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Treatment with Tildrakizumab Effective for Scalp Psoriasis in Phase 3b Study
TOPLINE:
METHODOLOGY:
- A 72-week, multicenter, randomized, double-blind, placebo-controlled phase 3b trial enrolled 231 patients with moderate to severe plaque psoriasis of the scalp.
- Patients were randomly assigned to receive placebo (n = 114) or tildrakizumab (n = 117) until week 16, when patients in the placebo group switched to receive tildrakizumab.
- The primary endpoint, Investigator Global Assessment modified 2011 (IGA) scalp response, was defined as a score of 0 (clear) or 1 (almost clear) or an improvement of at least two points at week 16.
- The treatment was stopped at week 52, and participants were observed for another 20 weeks for safety and tolerability.
TAKEAWAY:
- At week 16, the response rate was higher in the tildrakizumab group than in the placebo group (49.4% vs 7.3%; P < .00001), and it increased to 62.9% and 56.1% (after crossover), respectively, at week 52.
- Psoriasis Scalp Severity Index 90 (PSSI 90) response rates were 60.7% and 4.9% at week 16 in the tildrakizumab and placebo groups, rising to 65.2% and 57.3%, respectively, at week 52.
- More than 80% of the week 16 responders maintained IGA and PSSI 90 responses at week 52.
- More than 50% of patients in both groups experienced adverse events, with no treatment-related serious toxicity.
IN PRACTICE:
“Tildrakizumab maintains improvements in scalp psoriasis for up to 52 weeks,” the authors wrote.
SOURCE:
Howard L. Sofen, MD, University of California, Los Angeles, led the study, which was published online on December 22, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
This study excluded patients with predominantly scalp involvement and minimal whole body psoriasis, who might respond differently to the treatment. Results were obtained under controlled clinical conditions and may not be generalizable to clinical practice.
DISCLOSURES:
This study and analyses were funded by Sun Pharma. Sofen reported serving as a clinical investigator for various pharmaceutical companies, including Sun Pharma. Five authors were current or former employees of Sun Pharma and associated companies. Others also disclosed financial ties outside this work.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- A 72-week, multicenter, randomized, double-blind, placebo-controlled phase 3b trial enrolled 231 patients with moderate to severe plaque psoriasis of the scalp.
- Patients were randomly assigned to receive placebo (n = 114) or tildrakizumab (n = 117) until week 16, when patients in the placebo group switched to receive tildrakizumab.
- The primary endpoint, Investigator Global Assessment modified 2011 (IGA) scalp response, was defined as a score of 0 (clear) or 1 (almost clear) or an improvement of at least two points at week 16.
- The treatment was stopped at week 52, and participants were observed for another 20 weeks for safety and tolerability.
TAKEAWAY:
- At week 16, the response rate was higher in the tildrakizumab group than in the placebo group (49.4% vs 7.3%; P < .00001), and it increased to 62.9% and 56.1% (after crossover), respectively, at week 52.
- Psoriasis Scalp Severity Index 90 (PSSI 90) response rates were 60.7% and 4.9% at week 16 in the tildrakizumab and placebo groups, rising to 65.2% and 57.3%, respectively, at week 52.
- More than 80% of the week 16 responders maintained IGA and PSSI 90 responses at week 52.
- More than 50% of patients in both groups experienced adverse events, with no treatment-related serious toxicity.
IN PRACTICE:
“Tildrakizumab maintains improvements in scalp psoriasis for up to 52 weeks,” the authors wrote.
SOURCE:
Howard L. Sofen, MD, University of California, Los Angeles, led the study, which was published online on December 22, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
This study excluded patients with predominantly scalp involvement and minimal whole body psoriasis, who might respond differently to the treatment. Results were obtained under controlled clinical conditions and may not be generalizable to clinical practice.
DISCLOSURES:
This study and analyses were funded by Sun Pharma. Sofen reported serving as a clinical investigator for various pharmaceutical companies, including Sun Pharma. Five authors were current or former employees of Sun Pharma and associated companies. Others also disclosed financial ties outside this work.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- A 72-week, multicenter, randomized, double-blind, placebo-controlled phase 3b trial enrolled 231 patients with moderate to severe plaque psoriasis of the scalp.
- Patients were randomly assigned to receive placebo (n = 114) or tildrakizumab (n = 117) until week 16, when patients in the placebo group switched to receive tildrakizumab.
- The primary endpoint, Investigator Global Assessment modified 2011 (IGA) scalp response, was defined as a score of 0 (clear) or 1 (almost clear) or an improvement of at least two points at week 16.
- The treatment was stopped at week 52, and participants were observed for another 20 weeks for safety and tolerability.
TAKEAWAY:
- At week 16, the response rate was higher in the tildrakizumab group than in the placebo group (49.4% vs 7.3%; P < .00001), and it increased to 62.9% and 56.1% (after crossover), respectively, at week 52.
- Psoriasis Scalp Severity Index 90 (PSSI 90) response rates were 60.7% and 4.9% at week 16 in the tildrakizumab and placebo groups, rising to 65.2% and 57.3%, respectively, at week 52.
- More than 80% of the week 16 responders maintained IGA and PSSI 90 responses at week 52.
- More than 50% of patients in both groups experienced adverse events, with no treatment-related serious toxicity.
IN PRACTICE:
“Tildrakizumab maintains improvements in scalp psoriasis for up to 52 weeks,” the authors wrote.
SOURCE:
Howard L. Sofen, MD, University of California, Los Angeles, led the study, which was published online on December 22, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
This study excluded patients with predominantly scalp involvement and minimal whole body psoriasis, who might respond differently to the treatment. Results were obtained under controlled clinical conditions and may not be generalizable to clinical practice.
DISCLOSURES:
This study and analyses were funded by Sun Pharma. Sofen reported serving as a clinical investigator for various pharmaceutical companies, including Sun Pharma. Five authors were current or former employees of Sun Pharma and associated companies. Others also disclosed financial ties outside this work.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
New Ideas on PsA Pathogenesis May Drive New Treatments
NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.
Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.
Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.
Autoimmunity vs Immune Mediated
Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.
“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”
In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.
“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.
The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.
“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.
“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.
The ‘Additional Mechanism’
The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”
A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.
These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.
In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.
Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.
“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.
The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.
The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.”
Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.
An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”
Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.
A version of this article appeared on Medscape.com.
NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.
Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.
Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.
Autoimmunity vs Immune Mediated
Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.
“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”
In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.
“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.
The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.
“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.
“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.
The ‘Additional Mechanism’
The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”
A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.
These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.
In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.
Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.
“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.
The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.
The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.”
Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.
An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”
Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.
A version of this article appeared on Medscape.com.
NEW YORK — Over the past year, new evidence has emerged in support of the idea that psoriatic arthritis (PsA) is neither exclusively immune mediated nor a classic autoimmune disease, but that both mechanisms may be essential in disease pathogenesis, and that innate immune cells may possess adaptive properties that may lead to worsening of inflammation of the skin and joints.
Recent findings help dermatologists and rheumatologists to better understand the pathogenesis of PsA and may lead to more targeted and personalized therapies, Christopher Ritchlin, MD, MPH, who’s led research into the pathogenesis of inflammatory diseases, reported at the NYU Langone Advanced Seminar in Psoriasis and Psoriatic Arthritis.
Psoriasis and PsA, along with ankylosing spondylitis and Crohn’s disease, have been thought to be either immune mediated or a classic autoimmune disorder, Ritchlin, a rheumatologist and internist and director of the Clinical Immunology Research Unit at the University of Rochester in New York, said in an interview. “But emerging data reveal that these disorders might be triggered and sustained by both autoimmune and immune-mediated events,” he said.
Autoimmunity vs Immune Mediated
Autoimmune diseases are characterized by a specific autoantigen and antibody, such as the anti–cyclic citrullinated peptide antibody seen in rheumatoid arthritis, Ritchlin said. He cited a 2023 literature review from Italy that identified five autoantibodies and polymorphisms in PsA.
“In an immune-mediated disease, we demonstrate profound dysregulation of immune cells that promote inflammation, but we have not identified a specific autoantigen,” he said. “There’s an inflammatory response, which can be very severe, but we don’t know if it’s responding to an autoantigen or it’s just dysregulation of the T cells or the B cells or both.”
In a humanized mouse model developed by Maria Garcia-Hernandez, PhD, in Ritchlin’s lab, researchers found that both immunoglobulins and immune cells are required to recapitulate the skin and joint phenotypes. Ritchlin said that further analyses identified a putative autoantigen, which current experiments now underway are looking to confirm and should help discern distinctions in pathogenesis between a response to an autoantigen or cell dysregulation.
“There may be more than one type of immune inflammatory reaction that’s ongoing in individual tissue, and it may be different from one tissue to another,” Ritchlin said in an interview.
The immune-mediated and autoimmune properties of PsA are important to investigate, Jose U. Scher, MD, director of the Arthritis Clinic and Psoriatic Arthritis Center at NYU Langone Health in New York City, said in an interview.
“Classically considered an autoimmune disease, [PsA] may be better classified as an immune-mediated inflammatory disease,” Scher said. He noted one feature that makes PsA differ from classic autoimmunity is that it does not affect women predominantly.
“The fundamental question is whether there are elements of classic autoimmunity such as B cells that should be integrated into the research for future identification of novel therapeutics,” Scher said.
The ‘Additional Mechanism’
The additional mechanism Ritchlin referred to is “this idea of trained immunity,” he said, “where innate immune cells — fibroblasts, monocytes, keratinocytes — that are not considered to have [the] adaptive memory characteristic of T cells and B cells but act in an environment of inflammation and can actually develop sustained altered phenotypes in response to inflammation.”
A 2024 report from Europe outlined four characteristics of trained immunity, Ritchlin said, including that it is “antigen agnostic” and results from long-term reprogramming of cells through epigenetic and metabolic mechanisms. The effects of trained immunity are shorter in duration than that of classical adaptive immunity, he said.
These reprogrammed innate immune cells “retain a form of ‘memory’ after an initial stimulus, which can lead to enhanced or altered responses upon subsequent challenges,” Scher said.
In the context of PsA, Scher said, monocytes that express heightened inflammatory responses driven by metabolic and epigenetic reprogramming can become “trained” by triggers such as infections, cytokines (such as interleukin [IL]–1 beta and IL-17), or damage-associated molecular patterns that have been epigenetically modified to respond at higher rates in a future encounter with exacerbated production of proinflammatory cytokines, persistent inflammation, and flares.
Ritchlin explained how this emerging understanding of the mechanisms driving psoriasis and PsA is driving research into treatments.
“If you know that monocytes are undergoing change — these are innate cells, they’re not antigen driven — but that change is based on some type of pathway that makes the cell more inflammatory, then you can think about trying to block that pathway,” he said.
The goal would be to normalize the cellular environment that’s otherwise becoming activated to create the signs and symptoms of psoriasis and PsA, he said.
The other potential therapeutic target would be T cells, Ritchlin said. “There now are T cells that have been identified that have very specific alpha-beta receptors that are expanded in the peripheral blood, uveal fluid, and joints of HLAB27-positive patients with ankylosing spondylitis and anterior uveitis, which is thought to be immune mediated, not autoimmune.”
Those HLAB27-positive patients “have expansion of a certain subtype of T cells, they have a specific receptor, and specific autoantigens have been identified pointing to a potential autoimmune response,” Ritchlin added.
An antibody that binds and removes specific T-cell receptor subsets may be an effective strategy without being immunosuppressive, Ritchlin said. “That’s real exciting, and we’re all hoping that is going to be a therapeutic approach that could be successful.”
Ritchlin disclosed financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and UCB. Scher had no relevant financial relationships.
A version of this article appeared on Medscape.com.
Cardiac Risks of Newer Psoriasis Biologics vs. TNF Inhibitors Compared
TOPLINE:
The newer biologics — .
METHODOLOGY:
- In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
- Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
- A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
- The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).
TAKEAWAY:
- Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
- The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
- Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
- Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors.
IN PRACTICE:
“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”
SOURCE:
The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.
DISCLOSURES:
The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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 first appeared on Medscape.com.
TOPLINE:
The newer biologics — .
METHODOLOGY:
- In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
- Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
- A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
- The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).
TAKEAWAY:
- Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
- The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
- Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
- Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors.
IN PRACTICE:
“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”
SOURCE:
The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.
DISCLOSURES:
The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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 first appeared on Medscape.com.
TOPLINE:
The newer biologics — .
METHODOLOGY:
- In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
- Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
- A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
- The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).
TAKEAWAY:
- Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
- The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
- Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
- Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors.
IN PRACTICE:
“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”
SOURCE:
The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.
LIMITATIONS:
Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.
DISCLOSURES:
The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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 first appeared on Medscape.com.
Why Sex and Gender Are Important Biomarkers in PsA
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.
Combined Clinics, Personalized Medicine for Psoriatic Disease Face Barriers
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.
FDA Approves Ustekinumab Biosimilar Steqeyma, the Seventh of Its Kind
The Food and Drug Administration (FDA) has approved ustekinumab-stba (Steqeyma) as a biosimilar to the interleukin-12 and -23 inhibitor ustekinumab (Stelara) for the treatment of adults with active Crohn’s disease or ulcerative colitis and for both children aged ≥ 6 years and adults with moderate to severe plaque psoriasis or active psoriatic arthritis.
This is the seventh ustekinumab biosimilar approved by the FDA. The biosimilar, developed by Celltrion, has a license entry date in February 2025 as part of the settlement and license agreement with the manufacturer of the reference biologic, Johnson & Johnson.
Ustekinumab-stba will be available in two formulations: A subcutaneous injection in two strengths — a 45 mg/0.5 mL or 90 mg/1 mL solution in a single-dose, prefilled syringe — and an intravenous infusion of a 130 mg/26 mL (5 mg/mL) solution in a single-dose vial.
“The approval of Steqeyma reflects Celltrion’s continued investment in providing treatment options to patients diagnosed with ulcerative colitis, Crohn’s disease, psoriasis, and psoriatic arthritis,” said Thomas Nusbickel, Chief Commercial Officer at Celltrion USA, Jersey City, New Jersey, in a press release.
The FDA has previously approved the company’s adalimumab biosimilar Yuflyma and its infliximab biosimilar Zymfentra.
The full prescribing information for ustekinumab-stba is available here.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration (FDA) has approved ustekinumab-stba (Steqeyma) as a biosimilar to the interleukin-12 and -23 inhibitor ustekinumab (Stelara) for the treatment of adults with active Crohn’s disease or ulcerative colitis and for both children aged ≥ 6 years and adults with moderate to severe plaque psoriasis or active psoriatic arthritis.
This is the seventh ustekinumab biosimilar approved by the FDA. The biosimilar, developed by Celltrion, has a license entry date in February 2025 as part of the settlement and license agreement with the manufacturer of the reference biologic, Johnson & Johnson.
Ustekinumab-stba will be available in two formulations: A subcutaneous injection in two strengths — a 45 mg/0.5 mL or 90 mg/1 mL solution in a single-dose, prefilled syringe — and an intravenous infusion of a 130 mg/26 mL (5 mg/mL) solution in a single-dose vial.
“The approval of Steqeyma reflects Celltrion’s continued investment in providing treatment options to patients diagnosed with ulcerative colitis, Crohn’s disease, psoriasis, and psoriatic arthritis,” said Thomas Nusbickel, Chief Commercial Officer at Celltrion USA, Jersey City, New Jersey, in a press release.
The FDA has previously approved the company’s adalimumab biosimilar Yuflyma and its infliximab biosimilar Zymfentra.
The full prescribing information for ustekinumab-stba is available here.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration (FDA) has approved ustekinumab-stba (Steqeyma) as a biosimilar to the interleukin-12 and -23 inhibitor ustekinumab (Stelara) for the treatment of adults with active Crohn’s disease or ulcerative colitis and for both children aged ≥ 6 years and adults with moderate to severe plaque psoriasis or active psoriatic arthritis.
This is the seventh ustekinumab biosimilar approved by the FDA. The biosimilar, developed by Celltrion, has a license entry date in February 2025 as part of the settlement and license agreement with the manufacturer of the reference biologic, Johnson & Johnson.
Ustekinumab-stba will be available in two formulations: A subcutaneous injection in two strengths — a 45 mg/0.5 mL or 90 mg/1 mL solution in a single-dose, prefilled syringe — and an intravenous infusion of a 130 mg/26 mL (5 mg/mL) solution in a single-dose vial.
“The approval of Steqeyma reflects Celltrion’s continued investment in providing treatment options to patients diagnosed with ulcerative colitis, Crohn’s disease, psoriasis, and psoriatic arthritis,” said Thomas Nusbickel, Chief Commercial Officer at Celltrion USA, Jersey City, New Jersey, in a press release.
The FDA has previously approved the company’s adalimumab biosimilar Yuflyma and its infliximab biosimilar Zymfentra.
The full prescribing information for ustekinumab-stba is available here.
A version of this article first appeared on Medscape.com.
Adalimumab for Psoriasis: Study Compares Biosimilars Vs. Originator
TOPLINE:
rate than those who remained on Humira.
METHODOLOGY:
- Researchers conducted a cohort study using data on patients with psoriasis who were treated with adalimumab, a tumor necrosis factor alpha inhibitor used to treat moderate to severe psoriasis, from the French National Health Data System, British Association of Dermatologists Biologics and Immunomodulators Register, and Spanish Registry of Systemic Therapy in Psoriasis.
- The analysis included 7387 adalimumab-naive patients who were new users of an adalimumab biosimilar and 3654 patients (switchers) who switched from Humira to a biosimilar. Patients were matched and compared with patients receiving Humira.
- Co-primary outcomes of the study were drug discontinuation and serious adverse events.
- Researchers assessed the following adalimumab biosimilar brands: Amgevita, Imraldi, Hyrimoz, Idacio, and Hulio.
TAKEAWAY:
- All-cause drug discontinuation rates were similar between new users of biosimilars and Humira new users (hazard ratio [HR], 0.99; 95% CI, 0.94-1.04).
- Discontinuation rates were higher among those who switched from Humira to a biosimilar (HR, 1.35; 95% CI, 1.19-1.52) than among those who stayed on Humira. Switching to Amgevita (HR, 1.25; 95% CI, 1.13-1.27), Imraldi (HR, 1.53; 95% CI, 1.33-1.76), and Hyrimoz (HR, 1.80; 95% CI, 1.29-2.52) was associated with higher discontinuation rates.
- Serious adverse events were not significantly different between new users of Humira and biosimilar new users (incidence rate ratio [IRR], 0.91; 95% CI, 0.80-1.05), and between patients who switched from a biosimilar to Humira and those who stayed on Humira (IRR, 0.92; 95% CI, 0.83-1.01).
- No significant differences in discontinuation because of ineffectiveness were found between biosimilar and Humira new users (HR, 0.97; 95% CI, 0.88-1.08). Discontinuation because of adverse events was also comparable for all biosimilars among new users, except for Hyrimoz (HR, 0.54; 95% CI, 0.35-0.85), which showed fewer discontinuations than Humira.
IN PRACTICE:
“This study found comparable drug survival and safety between adalimumab biosimilars and Humira in adalimumab-naive patients, supporting the use of biosimilars as viable alternatives for new patients,” the authors wrote. However, noting that discontinuation was more likely among those who switched from Humira to a biosimilar, they added: “Changes in treatment response, skin or injection site reactions, and nocebo effects may contribute to treatment discontinuation post-switch. Thus, patients who switch from Humira to biosimilars may require closer monitoring and support to alleviate these challenges.”
SOURCE:
The study was led by Duc Binh Phan, Dermatology Centre, Northern Care Alliance NHS Foundation Trust in Manchester, England. It was published online in The British Journal of Dermatology.
LIMITATIONS:
Unmeasured factors including psychological perceptions, regional policies, and drug availability could influence drug survival, making the results not fully reflective of treatment effectiveness or safety. Most Humira users in registries were enrolled before biosimilars became available, making it impractical to match new users on the basis of treatment initiation years. Additionally, reasons for discontinuation were not available in the French National Health Data System.
DISCLOSURES:
In the United Kingdom, the research was funded by the Psoriasis Association PhD studentship and supported by the NIHR Manchester Biomedical Research Centre. In France, the authors are employees of the French National Health Insurance, the French National Agency for the Safety of Medicines and Health Products, and the Assistance Publique — Hôpitaux de Paris and received no funding. The authors reported receiving consulting and speaker fees and clinical trial sponsorship from various pharmaceutical companies. Additional disclosures are noted 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:
rate than those who remained on Humira.
METHODOLOGY:
- Researchers conducted a cohort study using data on patients with psoriasis who were treated with adalimumab, a tumor necrosis factor alpha inhibitor used to treat moderate to severe psoriasis, from the French National Health Data System, British Association of Dermatologists Biologics and Immunomodulators Register, and Spanish Registry of Systemic Therapy in Psoriasis.
- The analysis included 7387 adalimumab-naive patients who were new users of an adalimumab biosimilar and 3654 patients (switchers) who switched from Humira to a biosimilar. Patients were matched and compared with patients receiving Humira.
- Co-primary outcomes of the study were drug discontinuation and serious adverse events.
- Researchers assessed the following adalimumab biosimilar brands: Amgevita, Imraldi, Hyrimoz, Idacio, and Hulio.
TAKEAWAY:
- All-cause drug discontinuation rates were similar between new users of biosimilars and Humira new users (hazard ratio [HR], 0.99; 95% CI, 0.94-1.04).
- Discontinuation rates were higher among those who switched from Humira to a biosimilar (HR, 1.35; 95% CI, 1.19-1.52) than among those who stayed on Humira. Switching to Amgevita (HR, 1.25; 95% CI, 1.13-1.27), Imraldi (HR, 1.53; 95% CI, 1.33-1.76), and Hyrimoz (HR, 1.80; 95% CI, 1.29-2.52) was associated with higher discontinuation rates.
- Serious adverse events were not significantly different between new users of Humira and biosimilar new users (incidence rate ratio [IRR], 0.91; 95% CI, 0.80-1.05), and between patients who switched from a biosimilar to Humira and those who stayed on Humira (IRR, 0.92; 95% CI, 0.83-1.01).
- No significant differences in discontinuation because of ineffectiveness were found between biosimilar and Humira new users (HR, 0.97; 95% CI, 0.88-1.08). Discontinuation because of adverse events was also comparable for all biosimilars among new users, except for Hyrimoz (HR, 0.54; 95% CI, 0.35-0.85), which showed fewer discontinuations than Humira.
IN PRACTICE:
“This study found comparable drug survival and safety between adalimumab biosimilars and Humira in adalimumab-naive patients, supporting the use of biosimilars as viable alternatives for new patients,” the authors wrote. However, noting that discontinuation was more likely among those who switched from Humira to a biosimilar, they added: “Changes in treatment response, skin or injection site reactions, and nocebo effects may contribute to treatment discontinuation post-switch. Thus, patients who switch from Humira to biosimilars may require closer monitoring and support to alleviate these challenges.”
SOURCE:
The study was led by Duc Binh Phan, Dermatology Centre, Northern Care Alliance NHS Foundation Trust in Manchester, England. It was published online in The British Journal of Dermatology.
LIMITATIONS:
Unmeasured factors including psychological perceptions, regional policies, and drug availability could influence drug survival, making the results not fully reflective of treatment effectiveness or safety. Most Humira users in registries were enrolled before biosimilars became available, making it impractical to match new users on the basis of treatment initiation years. Additionally, reasons for discontinuation were not available in the French National Health Data System.
DISCLOSURES:
In the United Kingdom, the research was funded by the Psoriasis Association PhD studentship and supported by the NIHR Manchester Biomedical Research Centre. In France, the authors are employees of the French National Health Insurance, the French National Agency for the Safety of Medicines and Health Products, and the Assistance Publique — Hôpitaux de Paris and received no funding. The authors reported receiving consulting and speaker fees and clinical trial sponsorship from various pharmaceutical companies. Additional disclosures are noted 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:
rate than those who remained on Humira.
METHODOLOGY:
- Researchers conducted a cohort study using data on patients with psoriasis who were treated with adalimumab, a tumor necrosis factor alpha inhibitor used to treat moderate to severe psoriasis, from the French National Health Data System, British Association of Dermatologists Biologics and Immunomodulators Register, and Spanish Registry of Systemic Therapy in Psoriasis.
- The analysis included 7387 adalimumab-naive patients who were new users of an adalimumab biosimilar and 3654 patients (switchers) who switched from Humira to a biosimilar. Patients were matched and compared with patients receiving Humira.
- Co-primary outcomes of the study were drug discontinuation and serious adverse events.
- Researchers assessed the following adalimumab biosimilar brands: Amgevita, Imraldi, Hyrimoz, Idacio, and Hulio.
TAKEAWAY:
- All-cause drug discontinuation rates were similar between new users of biosimilars and Humira new users (hazard ratio [HR], 0.99; 95% CI, 0.94-1.04).
- Discontinuation rates were higher among those who switched from Humira to a biosimilar (HR, 1.35; 95% CI, 1.19-1.52) than among those who stayed on Humira. Switching to Amgevita (HR, 1.25; 95% CI, 1.13-1.27), Imraldi (HR, 1.53; 95% CI, 1.33-1.76), and Hyrimoz (HR, 1.80; 95% CI, 1.29-2.52) was associated with higher discontinuation rates.
- Serious adverse events were not significantly different between new users of Humira and biosimilar new users (incidence rate ratio [IRR], 0.91; 95% CI, 0.80-1.05), and between patients who switched from a biosimilar to Humira and those who stayed on Humira (IRR, 0.92; 95% CI, 0.83-1.01).
- No significant differences in discontinuation because of ineffectiveness were found between biosimilar and Humira new users (HR, 0.97; 95% CI, 0.88-1.08). Discontinuation because of adverse events was also comparable for all biosimilars among new users, except for Hyrimoz (HR, 0.54; 95% CI, 0.35-0.85), which showed fewer discontinuations than Humira.
IN PRACTICE:
“This study found comparable drug survival and safety between adalimumab biosimilars and Humira in adalimumab-naive patients, supporting the use of biosimilars as viable alternatives for new patients,” the authors wrote. However, noting that discontinuation was more likely among those who switched from Humira to a biosimilar, they added: “Changes in treatment response, skin or injection site reactions, and nocebo effects may contribute to treatment discontinuation post-switch. Thus, patients who switch from Humira to biosimilars may require closer monitoring and support to alleviate these challenges.”
SOURCE:
The study was led by Duc Binh Phan, Dermatology Centre, Northern Care Alliance NHS Foundation Trust in Manchester, England. It was published online in The British Journal of Dermatology.
LIMITATIONS:
Unmeasured factors including psychological perceptions, regional policies, and drug availability could influence drug survival, making the results not fully reflective of treatment effectiveness or safety. Most Humira users in registries were enrolled before biosimilars became available, making it impractical to match new users on the basis of treatment initiation years. Additionally, reasons for discontinuation were not available in the French National Health Data System.
DISCLOSURES:
In the United Kingdom, the research was funded by the Psoriasis Association PhD studentship and supported by the NIHR Manchester Biomedical Research Centre. In France, the authors are employees of the French National Health Insurance, the French National Agency for the Safety of Medicines and Health Products, and the Assistance Publique — Hôpitaux de Paris and received no funding. The authors reported receiving consulting and speaker fees and clinical trial sponsorship from various pharmaceutical companies. Additional disclosures are noted 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.
Commentary: Predicting PsA Progression, Managing Comorbidities, and Evaluating New Therapies, December 2024
Recently published clinical research in psoriatic arthritis (PsA) has continued to focus on the transition from psoriasis to PsA, comorbidities, and effects of treatments. Garcia-Salinas and colleagues reported results of a large study that investigated 1419 patients with joint pain who were carefully clinically evaluated with imaging (ultrasonography and MRI) and laboratory tests. They found that among patients with arthralgia, 8.4% were at risk of developing PsA (ie, had a personal or family history of psoriasis), with 29% of these patients progressing to PsA within 1 year. Significant predictors of progression included a family history of psoriasis, synovitis detected by power Doppler ultrasound, enthesopathy on ultrasonography, and a low tender joint count. Thus, more than one quarter of patients with psoriasis and joint pain developed PsA in 1 year. Patients with psoriasis and joint pain, especially those with findings on imaging, should be referred to rheumatologists and carefully followed up for early diagnosis of PsA and therefore better outcomes.
Chronic kidney disease (CKD) is a known comorbidity in psoriatic disease but is less well characterised. In a prospective observational cohort study that included 1336 patients with PsA, Kharouf and colleagues reported that 123 (9.2%) had CKD. They demonstrated that diabetes, kidney stones, joint damage, high uric acid levels, and daily use of nonsteroidal anti-inflammatory drugs were associated with development of CKD, whereas methotrexate use had a renoprotective effect. Thus, patients with severe PsA and comorbidities such as diabetes are at higher risk for CKD. Better management of PsA using disease-modifying antirheumatic drugs may reduce the risk. Replication of these findings, especially in terms of the renoprotective effect of methotrexate, is required.
Patients with PsA who do not respond to treatment with tumour necrosis factor (TNF) inhibitors are generally less likely to respond to subsequent therapy. Evaluating newer modes of action in this treatment-resistant PsA population is important. COSMOS was a phase 3b trial that included 285 patients with PsA who had inadequate response or intolerance to TNF inhibitors and were randomly assigned to receive 100 mg guselkumab (a monoclonal antibody targeting interleukin-23; n = 189) or placebo (n = 96). In a post hoc analysis, Gossec and colleagues showed that at week 24, a greater proportion of patients receiving guselkumab vs placebo achieved minimal disease activity (MDA) (14.8% vs 3.1%). Most of the patients who achieved MDA at week 24 maintained the response at week 48. Thus, guselkumab treatment led to sustained MDA over 1 year in patients with PsA who had inadequate response or intolerance to TNF inhibitors.
Achieving MDA was also evaluated in another novel drug for PsA. Deucravacitinib is an oral TYK2 inhibitor that is approved for the treatment of psoriasis and is currently being evaluated in phase 3 PsA trials. In a post hoc analysis of a phase 2 trial that included 203 adults with PsA who did not respond to or were intolerant to one or more prior therapies and were randomly assigned to receive 6 mg or 12 mg deucravacitinib or placebo, Kavanaugh and colleagues found that after 16 weeks, a significantly higher proportion of patients treated with deucravacitinib vs placebo achieved MDA (6 mg: 22.9% vs 7.6%; P = .01 and 12 mg: 23.9% vs 7.6%; P = .007). Achieving MDA reflects a state of low disease activity or remission; therefore, these results are very encouraging. Results from phase 3 trials and a formal comparison with other drugs will inform rheumatologists about the place of deucravacitinib in the management of PsA.
Recently published clinical research in psoriatic arthritis (PsA) has continued to focus on the transition from psoriasis to PsA, comorbidities, and effects of treatments. Garcia-Salinas and colleagues reported results of a large study that investigated 1419 patients with joint pain who were carefully clinically evaluated with imaging (ultrasonography and MRI) and laboratory tests. They found that among patients with arthralgia, 8.4% were at risk of developing PsA (ie, had a personal or family history of psoriasis), with 29% of these patients progressing to PsA within 1 year. Significant predictors of progression included a family history of psoriasis, synovitis detected by power Doppler ultrasound, enthesopathy on ultrasonography, and a low tender joint count. Thus, more than one quarter of patients with psoriasis and joint pain developed PsA in 1 year. Patients with psoriasis and joint pain, especially those with findings on imaging, should be referred to rheumatologists and carefully followed up for early diagnosis of PsA and therefore better outcomes.
Chronic kidney disease (CKD) is a known comorbidity in psoriatic disease but is less well characterised. In a prospective observational cohort study that included 1336 patients with PsA, Kharouf and colleagues reported that 123 (9.2%) had CKD. They demonstrated that diabetes, kidney stones, joint damage, high uric acid levels, and daily use of nonsteroidal anti-inflammatory drugs were associated with development of CKD, whereas methotrexate use had a renoprotective effect. Thus, patients with severe PsA and comorbidities such as diabetes are at higher risk for CKD. Better management of PsA using disease-modifying antirheumatic drugs may reduce the risk. Replication of these findings, especially in terms of the renoprotective effect of methotrexate, is required.
Patients with PsA who do not respond to treatment with tumour necrosis factor (TNF) inhibitors are generally less likely to respond to subsequent therapy. Evaluating newer modes of action in this treatment-resistant PsA population is important. COSMOS was a phase 3b trial that included 285 patients with PsA who had inadequate response or intolerance to TNF inhibitors and were randomly assigned to receive 100 mg guselkumab (a monoclonal antibody targeting interleukin-23; n = 189) or placebo (n = 96). In a post hoc analysis, Gossec and colleagues showed that at week 24, a greater proportion of patients receiving guselkumab vs placebo achieved minimal disease activity (MDA) (14.8% vs 3.1%). Most of the patients who achieved MDA at week 24 maintained the response at week 48. Thus, guselkumab treatment led to sustained MDA over 1 year in patients with PsA who had inadequate response or intolerance to TNF inhibitors.
Achieving MDA was also evaluated in another novel drug for PsA. Deucravacitinib is an oral TYK2 inhibitor that is approved for the treatment of psoriasis and is currently being evaluated in phase 3 PsA trials. In a post hoc analysis of a phase 2 trial that included 203 adults with PsA who did not respond to or were intolerant to one or more prior therapies and were randomly assigned to receive 6 mg or 12 mg deucravacitinib or placebo, Kavanaugh and colleagues found that after 16 weeks, a significantly higher proportion of patients treated with deucravacitinib vs placebo achieved MDA (6 mg: 22.9% vs 7.6%; P = .01 and 12 mg: 23.9% vs 7.6%; P = .007). Achieving MDA reflects a state of low disease activity or remission; therefore, these results are very encouraging. Results from phase 3 trials and a formal comparison with other drugs will inform rheumatologists about the place of deucravacitinib in the management of PsA.
Recently published clinical research in psoriatic arthritis (PsA) has continued to focus on the transition from psoriasis to PsA, comorbidities, and effects of treatments. Garcia-Salinas and colleagues reported results of a large study that investigated 1419 patients with joint pain who were carefully clinically evaluated with imaging (ultrasonography and MRI) and laboratory tests. They found that among patients with arthralgia, 8.4% were at risk of developing PsA (ie, had a personal or family history of psoriasis), with 29% of these patients progressing to PsA within 1 year. Significant predictors of progression included a family history of psoriasis, synovitis detected by power Doppler ultrasound, enthesopathy on ultrasonography, and a low tender joint count. Thus, more than one quarter of patients with psoriasis and joint pain developed PsA in 1 year. Patients with psoriasis and joint pain, especially those with findings on imaging, should be referred to rheumatologists and carefully followed up for early diagnosis of PsA and therefore better outcomes.
Chronic kidney disease (CKD) is a known comorbidity in psoriatic disease but is less well characterised. In a prospective observational cohort study that included 1336 patients with PsA, Kharouf and colleagues reported that 123 (9.2%) had CKD. They demonstrated that diabetes, kidney stones, joint damage, high uric acid levels, and daily use of nonsteroidal anti-inflammatory drugs were associated with development of CKD, whereas methotrexate use had a renoprotective effect. Thus, patients with severe PsA and comorbidities such as diabetes are at higher risk for CKD. Better management of PsA using disease-modifying antirheumatic drugs may reduce the risk. Replication of these findings, especially in terms of the renoprotective effect of methotrexate, is required.
Patients with PsA who do not respond to treatment with tumour necrosis factor (TNF) inhibitors are generally less likely to respond to subsequent therapy. Evaluating newer modes of action in this treatment-resistant PsA population is important. COSMOS was a phase 3b trial that included 285 patients with PsA who had inadequate response or intolerance to TNF inhibitors and were randomly assigned to receive 100 mg guselkumab (a monoclonal antibody targeting interleukin-23; n = 189) or placebo (n = 96). In a post hoc analysis, Gossec and colleagues showed that at week 24, a greater proportion of patients receiving guselkumab vs placebo achieved minimal disease activity (MDA) (14.8% vs 3.1%). Most of the patients who achieved MDA at week 24 maintained the response at week 48. Thus, guselkumab treatment led to sustained MDA over 1 year in patients with PsA who had inadequate response or intolerance to TNF inhibitors.
Achieving MDA was also evaluated in another novel drug for PsA. Deucravacitinib is an oral TYK2 inhibitor that is approved for the treatment of psoriasis and is currently being evaluated in phase 3 PsA trials. In a post hoc analysis of a phase 2 trial that included 203 adults with PsA who did not respond to or were intolerant to one or more prior therapies and were randomly assigned to receive 6 mg or 12 mg deucravacitinib or placebo, Kavanaugh and colleagues found that after 16 weeks, a significantly higher proportion of patients treated with deucravacitinib vs placebo achieved MDA (6 mg: 22.9% vs 7.6%; P = .01 and 12 mg: 23.9% vs 7.6%; P = .007). Achieving MDA reflects a state of low disease activity or remission; therefore, these results are very encouraging. Results from phase 3 trials and a formal comparison with other drugs will inform rheumatologists about the place of deucravacitinib in the management of PsA.
Guselkumab Lowers Serum Biomarker Levels and Improves Disease Activity in Biologic-Naive PsA Patients
Key clinical point: Guselkumab significantly reduced inflammatory and collagen biomarker levels, correlating with improvements in joint and overall disease activity over 2 years in biologic-naive patients with psoriatic arthritis (PsA).
Major finding: Over 2 years, reductions in C-reactive protein, interleukin-6, matrix metalloproteinase (MMP)–degradation type 1 collagen (C1M), and MMP-degradation type VI collagen (C6M) levels correlated with improved Disease Activity in Psoriatic Arthritis (correlation coefficient [r], 0.26-0.30; P < .05). Additionally, reductions in C1M, MMP-degradation type III collagen, MMP-degradation type IV collagen, and C6M levels correlated with improved Psoriatic Arthritis Disease Activity Scores (r, 0.27-0.31; P < .05).
Study details: This post hoc analysis of the phase 3 DISCOVER-2 trial included 739 biologic-naive patients with active PsA who were randomly assigned to receive guselkumab (100 mg every 4 or 8 weeks) or placebo with a crossover to 100 mg guselkumab every 4 weeks at week 24.
Disclosures: This DISCOVER-2 study was funded by Janssen Research & Development, LLC. Four authors reported being employees of Janssen and owning stock or stock options in Johnson & Johnson. Others declared having ties with various sources.
Source: Siebert S, Schett G, Raychaudhuri SP, et al. Correlation of changes in inflammatory and collagen biomarkers with durable guselkumab efficacy through 2 years in participants with active psoriatic arthritis: Results from a phase III randomized controlled trial. Ther Adv Musculoskelet Dis. 2024;16:1-20. Source
Key clinical point: Guselkumab significantly reduced inflammatory and collagen biomarker levels, correlating with improvements in joint and overall disease activity over 2 years in biologic-naive patients with psoriatic arthritis (PsA).
Major finding: Over 2 years, reductions in C-reactive protein, interleukin-6, matrix metalloproteinase (MMP)–degradation type 1 collagen (C1M), and MMP-degradation type VI collagen (C6M) levels correlated with improved Disease Activity in Psoriatic Arthritis (correlation coefficient [r], 0.26-0.30; P < .05). Additionally, reductions in C1M, MMP-degradation type III collagen, MMP-degradation type IV collagen, and C6M levels correlated with improved Psoriatic Arthritis Disease Activity Scores (r, 0.27-0.31; P < .05).
Study details: This post hoc analysis of the phase 3 DISCOVER-2 trial included 739 biologic-naive patients with active PsA who were randomly assigned to receive guselkumab (100 mg every 4 or 8 weeks) or placebo with a crossover to 100 mg guselkumab every 4 weeks at week 24.
Disclosures: This DISCOVER-2 study was funded by Janssen Research & Development, LLC. Four authors reported being employees of Janssen and owning stock or stock options in Johnson & Johnson. Others declared having ties with various sources.
Source: Siebert S, Schett G, Raychaudhuri SP, et al. Correlation of changes in inflammatory and collagen biomarkers with durable guselkumab efficacy through 2 years in participants with active psoriatic arthritis: Results from a phase III randomized controlled trial. Ther Adv Musculoskelet Dis. 2024;16:1-20. Source
Key clinical point: Guselkumab significantly reduced inflammatory and collagen biomarker levels, correlating with improvements in joint and overall disease activity over 2 years in biologic-naive patients with psoriatic arthritis (PsA).
Major finding: Over 2 years, reductions in C-reactive protein, interleukin-6, matrix metalloproteinase (MMP)–degradation type 1 collagen (C1M), and MMP-degradation type VI collagen (C6M) levels correlated with improved Disease Activity in Psoriatic Arthritis (correlation coefficient [r], 0.26-0.30; P < .05). Additionally, reductions in C1M, MMP-degradation type III collagen, MMP-degradation type IV collagen, and C6M levels correlated with improved Psoriatic Arthritis Disease Activity Scores (r, 0.27-0.31; P < .05).
Study details: This post hoc analysis of the phase 3 DISCOVER-2 trial included 739 biologic-naive patients with active PsA who were randomly assigned to receive guselkumab (100 mg every 4 or 8 weeks) or placebo with a crossover to 100 mg guselkumab every 4 weeks at week 24.
Disclosures: This DISCOVER-2 study was funded by Janssen Research & Development, LLC. Four authors reported being employees of Janssen and owning stock or stock options in Johnson & Johnson. Others declared having ties with various sources.
Source: Siebert S, Schett G, Raychaudhuri SP, et al. Correlation of changes in inflammatory and collagen biomarkers with durable guselkumab efficacy through 2 years in participants with active psoriatic arthritis: Results from a phase III randomized controlled trial. Ther Adv Musculoskelet Dis. 2024;16:1-20. Source
Predictors of Treatment Response to b/tsDMARDs in PsA
Key clinical point: Among patients with psoriatic arthritis (PsA), men and those with elevated baseline C-reactive protein (CRP) levels showed an improved response to biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), whereas older patients and those with severe baseline disease activity showed a worse response.
Major finding: Among patients with PsA, men (odds ratio [OR], 2.188; 95% CI, 1.912-2.503) and those with elevated baseline CRP levels (OR, 1.537; 95% CI, 1.111-2.125) showed an improved response to b/tsDMARDs. Conversely, older patients (OR, 0.982; 95% CI, 0.975-0.99) and those with increased baseline Disease Activity in Psoriatic Arthritis (OR, 0.789; 95% CI, 0.663-0.938), Health Assessment Questionnaire (OR, 0.483; 95% CI, 0.336-0.696), and joint count (OR, 0.97; 95% CI, 0.945-0.996) scores showed a significantly worse b/tsDMARD response.
Study details: This systematic review and meta-analysis of 37 studies included 17,042 patients with PsA.
Disclosures: Open access funding was provided by the University of Zurich. This study did not receive any funding. The authors declared no conflicts of interest.
Source: Künzler T, Bamert M, Sprott H. Factors predicting treatment response to biological and targeted synthetic disease-modifying antirheumatic drugs in psoriatic arthritis—A systematic review and meta-analysis. Clin Rheumatol. Published online October 28, 2024. Source
Key clinical point: Among patients with psoriatic arthritis (PsA), men and those with elevated baseline C-reactive protein (CRP) levels showed an improved response to biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), whereas older patients and those with severe baseline disease activity showed a worse response.
Major finding: Among patients with PsA, men (odds ratio [OR], 2.188; 95% CI, 1.912-2.503) and those with elevated baseline CRP levels (OR, 1.537; 95% CI, 1.111-2.125) showed an improved response to b/tsDMARDs. Conversely, older patients (OR, 0.982; 95% CI, 0.975-0.99) and those with increased baseline Disease Activity in Psoriatic Arthritis (OR, 0.789; 95% CI, 0.663-0.938), Health Assessment Questionnaire (OR, 0.483; 95% CI, 0.336-0.696), and joint count (OR, 0.97; 95% CI, 0.945-0.996) scores showed a significantly worse b/tsDMARD response.
Study details: This systematic review and meta-analysis of 37 studies included 17,042 patients with PsA.
Disclosures: Open access funding was provided by the University of Zurich. This study did not receive any funding. The authors declared no conflicts of interest.
Source: Künzler T, Bamert M, Sprott H. Factors predicting treatment response to biological and targeted synthetic disease-modifying antirheumatic drugs in psoriatic arthritis—A systematic review and meta-analysis. Clin Rheumatol. Published online October 28, 2024. Source
Key clinical point: Among patients with psoriatic arthritis (PsA), men and those with elevated baseline C-reactive protein (CRP) levels showed an improved response to biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), whereas older patients and those with severe baseline disease activity showed a worse response.
Major finding: Among patients with PsA, men (odds ratio [OR], 2.188; 95% CI, 1.912-2.503) and those with elevated baseline CRP levels (OR, 1.537; 95% CI, 1.111-2.125) showed an improved response to b/tsDMARDs. Conversely, older patients (OR, 0.982; 95% CI, 0.975-0.99) and those with increased baseline Disease Activity in Psoriatic Arthritis (OR, 0.789; 95% CI, 0.663-0.938), Health Assessment Questionnaire (OR, 0.483; 95% CI, 0.336-0.696), and joint count (OR, 0.97; 95% CI, 0.945-0.996) scores showed a significantly worse b/tsDMARD response.
Study details: This systematic review and meta-analysis of 37 studies included 17,042 patients with PsA.
Disclosures: Open access funding was provided by the University of Zurich. This study did not receive any funding. The authors declared no conflicts of interest.
Source: Künzler T, Bamert M, Sprott H. Factors predicting treatment response to biological and targeted synthetic disease-modifying antirheumatic drugs in psoriatic arthritis—A systematic review and meta-analysis. Clin Rheumatol. Published online October 28, 2024. Source