 patients with SLE who were undergoing kidney biopsy and 10 healthy controls and used proteomics to quantify the urinary levels of around 1,200 proteins at baseline, 3, 6, and 12 months after initiating treatment.

The team then analyzed these data to look for protein signatures that correlated with histologic phenotypes – particularly the amount of inflammation in the kidney – and clinical features such as response to treatment.

They found several protein biomarkers that appeared to be linked to histologic activity in the kidney, including interleukin (IL)-16, CD163, and neutrophil granule proteins.

Initially, the team looked at baseline levels of these proteins to see if they predicted who responded to treatment, but found no difference between responders and nonresponders.

However, when they looked at levels at 3 months after treatment, a pattern emerged. “We found that in patients who were not responding, there were no changes after 3 months of treatment in the urine proteome,” Dr. Fava said. Among those who did respond to treatment, the levels of these proteins – IL-16, CD163, galectin-1, and CD206 – decreased significantly.

“So the proteins that are linked to renal activity decrease only in responders, suggesting that effective immunosuppression is effective in reducing intrarenal inflammation, which eventually results in low proteinuria at 1 year.”

The decline in these biomarkers persisted at 1 year, and the study suggested it was a better predictor of which patients would respond to treatment at 1 year than proteinuria.

Dr. Fava said in an interview that better biomarkers could revolutionize the treatment and management of lupus nephritis.

“First of all, it can shift the management strategy from treatment to prevention, because at the very beginning we can nip it in the bud maybe with very gentle treatment,” he said. Different panels of urine biomarkers could identify patients at risk of treatment failure, and also help patients to taper off their immunosuppressive therapy without an increased risk of flare. “If we have a way to tell us there’s still inflammation that needs treatment, that could change the way we do it,” he said.

He acknowledged there are significant challenges to developing these biomarkers for clinical use; one is the decision of how to define disease activity without relying on proteinuria as a measure. “Why do I want a biomarker that can predict another biomarker?” he said.

Another presentation during the same session, by Huihua Ding, MD, of Shanghai Jiao Tong University in Shanghai, China, reported on the use of urinary L-selectin to assess renal disease activity and response to treatment in a multiethnic cohort.

This study, involving 474 patients with SLE with or without renal involvement in the United States and China, found levels of urinary L-selectin were elevated only in patients with active lupus nephritis and showed patterns that correlated with renal histologic characteristics.

Clinical rheumatologist Eric F. Morand, MD, PhD, and head of the School of Clinical Sciences at Monash University in Melbourne said one challenge with using urinary biomarkers was that it was not yet clear what these biomarkers reveal about the kidney. “It will be important to see whether this proteomic data actually link to renal outcomes,” Dr. Morand said in an interview. “I think predicting the response to treatment should be based around GFR [glomerular filtration rate] preservation, and I don’t think I’ve seen data yet that the urine biomarkers are going to tell us how to do that better.”

Dr. Morand is optimistic that urine biomarkers will one day be able to achieve that, but he stressed the importance of having urine biomarker tests available in the field at low cost. “You’re going to be doing the tests repeatedly, so therefore, you’re probably going to need to come down to a smaller list of proteins that you measure.”

Dr. Fava reported receiving support from Sanofi and Annexion Bio.

SEOUL, SOUTH KOREA – A panel of urinary biomarkers may do better than measuring proteinuria in predicting which patients with lupus nephritis are going to respond to treatment, according to a presentation at an international congress on systemic lupus erythematosus.

Physician-scientist Andrea Fava, MD, of the division of rheumatology at Johns Hopkins University, Baltimore, presented data from a study using urine proteomics to identify biomarkers present in the urine of patients with lupus nephritis at 3 months after starting treatment that were linked to better outcomes from that treatment at 1 year.

While proteinuria is the standard measure used to guide decisions about whether to do a kidney biopsy and how to treat lupus nephritis, it doesn’t always correlate with what’s actually going on inside the kidney in terms of histology and inflammation, Dr. Fava said.

Bianca Nogrady/MDedge News

He pointed to an earlier study in which researchers did kidney biopsies 6 months after patients with lupus nephritis started treatment with mycophenolate. This suggested that around half of patients who showed a clinical response to treatment – defined as proteinuria below 500 mg/day – still had significant histologic disease activity. Another study suggested that this elevated histologic disease activity is associated with a risk of flare, which can result in significant nephron loss. On the flip side, nearly two-thirds of patients in complete histologic remission still had elevated proteinuria.

Unfortunately, it’s not possible or practical to biopsy patients on a regular basis, Dr. Fava said. “So we need better biomarkers, and to do so, we need better knowledge of the pathophysiology because if we have biomarkers that reflect tissue biology in real-time, that may surely guide personalized treatments,” he said at the congress.

Dr. Fava and colleagues enrolled 225 patients with SLE who were undergoing kidney biopsy and 10 healthy controls and used proteomics to quantify the urinary levels of around 1,200 proteins at baseline, 3, 6, and 12 months after initiating treatment.

The team then analyzed these data to look for protein signatures that correlated with histologic phenotypes – particularly the amount of inflammation in the kidney – and clinical features such as response to treatment.

They found several protein biomarkers that appeared to be linked to histologic activity in the kidney, including interleukin (IL)-16, CD163, and neutrophil granule proteins.

Initially, the team looked at baseline levels of these proteins to see if they predicted who responded to treatment, but found no difference between responders and nonresponders.

However, when they looked at levels at 3 months after treatment, a pattern emerged. “We found that in patients who were not responding, there were no changes after 3 months of treatment in the urine proteome,” Dr. Fava said. Among those who did respond to treatment, the levels of these proteins – IL-16, CD163, galectin-1, and CD206 – decreased significantly.

“So the proteins that are linked to renal activity decrease only in responders, suggesting that effective immunosuppression is effective in reducing intrarenal inflammation, which eventually results in low proteinuria at 1 year.”

The decline in these biomarkers persisted at 1 year, and the study suggested it was a better predictor of which patients would respond to treatment at 1 year than proteinuria.

Dr. Fava said in an interview that better biomarkers could revolutionize the treatment and management of lupus nephritis.

“First of all, it can shift the management strategy from treatment to prevention, because at the very beginning we can nip it in the bud maybe with very gentle treatment,” he said. Different panels of urine biomarkers could identify patients at risk of treatment failure, and also help patients to taper off their immunosuppressive therapy without an increased risk of flare. “If we have a way to tell us there’s still inflammation that needs treatment, that could change the way we do it,” he said.

He acknowledged there are significant challenges to developing these biomarkers for clinical use; one is the decision of how to define disease activity without relying on proteinuria as a measure. “Why do I want a biomarker that can predict another biomarker?” he said.

Another presentation during the same session, by Huihua Ding, MD, of Shanghai Jiao Tong University in Shanghai, China, reported on the use of urinary L-selectin to assess renal disease activity and response to treatment in a multiethnic cohort.

This study, involving 474 patients with SLE with or without renal involvement in the United States and China, found levels of urinary L-selectin were elevated only in patients with active lupus nephritis and showed patterns that correlated with renal histologic characteristics.

Clinical rheumatologist Eric F. Morand, MD, PhD, and head of the School of Clinical Sciences at Monash University in Melbourne said one challenge with using urinary biomarkers was that it was not yet clear what these biomarkers reveal about the kidney. “It will be important to see whether this proteomic data actually link to renal outcomes,” Dr. Morand said in an interview. “I think predicting the response to treatment should be based around GFR [glomerular filtration rate] preservation, and I don’t think I’ve seen data yet that the urine biomarkers are going to tell us how to do that better.”

Dr. Morand is optimistic that urine biomarkers will one day be able to achieve that, but he stressed the importance of having urine biomarker tests available in the field at low cost. “You’re going to be doing the tests repeatedly, so therefore, you’re probably going to need to come down to a smaller list of proteins that you measure.”

Dr. Fava reported receiving support from Sanofi and Annexion Bio.

SEOUL, SOUTH KOREA – A panel of urinary biomarkers may do better than measuring proteinuria in predicting which patients with lupus nephritis are going to respond to treatment, according to a presentation at an international congress on systemic lupus erythematosus.

Physician-scientist Andrea Fava, MD, of the division of rheumatology at Johns Hopkins University, Baltimore, presented data from a study using urine proteomics to identify biomarkers present in the urine of patients with lupus nephritis at 3 months after starting treatment that were linked to better outcomes from that treatment at 1 year.

While proteinuria is the standard measure used to guide decisions about whether to do a kidney biopsy and how to treat lupus nephritis, it doesn’t always correlate with what’s actually going on inside the kidney in terms of histology and inflammation, Dr. Fava said.

Bianca Nogrady/MDedge News

He pointed to an earlier study in which researchers did kidney biopsies 6 months after patients with lupus nephritis started treatment with mycophenolate. This suggested that around half of patients who showed a clinical response to treatment – defined as proteinuria below 500 mg/day – still had significant histologic disease activity. Another study suggested that this elevated histologic disease activity is associated with a risk of flare, which can result in significant nephron loss. On the flip side, nearly two-thirds of patients in complete histologic remission still had elevated proteinuria.

Unfortunately, it’s not possible or practical to biopsy patients on a regular basis, Dr. Fava said. “So we need better biomarkers, and to do so, we need better knowledge of the pathophysiology because if we have biomarkers that reflect tissue biology in real-time, that may surely guide personalized treatments,” he said at the congress.

Dr. Fava and colleagues enrolled 225 patients with SLE who were undergoing kidney biopsy and 10 healthy controls and used proteomics to quantify the urinary levels of around 1,200 proteins at baseline, 3, 6, and 12 months after initiating treatment.

The team then analyzed these data to look for protein signatures that correlated with histologic phenotypes – particularly the amount of inflammation in the kidney – and clinical features such as response to treatment.

They found several protein biomarkers that appeared to be linked to histologic activity in the kidney, including interleukin (IL)-16, CD163, and neutrophil granule proteins.

Initially, the team looked at baseline levels of these proteins to see if they predicted who responded to treatment, but found no difference between responders and nonresponders.

However, when they looked at levels at 3 months after treatment, a pattern emerged. “We found that in patients who were not responding, there were no changes after 3 months of treatment in the urine proteome,” Dr. Fava said. Among those who did respond to treatment, the levels of these proteins – IL-16, CD163, galectin-1, and CD206 – decreased significantly.

“So the proteins that are linked to renal activity decrease only in responders, suggesting that effective immunosuppression is effective in reducing intrarenal inflammation, which eventually results in low proteinuria at 1 year.”

The decline in these biomarkers persisted at 1 year, and the study suggested it was a better predictor of which patients would respond to treatment at 1 year than proteinuria.

Dr. Fava said in an interview that better biomarkers could revolutionize the treatment and management of lupus nephritis.

“First of all, it can shift the management strategy from treatment to prevention, because at the very beginning we can nip it in the bud maybe with very gentle treatment,” he said. Different panels of urine biomarkers could identify patients at risk of treatment failure, and also help patients to taper off their immunosuppressive therapy without an increased risk of flare. “If we have a way to tell us there’s still inflammation that needs treatment, that could change the way we do it,” he said.

He acknowledged there are significant challenges to developing these biomarkers for clinical use; one is the decision of how to define disease activity without relying on proteinuria as a measure. “Why do I want a biomarker that can predict another biomarker?” he said.

Another presentation during the same session, by Huihua Ding, MD, of Shanghai Jiao Tong University in Shanghai, China, reported on the use of urinary L-selectin to assess renal disease activity and response to treatment in a multiethnic cohort.

This study, involving 474 patients with SLE with or without renal involvement in the United States and China, found levels of urinary L-selectin were elevated only in patients with active lupus nephritis and showed patterns that correlated with renal histologic characteristics.

Clinical rheumatologist Eric F. Morand, MD, PhD, and head of the School of Clinical Sciences at Monash University in Melbourne said one challenge with using urinary biomarkers was that it was not yet clear what these biomarkers reveal about the kidney. “It will be important to see whether this proteomic data actually link to renal outcomes,” Dr. Morand said in an interview. “I think predicting the response to treatment should be based around GFR [glomerular filtration rate] preservation, and I don’t think I’ve seen data yet that the urine biomarkers are going to tell us how to do that better.”

Dr. Morand is optimistic that urine biomarkers will one day be able to achieve that, but he stressed the importance of having urine biomarker tests available in the field at low cost. “You’re going to be doing the tests repeatedly, so therefore, you’re probably going to need to come down to a smaller list of proteins that you measure.”

Dr. Fava reported receiving support from Sanofi and Annexion Bio.