Psoriatic Arthritis

Female sex, hyperlipidemia, Medicaid insurance, earlier year of biologic initiation, shorter duration of psoriasis, and prior nonbiologic systemic therapy use were associated with multiple biologic failure in patients with psoriasis, results from a prospective cohort demonstrated.

“Prior cross-sectional and single-center studies have primarily analyzed therapeutic failure of a single biologic or biologics within one class,” researchers led by Wilson Liao, MD, professor and vice chair of research in the department of dermatology at the University of California, San Francisco, wrote in the study, published in the Journal of the American Academy of Dermatology. “However, failure of multiple biologics targeting different signaling pathways is common over the course of treatment. These ‘multiple biologic failure’ patients are not well-characterized, and the patterns of biologics attempted and sociodemographic or clinical features that may predict difficult treatment are incompletely studied.”

To bridge this gap, the researchers conducted a prospective cohort study from the CorEvitas Psoriasis Registry, which collected data from dermatologist-diagnosed patients with psoriasis who started or switched to a Food and Drug Administration (FDA)–approved systemic therapy for psoriasis during routine dermatology visits from April 15, 2015, to May 10, 2022. This period included data from 17,196 patients across 259 private and 209 academic sites from 580 physicians in the United States and Canada.

From this registry, Dr. Liao and colleagues identified 1,039 patients with 24 months or more of follow-up data, a confirmed index biologic start date, and valid baseline assessment data, and categorized them into three cohorts:

• 490 (47.2%) with good response (GR), defined as patients with 24 months or more of continued index biologic use by the last registry visit.
• 65 (6.3%) with multiple biologic failure (MBF), defined as patients administered two or more biologic agents of different mechanistic classes who discontinued these biologics because of physician-reported “inadequate initial response,” “failure to maintain initial response,” or “active disease” despite 90 or more days of use per biologic.
• 484 (46.6%) categorized as “other,” defined as patients failed by one biologic or who discontinued treatment for nonmedical reasons.

The researchers used multivariable logistic regression to identify sociodemographic, clinical, and patient-reported outcomes that differed between the MBF and GR groups. The mean age of the patients in the study was 49.1 years, 44.2% were female, 77.9% were White, 9.7% were Hispanic, and the mean duration of psoriasis was 11.5 years.

On multivariable logistic regression, factors associated with MBF, compared with those with GR, included female at birth (odds ratio [OR] = 2.29; confidence interval [CI], 1.11-4.72), history of hyperlipidemia (OR = 3.14; CI, 1.35-7.30), Medicaid insurance (OR = 4.53; CI, 1.40-14.60), prior nonbiologic systemic therapy (OR = 2.47; CI, 1.16-5.25), higher psoriasis duration (OR = 0.60 per standard deviation [SD]; CI, 0.38-0.94), and later index biologic initiation (OR = 0.37 per year; CI, 0.27-0.52). Sensitivity analysis revealed that the duration of prior nonbiologic systemic therapy use was not associated with MBF (OR = 0.99; CI, 0.94-1.02; P = 0.56).

“Interestingly, health-related behaviors (e.g., smoking, alcohol use) and location/extent of psoriasis were not important differentiators between MBF and GR,” the authors noted. “We might suspect these features to correlate with MBF, as numerous observational studies found associations between health-related behaviors or psoriasis severity and presence at difficult-to-treat locations, which often relates to biologic use.”

They acknowledged certain limitations of their study, including underrepresentation of ethnoracial minorities and male sex at birth relative to reported psoriasis epidemiology, “possibly reflecting participation bias and reduced access to specialty care, given that patients were enrolled into the registry by dermatologists,” they wrote. “Patient adherence to prescribed biologic regimens between registry visits was not evaluated.”

Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study, said that despite the rapid expansion in biologic therapies for psoriasis, “analysis of real-world use patterns and patient characteristics has been limited – particularly for those who have failed multiple treatments. These findings suggest that there indeed may be some key differences between patients who have had to cycle through multiple biologics versus those who have had a sustained satisfactory response on a single therapy, such as disease duration and previous nonbiologic treatments.”

Dr. Chovatiya

Female sex, hyperlipidemia, Medicaid insurance, earlier year of biologic initiation, shorter duration of psoriasis, and prior nonbiologic systemic therapy use were associated with multiple biologic failure in patients with psoriasis, results from a prospective cohort demonstrated.

“Prior cross-sectional and single-center studies have primarily analyzed therapeutic failure of a single biologic or biologics within one class,” researchers led by Wilson Liao, MD, professor and vice chair of research in the department of dermatology at the University of California, San Francisco, wrote in the study, published in the Journal of the American Academy of Dermatology. “However, failure of multiple biologics targeting different signaling pathways is common over the course of treatment. These ‘multiple biologic failure’ patients are not well-characterized, and the patterns of biologics attempted and sociodemographic or clinical features that may predict difficult treatment are incompletely studied.”

To bridge this gap, the researchers conducted a prospective cohort study from the CorEvitas Psoriasis Registry, which collected data from dermatologist-diagnosed patients with psoriasis who started or switched to a Food and Drug Administration (FDA)–approved systemic therapy for psoriasis during routine dermatology visits from April 15, 2015, to May 10, 2022. This period included data from 17,196 patients across 259 private and 209 academic sites from 580 physicians in the United States and Canada.

From this registry, Dr. Liao and colleagues identified 1,039 patients with 24 months or more of follow-up data, a confirmed index biologic start date, and valid baseline assessment data, and categorized them into three cohorts:

• 490 (47.2%) with good response (GR), defined as patients with 24 months or more of continued index biologic use by the last registry visit.
• 65 (6.3%) with multiple biologic failure (MBF), defined as patients administered two or more biologic agents of different mechanistic classes who discontinued these biologics because of physician-reported “inadequate initial response,” “failure to maintain initial response,” or “active disease” despite 90 or more days of use per biologic.
• 484 (46.6%) categorized as “other,” defined as patients failed by one biologic or who discontinued treatment for nonmedical reasons.

The researchers used multivariable logistic regression to identify sociodemographic, clinical, and patient-reported outcomes that differed between the MBF and GR groups. The mean age of the patients in the study was 49.1 years, 44.2% were female, 77.9% were White, 9.7% were Hispanic, and the mean duration of psoriasis was 11.5 years.

On multivariable logistic regression, factors associated with MBF, compared with those with GR, included female at birth (odds ratio [OR] = 2.29; confidence interval [CI], 1.11-4.72), history of hyperlipidemia (OR = 3.14; CI, 1.35-7.30), Medicaid insurance (OR = 4.53; CI, 1.40-14.60), prior nonbiologic systemic therapy (OR = 2.47; CI, 1.16-5.25), higher psoriasis duration (OR = 0.60 per standard deviation [SD]; CI, 0.38-0.94), and later index biologic initiation (OR = 0.37 per year; CI, 0.27-0.52). Sensitivity analysis revealed that the duration of prior nonbiologic systemic therapy use was not associated with MBF (OR = 0.99; CI, 0.94-1.02; P = 0.56).

“Interestingly, health-related behaviors (e.g., smoking, alcohol use) and location/extent of psoriasis were not important differentiators between MBF and GR,” the authors noted. “We might suspect these features to correlate with MBF, as numerous observational studies found associations between health-related behaviors or psoriasis severity and presence at difficult-to-treat locations, which often relates to biologic use.”

They acknowledged certain limitations of their study, including underrepresentation of ethnoracial minorities and male sex at birth relative to reported psoriasis epidemiology, “possibly reflecting participation bias and reduced access to specialty care, given that patients were enrolled into the registry by dermatologists,” they wrote. “Patient adherence to prescribed biologic regimens between registry visits was not evaluated.”

Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study, said that despite the rapid expansion in biologic therapies for psoriasis, “analysis of real-world use patterns and patient characteristics has been limited – particularly for those who have failed multiple treatments. These findings suggest that there indeed may be some key differences between patients who have had to cycle through multiple biologics versus those who have had a sustained satisfactory response on a single therapy, such as disease duration and previous nonbiologic treatments.”

Dr. Chovatiya

Female sex, hyperlipidemia, Medicaid insurance, earlier year of biologic initiation, shorter duration of psoriasis, and prior nonbiologic systemic therapy use were associated with multiple biologic failure in patients with psoriasis, results from a prospective cohort demonstrated.

“Prior cross-sectional and single-center studies have primarily analyzed therapeutic failure of a single biologic or biologics within one class,” researchers led by Wilson Liao, MD, professor and vice chair of research in the department of dermatology at the University of California, San Francisco, wrote in the study, published in the Journal of the American Academy of Dermatology. “However, failure of multiple biologics targeting different signaling pathways is common over the course of treatment. These ‘multiple biologic failure’ patients are not well-characterized, and the patterns of biologics attempted and sociodemographic or clinical features that may predict difficult treatment are incompletely studied.”

To bridge this gap, the researchers conducted a prospective cohort study from the CorEvitas Psoriasis Registry, which collected data from dermatologist-diagnosed patients with psoriasis who started or switched to a Food and Drug Administration (FDA)–approved systemic therapy for psoriasis during routine dermatology visits from April 15, 2015, to May 10, 2022. This period included data from 17,196 patients across 259 private and 209 academic sites from 580 physicians in the United States and Canada.

From this registry, Dr. Liao and colleagues identified 1,039 patients with 24 months or more of follow-up data, a confirmed index biologic start date, and valid baseline assessment data, and categorized them into three cohorts:

• 490 (47.2%) with good response (GR), defined as patients with 24 months or more of continued index biologic use by the last registry visit.
• 65 (6.3%) with multiple biologic failure (MBF), defined as patients administered two or more biologic agents of different mechanistic classes who discontinued these biologics because of physician-reported “inadequate initial response,” “failure to maintain initial response,” or “active disease” despite 90 or more days of use per biologic.
• 484 (46.6%) categorized as “other,” defined as patients failed by one biologic or who discontinued treatment for nonmedical reasons.

The researchers used multivariable logistic regression to identify sociodemographic, clinical, and patient-reported outcomes that differed between the MBF and GR groups. The mean age of the patients in the study was 49.1 years, 44.2% were female, 77.9% were White, 9.7% were Hispanic, and the mean duration of psoriasis was 11.5 years.

On multivariable logistic regression, factors associated with MBF, compared with those with GR, included female at birth (odds ratio [OR] = 2.29; confidence interval [CI], 1.11-4.72), history of hyperlipidemia (OR = 3.14; CI, 1.35-7.30), Medicaid insurance (OR = 4.53; CI, 1.40-14.60), prior nonbiologic systemic therapy (OR = 2.47; CI, 1.16-5.25), higher psoriasis duration (OR = 0.60 per standard deviation [SD]; CI, 0.38-0.94), and later index biologic initiation (OR = 0.37 per year; CI, 0.27-0.52). Sensitivity analysis revealed that the duration of prior nonbiologic systemic therapy use was not associated with MBF (OR = 0.99; CI, 0.94-1.02; P = 0.56).

“Interestingly, health-related behaviors (e.g., smoking, alcohol use) and location/extent of psoriasis were not important differentiators between MBF and GR,” the authors noted. “We might suspect these features to correlate with MBF, as numerous observational studies found associations between health-related behaviors or psoriasis severity and presence at difficult-to-treat locations, which often relates to biologic use.”

They acknowledged certain limitations of their study, including underrepresentation of ethnoracial minorities and male sex at birth relative to reported psoriasis epidemiology, “possibly reflecting participation bias and reduced access to specialty care, given that patients were enrolled into the registry by dermatologists,” they wrote. “Patient adherence to prescribed biologic regimens between registry visits was not evaluated.”

Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study, said that despite the rapid expansion in biologic therapies for psoriasis, “analysis of real-world use patterns and patient characteristics has been limited – particularly for those who have failed multiple treatments. These findings suggest that there indeed may be some key differences between patients who have had to cycle through multiple biologics versus those who have had a sustained satisfactory response on a single therapy, such as disease duration and previous nonbiologic treatments.”

Dr. Chovatiya

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Although there are several treatment options for PsA, there have been few head-to-head studies conducted to determine comparative efficacy. Ustekinumab, a biologic agent targeting IL-p40, and therefore both IL-12 and IL-23, has proven efficacy in PsA, but the impression is that this drug is less effective than are TNF inhibitors for the treatment of the peripheral arthritis domain. However, in a prospective, observational study, Gossec and colleagues report that the improvements in patient-reported outcomes were generally comparable between ustekinumab and TNF inhibitor treatments. This study evaluated 437 patients with PsA from the PsABio study who initiated first- to third-line ustekinumab (n = 219) or TNF inhibitors (n = 218) and continued the initial treatment for 3 years. At 3 years, ustekinumab and TNF inhibitors were associated with comparable improvements in the EuroQol-5 dimensions health state visual analog scale scores, Psoriatic Arthritis Impact of Disease 12-item scores, and work productivity, although the improvements were generally greater in the TNF inhibitor–treated group. A randomized trial comparing ustekinumab to TNF inhibitors in PsA is warranted to confirm these findings and inform treatment decisions.

Targeted therapies, such as biologics, are proven to be more efficacious than are conventional therapies; however, only about 60% of patients initiating targeted therapies demonstrate treatment response. Identifying the predictors of treatment response is an active area of research. Linde and colleagues looked at data from 13,369 biologic-naive patients registered with a PsA diagnosis from 13 European registries who initiated a first TNF inhibitor treatment. The study demonstrated that sex, disease duration, C-reactive protein level, age at treatment initiation, and fatigue predicted the achievement of the Disease Activity in Psoriatic Arthritis in 28 joints remission at 6 months.

Could biomarkers help predict response beyond clinical predictors? An interesting study indicates that beta–defensin 2 (BD-2) may serve as a predictive biomarker for clinical response to secukinumab in PsA. BD-2 is an antimicrobial peptide and an important protein in innate immune response. Cardner and colleagues analyzed protein expression data in serum samples from the phase 3 FUTURE 1-5 trials that included 1989 patients with PsA who received secukinumab or placebo. Baseline BD-2 levels were associated with early as well as sustained PsA treatment response to secukinumab, independent of psoriasis severity. BD-2 levels did not predict response to adalimumab in PsA nor was it associated with treatment response to secukinumab in RA. The addition of BD-2 to the clinical prediction model significantly improved the prediction of the 16-week American College of Rheumatology 20 response. Thus, BD-2 seems to be a secukinumab treatment response biomarker and requires further evaluation.

Janus kinase inhibitors (JAKi) are a novel class of oral, targeted small-molecule inhibitors that are increasingly used to treat several different autoimmune conditions. In terms of rheumatologic indications, the FDA first approved tofacitinib (TOF) for use in moderate to severe rheumatoid arthritis (RA) unresponsive to methotrexate therapy. Eleven years later, the indications for JAKi use have expanded to include ulcerative colitis, ankylosing spondylitis, and psoriatic arthritis (PsA), among other diseases. As with any new therapeutic mechanism, there are questions as to how JAKi should be incorporated into the treatment paradigm of PsA. In this article, we briefly review the efficacy and safety data of these agents and discuss our approach to their use in PsA.

Two JAKi are currently FDA approved for the treatment of PsA: tofacitinib (TOF) and upadacitinib (UPA). Other JAKi, such as filgotinib and peficitinib, are only approved outside the United States and will not be discussed here. 

TOF was originally studied in skin psoriasis (PsO) before 2 pivotal studies demonstrated efficacy in PsA. TOF or adalimumab (ADA) were compared with placebo in patients who had failed conventional synthetic disease-modifying antirheumatic drugs (DMARD).¹ ACR20 response was superior with TOF 5 mg twice daily (BID) (50%) and 10 mg BID (61%) vs placebo (33%), and it was comparable to ADA (52%), which was used in this study as an active comparator. The overall rate of adverse events was similar with both doses of TOF when compared with ADA; however, patients taking TOF had numerically more cases of cancer, serious infection, and herpes zoster. 

Another study evaluated TOF compared with placebo in patients with PsA who had an inadequate response to tumor necrosis factor inhibitor (TNFi) therapy.² The study showed an ACR20 response of 50% in patients taking TOF 5 mg BID and 47% in patients taking 10 mg BID, compared with 24% in those taking placebo. Patients who received the 10 mg TOF dose continuously had higher rates of adverse events compared to TOF 5 mg, placebo, and patients who crossed over from placebo to TOF at either dose. In the TOF groups, there were cases of serious infection and herpes zoster, as well as 2 patients with major adverse cardiovascular events (MACE). Following review of these data, the FDA approved only the 5 mg BID dose, and later an 11-mg daily extended-release formulation that was pharmacokinetically similar.

The efficacy for UPA in PsA was shown in 2 pivotal phase 3 trials. SELECT-PsA1 compared UPA at 2 doses, 15 mg and 30 mg daily, vs placebo and vs ADA in patients with biologic DMARD (bDMARD)-naïve PsA.³ This trial demonstrated superiority of UPA in the ACR20 response at both doses (71% and 79%, respectively) compared with placebo (36%). The 15-mg dose of UPA was comparable to ADA (65%), while the 30-mg dose achieved superiority compared to ADA. Secondary outcomes including skin activity, patient-reported symptoms, and inhibition of radiographic progression were also superior in UPA compared with placebo and similar or greater with UPA compared with ADA, depending on the specific outcome.⁴ SELECT-PsA2 compared UPA 15 mg, 30 mg, and placebo in patients with prior incomplete response or intolerance to a bDMARD.⁵ At week 12 of the study, patients taking UPA 15 mg and 30 mg had an ACR20 response of 57% and 64%, respectively, compared with placebo (24%). At week 24, minimal disease activity was achieved by 25% of patients taking UPA 15 mg and 29% of patients taking UPA 30 mg, which was superior to placebo (3%). 

Both studies found a significant increase in infections, including serious infections, at the 30-mg UPA dose compared with the placebo and adalimumab groups. Cytopenia and elevated creatine kinase (CK) level also occurred more frequently in the UPA 30-mg group. Rates of cancer were low overall and comparable between the patients treated with UPA and ADA. Given the higher incidence of adverse events with the 30-mg dose and the relatively similar efficacy, the sponsor elected to submit only the lower dose to the FDA for approval.

In the last few years, concerns for safety with JAKi use grew after the publication of data from the ORAL SURVEILLANCE trial, an FDA-mandated, post-approval safety study of TOF in RA. In this trial, patients with active RA over 50 years of age and with at least 1 additional cardiovascular risk factor were randomized to TOF at 1 of 2 doses, 5 mg or 10 mg BID, or a TNFi.⁶ This trial was designed as a noninferiority study, and TOF did not meet the noninferiority threshold compared to TNFi, with hazard ratios of 1.33 and 1.48 for MACE and malignancy, respectively. The results of this trial prompted the FDA to add a black box warning to the label for all JAKi, pointing out the risk of malignancy and MACE, as well as infection, mortality, and thrombosis. 

In the ORAL SURVEILLANCE trial, the increased risk of MACE and malignancy was primarily seen in the study patients with high risk for a cardiovascular event. To address the question of whether a similar risk profile exists when using JAKi to treat PsA, or whether this is a disease-specific process related to RA, a post hoc analysis of 3 PsA trials and 7 PsO trials of patients treated with TOF was conducted.⁷ The analysis found that patients with a history of atherosclerotic cardiovascular disease (ASCVD) or metabolic syndrome, or patients at high risk for ASCVD (score > 20%) had increased incidence rates of MACE compared with those with low risk scores for ASCVD. Interestingly, as in RA, increased incidence rates of malignancy were seen in patients with preexisting or at high risk for ASCVD.

While the FDA recommends JAKi use in patients who have failed or are inappropriate for treatment with a TNFi, we would consider the use of JAKi for first-line therapy in PsA on an individual basis. One advantage of JAKi is their efficacy across multiple PsA domains, including peripheral arthritis, axial disease, enthesitis, dactylitis, and skin disease (although the approved dose of TOF was not statistically effective for PsO in the pivotal trials). Based on this efficacy, we believe that patients with overlapping, multifaceted disease may benefit the most from these medications. Patient risk factors and comorbidities are a prominent consideration in our use of JAKi to ensure safety, as the risk for MACE and malignancy is informed partly by baseline cardiovascular status. In younger patients without cardiovascular risk factors, JAKi may be a strong candidate for first-line therapy, particularly in patients averse to subcutaneous or intravenous therapy. We do counsel all patients on the increased risk of infection, and we do recommend inactivated herpes zoster vaccination in previously unvaccinated patients planning to start JAKi therapy. 

On the horizon are the development of novel, oral agents targeting tyrosine kinase 2 (TYK2), which is a member of the JAK family of signaling proteins. In fact, the TYK2 inhibitor deucravacitinib was approved by the FDA in 2022 for the treatment of PsO. TYK2 inhibitors appear to have the advantage of a more selective mechanism of action, with fewer off-target effects. There were fewer adverse events in the deucravacitinib trials, which led to its prompt PsO authorization, and the FDA approval for the drug did not include the same black box warning that appears in the label for other JAKi.⁸ A phase 2 study showed early promise for the efficacy and safety of deucravacitinib in PsA.⁹ Further investigation will be needed to better understand the role of deucravacitinib and other TYK2 inhibitors being developed for the treatment of PsA. In the meantime, JAKi continue to be a prominent consideration for first-line PsA therapy in a carefully selected patient population. 

Janus kinase inhibitors (JAKi) are a novel class of oral, targeted small-molecule inhibitors that are increasingly used to treat several different autoimmune conditions. In terms of rheumatologic indications, the FDA first approved tofacitinib (TOF) for use in moderate to severe rheumatoid arthritis (RA) unresponsive to methotrexate therapy. Eleven years later, the indications for JAKi use have expanded to include ulcerative colitis, ankylosing spondylitis, and psoriatic arthritis (PsA), among other diseases. As with any new therapeutic mechanism, there are questions as to how JAKi should be incorporated into the treatment paradigm of PsA. In this article, we briefly review the efficacy and safety data of these agents and discuss our approach to their use in PsA.

Two JAKi are currently FDA approved for the treatment of PsA: tofacitinib (TOF) and upadacitinib (UPA). Other JAKi, such as filgotinib and peficitinib, are only approved outside the United States and will not be discussed here. 

TOF was originally studied in skin psoriasis (PsO) before 2 pivotal studies demonstrated efficacy in PsA. TOF or adalimumab (ADA) were compared with placebo in patients who had failed conventional synthetic disease-modifying antirheumatic drugs (DMARD).¹ ACR20 response was superior with TOF 5 mg twice daily (BID) (50%) and 10 mg BID (61%) vs placebo (33%), and it was comparable to ADA (52%), which was used in this study as an active comparator. The overall rate of adverse events was similar with both doses of TOF when compared with ADA; however, patients taking TOF had numerically more cases of cancer, serious infection, and herpes zoster. 

Another study evaluated TOF compared with placebo in patients with PsA who had an inadequate response to tumor necrosis factor inhibitor (TNFi) therapy.² The study showed an ACR20 response of 50% in patients taking TOF 5 mg BID and 47% in patients taking 10 mg BID, compared with 24% in those taking placebo. Patients who received the 10 mg TOF dose continuously had higher rates of adverse events compared to TOF 5 mg, placebo, and patients who crossed over from placebo to TOF at either dose. In the TOF groups, there were cases of serious infection and herpes zoster, as well as 2 patients with major adverse cardiovascular events (MACE). Following review of these data, the FDA approved only the 5 mg BID dose, and later an 11-mg daily extended-release formulation that was pharmacokinetically similar.

The efficacy for UPA in PsA was shown in 2 pivotal phase 3 trials. SELECT-PsA1 compared UPA at 2 doses, 15 mg and 30 mg daily, vs placebo and vs ADA in patients with biologic DMARD (bDMARD)-naïve PsA.³ This trial demonstrated superiority of UPA in the ACR20 response at both doses (71% and 79%, respectively) compared with placebo (36%). The 15-mg dose of UPA was comparable to ADA (65%), while the 30-mg dose achieved superiority compared to ADA. Secondary outcomes including skin activity, patient-reported symptoms, and inhibition of radiographic progression were also superior in UPA compared with placebo and similar or greater with UPA compared with ADA, depending on the specific outcome.⁴ SELECT-PsA2 compared UPA 15 mg, 30 mg, and placebo in patients with prior incomplete response or intolerance to a bDMARD.⁵ At week 12 of the study, patients taking UPA 15 mg and 30 mg had an ACR20 response of 57% and 64%, respectively, compared with placebo (24%). At week 24, minimal disease activity was achieved by 25% of patients taking UPA 15 mg and 29% of patients taking UPA 30 mg, which was superior to placebo (3%). 

Both studies found a significant increase in infections, including serious infections, at the 30-mg UPA dose compared with the placebo and adalimumab groups. Cytopenia and elevated creatine kinase (CK) level also occurred more frequently in the UPA 30-mg group. Rates of cancer were low overall and comparable between the patients treated with UPA and ADA. Given the higher incidence of adverse events with the 30-mg dose and the relatively similar efficacy, the sponsor elected to submit only the lower dose to the FDA for approval.

In the last few years, concerns for safety with JAKi use grew after the publication of data from the ORAL SURVEILLANCE trial, an FDA-mandated, post-approval safety study of TOF in RA. In this trial, patients with active RA over 50 years of age and with at least 1 additional cardiovascular risk factor were randomized to TOF at 1 of 2 doses, 5 mg or 10 mg BID, or a TNFi.⁶ This trial was designed as a noninferiority study, and TOF did not meet the noninferiority threshold compared to TNFi, with hazard ratios of 1.33 and 1.48 for MACE and malignancy, respectively. The results of this trial prompted the FDA to add a black box warning to the label for all JAKi, pointing out the risk of malignancy and MACE, as well as infection, mortality, and thrombosis. 

In the ORAL SURVEILLANCE trial, the increased risk of MACE and malignancy was primarily seen in the study patients with high risk for a cardiovascular event. To address the question of whether a similar risk profile exists when using JAKi to treat PsA, or whether this is a disease-specific process related to RA, a post hoc analysis of 3 PsA trials and 7 PsO trials of patients treated with TOF was conducted.⁷ The analysis found that patients with a history of atherosclerotic cardiovascular disease (ASCVD) or metabolic syndrome, or patients at high risk for ASCVD (score > 20%) had increased incidence rates of MACE compared with those with low risk scores for ASCVD. Interestingly, as in RA, increased incidence rates of malignancy were seen in patients with preexisting or at high risk for ASCVD.

While the FDA recommends JAKi use in patients who have failed or are inappropriate for treatment with a TNFi, we would consider the use of JAKi for first-line therapy in PsA on an individual basis. One advantage of JAKi is their efficacy across multiple PsA domains, including peripheral arthritis, axial disease, enthesitis, dactylitis, and skin disease (although the approved dose of TOF was not statistically effective for PsO in the pivotal trials). Based on this efficacy, we believe that patients with overlapping, multifaceted disease may benefit the most from these medications. Patient risk factors and comorbidities are a prominent consideration in our use of JAKi to ensure safety, as the risk for MACE and malignancy is informed partly by baseline cardiovascular status. In younger patients without cardiovascular risk factors, JAKi may be a strong candidate for first-line therapy, particularly in patients averse to subcutaneous or intravenous therapy. We do counsel all patients on the increased risk of infection, and we do recommend inactivated herpes zoster vaccination in previously unvaccinated patients planning to start JAKi therapy. 

On the horizon are the development of novel, oral agents targeting tyrosine kinase 2 (TYK2), which is a member of the JAK family of signaling proteins. In fact, the TYK2 inhibitor deucravacitinib was approved by the FDA in 2022 for the treatment of PsO. TYK2 inhibitors appear to have the advantage of a more selective mechanism of action, with fewer off-target effects. There were fewer adverse events in the deucravacitinib trials, which led to its prompt PsO authorization, and the FDA approval for the drug did not include the same black box warning that appears in the label for other JAKi.⁸ A phase 2 study showed early promise for the efficacy and safety of deucravacitinib in PsA.⁹ Further investigation will be needed to better understand the role of deucravacitinib and other TYK2 inhibitors being developed for the treatment of PsA. In the meantime, JAKi continue to be a prominent consideration for first-line PsA therapy in a carefully selected patient population. 

Janus kinase inhibitors (JAKi) are a novel class of oral, targeted small-molecule inhibitors that are increasingly used to treat several different autoimmune conditions. In terms of rheumatologic indications, the FDA first approved tofacitinib (TOF) for use in moderate to severe rheumatoid arthritis (RA) unresponsive to methotrexate therapy. Eleven years later, the indications for JAKi use have expanded to include ulcerative colitis, ankylosing spondylitis, and psoriatic arthritis (PsA), among other diseases. As with any new therapeutic mechanism, there are questions as to how JAKi should be incorporated into the treatment paradigm of PsA. In this article, we briefly review the efficacy and safety data of these agents and discuss our approach to their use in PsA.

Two JAKi are currently FDA approved for the treatment of PsA: tofacitinib (TOF) and upadacitinib (UPA). Other JAKi, such as filgotinib and peficitinib, are only approved outside the United States and will not be discussed here. 

TOF was originally studied in skin psoriasis (PsO) before 2 pivotal studies demonstrated efficacy in PsA. TOF or adalimumab (ADA) were compared with placebo in patients who had failed conventional synthetic disease-modifying antirheumatic drugs (DMARD).¹ ACR20 response was superior with TOF 5 mg twice daily (BID) (50%) and 10 mg BID (61%) vs placebo (33%), and it was comparable to ADA (52%), which was used in this study as an active comparator. The overall rate of adverse events was similar with both doses of TOF when compared with ADA; however, patients taking TOF had numerically more cases of cancer, serious infection, and herpes zoster. 

Another study evaluated TOF compared with placebo in patients with PsA who had an inadequate response to tumor necrosis factor inhibitor (TNFi) therapy.² The study showed an ACR20 response of 50% in patients taking TOF 5 mg BID and 47% in patients taking 10 mg BID, compared with 24% in those taking placebo. Patients who received the 10 mg TOF dose continuously had higher rates of adverse events compared to TOF 5 mg, placebo, and patients who crossed over from placebo to TOF at either dose. In the TOF groups, there were cases of serious infection and herpes zoster, as well as 2 patients with major adverse cardiovascular events (MACE). Following review of these data, the FDA approved only the 5 mg BID dose, and later an 11-mg daily extended-release formulation that was pharmacokinetically similar.

The efficacy for UPA in PsA was shown in 2 pivotal phase 3 trials. SELECT-PsA1 compared UPA at 2 doses, 15 mg and 30 mg daily, vs placebo and vs ADA in patients with biologic DMARD (bDMARD)-naïve PsA.³ This trial demonstrated superiority of UPA in the ACR20 response at both doses (71% and 79%, respectively) compared with placebo (36%). The 15-mg dose of UPA was comparable to ADA (65%), while the 30-mg dose achieved superiority compared to ADA. Secondary outcomes including skin activity, patient-reported symptoms, and inhibition of radiographic progression were also superior in UPA compared with placebo and similar or greater with UPA compared with ADA, depending on the specific outcome.⁴ SELECT-PsA2 compared UPA 15 mg, 30 mg, and placebo in patients with prior incomplete response or intolerance to a bDMARD.⁵ At week 12 of the study, patients taking UPA 15 mg and 30 mg had an ACR20 response of 57% and 64%, respectively, compared with placebo (24%). At week 24, minimal disease activity was achieved by 25% of patients taking UPA 15 mg and 29% of patients taking UPA 30 mg, which was superior to placebo (3%). 

Both studies found a significant increase in infections, including serious infections, at the 30-mg UPA dose compared with the placebo and adalimumab groups. Cytopenia and elevated creatine kinase (CK) level also occurred more frequently in the UPA 30-mg group. Rates of cancer were low overall and comparable between the patients treated with UPA and ADA. Given the higher incidence of adverse events with the 30-mg dose and the relatively similar efficacy, the sponsor elected to submit only the lower dose to the FDA for approval.

In the last few years, concerns for safety with JAKi use grew after the publication of data from the ORAL SURVEILLANCE trial, an FDA-mandated, post-approval safety study of TOF in RA. In this trial, patients with active RA over 50 years of age and with at least 1 additional cardiovascular risk factor were randomized to TOF at 1 of 2 doses, 5 mg or 10 mg BID, or a TNFi.⁶ This trial was designed as a noninferiority study, and TOF did not meet the noninferiority threshold compared to TNFi, with hazard ratios of 1.33 and 1.48 for MACE and malignancy, respectively. The results of this trial prompted the FDA to add a black box warning to the label for all JAKi, pointing out the risk of malignancy and MACE, as well as infection, mortality, and thrombosis. 

In the ORAL SURVEILLANCE trial, the increased risk of MACE and malignancy was primarily seen in the study patients with high risk for a cardiovascular event. To address the question of whether a similar risk profile exists when using JAKi to treat PsA, or whether this is a disease-specific process related to RA, a post hoc analysis of 3 PsA trials and 7 PsO trials of patients treated with TOF was conducted.⁷ The analysis found that patients with a history of atherosclerotic cardiovascular disease (ASCVD) or metabolic syndrome, or patients at high risk for ASCVD (score > 20%) had increased incidence rates of MACE compared with those with low risk scores for ASCVD. Interestingly, as in RA, increased incidence rates of malignancy were seen in patients with preexisting or at high risk for ASCVD.

While the FDA recommends JAKi use in patients who have failed or are inappropriate for treatment with a TNFi, we would consider the use of JAKi for first-line therapy in PsA on an individual basis. One advantage of JAKi is their efficacy across multiple PsA domains, including peripheral arthritis, axial disease, enthesitis, dactylitis, and skin disease (although the approved dose of TOF was not statistically effective for PsO in the pivotal trials). Based on this efficacy, we believe that patients with overlapping, multifaceted disease may benefit the most from these medications. Patient risk factors and comorbidities are a prominent consideration in our use of JAKi to ensure safety, as the risk for MACE and malignancy is informed partly by baseline cardiovascular status. In younger patients without cardiovascular risk factors, JAKi may be a strong candidate for first-line therapy, particularly in patients averse to subcutaneous or intravenous therapy. We do counsel all patients on the increased risk of infection, and we do recommend inactivated herpes zoster vaccination in previously unvaccinated patients planning to start JAKi therapy. 

On the horizon are the development of novel, oral agents targeting tyrosine kinase 2 (TYK2), which is a member of the JAK family of signaling proteins. In fact, the TYK2 inhibitor deucravacitinib was approved by the FDA in 2022 for the treatment of PsO. TYK2 inhibitors appear to have the advantage of a more selective mechanism of action, with fewer off-target effects. There were fewer adverse events in the deucravacitinib trials, which led to its prompt PsO authorization, and the FDA approval for the drug did not include the same black box warning that appears in the label for other JAKi.⁸ A phase 2 study showed early promise for the efficacy and safety of deucravacitinib in PsA.⁹ Further investigation will be needed to better understand the role of deucravacitinib and other TYK2 inhibitors being developed for the treatment of PsA. In the meantime, JAKi continue to be a prominent consideration for first-line PsA therapy in a carefully selected patient population. 

A new model can predict which patients are more likely to experience side effects from long-term methotrexate (MTX) use, research suggests. Patients with a lower risk profile may benefit from less frequent testing, the authors hypothesize.

Most recommendations advise that patients initiating MTX therapy should get blood testing every 2-4 weeks to monitor for full blood count, liver function, urea electrolytes, and creatinine. After 6 months taking MTX, monitoring can be tapered to every 3 months. But Abhishek Abhishek, MD, PhD, professor of rheumatology and honorary consultant rheumatologist at Nottingham (England) University Hospitals NHS Trust and colleagues argue that abnormal results after the initial 6 months of treatment are “infrequent,” and patients may benefit from fewer tests throughout the year.

ftwitty/E+/Getty Images

“Unnecessary blood tests waste patients’ time and health care resources, including the time of general practitioners and phlebotomists,” Dr. Abhishek and associates write. “It would be beneficial to predict the risk of clinically significant abnormal blood test results during long-term methotrexate treatment to inform the frequency of testing for individuals.”
 

Stratifying risk

In the study, published in the BMJ, researchers used the UK’s Clinical Practice Research Datalink (CPRD) to identify the electronic medical records of over 37,000 adult patients with an immune-mediated inflammatory disease who were prescribed MTX during 2007-2019. All included patients were prescribed MTX for at least 6 months. The main outcome was discontinuation of methotrexate because of abnormal blood test results. Around 62% of patients had rheumatoid arthritis and 22% had psoriasis or psoriatic arthritis.

Using these anonymized data, the group developed a risk stratification model using 11 clinical predictors. “The factors that went in the model are simple things that most patients can self-report or doctors can get from their patient’s medical records,” Dr. Abhishek told this news organization, including methotrexate dose, age, sex, and comorbidities. Dr. Abhishek emphasized that the model should be used only in patients who have continued taking MTX for at least 6 months and have already undergone more frequent initial testing.

The strongest individual predictors were diabetes (hazard ratio, 1.25), chronic kidney disease stage 3 (HR, 2.01), and previous cytopenia or raised liver enzyme levels during the first 6 months of MTX therapy (HR, 2.97). However, Dr. Abhishek emphasized that the individual factors were less important, noting that the model sums the risks to predict outcomes more accurately. Most patients (68.4%) were sorted into the low-risk cohort, with a less than 10% estimated risk of discontinuing MTX over the next 5 years. About one-fifth (20.9%) were categorized as moderate risk (10%-20% estimated risk over 5 years), and 10.7% were high risk, with a greater than 20% estimated risk of discontinuing the drug over 5 years.

The authors argue that low-risk patients could receive less frequent testing – perhaps every 6 months or annually, while moderate-risk patients would continue to be tested every 3 months. High-risk patients could potentially be tested with even greater frequently.
 

More research needed

The research involved “incredibly sophisticated statistical analysis,” said Daniel E. Furst, MD, professor emeritus of medicine at the University of California, Los Angeles, who was not involved with the study. However, the data do not yet support altering blood testing frequency based on this model.

“The hypothesis that not all patients have to be examined so frequently is a very reasonable hypothesis,” Dr. Furst said in an interview, and additional research is needed to corroborate it. The model also needs to be validated in patient populations outside of the United Kingdom, he added.

Dr. Abhishek agreed that validating the model in other patient populations is an important next step. “When we develop a tool [using] a one-nation data set, we want other researchers to then validate it in other countries’ data sets to make sure there is nothing odd about patients in the U.K. that makes the tool work well here but not in [the] U.S., Europe, or Asia, for example,” he said. Doing so should be relatively easy, he said, as the model is publicly available, and the information required is routinely collected during clinic visits.

To understand if less frequent testing might be appropriate for some patients, researchers would need to look at data registries like the Brigham and Women’s Hospital Rheumatoid Arthritis Sequential Study (BRASS) registry or CorEvitas registries “where the testing is done in a very regular way over the long haul,” Dr. Furst said. Analyzing these datasets, researchers could determine the testing intervals that would be most efficient for low- and high-risk patients.
 

A word of caution

While less frequent testing for long-term MTX therapy could likely have benefits, there is still some risk involved, cautioned Prabha Ranganathan, MD, professor of medicine at Washington University in St. Louis.

“Although most methotrexate toxicity occurs within the first 6 months of starting treatment, rare idiosyncratic toxicity can occur that does not correlate with the dose, duration, or method of how methotrexate is administered,” she wrote in an accompanying editorial. “Most rheumatologists can identify a handful of patients who receive methotrexate in their practice who develop sudden leukopenia or thrombocytopenia or transaminitis that is severe enough to warrant drug discontinuation.” While tools like this prediction model can be useful, clinicians need to consider each patient individually and use shared decision-making when monitoring for MTX toxicity, she advised.

“As in most of areas of medicine, the one-size-fits-all approach does not work for methotrexate users,” she noted.

This study was funded by the U.K. National Institute for Health and Care Research and Health Technology Assessment. Dr. Abhishek has received institutional research grants from AstraZeneca and Oxford Immunotech and personal fees from UpToDate, Springer, Cadila Pharmaceuticals, NGM Bio, Limbic, and Inflazome. Dr. Furst and Dr. Ranganathan report no relevant financial relationships.

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

A new model can predict which patients are more likely to experience side effects from long-term methotrexate (MTX) use, research suggests. Patients with a lower risk profile may benefit from less frequent testing, the authors hypothesize.

Most recommendations advise that patients initiating MTX therapy should get blood testing every 2-4 weeks to monitor for full blood count, liver function, urea electrolytes, and creatinine. After 6 months taking MTX, monitoring can be tapered to every 3 months. But Abhishek Abhishek, MD, PhD, professor of rheumatology and honorary consultant rheumatologist at Nottingham (England) University Hospitals NHS Trust and colleagues argue that abnormal results after the initial 6 months of treatment are “infrequent,” and patients may benefit from fewer tests throughout the year.

ftwitty/E+/Getty Images

“Unnecessary blood tests waste patients’ time and health care resources, including the time of general practitioners and phlebotomists,” Dr. Abhishek and associates write. “It would be beneficial to predict the risk of clinically significant abnormal blood test results during long-term methotrexate treatment to inform the frequency of testing for individuals.”
 

Stratifying risk

In the study, published in the BMJ, researchers used the UK’s Clinical Practice Research Datalink (CPRD) to identify the electronic medical records of over 37,000 adult patients with an immune-mediated inflammatory disease who were prescribed MTX during 2007-2019. All included patients were prescribed MTX for at least 6 months. The main outcome was discontinuation of methotrexate because of abnormal blood test results. Around 62% of patients had rheumatoid arthritis and 22% had psoriasis or psoriatic arthritis.

Using these anonymized data, the group developed a risk stratification model using 11 clinical predictors. “The factors that went in the model are simple things that most patients can self-report or doctors can get from their patient’s medical records,” Dr. Abhishek told this news organization, including methotrexate dose, age, sex, and comorbidities. Dr. Abhishek emphasized that the model should be used only in patients who have continued taking MTX for at least 6 months and have already undergone more frequent initial testing.

The strongest individual predictors were diabetes (hazard ratio, 1.25), chronic kidney disease stage 3 (HR, 2.01), and previous cytopenia or raised liver enzyme levels during the first 6 months of MTX therapy (HR, 2.97). However, Dr. Abhishek emphasized that the individual factors were less important, noting that the model sums the risks to predict outcomes more accurately. Most patients (68.4%) were sorted into the low-risk cohort, with a less than 10% estimated risk of discontinuing MTX over the next 5 years. About one-fifth (20.9%) were categorized as moderate risk (10%-20% estimated risk over 5 years), and 10.7% were high risk, with a greater than 20% estimated risk of discontinuing the drug over 5 years.

The authors argue that low-risk patients could receive less frequent testing – perhaps every 6 months or annually, while moderate-risk patients would continue to be tested every 3 months. High-risk patients could potentially be tested with even greater frequently.
 

More research needed

The research involved “incredibly sophisticated statistical analysis,” said Daniel E. Furst, MD, professor emeritus of medicine at the University of California, Los Angeles, who was not involved with the study. However, the data do not yet support altering blood testing frequency based on this model.

“The hypothesis that not all patients have to be examined so frequently is a very reasonable hypothesis,” Dr. Furst said in an interview, and additional research is needed to corroborate it. The model also needs to be validated in patient populations outside of the United Kingdom, he added.

Dr. Abhishek agreed that validating the model in other patient populations is an important next step. “When we develop a tool [using] a one-nation data set, we want other researchers to then validate it in other countries’ data sets to make sure there is nothing odd about patients in the U.K. that makes the tool work well here but not in [the] U.S., Europe, or Asia, for example,” he said. Doing so should be relatively easy, he said, as the model is publicly available, and the information required is routinely collected during clinic visits.

To understand if less frequent testing might be appropriate for some patients, researchers would need to look at data registries like the Brigham and Women’s Hospital Rheumatoid Arthritis Sequential Study (BRASS) registry or CorEvitas registries “where the testing is done in a very regular way over the long haul,” Dr. Furst said. Analyzing these datasets, researchers could determine the testing intervals that would be most efficient for low- and high-risk patients.
 

A word of caution

While less frequent testing for long-term MTX therapy could likely have benefits, there is still some risk involved, cautioned Prabha Ranganathan, MD, professor of medicine at Washington University in St. Louis.

“Although most methotrexate toxicity occurs within the first 6 months of starting treatment, rare idiosyncratic toxicity can occur that does not correlate with the dose, duration, or method of how methotrexate is administered,” she wrote in an accompanying editorial. “Most rheumatologists can identify a handful of patients who receive methotrexate in their practice who develop sudden leukopenia or thrombocytopenia or transaminitis that is severe enough to warrant drug discontinuation.” While tools like this prediction model can be useful, clinicians need to consider each patient individually and use shared decision-making when monitoring for MTX toxicity, she advised.

“As in most of areas of medicine, the one-size-fits-all approach does not work for methotrexate users,” she noted.

This study was funded by the U.K. National Institute for Health and Care Research and Health Technology Assessment. Dr. Abhishek has received institutional research grants from AstraZeneca and Oxford Immunotech and personal fees from UpToDate, Springer, Cadila Pharmaceuticals, NGM Bio, Limbic, and Inflazome. Dr. Furst and Dr. Ranganathan report no relevant financial relationships.

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

A new model can predict which patients are more likely to experience side effects from long-term methotrexate (MTX) use, research suggests. Patients with a lower risk profile may benefit from less frequent testing, the authors hypothesize.

Most recommendations advise that patients initiating MTX therapy should get blood testing every 2-4 weeks to monitor for full blood count, liver function, urea electrolytes, and creatinine. After 6 months taking MTX, monitoring can be tapered to every 3 months. But Abhishek Abhishek, MD, PhD, professor of rheumatology and honorary consultant rheumatologist at Nottingham (England) University Hospitals NHS Trust and colleagues argue that abnormal results after the initial 6 months of treatment are “infrequent,” and patients may benefit from fewer tests throughout the year.

ftwitty/E+/Getty Images

“Unnecessary blood tests waste patients’ time and health care resources, including the time of general practitioners and phlebotomists,” Dr. Abhishek and associates write. “It would be beneficial to predict the risk of clinically significant abnormal blood test results during long-term methotrexate treatment to inform the frequency of testing for individuals.”
 

Stratifying risk

In the study, published in the BMJ, researchers used the UK’s Clinical Practice Research Datalink (CPRD) to identify the electronic medical records of over 37,000 adult patients with an immune-mediated inflammatory disease who were prescribed MTX during 2007-2019. All included patients were prescribed MTX for at least 6 months. The main outcome was discontinuation of methotrexate because of abnormal blood test results. Around 62% of patients had rheumatoid arthritis and 22% had psoriasis or psoriatic arthritis.

Using these anonymized data, the group developed a risk stratification model using 11 clinical predictors. “The factors that went in the model are simple things that most patients can self-report or doctors can get from their patient’s medical records,” Dr. Abhishek told this news organization, including methotrexate dose, age, sex, and comorbidities. Dr. Abhishek emphasized that the model should be used only in patients who have continued taking MTX for at least 6 months and have already undergone more frequent initial testing.

The strongest individual predictors were diabetes (hazard ratio, 1.25), chronic kidney disease stage 3 (HR, 2.01), and previous cytopenia or raised liver enzyme levels during the first 6 months of MTX therapy (HR, 2.97). However, Dr. Abhishek emphasized that the individual factors were less important, noting that the model sums the risks to predict outcomes more accurately. Most patients (68.4%) were sorted into the low-risk cohort, with a less than 10% estimated risk of discontinuing MTX over the next 5 years. About one-fifth (20.9%) were categorized as moderate risk (10%-20% estimated risk over 5 years), and 10.7% were high risk, with a greater than 20% estimated risk of discontinuing the drug over 5 years.

The authors argue that low-risk patients could receive less frequent testing – perhaps every 6 months or annually, while moderate-risk patients would continue to be tested every 3 months. High-risk patients could potentially be tested with even greater frequently.
 

More research needed

The research involved “incredibly sophisticated statistical analysis,” said Daniel E. Furst, MD, professor emeritus of medicine at the University of California, Los Angeles, who was not involved with the study. However, the data do not yet support altering blood testing frequency based on this model.

“The hypothesis that not all patients have to be examined so frequently is a very reasonable hypothesis,” Dr. Furst said in an interview, and additional research is needed to corroborate it. The model also needs to be validated in patient populations outside of the United Kingdom, he added.

Dr. Abhishek agreed that validating the model in other patient populations is an important next step. “When we develop a tool [using] a one-nation data set, we want other researchers to then validate it in other countries’ data sets to make sure there is nothing odd about patients in the U.K. that makes the tool work well here but not in [the] U.S., Europe, or Asia, for example,” he said. Doing so should be relatively easy, he said, as the model is publicly available, and the information required is routinely collected during clinic visits.

To understand if less frequent testing might be appropriate for some patients, researchers would need to look at data registries like the Brigham and Women’s Hospital Rheumatoid Arthritis Sequential Study (BRASS) registry or CorEvitas registries “where the testing is done in a very regular way over the long haul,” Dr. Furst said. Analyzing these datasets, researchers could determine the testing intervals that would be most efficient for low- and high-risk patients.
 

A word of caution

While less frequent testing for long-term MTX therapy could likely have benefits, there is still some risk involved, cautioned Prabha Ranganathan, MD, professor of medicine at Washington University in St. Louis.

“Although most methotrexate toxicity occurs within the first 6 months of starting treatment, rare idiosyncratic toxicity can occur that does not correlate with the dose, duration, or method of how methotrexate is administered,” she wrote in an accompanying editorial. “Most rheumatologists can identify a handful of patients who receive methotrexate in their practice who develop sudden leukopenia or thrombocytopenia or transaminitis that is severe enough to warrant drug discontinuation.” While tools like this prediction model can be useful, clinicians need to consider each patient individually and use shared decision-making when monitoring for MTX toxicity, she advised.

“As in most of areas of medicine, the one-size-fits-all approach does not work for methotrexate users,” she noted.

This study was funded by the U.K. National Institute for Health and Care Research and Health Technology Assessment. Dr. Abhishek has received institutional research grants from AstraZeneca and Oxford Immunotech and personal fees from UpToDate, Springer, Cadila Pharmaceuticals, NGM Bio, Limbic, and Inflazome. Dr. Furst and Dr. Ranganathan report no relevant financial relationships.

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

Investigators have found a correlation between vitamin D deficiency and psoriasis severity, suggesting that some people who increase their intake of the vitamin could better control this skin condition that affects up to 8 million people in the United States alone. 

Brown University researchers studied almost 500 psoriasis cases taken from the National Health and Nutrition Examination Survey (NHANES), the scientists told attendees at the conference of the American Society for Nutrition. They compared the peoples’ reports on how much of their body surface was affected by psoriasis to vitamin D levels collected in blood samples.

“After adjusting for lifestyle factors such as smoking, the analysis showed that lower vitamin D levels and vitamin D deficiency were significantly associated with greater psoriasis severity,” the ASN said in a news release. “The researchers also found that patients with the least amount of body surface affected by psoriasis had the highest average vitamin D levels while those with the greatest affected area had the lowest average levels of vitamin D.”

The researchers said that people with psoriasis might improve their condition by getting more vitamin D in their diet and through supplements.

“Topical synthetic vitamin D creams are emerging as new therapies for psoriasis, but these usually require a doctor’s prescription,” said researcher Rachel K. Lim, an MD candidate at Brown University, Providence, R.I. “Our results suggest that a vitamin D–rich diet or oral vitamin D supplementation may also provide some benefit to psoriasis patients.”

The researchers said that vitamin D toxicity is rare but that people should consult with their medical caregivers before they start taking supplements.

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

Investigators have found a correlation between vitamin D deficiency and psoriasis severity, suggesting that some people who increase their intake of the vitamin could better control this skin condition that affects up to 8 million people in the United States alone. 

Brown University researchers studied almost 500 psoriasis cases taken from the National Health and Nutrition Examination Survey (NHANES), the scientists told attendees at the conference of the American Society for Nutrition. They compared the peoples’ reports on how much of their body surface was affected by psoriasis to vitamin D levels collected in blood samples.

“After adjusting for lifestyle factors such as smoking, the analysis showed that lower vitamin D levels and vitamin D deficiency were significantly associated with greater psoriasis severity,” the ASN said in a news release. “The researchers also found that patients with the least amount of body surface affected by psoriasis had the highest average vitamin D levels while those with the greatest affected area had the lowest average levels of vitamin D.”

The researchers said that people with psoriasis might improve their condition by getting more vitamin D in their diet and through supplements.

“Topical synthetic vitamin D creams are emerging as new therapies for psoriasis, but these usually require a doctor’s prescription,” said researcher Rachel K. Lim, an MD candidate at Brown University, Providence, R.I. “Our results suggest that a vitamin D–rich diet or oral vitamin D supplementation may also provide some benefit to psoriasis patients.”

The researchers said that vitamin D toxicity is rare but that people should consult with their medical caregivers before they start taking supplements.

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

Investigators have found a correlation between vitamin D deficiency and psoriasis severity, suggesting that some people who increase their intake of the vitamin could better control this skin condition that affects up to 8 million people in the United States alone. 

Brown University researchers studied almost 500 psoriasis cases taken from the National Health and Nutrition Examination Survey (NHANES), the scientists told attendees at the conference of the American Society for Nutrition. They compared the peoples’ reports on how much of their body surface was affected by psoriasis to vitamin D levels collected in blood samples.

“After adjusting for lifestyle factors such as smoking, the analysis showed that lower vitamin D levels and vitamin D deficiency were significantly associated with greater psoriasis severity,” the ASN said in a news release. “The researchers also found that patients with the least amount of body surface affected by psoriasis had the highest average vitamin D levels while those with the greatest affected area had the lowest average levels of vitamin D.”

The researchers said that people with psoriasis might improve their condition by getting more vitamin D in their diet and through supplements.

“Topical synthetic vitamin D creams are emerging as new therapies for psoriasis, but these usually require a doctor’s prescription,” said researcher Rachel K. Lim, an MD candidate at Brown University, Providence, R.I. “Our results suggest that a vitamin D–rich diet or oral vitamin D supplementation may also provide some benefit to psoriasis patients.”

The researchers said that vitamin D toxicity is rare but that people should consult with their medical caregivers before they start taking supplements.

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

Key clinical point: Serum neutrophil gelatinase-associated lipocalin (NGAL) showed no value as a biomarker either for disease activity or for monitoring in relation to anti-inflammatory treatment in patients with peripheral psoriatic arthritis (PsA).

Major finding: Overall, the mean serum NGAL reduced by 11% after 12 months of treatment with any disease-modifying antirheumatic drug (DMARD), with no clear trend of a clinically significant increase or decrease after 12 months of treatment with conventional-synthetic DMARDs, tumor necrosis factor-alpha inhibitors, or interleukin-17 inhibitors. The changes in NGAL levels showed no correlation with changes in PsA outcomes (Spearman correlation coefficients close to 0.0).

Study details: This exploratory prospective cohort study included 117 patients with peripheral PsA who initiated conventional synthetic or biologic DMARDs, 20 patients with psoriasis without arthritis who did not receive systemic treatment, and 20 control individuals.

Disclosures: This study was supported by the Danish Rheumatism Association and others. Five authors reported ties with various sources. The other authors declared no conflict of interests.

Source: Stisen ZR et al. Treatment-related changes in serum neutrophil gelatinase-associated lipocalin (NGAL) in psoriatic arthritis: Results from the PIPA cohort study. Scand J Rheumatol. 2023;1-8 (Jun 20). Doi: 10.1080/03009742.2023.2216046.

Key clinical point: Serum neutrophil gelatinase-associated lipocalin (NGAL) showed no value as a biomarker either for disease activity or for monitoring in relation to anti-inflammatory treatment in patients with peripheral psoriatic arthritis (PsA).

Major finding: Overall, the mean serum NGAL reduced by 11% after 12 months of treatment with any disease-modifying antirheumatic drug (DMARD), with no clear trend of a clinically significant increase or decrease after 12 months of treatment with conventional-synthetic DMARDs, tumor necrosis factor-alpha inhibitors, or interleukin-17 inhibitors. The changes in NGAL levels showed no correlation with changes in PsA outcomes (Spearman correlation coefficients close to 0.0).

Study details: This exploratory prospective cohort study included 117 patients with peripheral PsA who initiated conventional synthetic or biologic DMARDs, 20 patients with psoriasis without arthritis who did not receive systemic treatment, and 20 control individuals.

Disclosures: This study was supported by the Danish Rheumatism Association and others. Five authors reported ties with various sources. The other authors declared no conflict of interests.

Source: Stisen ZR et al. Treatment-related changes in serum neutrophil gelatinase-associated lipocalin (NGAL) in psoriatic arthritis: Results from the PIPA cohort study. Scand J Rheumatol. 2023;1-8 (Jun 20). Doi: 10.1080/03009742.2023.2216046.

Key clinical point: Serum neutrophil gelatinase-associated lipocalin (NGAL) showed no value as a biomarker either for disease activity or for monitoring in relation to anti-inflammatory treatment in patients with peripheral psoriatic arthritis (PsA).

Major finding: Overall, the mean serum NGAL reduced by 11% after 12 months of treatment with any disease-modifying antirheumatic drug (DMARD), with no clear trend of a clinically significant increase or decrease after 12 months of treatment with conventional-synthetic DMARDs, tumor necrosis factor-alpha inhibitors, or interleukin-17 inhibitors. The changes in NGAL levels showed no correlation with changes in PsA outcomes (Spearman correlation coefficients close to 0.0).

Study details: This exploratory prospective cohort study included 117 patients with peripheral PsA who initiated conventional synthetic or biologic DMARDs, 20 patients with psoriasis without arthritis who did not receive systemic treatment, and 20 control individuals.

Disclosures: This study was supported by the Danish Rheumatism Association and others. Five authors reported ties with various sources. The other authors declared no conflict of interests.

Source: Stisen ZR et al. Treatment-related changes in serum neutrophil gelatinase-associated lipocalin (NGAL) in psoriatic arthritis: Results from the PIPA cohort study. Scand J Rheumatol. 2023;1-8 (Jun 20). Doi: 10.1080/03009742.2023.2216046.

Key clinical point: The combination of serum interleukin-6 (IL-6), platelet to lymphocyte ratio (PLR), and nail psoriasis can help screen and predict early stage of psoriatic arthritis (PsA).

Major finding: The proportion of patients with elevated serum IL-6 levels was significantly higher in the PsA vs. plaque psoriasis group (P < .0167), with the elevations in PLR levels and systemic immune-inflammation index being significantly higher among patients with PsA and early PsA vs. plaque psoriasis (P < .05 for all). The combination of nail psoriasis (P = .002), IL-6 (P < .001), and PLR (P < .001) as a predictor for early PsA diagnosis showed an area under curve of 0.84 (95% CI, 0.77-0.90).

Study details: Findings are from a case-control study including 109 patients with plaque psoriasis without joint involvement, 47 patients with PsA, and 41 patients with rheumatoid arthritis.

Disclosures: This study did not receive any funding. The authors declared no conflict of interests.

Source: Liu X et al. The combination of IL-6, PLR and nail psoriasis: Screen for the early diagnosis of psoriatic arthritis. Clin Cosmet Investig Dermatol. 2023;16:1703-1713 (Jun 28). Doi: 10.2147/CCID.S413853.

Key clinical point: The combination of serum interleukin-6 (IL-6), platelet to lymphocyte ratio (PLR), and nail psoriasis can help screen and predict early stage of psoriatic arthritis (PsA).

Major finding: The proportion of patients with elevated serum IL-6 levels was significantly higher in the PsA vs. plaque psoriasis group (P < .0167), with the elevations in PLR levels and systemic immune-inflammation index being significantly higher among patients with PsA and early PsA vs. plaque psoriasis (P < .05 for all). The combination of nail psoriasis (P = .002), IL-6 (P < .001), and PLR (P < .001) as a predictor for early PsA diagnosis showed an area under curve of 0.84 (95% CI, 0.77-0.90).

Study details: Findings are from a case-control study including 109 patients with plaque psoriasis without joint involvement, 47 patients with PsA, and 41 patients with rheumatoid arthritis.

Disclosures: This study did not receive any funding. The authors declared no conflict of interests.

Source: Liu X et al. The combination of IL-6, PLR and nail psoriasis: Screen for the early diagnosis of psoriatic arthritis. Clin Cosmet Investig Dermatol. 2023;16:1703-1713 (Jun 28). Doi: 10.2147/CCID.S413853.

Key clinical point: The combination of serum interleukin-6 (IL-6), platelet to lymphocyte ratio (PLR), and nail psoriasis can help screen and predict early stage of psoriatic arthritis (PsA).

Major finding: The proportion of patients with elevated serum IL-6 levels was significantly higher in the PsA vs. plaque psoriasis group (P < .0167), with the elevations in PLR levels and systemic immune-inflammation index being significantly higher among patients with PsA and early PsA vs. plaque psoriasis (P < .05 for all). The combination of nail psoriasis (P = .002), IL-6 (P < .001), and PLR (P < .001) as a predictor for early PsA diagnosis showed an area under curve of 0.84 (95% CI, 0.77-0.90).

Study details: Findings are from a case-control study including 109 patients with plaque psoriasis without joint involvement, 47 patients with PsA, and 41 patients with rheumatoid arthritis.

Disclosures: This study did not receive any funding. The authors declared no conflict of interests.

Source: Liu X et al. The combination of IL-6, PLR and nail psoriasis: Screen for the early diagnosis of psoriatic arthritis. Clin Cosmet Investig Dermatol. 2023;16:1703-1713 (Jun 28). Doi: 10.2147/CCID.S413853.

Key clinical point: The presentation of disease domains is heterogenous in psoriatic arthritis (PsA) making assessment of all domains important for optimal disease management.

Major finding: Peripheral arthritis (86%) and skin disease (82%) were the most common, whereas dactylitis (23%) and axial disease (20%) were the least common disease domains identified in the overall PsA population and across treatment groups. The triad of peripheral arthritis, nail psoriasis, and skin disease was the most common domain combination (13.7%) not only in the overall PsA population but also when stratified by those who initiated tumor necrosis factor inhibitors (TNFis; 14.4%) or interleukin-17 inhibitors (IL-17is; 12.6%). At 6 months, the minimal disease activity improved across PsA domains.

Study details: This real-world analysis included 1,005 patients with PsA from the CorEvitas PsA/Spondyloarthritis Registry who initiated either TNFis or IL-17is at baseline.

Disclosures: This study was sponsored by Amgen Inc. Three authors declared being employees of and owning stocks or options in Amgen. Two authors declared being employees of CorEvitas, LLC. PJ Mease and A Ogdie declared ties with various sources, including Amgen.

Source: Mease PJ et al. Real-world evidence assessing psoriatic arthritis by disease domain: An evaluation of the CorEvitas Psoriatic Arthritis/Spondyloarthritis Registry. ACR Open Rheumatol. 2023 (Jun 25). Doi: 10.1002/acr2.11556.

Key clinical point: The presentation of disease domains is heterogenous in psoriatic arthritis (PsA) making assessment of all domains important for optimal disease management.

Major finding: Peripheral arthritis (86%) and skin disease (82%) were the most common, whereas dactylitis (23%) and axial disease (20%) were the least common disease domains identified in the overall PsA population and across treatment groups. The triad of peripheral arthritis, nail psoriasis, and skin disease was the most common domain combination (13.7%) not only in the overall PsA population but also when stratified by those who initiated tumor necrosis factor inhibitors (TNFis; 14.4%) or interleukin-17 inhibitors (IL-17is; 12.6%). At 6 months, the minimal disease activity improved across PsA domains.

Study details: This real-world analysis included 1,005 patients with PsA from the CorEvitas PsA/Spondyloarthritis Registry who initiated either TNFis or IL-17is at baseline.

Disclosures: This study was sponsored by Amgen Inc. Three authors declared being employees of and owning stocks or options in Amgen. Two authors declared being employees of CorEvitas, LLC. PJ Mease and A Ogdie declared ties with various sources, including Amgen.

Source: Mease PJ et al. Real-world evidence assessing psoriatic arthritis by disease domain: An evaluation of the CorEvitas Psoriatic Arthritis/Spondyloarthritis Registry. ACR Open Rheumatol. 2023 (Jun 25). Doi: 10.1002/acr2.11556.

Key clinical point: The presentation of disease domains is heterogenous in psoriatic arthritis (PsA) making assessment of all domains important for optimal disease management.

Major finding: Peripheral arthritis (86%) and skin disease (82%) were the most common, whereas dactylitis (23%) and axial disease (20%) were the least common disease domains identified in the overall PsA population and across treatment groups. The triad of peripheral arthritis, nail psoriasis, and skin disease was the most common domain combination (13.7%) not only in the overall PsA population but also when stratified by those who initiated tumor necrosis factor inhibitors (TNFis; 14.4%) or interleukin-17 inhibitors (IL-17is; 12.6%). At 6 months, the minimal disease activity improved across PsA domains.

Study details: This real-world analysis included 1,005 patients with PsA from the CorEvitas PsA/Spondyloarthritis Registry who initiated either TNFis or IL-17is at baseline.

Disclosures: This study was sponsored by Amgen Inc. Three authors declared being employees of and owning stocks or options in Amgen. Two authors declared being employees of CorEvitas, LLC. PJ Mease and A Ogdie declared ties with various sources, including Amgen.

Source: Mease PJ et al. Real-world evidence assessing psoriatic arthritis by disease domain: An evaluation of the CorEvitas Psoriatic Arthritis/Spondyloarthritis Registry. ACR Open Rheumatol. 2023 (Jun 25). Doi: 10.1002/acr2.11556.

Key clinical point: Patients with moderate-high psoriatic arthritis (PsA) disease activity without traditional cardiovascular risk factors had an increased prevalence of subclinical myocardial dysfunction, lower adiponectin levels, and higher serum interleukin-17A (IL-17A) levels.

Major finding: Patients with moderate and high PsA disease activity had lower global longitudinal strain (GLS), tricuspid annular plane systolic excursion, left ventricular ejection fraction, and adiponectin levels and higher IL-17A levels compared with patients with low PsA disease activity and control individuals (all P < .05). GLS was significantly associated with serum IL-17A (P = .001) and adiponectin (P = .032) levels.

Study details: This study included 55 patients with PsA and 25 control individuals without cardiovascular disease.

Disclosures: This study did not disclose the funding source. The authors declared no conflict of interests.

Source: Pletikosic I et al. Association of inflammatory biomarkers and disease activity with subclinical myocardial dysfunction in psoriatic arthritis. Sci Rep. 2023;13(1):10371 (Jun 26). Doi: 10.1038/s41598-023-37412-6.

Key clinical point: Patients with moderate-high psoriatic arthritis (PsA) disease activity without traditional cardiovascular risk factors had an increased prevalence of subclinical myocardial dysfunction, lower adiponectin levels, and higher serum interleukin-17A (IL-17A) levels.

Major finding: Patients with moderate and high PsA disease activity had lower global longitudinal strain (GLS), tricuspid annular plane systolic excursion, left ventricular ejection fraction, and adiponectin levels and higher IL-17A levels compared with patients with low PsA disease activity and control individuals (all P < .05). GLS was significantly associated with serum IL-17A (P = .001) and adiponectin (P = .032) levels.

Study details: This study included 55 patients with PsA and 25 control individuals without cardiovascular disease.

Disclosures: This study did not disclose the funding source. The authors declared no conflict of interests.

Source: Pletikosic I et al. Association of inflammatory biomarkers and disease activity with subclinical myocardial dysfunction in psoriatic arthritis. Sci Rep. 2023;13(1):10371 (Jun 26). Doi: 10.1038/s41598-023-37412-6.

Key clinical point: Patients with moderate-high psoriatic arthritis (PsA) disease activity without traditional cardiovascular risk factors had an increased prevalence of subclinical myocardial dysfunction, lower adiponectin levels, and higher serum interleukin-17A (IL-17A) levels.

Major finding: Patients with moderate and high PsA disease activity had lower global longitudinal strain (GLS), tricuspid annular plane systolic excursion, left ventricular ejection fraction, and adiponectin levels and higher IL-17A levels compared with patients with low PsA disease activity and control individuals (all P < .05). GLS was significantly associated with serum IL-17A (P = .001) and adiponectin (P = .032) levels.

Study details: This study included 55 patients with PsA and 25 control individuals without cardiovascular disease.

Disclosures: This study did not disclose the funding source. The authors declared no conflict of interests.

Source: Pletikosic I et al. Association of inflammatory biomarkers and disease activity with subclinical myocardial dysfunction in psoriatic arthritis. Sci Rep. 2023;13(1):10371 (Jun 26). Doi: 10.1038/s41598-023-37412-6.