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NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — Rheumatologists, dermatologists, drug manufacturers, and researchers do not pay enough attention to the role sex and gender play in the pathogenesis and presentation of psoriatic arthritis (PsA), Lihi Eder, MD, PhD, said at the Tenth Annual NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Being mindful that the disease and treatments affect men and women differently makes patient management more personalized and effective, she noted.

“We tend to ignore sex and gender when we manage our patients in our approach to psoriatic arthritis as well as other rheumatic diseases,” Eder said. “We have to start thinking about sex of the patient as a biomarker that can potentially help us personalize care and move from a gender-blinded to a gender-specific approach.”

Eder, the Canada Research Chair in Inflammatory Rheumatic Diseases at the Women’s College Hospital of the University of Toronto, in Ontario, Canada, said much of the obfuscation of the role gender plays in PsA begins with research. “There’s very little research into sex differences in PsA,” she said. A meta-analysis published last year by her group found that while 51% of participants in 54 PsA trials were women, only nine (17%) reported baseline characteristics by sex, 18 (33%) reported efficacy by sex, and two (4%) reported safety endpoints by sex.

Eder said sex is a biological factor, whereas gender is a “more complex” factor based on social and cultural aspects of men and women.

 

PsA Differences in Women vs Men

Although the prevalence of PsA in men and women is similar, sex affects the risk of developing rheumatic disease. For example, Eder cited a host of studies that showed Sjögren’s syndrome and systemic lupus erythematosus have a 9:1 and 7:1 prevalence in women vs men, whereas gout has a 1:4 prevalence.

Her group’s 2013 study, along with a 2023 study from Italy, found significant differences in how PsA disease activity and quality of life differ between the two sexes.

“Females tend to have a higher tender joint count and more clinical entheses,” Eder said. “They also have worse patient-reported outcomes when it comes to pain, fatigue, and physical dysfunction, and these are things that would influence quality of life.

“On the other hand, when we look at male patients, they tend to have higher CRP [C-reactive protein] levels, they tend to have more severe restriction in the spine, and they also tend to have more severe psoriasis.”

She added that women are less likely than men to develop joint damage that’s picked up on x-rays.

 

Questioning Drug Development 

A gender gap exists across four phases of drug development, Eder said. Preclinical studies tend to rely on single-sex models, phase 1 clinical trials target a standard 70-kg healthy male, and phase 2 and 3 trials as well as postmarketing surveillance do not consider gender in study design and have limited reporting of sex-specific endpoints, she said.

“So, it’s very hard to pick up these signals, and this may explain why most of the drugs that are withdrawn from the market pose a greater risk for women than for men,” she said, citing a 2001 Government Accountability Office report that found that 80% of prescription drugs withdrawn from the market pose a greater risk for women.

That gender bias also carries over to drug commercialization, she said. The sleeping pill zolpidem remains one of the few drugs for which the Food and Drug Administration has approved sex-specific dosing, Eder noted.

Her group’s 2023 meta-analysis showed that men and women respond differently to approved biological disease-modifying antirheumatic drugs. That research, which included a subanalysis of 18 trials and 6821 patients, found that men had a better American College of Rheumatology 20 response to tumor necrosis factor (TNF), interleukin-17 (IL-17), and IL-23 inhibitors, but there was no difference between the sexes in response to Janus-activated kinase (JAK) and tyrosine kinase 2 inhibitors. The same subanalysis also found no difference in the placebo response between men and women in those trials.

“So this raises the question: Should we consider the sex of the patient when we select treatments?” Eder said.

A French study last year reported that men had higher rates of persistence after 1 year: 62% vs 52% for women for TNF inhibitor, IL-17 inhibitor, and IL-23 inhibitor agents, but persistence rates for JAK inhibitors were similar between sexes.

“People ask me should we start favoring JAK inhibitors for females,” Eder said. “I think it’s premature. We need to do more research, but it does raise the question.”

A study by Eder and her group reported that women were more likely than men to discontinue their medications because their symptoms did not improve or the side effects were intolerable.

Another sex-differentiating factor of PsA that clinicians should take into account, Eder said, is the way men and women experience pain. “Women tend to report higher levels of pain across different rheumatic conditions,” she said, citing her own group’s 2022 study and a 2020 Dutch study. Cultural differences in how the sexes approach pain may also come into play, with men expected to be more tolerant and women more susceptible to it, Eder added. 

 

Evidence Is Mounting, but More Is Needed

The evidence that explains why these apparent differences exist between men and women with PsA is still lacking, Eder said in an interview with Medscape Medical News. “It’s very hard now because we don’t know the differences,” she said. “It’s very hard to know the solutions when you don’t know why things are happening.”

Nonetheless, she said, in her own practice she tries to be attuned to pain in women and is trying to stay unbiased when her patients talk about pain.

“I’ve also started asking females as they go into menopause or around the age of the mid-40s — those that complain about pain — about other menopausal-related symptoms, which I didn’t do before,” Eder said. She said she counsels patients whose pain might be driven by potentially menopausal transition, especially if they’re taking hormone-replacement therapy. She added that she is also using objective measures to differentiate PsA-related pain from other causes, such as fibromyalgia or depression.

Asked to comment on this topic, Iannis Adamopoulos, PhD, associate professor of medicine and director of the Arthritis Program and Head of the Osteoimmunology Laboratory at Beth Israel Deaconess Medical Center, Boston, told Medscape Medical News, “the science is now building” to better understand how sex and gender influence PsA. He noted that the National Institutes of Health already mandates sex-specific mouse studies in any research it funds.

Human studies, however, must take into account a host of variables, Adamopoulos said. “You have more variation within the groups because you don’t control 100% of people; you don’t put them in cages,” he said.

In her presentation, Eder noted that her group’s research into sex dimorphisms in the proteomic profile in PsA found that men have 20 times more sex-specific differentially expressed proteins than women. But Adamopoulos said that “there are no male and female proteins at all. There could be different levels but not different proteins.”

The research into sex differences in PsA is nascent, he said, adding, “There’s still a lot to uncover.” 

Eder disclosed financial relationships with AbbVie, Eli Lilly, Pfizer, Novartis, Johnson & Johnson, Bristol Myers Squibb, UCB, Fresenius Kabi, and Sandoz. Adamopoulos had no relevant financial disclosures.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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

NEW YORK CITY — The idea of having dermatologists and rheumatologists under one roof to see patients with psoriasis prone to psoriatic arthritis (PsA) — a concept known as combined clinics — has been around for more than a decade, and the idea of personalized medicine for these patients even longer than that, yet both approaches to care have encountered a host of obstacles, a longtime research rheumatologist said.

“It’s important that we work together, but there is a problem in terms of staffing — managing the meetings with patients together — and in the states in particular it’s a matter of who’s charging for what,” Dafna Gladman, MD, a rheumatologist at the University of Toronto, in Ontario, Canada, told attendees at the annual New York University (NYU) Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis. Her institution has one of the 44 worldwide combined clinics registered in the Psoriasis & Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), of which Gladman is an advisory board member.

 

Barriers to Combined Clinics

“Some of the barriers are physical in the sense that, for the dermatologists and rheumatologists to work at the same time, you need the right space, and in many places, you just don’t have the space to have the two specialists sitting at the same time,” Gladman told Medscape Medical News.

Some centers get around this by having the dermatology and rheumatology clinics next to or near each other. “So these two specialists are close enough to be able to go from room to room,” she added.

Another challenge facing combined clinics lies in the nature of how dermatologists and rheumatologists see patients. “The dermatologist sees patients a lot faster than the rheumatologist, so if the dermatologist and rheumatologist are sitting together, the dermatologist may not see as many patients as they would otherwise and therefore may not get reimbursed properly,” Gladman said.

To overcome these challenges, different models have emerged, Gladman said. If space allows, the ideal model is to have both specialties in one clinic, she said, while compensating for the different pace at which dermatologists and rheumatologists see patients.

The other model is to locate the two clinics close enough so that a person with suspected PsA can get to the rheumatology clinic soon after their dermatologic consult, or the rheumatologist can go to the dermatology clinic, Gladman said. Or the situation may be reversed when the rheumatologist needs a dermatology consult, she added.

When that’s not possible, a virtual visit may be the solution, Gladman said. She noted that PPACMAN offers ways to overcome the challenges of running a combined clinic.

Whatever combined clinic model a center chooses, clinicians must be mindful of preventing patients from falling through the cracks, Gladman said.

“When you treat patients separately, the patient sees the rheumatologist, and the rheumatologist wants to do one thing; then they go to the dermatologist and the dermatologist wants to do another thing, and the patient doesn’t do anything because they don’t know what to choose,” she said.

The combined clinic allows the patient to get the opinions of both specialists and avoid the uncertainty about the course of treatment, Gladman added.

Some combined clinics may also house other specialists, such as gastroenterologists, cardiologists, and nurse practitioners, noted Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City. Such centers are typically in academic centers “given challenges with space, scheduling, and reimbursement,” he told Medscape Medical News. NYU has a PPACMAN-registered combined clinic.

Regardless of how combined clinics are organized, Scher said, “We have found that the most important aspect of combined clinics is the open communication and integration of care between and amongst specialists and patients.”

 

The Potential of Personalized Medicine

“Personalized medicine is where we need to get to,” Gladman told seminar attendees. She said she had hoped it would be further along by now and be more integrated into the care of patients with psoriasis and PsA. “The idea is to identify psoriasis patients that are destined to develop psoriatic arthritis,” she said.

Besides that, identifying biomarkers is key to advancing personalized medicine for psoriasis, Gladman noted.

“In the skin, it’s easy; even the patient can assess their psoriasis,” she said. “But in the joints, it’s very difficult, so it would be nice to have some kind of biomarker, whether it’s the blood or an imaging modality. We want to identify the biomarkers for drug response or lack thereof so we know what drugs would be appropriate for the individual patient, and therefore, we can provide the right drug for the right person and fortunately at the right time.”

In explaining why personalized medicine isn’t further along in dermatology and rheumatology, Gladman told Medscape Medical News, “It’s a matter of finding the right things; we haven’t solved the mystery.” She cited a previous discussion at the seminar about the pathogenesis of PsA. “One person thinks it’s the bone marrow and another thinks it’s the T cells, so we haven’t quite put it all together to have a definitive answer.”

Personalized medicine in psoriasis and PsA is a “key unmet need,” Scher said. “Multiomics” — a biological analysis approach that uses multiple “omes,” such as the genome and microbiome — digital features, and wearables “can unlock novel diagnostic and therapeutic pathways that are desperately needed to enhance clinical response in PsA,” he said.

Also emerging are humanized animal models for laboratory research, which Scher called “potentially very useful tools to personalize approaches to PsA pathogenesis and treatment.”

Gladman disclosed financial relationships with AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.

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

TOPLINE:

Patients who require biologic disease-modifying antirheumatic drugs (DMARDs) for severe RA are less likely to achieve sustained DMARD-free remission than those not needing the medication.

METHODOLOGY:

• Patients with early RA from the Leiden Early Arthritis Clinic (EAC; n = 627) and the Rotterdam Early Arthritis Cohort (tREACH) trial (n = 425) were followed for 5 years and 3 years, respectively.
• Most patients in both the EAC (86%) and tREACH (64%) cohorts had never used a biologic DMARD during the follow-up period.
• The primary outcome measure was sustained DMARD-free remission, defined as the absence of clinical synovitis after discontinuation of DMARDs for at least 1 year.

TAKEAWAY:

• None of the EAC patients using a biologic DMARD achieved sustained DMARD-free remission, but 37% of those who never used the drug reached remission at 5 years (hazard ratio [HR], 0.02; P < .0001).
• No tREACH patients using a biologic DMARD reached sustained DMARD-free remission, but 15% of those who never used the drug achieved remission at 3 years (HR, 0.03; P < .0001).
• Sustained DMARD-free remission was higher in EAC patients who were negative for anti-citrullinated protein antibody (ACPA) than in those who were ACPA-positive at 5 years (56% vs 14%; P < .0001).
• During follow-up, some patients in both the EAC (9%) and tREACH (14%) cohorts experienced late flares after more than 1 year of discontinuing DMARDs.

IN PRACTICE:

“Sustained DMARD-free remission is unlikely in patients needing a biologic DMARD,” the authors said.

SOURCE:

Judith W. Heutz, MD, Erasmus Medical Center, Rotterdam, the Netherlands, led the study, published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Because both cohorts were defined during follow-up rather than at baseline, outcomes related to the use of DMARDs and remission status could have been misinterpreted. Although the study adjusted for ACPA status, other factors such as disease activity were not corrected, which could have potentially led to residual confounding. Sparse data bias was present, especially in the biologic DMARD user group, in which none of the patients reached sustained DMARD-free remission.

DISCLOSURES:

The EAC received funding from the Dutch Arthritis Foundation and the European Research Council under the European Union’s Horizon 2020 research and innovation program. The tREACH trial was supported by an unrestricted grant from Pfizer. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Patients who require biologic disease-modifying antirheumatic drugs (DMARDs) for severe RA are less likely to achieve sustained DMARD-free remission than those not needing the medication.

METHODOLOGY:

• Patients with early RA from the Leiden Early Arthritis Clinic (EAC; n = 627) and the Rotterdam Early Arthritis Cohort (tREACH) trial (n = 425) were followed for 5 years and 3 years, respectively.
• Most patients in both the EAC (86%) and tREACH (64%) cohorts had never used a biologic DMARD during the follow-up period.
• The primary outcome measure was sustained DMARD-free remission, defined as the absence of clinical synovitis after discontinuation of DMARDs for at least 1 year.

TAKEAWAY:

• None of the EAC patients using a biologic DMARD achieved sustained DMARD-free remission, but 37% of those who never used the drug reached remission at 5 years (hazard ratio [HR], 0.02; P < .0001).
• No tREACH patients using a biologic DMARD reached sustained DMARD-free remission, but 15% of those who never used the drug achieved remission at 3 years (HR, 0.03; P < .0001).
• Sustained DMARD-free remission was higher in EAC patients who were negative for anti-citrullinated protein antibody (ACPA) than in those who were ACPA-positive at 5 years (56% vs 14%; P < .0001).
• During follow-up, some patients in both the EAC (9%) and tREACH (14%) cohorts experienced late flares after more than 1 year of discontinuing DMARDs.

IN PRACTICE:

“Sustained DMARD-free remission is unlikely in patients needing a biologic DMARD,” the authors said.

SOURCE:

Judith W. Heutz, MD, Erasmus Medical Center, Rotterdam, the Netherlands, led the study, published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Because both cohorts were defined during follow-up rather than at baseline, outcomes related to the use of DMARDs and remission status could have been misinterpreted. Although the study adjusted for ACPA status, other factors such as disease activity were not corrected, which could have potentially led to residual confounding. Sparse data bias was present, especially in the biologic DMARD user group, in which none of the patients reached sustained DMARD-free remission.

DISCLOSURES:

The EAC received funding from the Dutch Arthritis Foundation and the European Research Council under the European Union’s Horizon 2020 research and innovation program. The tREACH trial was supported by an unrestricted grant from Pfizer. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Patients who require biologic disease-modifying antirheumatic drugs (DMARDs) for severe RA are less likely to achieve sustained DMARD-free remission than those not needing the medication.

METHODOLOGY:

• Patients with early RA from the Leiden Early Arthritis Clinic (EAC; n = 627) and the Rotterdam Early Arthritis Cohort (tREACH) trial (n = 425) were followed for 5 years and 3 years, respectively.
• Most patients in both the EAC (86%) and tREACH (64%) cohorts had never used a biologic DMARD during the follow-up period.
• The primary outcome measure was sustained DMARD-free remission, defined as the absence of clinical synovitis after discontinuation of DMARDs for at least 1 year.

TAKEAWAY:

• None of the EAC patients using a biologic DMARD achieved sustained DMARD-free remission, but 37% of those who never used the drug reached remission at 5 years (hazard ratio [HR], 0.02; P < .0001).
• No tREACH patients using a biologic DMARD reached sustained DMARD-free remission, but 15% of those who never used the drug achieved remission at 3 years (HR, 0.03; P < .0001).
• Sustained DMARD-free remission was higher in EAC patients who were negative for anti-citrullinated protein antibody (ACPA) than in those who were ACPA-positive at 5 years (56% vs 14%; P < .0001).
• During follow-up, some patients in both the EAC (9%) and tREACH (14%) cohorts experienced late flares after more than 1 year of discontinuing DMARDs.

IN PRACTICE:

“Sustained DMARD-free remission is unlikely in patients needing a biologic DMARD,” the authors said.

SOURCE:

Judith W. Heutz, MD, Erasmus Medical Center, Rotterdam, the Netherlands, led the study, published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Because both cohorts were defined during follow-up rather than at baseline, outcomes related to the use of DMARDs and remission status could have been misinterpreted. Although the study adjusted for ACPA status, other factors such as disease activity were not corrected, which could have potentially led to residual confounding. Sparse data bias was present, especially in the biologic DMARD user group, in which none of the patients reached sustained DMARD-free remission.

DISCLOSURES:

The EAC received funding from the Dutch Arthritis Foundation and the European Research Council under the European Union’s Horizon 2020 research and innovation program. The tREACH trial was supported by an unrestricted grant from Pfizer. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors protect patients with axial spondyloarthritis (axSpA) from hip and spine fractures better than other drugs.

METHODOLOGY:

• Large US insurance claims database study comparing protective effects of TNF inhibitors vs other drugs on fractures in patients with axSpA.
• The study included 13,519 patients with axSpA aged 18-65 years, of whom 1229 had hip or spine fractures (mean age, 53 years; 38% women) and 12,290 were control participants without fractures.
• Effects of TNF inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), or no medication before the fracture were compared.
• The primary outcome was a composite hip and/or spine fracture, and the secondary outcome was a spine fracture.

TAKEAWAY:

• TNF inhibitor users had a lower risk for hip and spine fractures (adjusted odds ratio [aOR], 0.75; 95% CI, 0.62-0.91) than NSAID users, but this protective association was not seen in csDMARD users.
• Sex-stratified analysis showed similar protective effects of TNF inhibitors in both women and men.
• TNF inhibitor users showed a significantly lower risk for spine fractures than NSAID users (aOR, 0.81; 95% CI, 0.66-0.99).
• The protective effect of TNF inhibitors on hip and spine fractures was also seen in patients with a history of prior fractures; however, the effect was not statistically significant.

IN PRACTICE:

“Our findings underscore the multifaceted benefits of TNF inhibitors in axSpA,” the authors wrote.

SOURCE:

Devin Driscoll, MD, Section of Rheumatology, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, led the study, published online in Arthritis & Rheumatology.

LIMITATIONS:

Identification of the axSpA cohort and fracture outcomes was based solely on diagnostic and procedure codes, which may have led to misclassification. The administrative database lacked detailed information on disease activity levels, and the high proportion of missing data for body mass index, a known strong confounder for fracture risk, may have introduced bias. There were insufficient numbers of hip fractures to conduct analyses limited solely to hip fractures.

DISCLOSURES:

The study was supported by R03 AR076495 and NIH P30 AR072571. Two authors declared receiving grants, contracts, payments, honoraria, and other affiliations with various institutions and pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors protect patients with axial spondyloarthritis (axSpA) from hip and spine fractures better than other drugs.

METHODOLOGY:

• Large US insurance claims database study comparing protective effects of TNF inhibitors vs other drugs on fractures in patients with axSpA.
• The study included 13,519 patients with axSpA aged 18-65 years, of whom 1229 had hip or spine fractures (mean age, 53 years; 38% women) and 12,290 were control participants without fractures.
• Effects of TNF inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), or no medication before the fracture were compared.
• The primary outcome was a composite hip and/or spine fracture, and the secondary outcome was a spine fracture.

TAKEAWAY:

• TNF inhibitor users had a lower risk for hip and spine fractures (adjusted odds ratio [aOR], 0.75; 95% CI, 0.62-0.91) than NSAID users, but this protective association was not seen in csDMARD users.
• Sex-stratified analysis showed similar protective effects of TNF inhibitors in both women and men.
• TNF inhibitor users showed a significantly lower risk for spine fractures than NSAID users (aOR, 0.81; 95% CI, 0.66-0.99).
• The protective effect of TNF inhibitors on hip and spine fractures was also seen in patients with a history of prior fractures; however, the effect was not statistically significant.

IN PRACTICE:

“Our findings underscore the multifaceted benefits of TNF inhibitors in axSpA,” the authors wrote.

SOURCE:

Devin Driscoll, MD, Section of Rheumatology, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, led the study, published online in Arthritis & Rheumatology.

LIMITATIONS:

Identification of the axSpA cohort and fracture outcomes was based solely on diagnostic and procedure codes, which may have led to misclassification. The administrative database lacked detailed information on disease activity levels, and the high proportion of missing data for body mass index, a known strong confounder for fracture risk, may have introduced bias. There were insufficient numbers of hip fractures to conduct analyses limited solely to hip fractures.

DISCLOSURES:

The study was supported by R03 AR076495 and NIH P30 AR072571. Two authors declared receiving grants, contracts, payments, honoraria, and other affiliations with various institutions and pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors protect patients with axial spondyloarthritis (axSpA) from hip and spine fractures better than other drugs.

METHODOLOGY:

• Large US insurance claims database study comparing protective effects of TNF inhibitors vs other drugs on fractures in patients with axSpA.
• The study included 13,519 patients with axSpA aged 18-65 years, of whom 1229 had hip or spine fractures (mean age, 53 years; 38% women) and 12,290 were control participants without fractures.
• Effects of TNF inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), or no medication before the fracture were compared.
• The primary outcome was a composite hip and/or spine fracture, and the secondary outcome was a spine fracture.

TAKEAWAY:

• TNF inhibitor users had a lower risk for hip and spine fractures (adjusted odds ratio [aOR], 0.75; 95% CI, 0.62-0.91) than NSAID users, but this protective association was not seen in csDMARD users.
• Sex-stratified analysis showed similar protective effects of TNF inhibitors in both women and men.
• TNF inhibitor users showed a significantly lower risk for spine fractures than NSAID users (aOR, 0.81; 95% CI, 0.66-0.99).
• The protective effect of TNF inhibitors on hip and spine fractures was also seen in patients with a history of prior fractures; however, the effect was not statistically significant.

IN PRACTICE:

“Our findings underscore the multifaceted benefits of TNF inhibitors in axSpA,” the authors wrote.

SOURCE:

Devin Driscoll, MD, Section of Rheumatology, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, led the study, published online in Arthritis & Rheumatology.

LIMITATIONS:

Identification of the axSpA cohort and fracture outcomes was based solely on diagnostic and procedure codes, which may have led to misclassification. The administrative database lacked detailed information on disease activity levels, and the high proportion of missing data for body mass index, a known strong confounder for fracture risk, may have introduced bias. There were insufficient numbers of hip fractures to conduct analyses limited solely to hip fractures.

DISCLOSURES:

The study was supported by R03 AR076495 and NIH P30 AR072571. Two authors declared receiving grants, contracts, payments, honoraria, and other affiliations with various institutions and pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Stem cell transplantation tames some refractory systemic juvenile idiopathic arthritis–related lung disease that does not respond to other treatment.

METHODOLOGY:

• Retrospective cohort study of 13 children with refractory systemic juvenile idiopathic arthritis–related lung disease (sJIA-LD) who had allogeneic hematopoietic stem cell transplantation (HSCT).
• Children whose median age was 9 years at transplantation underwent HSCT at nine hospitals in the United States and Europe between January 2018 and October 2022, with a median follow-up of 16 months.
• Outcomes included transplant-related complications, pulmonary outcomes (eg, oxygen dependence and chest CT findings), and overall outcomes (eg, complete response, partial response, and death).

TAKEAWAY:

• Five patients developed acute graft vs host disease of varying grades, but none experienced chronic disease.
• All nine surviving patients achieved a complete response at the last follow-up, with no sJIA characteristics or need for immunosuppressive therapy or supplemental oxygen.
• Four patients died from complications including cytomegalovirus pneumonitis (n = 2), intracranial hemorrhage (n = 1), and progressive sJIA-LD (n = 1).
• Of six patients who underwent posttransplant chest CT, three had improved lung health, two had stable lung disease, and one experienced worsening lung disease, ultimately resulting in death.

IN PRACTICE:

“Allogeneic HSCT should be considered for treatment-refractory sJIA-LD,” the authors wrote.

“Efforts are being pursued for earlier recognition of patients with sJIA-LD at risk of adverse reactions to biologics. Early detection should help to avoid repeated treatments that are less effective and possibly deleterious and consider therapeutic approaches (eg, anti–[interleukin]-18 or [interferon]-delta–targeted treatments) that might act as a bridge therapy to control disease activity before HSCT,” wrote the author of an accompanying editorial.

SOURCE:

Michael G. Matt, MD, and Daniel Drozdov, MD, led the study, which was published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Limitations included sampling bias and heterogeneity in clinical follow-up. The small sample size made it difficult to identify variables affecting survival and the achievement of a complete response. Additionally, many patients had relatively short follow-up periods.

DISCLOSURES:

This study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. Several authors reported receiving advisory board fees, consulting fees, honoraria, grant funds, and stocks and shares from various research institutes and pharmaceutical organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Stem cell transplantation tames some refractory systemic juvenile idiopathic arthritis–related lung disease that does not respond to other treatment.

METHODOLOGY:

• Retrospective cohort study of 13 children with refractory systemic juvenile idiopathic arthritis–related lung disease (sJIA-LD) who had allogeneic hematopoietic stem cell transplantation (HSCT).
• Children whose median age was 9 years at transplantation underwent HSCT at nine hospitals in the United States and Europe between January 2018 and October 2022, with a median follow-up of 16 months.
• Outcomes included transplant-related complications, pulmonary outcomes (eg, oxygen dependence and chest CT findings), and overall outcomes (eg, complete response, partial response, and death).

TAKEAWAY:

• Five patients developed acute graft vs host disease of varying grades, but none experienced chronic disease.
• All nine surviving patients achieved a complete response at the last follow-up, with no sJIA characteristics or need for immunosuppressive therapy or supplemental oxygen.
• Four patients died from complications including cytomegalovirus pneumonitis (n = 2), intracranial hemorrhage (n = 1), and progressive sJIA-LD (n = 1).
• Of six patients who underwent posttransplant chest CT, three had improved lung health, two had stable lung disease, and one experienced worsening lung disease, ultimately resulting in death.

IN PRACTICE:

“Allogeneic HSCT should be considered for treatment-refractory sJIA-LD,” the authors wrote.

“Efforts are being pursued for earlier recognition of patients with sJIA-LD at risk of adverse reactions to biologics. Early detection should help to avoid repeated treatments that are less effective and possibly deleterious and consider therapeutic approaches (eg, anti–[interleukin]-18 or [interferon]-delta–targeted treatments) that might act as a bridge therapy to control disease activity before HSCT,” wrote the author of an accompanying editorial.

SOURCE:

Michael G. Matt, MD, and Daniel Drozdov, MD, led the study, which was published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Limitations included sampling bias and heterogeneity in clinical follow-up. The small sample size made it difficult to identify variables affecting survival and the achievement of a complete response. Additionally, many patients had relatively short follow-up periods.

DISCLOSURES:

This study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. Several authors reported receiving advisory board fees, consulting fees, honoraria, grant funds, and stocks and shares from various research institutes and pharmaceutical organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Stem cell transplantation tames some refractory systemic juvenile idiopathic arthritis–related lung disease that does not respond to other treatment.

METHODOLOGY:

• Retrospective cohort study of 13 children with refractory systemic juvenile idiopathic arthritis–related lung disease (sJIA-LD) who had allogeneic hematopoietic stem cell transplantation (HSCT).
• Children whose median age was 9 years at transplantation underwent HSCT at nine hospitals in the United States and Europe between January 2018 and October 2022, with a median follow-up of 16 months.
• Outcomes included transplant-related complications, pulmonary outcomes (eg, oxygen dependence and chest CT findings), and overall outcomes (eg, complete response, partial response, and death).

TAKEAWAY:

• Five patients developed acute graft vs host disease of varying grades, but none experienced chronic disease.
• All nine surviving patients achieved a complete response at the last follow-up, with no sJIA characteristics or need for immunosuppressive therapy or supplemental oxygen.
• Four patients died from complications including cytomegalovirus pneumonitis (n = 2), intracranial hemorrhage (n = 1), and progressive sJIA-LD (n = 1).
• Of six patients who underwent posttransplant chest CT, three had improved lung health, two had stable lung disease, and one experienced worsening lung disease, ultimately resulting in death.

IN PRACTICE:

“Allogeneic HSCT should be considered for treatment-refractory sJIA-LD,” the authors wrote.

“Efforts are being pursued for earlier recognition of patients with sJIA-LD at risk of adverse reactions to biologics. Early detection should help to avoid repeated treatments that are less effective and possibly deleterious and consider therapeutic approaches (eg, anti–[interleukin]-18 or [interferon]-delta–targeted treatments) that might act as a bridge therapy to control disease activity before HSCT,” wrote the author of an accompanying editorial.

SOURCE:

Michael G. Matt, MD, and Daniel Drozdov, MD, led the study, which was published online on December 20, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Limitations included sampling bias and heterogeneity in clinical follow-up. The small sample size made it difficult to identify variables affecting survival and the achievement of a complete response. Additionally, many patients had relatively short follow-up periods.

DISCLOSURES:

This study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. Several authors reported receiving advisory board fees, consulting fees, honoraria, grant funds, and stocks and shares from various research institutes and pharmaceutical organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Higher levels of environmental metals in urine are associated with poorer cognitive performance and an increased risk for dementia, new research suggests.

METHODOLOGY:

• This multicenter prospective cohort study included 6303 participants from six US study centers from 2000 to 2002, with follow-up through 2018.
• Participants were aged 45-84 years (median age at baseline, 60 years; 52% women) and were free of diagnosed cardiovascular disease.
• Researchers measured urinary levels of arsenic, cadmium, cobalt, copper, lead, manganese, tungsten, uranium, and zinc.
• Neuropsychological assessments included the Digit Symbol Coding, Cognitive Abilities Screening Instrument, and Digit Span tests.
• The median follow-up duration was 11.7 years for participants with dementia and 16.8 years for those without; 559 cases of dementia were identified during the study.

TAKEAWAY:

• Lower Digit Symbol Coding scores were associated with higher urinary concentrations of arsenic (mean difference [MD] in score per interquartile range [IQR] increase, –0.03), cobalt (MD per IQR increase, –0.05), copper (MD per IQR increase, –0.05), uranium (MD per IQR increase, –0.04), and zinc (MD per IQR increase, –0.03).
• Effects for cobalt, uranium, and zinc were stronger in apolipoprotein epsilon 4 allele (APOE4) carriers vs noncarriers.
• Higher urinary levels of copper were associated with lower Digit Span scores (MD, –0.043) and elevated levels of copper (MD, –0.028) and zinc (MD, –0.024) were associated with lower global cognitive scores.
• Individuals with urinary levels of the nine-metal mixture at the 95th percentile had a 71% higher risk for dementia compared to those with levels at the 25th percentile, with the risk more pronounced in APOE4 carriers than in noncarriers (MD, –0.30 vs –0.10, respectively).

IN PRACTICE:

“We found an inverse association of essential and nonessential metals in urine, both individually and as a mixture, with the speed of mental operations, as well as a positive association of urinary metal levels with dementia risk. As metal exposure and levels in the body are modifiable, these findings could inform early screening and precision interventions for dementia prevention based on individuals’ metal exposure and genetic profiles,” the investigators wrote.

 

SOURCE:

The study was led by Arce Domingo-Relloso, PhD, Columbia University Mailman School of Public Health, New York City. It was published online in JAMA Network Open.

 

LIMITATIONS:

Data may have been missed for patients with dementia who were never hospitalized, died, or were lost to follow-up. The dementia diagnosis included nonspecific International Classification of Diseases codes, potentially leading to false-positive reports. In addition, the sample size was not sufficient to evaluate the associations between metal exposure and cognitive test scores for carriers of two APOE4 alleles.

 

DISCLOSURES:

The study was supported by the National Heart, Lung, and Blood Institute. Several authors reported receiving grants from the National Institutes of Health and consulting fees, editorial stipends, teaching fees, or unrelated grant funding from various sources, which are fully listed in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Higher levels of environmental metals in urine are associated with poorer cognitive performance and an increased risk for dementia, new research suggests.

METHODOLOGY:

• This multicenter prospective cohort study included 6303 participants from six US study centers from 2000 to 2002, with follow-up through 2018.
• Participants were aged 45-84 years (median age at baseline, 60 years; 52% women) and were free of diagnosed cardiovascular disease.
• Researchers measured urinary levels of arsenic, cadmium, cobalt, copper, lead, manganese, tungsten, uranium, and zinc.
• Neuropsychological assessments included the Digit Symbol Coding, Cognitive Abilities Screening Instrument, and Digit Span tests.
• The median follow-up duration was 11.7 years for participants with dementia and 16.8 years for those without; 559 cases of dementia were identified during the study.

TAKEAWAY:

• Lower Digit Symbol Coding scores were associated with higher urinary concentrations of arsenic (mean difference [MD] in score per interquartile range [IQR] increase, –0.03), cobalt (MD per IQR increase, –0.05), copper (MD per IQR increase, –0.05), uranium (MD per IQR increase, –0.04), and zinc (MD per IQR increase, –0.03).
• Effects for cobalt, uranium, and zinc were stronger in apolipoprotein epsilon 4 allele (APOE4) carriers vs noncarriers.
• Higher urinary levels of copper were associated with lower Digit Span scores (MD, –0.043) and elevated levels of copper (MD, –0.028) and zinc (MD, –0.024) were associated with lower global cognitive scores.
• Individuals with urinary levels of the nine-metal mixture at the 95th percentile had a 71% higher risk for dementia compared to those with levels at the 25th percentile, with the risk more pronounced in APOE4 carriers than in noncarriers (MD, –0.30 vs –0.10, respectively).

IN PRACTICE:

“We found an inverse association of essential and nonessential metals in urine, both individually and as a mixture, with the speed of mental operations, as well as a positive association of urinary metal levels with dementia risk. As metal exposure and levels in the body are modifiable, these findings could inform early screening and precision interventions for dementia prevention based on individuals’ metal exposure and genetic profiles,” the investigators wrote.

 

SOURCE:

The study was led by Arce Domingo-Relloso, PhD, Columbia University Mailman School of Public Health, New York City. It was published online in JAMA Network Open.

 

LIMITATIONS:

Data may have been missed for patients with dementia who were never hospitalized, died, or were lost to follow-up. The dementia diagnosis included nonspecific International Classification of Diseases codes, potentially leading to false-positive reports. In addition, the sample size was not sufficient to evaluate the associations between metal exposure and cognitive test scores for carriers of two APOE4 alleles.

 

DISCLOSURES:

The study was supported by the National Heart, Lung, and Blood Institute. Several authors reported receiving grants from the National Institutes of Health and consulting fees, editorial stipends, teaching fees, or unrelated grant funding from various sources, which are fully listed in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Higher levels of environmental metals in urine are associated with poorer cognitive performance and an increased risk for dementia, new research suggests.

METHODOLOGY:

• This multicenter prospective cohort study included 6303 participants from six US study centers from 2000 to 2002, with follow-up through 2018.
• Participants were aged 45-84 years (median age at baseline, 60 years; 52% women) and were free of diagnosed cardiovascular disease.
• Researchers measured urinary levels of arsenic, cadmium, cobalt, copper, lead, manganese, tungsten, uranium, and zinc.
• Neuropsychological assessments included the Digit Symbol Coding, Cognitive Abilities Screening Instrument, and Digit Span tests.
• The median follow-up duration was 11.7 years for participants with dementia and 16.8 years for those without; 559 cases of dementia were identified during the study.

TAKEAWAY:

• Lower Digit Symbol Coding scores were associated with higher urinary concentrations of arsenic (mean difference [MD] in score per interquartile range [IQR] increase, –0.03), cobalt (MD per IQR increase, –0.05), copper (MD per IQR increase, –0.05), uranium (MD per IQR increase, –0.04), and zinc (MD per IQR increase, –0.03).
• Effects for cobalt, uranium, and zinc were stronger in apolipoprotein epsilon 4 allele (APOE4) carriers vs noncarriers.
• Higher urinary levels of copper were associated with lower Digit Span scores (MD, –0.043) and elevated levels of copper (MD, –0.028) and zinc (MD, –0.024) were associated with lower global cognitive scores.
• Individuals with urinary levels of the nine-metal mixture at the 95th percentile had a 71% higher risk for dementia compared to those with levels at the 25th percentile, with the risk more pronounced in APOE4 carriers than in noncarriers (MD, –0.30 vs –0.10, respectively).

IN PRACTICE:

“We found an inverse association of essential and nonessential metals in urine, both individually and as a mixture, with the speed of mental operations, as well as a positive association of urinary metal levels with dementia risk. As metal exposure and levels in the body are modifiable, these findings could inform early screening and precision interventions for dementia prevention based on individuals’ metal exposure and genetic profiles,” the investigators wrote.

 

SOURCE:

The study was led by Arce Domingo-Relloso, PhD, Columbia University Mailman School of Public Health, New York City. It was published online in JAMA Network Open.

 

LIMITATIONS:

Data may have been missed for patients with dementia who were never hospitalized, died, or were lost to follow-up. The dementia diagnosis included nonspecific International Classification of Diseases codes, potentially leading to false-positive reports. In addition, the sample size was not sufficient to evaluate the associations between metal exposure and cognitive test scores for carriers of two APOE4 alleles.

 

DISCLOSURES:

The study was supported by the National Heart, Lung, and Blood Institute. Several authors reported receiving grants from the National Institutes of Health and consulting fees, editorial stipends, teaching fees, or unrelated grant funding from various sources, which are fully listed in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A rare coin-shaped headache long viewed as a primary headache disorder frequently has underlying causes, according to new research, and clinicians should refer people who present with it for imaging.

First described in 2003, nummular or coin-shaped headache comprises an intermittent or constant pain limited to a rounded region between 1 and 6 cm in diameter. Classed as a primary headache by the International Classification of Headache Disorders (ICHD-3), it usually occurs in the parietal, or top rear, region of the head.

Despite nummular headache’s classification as a primary disorder, studies have linked some cases of coin-shaped headache to cranial or intracranial lesions. Now, a group of Spanish researchers has revised 20 years’ worth of cases, representing the largest series to date, and found a wide variety of causes, some of which, they say, had not been reported before in connection to this headache type.

For their research, published online in Headache, Antonio Sánchez-Soblechero, MD, and colleagues at the University Hospital Gregorio Marañón in Madrid, Spain, looked at clinical and imaging findings from 131 patients (67% women, median age at onset 52) seen from 2002 to 2022 at their center, seeking to identify any differences among primary and secondary or symptomatic coin-shaped headache cases. All patients underwent cranial MRI, CT, or both.

Altogether, 26% of the nummular headaches (n = 34) were found associated with trauma, vascular malformations, cranial bone disorders, neoplasia, arachnoid cysts, hypertension, aneurysm, or skin disorders including, in one case, a psoriasis plaque. Hypertension, aneurysm, and psoriasis were not previously described as causes of this headache, the authors said.

The definition of a nummular headache includes that secondary causes need to be excluded, according to the ICHD-3. The study authors proposed that “definite” secondary cases should meet ICHD-3 diagnostic criteria for nummular headache as well as for secondary headache, while “probable” cases meet all criteria for the former and all but one of the criteria for the latter. In their study, eight patients met the proposed criteria for “definite,” while the rest were deemed “probable” secondary cases.

Headache symptoms remained similar regardless of etiology, Sánchez-Soblechero and colleagues found, but coin-shaped headaches deemed to have secondary etiologies were significantly more likely to be associated with previous headache, remote head trauma, and longer symptom duration. The authors described treatments, including surgical interventions, for cases with secondary causes.

Preventive treatment was more effective in patients with determined causes for their headaches, Sánchez-Soblechero and colleagues found, with 72% seeing their monthly headache days halved, compared with just 30% of patients in whom a cause was not identified.

“The presence of any previous headache or remote head trauma may suggest a diagnosis of symptomatic nummular headache; however, as certain nummular headache might be an early symptom of intracranial mass lesions, neuroimaging is necessary. Finding the cause of nummular headache is essential to offer the most effective targeted treatment,” the investigators wrote in their analysis.

 

Primary Headache or Secondary?

In an interview, neurologist and headache specialist Nina Riggins, MD, PhD, of VA Palo Alto Health Care in California, praised the new findings as underscoring the importance of a thorough clinical approach.

“What this study shows is applicable to many primary headache disorders, whether migraine or cluster or nummular,” Riggins said. “Secondary headache can look like all of these headache types.”

Understanding what should be done to rule out secondary causes of headache is key for the correct diagnosis, she said. “In cases of coin-shaped headache, one should do a detailed neurological exam, consider imaging, check blood pressure, do blood work, and consider exams to exclude autoimmune psoriasis and other disorders as appropriate.”

Despite the inherent limits of its retrospective, single-center design, the study by Sánchez-Soblechero and colleagues is “extremely helpful in emphasizing that we should not dismiss [nummular headache] because it’s a little area of 1-6 centimeters,” Riggins said. “We absolutely have to make sure that we have ruled out secondary causes.” And while it would be useful to have evidence from prospective studies of nummular headache, “with such a rare headache, it’s hard. That’s why it’s so precious to have a study like this one, with 131 patients.”

Riggins acknowledged that the study emphasized the challenges of classifying and diagnosing nummular headache. The ICHD, last revised in 2018, “is a living, breathing document,” she said. “The idea is that as we learn more about headache disorders over time, this may mean changing some primary headaches to secondary, but we are clearly not there with this research: Most participants did not have a secondary cause for their coin-shaped headache.”

For now, Riggins said, “I think it’s best to keep classification straightforward for primary and secondary headache. It’s helpful for my day-to-day clinic life to have this neat division in place. But we do have to exclude secondary headache whenever possible in order to say that this is primary headache.”

Sánchez-Soblechero and coauthors disclosed no financial conflicts of interest related to their findings. Riggins disclosed consulting work for Gerson Lehrman Group, receiving research support from electroCore, Theranica, and Eli Lilly, and serving on advisory boards for Theranica, Teva Pharmaceuticals, Lundbeck, and Amneal Pharmaceuticals.

A version of this article appeared on Medscape.com.

A rare coin-shaped headache long viewed as a primary headache disorder frequently has underlying causes, according to new research, and clinicians should refer people who present with it for imaging.

First described in 2003, nummular or coin-shaped headache comprises an intermittent or constant pain limited to a rounded region between 1 and 6 cm in diameter. Classed as a primary headache by the International Classification of Headache Disorders (ICHD-3), it usually occurs in the parietal, or top rear, region of the head.

Despite nummular headache’s classification as a primary disorder, studies have linked some cases of coin-shaped headache to cranial or intracranial lesions. Now, a group of Spanish researchers has revised 20 years’ worth of cases, representing the largest series to date, and found a wide variety of causes, some of which, they say, had not been reported before in connection to this headache type.

For their research, published online in Headache, Antonio Sánchez-Soblechero, MD, and colleagues at the University Hospital Gregorio Marañón in Madrid, Spain, looked at clinical and imaging findings from 131 patients (67% women, median age at onset 52) seen from 2002 to 2022 at their center, seeking to identify any differences among primary and secondary or symptomatic coin-shaped headache cases. All patients underwent cranial MRI, CT, or both.

Altogether, 26% of the nummular headaches (n = 34) were found associated with trauma, vascular malformations, cranial bone disorders, neoplasia, arachnoid cysts, hypertension, aneurysm, or skin disorders including, in one case, a psoriasis plaque. Hypertension, aneurysm, and psoriasis were not previously described as causes of this headache, the authors said.

The definition of a nummular headache includes that secondary causes need to be excluded, according to the ICHD-3. The study authors proposed that “definite” secondary cases should meet ICHD-3 diagnostic criteria for nummular headache as well as for secondary headache, while “probable” cases meet all criteria for the former and all but one of the criteria for the latter. In their study, eight patients met the proposed criteria for “definite,” while the rest were deemed “probable” secondary cases.

Headache symptoms remained similar regardless of etiology, Sánchez-Soblechero and colleagues found, but coin-shaped headaches deemed to have secondary etiologies were significantly more likely to be associated with previous headache, remote head trauma, and longer symptom duration. The authors described treatments, including surgical interventions, for cases with secondary causes.

Preventive treatment was more effective in patients with determined causes for their headaches, Sánchez-Soblechero and colleagues found, with 72% seeing their monthly headache days halved, compared with just 30% of patients in whom a cause was not identified.

“The presence of any previous headache or remote head trauma may suggest a diagnosis of symptomatic nummular headache; however, as certain nummular headache might be an early symptom of intracranial mass lesions, neuroimaging is necessary. Finding the cause of nummular headache is essential to offer the most effective targeted treatment,” the investigators wrote in their analysis.

 

Primary Headache or Secondary?

In an interview, neurologist and headache specialist Nina Riggins, MD, PhD, of VA Palo Alto Health Care in California, praised the new findings as underscoring the importance of a thorough clinical approach.

“What this study shows is applicable to many primary headache disorders, whether migraine or cluster or nummular,” Riggins said. “Secondary headache can look like all of these headache types.”

Understanding what should be done to rule out secondary causes of headache is key for the correct diagnosis, she said. “In cases of coin-shaped headache, one should do a detailed neurological exam, consider imaging, check blood pressure, do blood work, and consider exams to exclude autoimmune psoriasis and other disorders as appropriate.”

Despite the inherent limits of its retrospective, single-center design, the study by Sánchez-Soblechero and colleagues is “extremely helpful in emphasizing that we should not dismiss [nummular headache] because it’s a little area of 1-6 centimeters,” Riggins said. “We absolutely have to make sure that we have ruled out secondary causes.” And while it would be useful to have evidence from prospective studies of nummular headache, “with such a rare headache, it’s hard. That’s why it’s so precious to have a study like this one, with 131 patients.”

Riggins acknowledged that the study emphasized the challenges of classifying and diagnosing nummular headache. The ICHD, last revised in 2018, “is a living, breathing document,” she said. “The idea is that as we learn more about headache disorders over time, this may mean changing some primary headaches to secondary, but we are clearly not there with this research: Most participants did not have a secondary cause for their coin-shaped headache.”

For now, Riggins said, “I think it’s best to keep classification straightforward for primary and secondary headache. It’s helpful for my day-to-day clinic life to have this neat division in place. But we do have to exclude secondary headache whenever possible in order to say that this is primary headache.”

Sánchez-Soblechero and coauthors disclosed no financial conflicts of interest related to their findings. Riggins disclosed consulting work for Gerson Lehrman Group, receiving research support from electroCore, Theranica, and Eli Lilly, and serving on advisory boards for Theranica, Teva Pharmaceuticals, Lundbeck, and Amneal Pharmaceuticals.

A version of this article appeared on Medscape.com.

A rare coin-shaped headache long viewed as a primary headache disorder frequently has underlying causes, according to new research, and clinicians should refer people who present with it for imaging.

First described in 2003, nummular or coin-shaped headache comprises an intermittent or constant pain limited to a rounded region between 1 and 6 cm in diameter. Classed as a primary headache by the International Classification of Headache Disorders (ICHD-3), it usually occurs in the parietal, or top rear, region of the head.

Despite nummular headache’s classification as a primary disorder, studies have linked some cases of coin-shaped headache to cranial or intracranial lesions. Now, a group of Spanish researchers has revised 20 years’ worth of cases, representing the largest series to date, and found a wide variety of causes, some of which, they say, had not been reported before in connection to this headache type.

For their research, published online in Headache, Antonio Sánchez-Soblechero, MD, and colleagues at the University Hospital Gregorio Marañón in Madrid, Spain, looked at clinical and imaging findings from 131 patients (67% women, median age at onset 52) seen from 2002 to 2022 at their center, seeking to identify any differences among primary and secondary or symptomatic coin-shaped headache cases. All patients underwent cranial MRI, CT, or both.

Altogether, 26% of the nummular headaches (n = 34) were found associated with trauma, vascular malformations, cranial bone disorders, neoplasia, arachnoid cysts, hypertension, aneurysm, or skin disorders including, in one case, a psoriasis plaque. Hypertension, aneurysm, and psoriasis were not previously described as causes of this headache, the authors said.

The definition of a nummular headache includes that secondary causes need to be excluded, according to the ICHD-3. The study authors proposed that “definite” secondary cases should meet ICHD-3 diagnostic criteria for nummular headache as well as for secondary headache, while “probable” cases meet all criteria for the former and all but one of the criteria for the latter. In their study, eight patients met the proposed criteria for “definite,” while the rest were deemed “probable” secondary cases.

Headache symptoms remained similar regardless of etiology, Sánchez-Soblechero and colleagues found, but coin-shaped headaches deemed to have secondary etiologies were significantly more likely to be associated with previous headache, remote head trauma, and longer symptom duration. The authors described treatments, including surgical interventions, for cases with secondary causes.

Preventive treatment was more effective in patients with determined causes for their headaches, Sánchez-Soblechero and colleagues found, with 72% seeing their monthly headache days halved, compared with just 30% of patients in whom a cause was not identified.

“The presence of any previous headache or remote head trauma may suggest a diagnosis of symptomatic nummular headache; however, as certain nummular headache might be an early symptom of intracranial mass lesions, neuroimaging is necessary. Finding the cause of nummular headache is essential to offer the most effective targeted treatment,” the investigators wrote in their analysis.

 

Primary Headache or Secondary?

In an interview, neurologist and headache specialist Nina Riggins, MD, PhD, of VA Palo Alto Health Care in California, praised the new findings as underscoring the importance of a thorough clinical approach.

“What this study shows is applicable to many primary headache disorders, whether migraine or cluster or nummular,” Riggins said. “Secondary headache can look like all of these headache types.”

Understanding what should be done to rule out secondary causes of headache is key for the correct diagnosis, she said. “In cases of coin-shaped headache, one should do a detailed neurological exam, consider imaging, check blood pressure, do blood work, and consider exams to exclude autoimmune psoriasis and other disorders as appropriate.”

Despite the inherent limits of its retrospective, single-center design, the study by Sánchez-Soblechero and colleagues is “extremely helpful in emphasizing that we should not dismiss [nummular headache] because it’s a little area of 1-6 centimeters,” Riggins said. “We absolutely have to make sure that we have ruled out secondary causes.” And while it would be useful to have evidence from prospective studies of nummular headache, “with such a rare headache, it’s hard. That’s why it’s so precious to have a study like this one, with 131 patients.”

Riggins acknowledged that the study emphasized the challenges of classifying and diagnosing nummular headache. The ICHD, last revised in 2018, “is a living, breathing document,” she said. “The idea is that as we learn more about headache disorders over time, this may mean changing some primary headaches to secondary, but we are clearly not there with this research: Most participants did not have a secondary cause for their coin-shaped headache.”

For now, Riggins said, “I think it’s best to keep classification straightforward for primary and secondary headache. It’s helpful for my day-to-day clinic life to have this neat division in place. But we do have to exclude secondary headache whenever possible in order to say that this is primary headache.”

Sánchez-Soblechero and coauthors disclosed no financial conflicts of interest related to their findings. Riggins disclosed consulting work for Gerson Lehrman Group, receiving research support from electroCore, Theranica, and Eli Lilly, and serving on advisory boards for Theranica, Teva Pharmaceuticals, Lundbeck, and Amneal Pharmaceuticals.

A version of this article appeared on Medscape.com.

TOPLINE:

Gout patients who take colchicine at the start of urate-lowering therapy have a lower risk for cardiovascular events than those who do not receive prophylaxis.

METHODOLOGY:

• Retrospective cohort study of 99,800 patients (mean age, 62.8 years; 74.4% men; 85.1% White) newly diagnosed with gout between January 1997 and March 2021 who initiated urate-lowering therapy.
• Gout flare prophylaxis, defined as a colchicine prescription for 21 days or more, was prescribed to 16,028 patients for a mean duration of 47.3 days at a mean daily dose of 0.97 mg.
• Patients who received colchicine prophylaxis and 83,772 patients who did not receive prophylaxis were followed for a mean of 175.5 and 176.9 days, respectively, in the intention-to-treat analysis.
• The primary outcome was the occurrence of the first cardiovascular event (fatal or nonfatal myocardial infarction or stroke) within 180 days of initiation of urate-lowering therapy.

TAKEAWAY:

• The risk for cardiovascular events was significantly lower with colchicine prophylaxis than without it (weighted hazard ratio [HR], 0.82; 95% CI, 0.69-0.94).
• The risk for a first-ever cardiovascular event was significantly lower with colchicine prophylaxis than without it (adjusted HR, 0.80; 95% CI, 0.62-0.97).
• The findings were similar regardless of analytical approach, and the intention-to-treat analysis did not show an increased risk for diarrhea with colchicine.

IN PRACTICE:

“The findings support consideration for the use of colchicine in people with gout and cardiovascular diseases,” the authors wrote. 

“The observed beneficial effect of colchicine concerns a huge group of patients worldwide. In addition, it is conceivable that, if a cardiovascular risk reduction is indeed confirmed, a strong argument arises to recommend the prescription of a course of colchicine to all [flaring] patients with gout, independently of their preference for urate-lowering therapy in general or urate-lowering therapy with or without colchicine prophylaxis more specifically,” experts wrote in a linked commentary.

SOURCE:

Edoardo Cipolletta, MD, Academic Rheumatology, School of Medicine, Nottingham City Hospital, University of Nottingham, England, led the study, which was published online in The Lancet Rheumatology.

LIMITATIONS: 

Because of the retrospective nature of the data extraction from a prospective database, the study had variations in follow-up and data completeness. Potential surveillance bias could have been introduced because patients with prior cardiovascular events were included in the study, and patients’ adherence to prescribed medications could not be verified.

DISCLOSURES:

This study was funded by the Foundation for Research in Rheumatology. Some authors reported receiving consulting fees, lecturing fees, and travel grants from various pharmaceutical companies and other additional sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Gout patients who take colchicine at the start of urate-lowering therapy have a lower risk for cardiovascular events than those who do not receive prophylaxis.

METHODOLOGY:

• Retrospective cohort study of 99,800 patients (mean age, 62.8 years; 74.4% men; 85.1% White) newly diagnosed with gout between January 1997 and March 2021 who initiated urate-lowering therapy.
• Gout flare prophylaxis, defined as a colchicine prescription for 21 days or more, was prescribed to 16,028 patients for a mean duration of 47.3 days at a mean daily dose of 0.97 mg.
• Patients who received colchicine prophylaxis and 83,772 patients who did not receive prophylaxis were followed for a mean of 175.5 and 176.9 days, respectively, in the intention-to-treat analysis.
• The primary outcome was the occurrence of the first cardiovascular event (fatal or nonfatal myocardial infarction or stroke) within 180 days of initiation of urate-lowering therapy.

TAKEAWAY:

• The risk for cardiovascular events was significantly lower with colchicine prophylaxis than without it (weighted hazard ratio [HR], 0.82; 95% CI, 0.69-0.94).
• The risk for a first-ever cardiovascular event was significantly lower with colchicine prophylaxis than without it (adjusted HR, 0.80; 95% CI, 0.62-0.97).
• The findings were similar regardless of analytical approach, and the intention-to-treat analysis did not show an increased risk for diarrhea with colchicine.

IN PRACTICE:

“The findings support consideration for the use of colchicine in people with gout and cardiovascular diseases,” the authors wrote. 

“The observed beneficial effect of colchicine concerns a huge group of patients worldwide. In addition, it is conceivable that, if a cardiovascular risk reduction is indeed confirmed, a strong argument arises to recommend the prescription of a course of colchicine to all [flaring] patients with gout, independently of their preference for urate-lowering therapy in general or urate-lowering therapy with or without colchicine prophylaxis more specifically,” experts wrote in a linked commentary.

SOURCE:

Edoardo Cipolletta, MD, Academic Rheumatology, School of Medicine, Nottingham City Hospital, University of Nottingham, England, led the study, which was published online in The Lancet Rheumatology.

LIMITATIONS: 

Because of the retrospective nature of the data extraction from a prospective database, the study had variations in follow-up and data completeness. Potential surveillance bias could have been introduced because patients with prior cardiovascular events were included in the study, and patients’ adherence to prescribed medications could not be verified.

DISCLOSURES:

This study was funded by the Foundation for Research in Rheumatology. Some authors reported receiving consulting fees, lecturing fees, and travel grants from various pharmaceutical companies and other additional sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Gout patients who take colchicine at the start of urate-lowering therapy have a lower risk for cardiovascular events than those who do not receive prophylaxis.

METHODOLOGY:

• Retrospective cohort study of 99,800 patients (mean age, 62.8 years; 74.4% men; 85.1% White) newly diagnosed with gout between January 1997 and March 2021 who initiated urate-lowering therapy.
• Gout flare prophylaxis, defined as a colchicine prescription for 21 days or more, was prescribed to 16,028 patients for a mean duration of 47.3 days at a mean daily dose of 0.97 mg.
• Patients who received colchicine prophylaxis and 83,772 patients who did not receive prophylaxis were followed for a mean of 175.5 and 176.9 days, respectively, in the intention-to-treat analysis.
• The primary outcome was the occurrence of the first cardiovascular event (fatal or nonfatal myocardial infarction or stroke) within 180 days of initiation of urate-lowering therapy.

TAKEAWAY:

• The risk for cardiovascular events was significantly lower with colchicine prophylaxis than without it (weighted hazard ratio [HR], 0.82; 95% CI, 0.69-0.94).
• The risk for a first-ever cardiovascular event was significantly lower with colchicine prophylaxis than without it (adjusted HR, 0.80; 95% CI, 0.62-0.97).
• The findings were similar regardless of analytical approach, and the intention-to-treat analysis did not show an increased risk for diarrhea with colchicine.

IN PRACTICE:

“The findings support consideration for the use of colchicine in people with gout and cardiovascular diseases,” the authors wrote. 

“The observed beneficial effect of colchicine concerns a huge group of patients worldwide. In addition, it is conceivable that, if a cardiovascular risk reduction is indeed confirmed, a strong argument arises to recommend the prescription of a course of colchicine to all [flaring] patients with gout, independently of their preference for urate-lowering therapy in general or urate-lowering therapy with or without colchicine prophylaxis more specifically,” experts wrote in a linked commentary.

SOURCE:

Edoardo Cipolletta, MD, Academic Rheumatology, School of Medicine, Nottingham City Hospital, University of Nottingham, England, led the study, which was published online in The Lancet Rheumatology.

LIMITATIONS: 

Because of the retrospective nature of the data extraction from a prospective database, the study had variations in follow-up and data completeness. Potential surveillance bias could have been introduced because patients with prior cardiovascular events were included in the study, and patients’ adherence to prescribed medications could not be verified.

DISCLOSURES:

This study was funded by the Foundation for Research in Rheumatology. Some authors reported receiving consulting fees, lecturing fees, and travel grants from various pharmaceutical companies and other additional sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.