TBD Meeting (5318-20)

Polycystic ovarian syndrome (PCOS) was associated with a nearly doubled risk of developing psoriasis in a propensity score–matched analysis conducted in Taiwan.

PCOS is characterized by androgen elevation that can lead to insulin resistance and metabolic syndrome, which have also been associated with an increased risk of psoriasis. Previous retrospective analyses have suggested an increased risk of psoriasis associated with PCOS, and psoriasis patients with PCOS have been reported to have more severe skin lesions, compared with those who do not have PCOS.

“The incidence of psoriasis is indeed higher in the PCOS group than in the control group, and the comorbidities related to metabolic syndrome did not modify the adjusted hazard ratio,” said Ming-Li Chen, during her presentation of the study results at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. Dr. Chen is at Chung Shan Medical University in Taiwan.

The researchers analyzed 1 million randomly selected records from Taiwan’s Longitudinal Health Insurance database, a subset of the country’s National Health Insurance Program. Between 2000 and 2012, they identified a case group with at least three outpatient diagnoses or one inpatient diagnosis of PCOS; they then compared each with four patients who did not have PCOS who were matched by age and index year. The mean age in both groups was about 27 years.

The mean follow-up times were 6.99 years for 4,707 cases and 6.94 years for 18,828 controls. Comorbidities were slightly higher in the PCOS group, including asthma (6.7% vs. 4.9%; P less than .001), chronic obstructive pulmonary disease (14% vs. 11%; P less than .001), chronic liver disease (8.0% vs. 5.0%; P less than .001), diabetes mellitus (3.0% vs. 1.4%; P less than .001), hypertension (2.4% vs. 1.5%; P less than .001), hyperlipidemia (5.4% vs. 2.5%; P less than .001), depression (5.4% vs. 3.9%; P less than .001), and sleep apnea (0.23% vs. 0.10%; P = .040).

There was a higher cumulative incidence of psoriasis in the PCOS group (adjusted hazard ratio, 2.07; 95% confidence interval, 1.25-3.44). Other factors associated with increased risk of psoriasis were advanced age (greater than 50 years old; aHR, 14.13; 95% CI, 1.8-110.7) and having a cancer diagnosis (aHR, 11.72; 95% CI, 2.87-47.9).

When PCOS patients were stratified by age, the researchers noted a higher risk of psoriasis among those 20 years or younger (aHR, 4.02; 95% CI, 1.16-13.9) than among those aged 20-50 years (aHR, 1.88; 95% CI, 1.07-3.29). Among those older than 50 years, there was no significantly increased risk, although the number of psoriasis diagnoses and population sizes were small in the latter category. Among patients with PCOS, a cancer diagnosis was not associated with a statistically significant increased risk of psoriasis.

The mechanisms underlying the association between PCOS and psoriasis should be studied further, she noted.

Following Dr. Chen’s prerecorded presentation, there was a live discussion session led by Alice Gottlieb, MD, PhD, medical director of Mount Sinai Beth Israel Dermatology, New York, and Ennio Lubrano, MD, associate professor of rheumatology at the University of Molise (Italy). Dr. Gottlieb noted that the study did not appear to account for weight in the association between PCOS and psoriasis, since heavier people are known to be at greater risk of developing psoriasis. Dr. Chen acknowledged that the study had no records of BMI or weight.

Dr. Gottlieb also wondered if treatment of PCOS led to any improvements in psoriasis in patients with the two diagnoses. “If we treat PCOS, does the psoriasis get better?” Again, the study did not address the question. “We didn’t follow up on therapies,” Dr. Chen said.

Dr. Chen reported no relevant financial disclosures. Dr. Gottlieb is a consultant, advisory board member and/or speaker for AbbVie, Allergan, Avotres Therapeutics, Beiersdorf, Bristol-Myers Squibb, Celgene, Dermira, Eli Lilly, Incyte, Janssen, Leo, Novartis, Reddy Labs, Sun Pharmaceutical Industries, UCB Pharma and Xbiotech. She has received research or educational grants from Boehringer Ingelheim, Incyte, Janssen, Novartis and Xbiotech.

Polycystic ovarian syndrome (PCOS) was associated with a nearly doubled risk of developing psoriasis in a propensity score–matched analysis conducted in Taiwan.

PCOS is characterized by androgen elevation that can lead to insulin resistance and metabolic syndrome, which have also been associated with an increased risk of psoriasis. Previous retrospective analyses have suggested an increased risk of psoriasis associated with PCOS, and psoriasis patients with PCOS have been reported to have more severe skin lesions, compared with those who do not have PCOS.

“The incidence of psoriasis is indeed higher in the PCOS group than in the control group, and the comorbidities related to metabolic syndrome did not modify the adjusted hazard ratio,” said Ming-Li Chen, during her presentation of the study results at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. Dr. Chen is at Chung Shan Medical University in Taiwan.

The researchers analyzed 1 million randomly selected records from Taiwan’s Longitudinal Health Insurance database, a subset of the country’s National Health Insurance Program. Between 2000 and 2012, they identified a case group with at least three outpatient diagnoses or one inpatient diagnosis of PCOS; they then compared each with four patients who did not have PCOS who were matched by age and index year. The mean age in both groups was about 27 years.

The mean follow-up times were 6.99 years for 4,707 cases and 6.94 years for 18,828 controls. Comorbidities were slightly higher in the PCOS group, including asthma (6.7% vs. 4.9%; P less than .001), chronic obstructive pulmonary disease (14% vs. 11%; P less than .001), chronic liver disease (8.0% vs. 5.0%; P less than .001), diabetes mellitus (3.0% vs. 1.4%; P less than .001), hypertension (2.4% vs. 1.5%; P less than .001), hyperlipidemia (5.4% vs. 2.5%; P less than .001), depression (5.4% vs. 3.9%; P less than .001), and sleep apnea (0.23% vs. 0.10%; P = .040).

There was a higher cumulative incidence of psoriasis in the PCOS group (adjusted hazard ratio, 2.07; 95% confidence interval, 1.25-3.44). Other factors associated with increased risk of psoriasis were advanced age (greater than 50 years old; aHR, 14.13; 95% CI, 1.8-110.7) and having a cancer diagnosis (aHR, 11.72; 95% CI, 2.87-47.9).

When PCOS patients were stratified by age, the researchers noted a higher risk of psoriasis among those 20 years or younger (aHR, 4.02; 95% CI, 1.16-13.9) than among those aged 20-50 years (aHR, 1.88; 95% CI, 1.07-3.29). Among those older than 50 years, there was no significantly increased risk, although the number of psoriasis diagnoses and population sizes were small in the latter category. Among patients with PCOS, a cancer diagnosis was not associated with a statistically significant increased risk of psoriasis.

The mechanisms underlying the association between PCOS and psoriasis should be studied further, she noted.

Following Dr. Chen’s prerecorded presentation, there was a live discussion session led by Alice Gottlieb, MD, PhD, medical director of Mount Sinai Beth Israel Dermatology, New York, and Ennio Lubrano, MD, associate professor of rheumatology at the University of Molise (Italy). Dr. Gottlieb noted that the study did not appear to account for weight in the association between PCOS and psoriasis, since heavier people are known to be at greater risk of developing psoriasis. Dr. Chen acknowledged that the study had no records of BMI or weight.

Dr. Gottlieb also wondered if treatment of PCOS led to any improvements in psoriasis in patients with the two diagnoses. “If we treat PCOS, does the psoriasis get better?” Again, the study did not address the question. “We didn’t follow up on therapies,” Dr. Chen said.

Dr. Chen reported no relevant financial disclosures. Dr. Gottlieb is a consultant, advisory board member and/or speaker for AbbVie, Allergan, Avotres Therapeutics, Beiersdorf, Bristol-Myers Squibb, Celgene, Dermira, Eli Lilly, Incyte, Janssen, Leo, Novartis, Reddy Labs, Sun Pharmaceutical Industries, UCB Pharma and Xbiotech. She has received research or educational grants from Boehringer Ingelheim, Incyte, Janssen, Novartis and Xbiotech.

Polycystic ovarian syndrome (PCOS) was associated with a nearly doubled risk of developing psoriasis in a propensity score–matched analysis conducted in Taiwan.

PCOS is characterized by androgen elevation that can lead to insulin resistance and metabolic syndrome, which have also been associated with an increased risk of psoriasis. Previous retrospective analyses have suggested an increased risk of psoriasis associated with PCOS, and psoriasis patients with PCOS have been reported to have more severe skin lesions, compared with those who do not have PCOS.

“The incidence of psoriasis is indeed higher in the PCOS group than in the control group, and the comorbidities related to metabolic syndrome did not modify the adjusted hazard ratio,” said Ming-Li Chen, during her presentation of the study results at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. Dr. Chen is at Chung Shan Medical University in Taiwan.

The researchers analyzed 1 million randomly selected records from Taiwan’s Longitudinal Health Insurance database, a subset of the country’s National Health Insurance Program. Between 2000 and 2012, they identified a case group with at least three outpatient diagnoses or one inpatient diagnosis of PCOS; they then compared each with four patients who did not have PCOS who were matched by age and index year. The mean age in both groups was about 27 years.

The mean follow-up times were 6.99 years for 4,707 cases and 6.94 years for 18,828 controls. Comorbidities were slightly higher in the PCOS group, including asthma (6.7% vs. 4.9%; P less than .001), chronic obstructive pulmonary disease (14% vs. 11%; P less than .001), chronic liver disease (8.0% vs. 5.0%; P less than .001), diabetes mellitus (3.0% vs. 1.4%; P less than .001), hypertension (2.4% vs. 1.5%; P less than .001), hyperlipidemia (5.4% vs. 2.5%; P less than .001), depression (5.4% vs. 3.9%; P less than .001), and sleep apnea (0.23% vs. 0.10%; P = .040).

There was a higher cumulative incidence of psoriasis in the PCOS group (adjusted hazard ratio, 2.07; 95% confidence interval, 1.25-3.44). Other factors associated with increased risk of psoriasis were advanced age (greater than 50 years old; aHR, 14.13; 95% CI, 1.8-110.7) and having a cancer diagnosis (aHR, 11.72; 95% CI, 2.87-47.9).

When PCOS patients were stratified by age, the researchers noted a higher risk of psoriasis among those 20 years or younger (aHR, 4.02; 95% CI, 1.16-13.9) than among those aged 20-50 years (aHR, 1.88; 95% CI, 1.07-3.29). Among those older than 50 years, there was no significantly increased risk, although the number of psoriasis diagnoses and population sizes were small in the latter category. Among patients with PCOS, a cancer diagnosis was not associated with a statistically significant increased risk of psoriasis.

The mechanisms underlying the association between PCOS and psoriasis should be studied further, she noted.

Following Dr. Chen’s prerecorded presentation, there was a live discussion session led by Alice Gottlieb, MD, PhD, medical director of Mount Sinai Beth Israel Dermatology, New York, and Ennio Lubrano, MD, associate professor of rheumatology at the University of Molise (Italy). Dr. Gottlieb noted that the study did not appear to account for weight in the association between PCOS and psoriasis, since heavier people are known to be at greater risk of developing psoriasis. Dr. Chen acknowledged that the study had no records of BMI or weight.

Dr. Gottlieb also wondered if treatment of PCOS led to any improvements in psoriasis in patients with the two diagnoses. “If we treat PCOS, does the psoriasis get better?” Again, the study did not address the question. “We didn’t follow up on therapies,” Dr. Chen said.

Dr. Chen reported no relevant financial disclosures. Dr. Gottlieb is a consultant, advisory board member and/or speaker for AbbVie, Allergan, Avotres Therapeutics, Beiersdorf, Bristol-Myers Squibb, Celgene, Dermira, Eli Lilly, Incyte, Janssen, Leo, Novartis, Reddy Labs, Sun Pharmaceutical Industries, UCB Pharma and Xbiotech. She has received research or educational grants from Boehringer Ingelheim, Incyte, Janssen, Novartis and Xbiotech.

Treatment of psoriasis with biologics was associated with a reduced risk of developing psoriatic arthritis compared with conventional disease-modifying antirheumatic drugs (DMARDs), in a single center retrospective analysis in Argentina that followed patients for almost 2 decades.

About 30%-40% of patients with psoriasis go on to develop psoriatic arthritis (PsA), usually on average about 10 years after the onset of psoriasis. One potential mechanism of PsA onset is through enthesitis, which has been described at subclinical levels in psoriasis.

“It could be speculated that treatment with biologics in patients with psoriasis could prevent the development of psoriatic arthritis, perhaps by inhibiting the subclinical development of enthesitis,” Luciano Lo Giudice, MD, a rheumatology fellow at Hospital Italiano de Buenos Aires, said during his presentation at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

Although these results do not prove that treatment of the underlying disease delays progression to PsA, it is suggestive, and highlights an emerging field of research, according to Diamant Thaçi, MD, PhD, professor of medicine at University Hospital Schleswig-Holstein, Germany, who led a live discussion following a prerecorded presentation of the results. “We’re going in this direction – how can we prevent psoriatic arthritis, how can we delay it. We are just starting to think about this,” Dr. Thaçi said in an interview.

The researchers examined medical records of 1,626 patients with psoriasis treated at their center between 2000 and 2019, with a total of 15,152 years of follow-up. Of these patients, 1,293 were treated with topical medication, 229 with conventional DMARDs (methotrexate in 77%, cyclosporine in 13%, and both in 10%), and 104 with biologics, including etanercept (34%), secukinumab (20%), adalimumab (20%), ustekinumab (12%), ixekizumab (9%), and infliximab (5%).

They found that 11% in the topical treatment group developed PsA, as did 3.5% in the conventional DMARD group, 1.9% in the biologics group, and 9.1% overall. Treatment with biologics was associated with a significantly lower odds of developing PsA compared with treatment with conventional DMARDs (3 versus 17.2 per 1,000 patient-years; incidence rate ratio [IRR], 0.17; P = .0177). There was a trend toward reduced odds of developing PsA among those on biologic therapy compared with those on topicals (3 versus 9.8 per 1,000 patient-years; IRR, 0.3; P = .0588).

The researchers confirmed all medical encounters using electronic medical records and the study had a long follow-up time, but was limited by the single center and its retrospective nature. It also could not associate reduced risk with specific biologics.

The findings probably reflect the presence of subclinical PsA that many clinicians don’t see, according to Dr. Thaçi. While a dermatology practice might find PsA in 2% or 3%, or at most, 10% of patients with psoriasis, “in our department it’s about 50 to 60 percent of patients who have psoriatic arthritis, because we diagnose it early,” he said.

He found the results of the study encouraging. “It looks like some of the biologics, for example IL [interleukin]-17 or even IL-23 [blockers] may have an influence on occurrence or delay the occurrence of psoriatic arthritis.”

Dr. Thaçi noted that early treatment of skin lesions can increase the probability of longer remissions, especially with IL-23 blockers. Still, that’s no guarantee the same would hold true for PsA risk. “Skin is skin and joints are joints,” Dr. Thaçi said.

Dr. Thaçi and Dr. Lo Giudice had no relevant financial disclosures.

Treatment of psoriasis with biologics was associated with a reduced risk of developing psoriatic arthritis compared with conventional disease-modifying antirheumatic drugs (DMARDs), in a single center retrospective analysis in Argentina that followed patients for almost 2 decades.

About 30%-40% of patients with psoriasis go on to develop psoriatic arthritis (PsA), usually on average about 10 years after the onset of psoriasis. One potential mechanism of PsA onset is through enthesitis, which has been described at subclinical levels in psoriasis.

“It could be speculated that treatment with biologics in patients with psoriasis could prevent the development of psoriatic arthritis, perhaps by inhibiting the subclinical development of enthesitis,” Luciano Lo Giudice, MD, a rheumatology fellow at Hospital Italiano de Buenos Aires, said during his presentation at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

Although these results do not prove that treatment of the underlying disease delays progression to PsA, it is suggestive, and highlights an emerging field of research, according to Diamant Thaçi, MD, PhD, professor of medicine at University Hospital Schleswig-Holstein, Germany, who led a live discussion following a prerecorded presentation of the results. “We’re going in this direction – how can we prevent psoriatic arthritis, how can we delay it. We are just starting to think about this,” Dr. Thaçi said in an interview.

The researchers examined medical records of 1,626 patients with psoriasis treated at their center between 2000 and 2019, with a total of 15,152 years of follow-up. Of these patients, 1,293 were treated with topical medication, 229 with conventional DMARDs (methotrexate in 77%, cyclosporine in 13%, and both in 10%), and 104 with biologics, including etanercept (34%), secukinumab (20%), adalimumab (20%), ustekinumab (12%), ixekizumab (9%), and infliximab (5%).

They found that 11% in the topical treatment group developed PsA, as did 3.5% in the conventional DMARD group, 1.9% in the biologics group, and 9.1% overall. Treatment with biologics was associated with a significantly lower odds of developing PsA compared with treatment with conventional DMARDs (3 versus 17.2 per 1,000 patient-years; incidence rate ratio [IRR], 0.17; P = .0177). There was a trend toward reduced odds of developing PsA among those on biologic therapy compared with those on topicals (3 versus 9.8 per 1,000 patient-years; IRR, 0.3; P = .0588).

The researchers confirmed all medical encounters using electronic medical records and the study had a long follow-up time, but was limited by the single center and its retrospective nature. It also could not associate reduced risk with specific biologics.

The findings probably reflect the presence of subclinical PsA that many clinicians don’t see, according to Dr. Thaçi. While a dermatology practice might find PsA in 2% or 3%, or at most, 10% of patients with psoriasis, “in our department it’s about 50 to 60 percent of patients who have psoriatic arthritis, because we diagnose it early,” he said.

He found the results of the study encouraging. “It looks like some of the biologics, for example IL [interleukin]-17 or even IL-23 [blockers] may have an influence on occurrence or delay the occurrence of psoriatic arthritis.”

Dr. Thaçi noted that early treatment of skin lesions can increase the probability of longer remissions, especially with IL-23 blockers. Still, that’s no guarantee the same would hold true for PsA risk. “Skin is skin and joints are joints,” Dr. Thaçi said.

Dr. Thaçi and Dr. Lo Giudice had no relevant financial disclosures.

Treatment of psoriasis with biologics was associated with a reduced risk of developing psoriatic arthritis compared with conventional disease-modifying antirheumatic drugs (DMARDs), in a single center retrospective analysis in Argentina that followed patients for almost 2 decades.

About 30%-40% of patients with psoriasis go on to develop psoriatic arthritis (PsA), usually on average about 10 years after the onset of psoriasis. One potential mechanism of PsA onset is through enthesitis, which has been described at subclinical levels in psoriasis.

“It could be speculated that treatment with biologics in patients with psoriasis could prevent the development of psoriatic arthritis, perhaps by inhibiting the subclinical development of enthesitis,” Luciano Lo Giudice, MD, a rheumatology fellow at Hospital Italiano de Buenos Aires, said during his presentation at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

Although these results do not prove that treatment of the underlying disease delays progression to PsA, it is suggestive, and highlights an emerging field of research, according to Diamant Thaçi, MD, PhD, professor of medicine at University Hospital Schleswig-Holstein, Germany, who led a live discussion following a prerecorded presentation of the results. “We’re going in this direction – how can we prevent psoriatic arthritis, how can we delay it. We are just starting to think about this,” Dr. Thaçi said in an interview.

The researchers examined medical records of 1,626 patients with psoriasis treated at their center between 2000 and 2019, with a total of 15,152 years of follow-up. Of these patients, 1,293 were treated with topical medication, 229 with conventional DMARDs (methotrexate in 77%, cyclosporine in 13%, and both in 10%), and 104 with biologics, including etanercept (34%), secukinumab (20%), adalimumab (20%), ustekinumab (12%), ixekizumab (9%), and infliximab (5%).

They found that 11% in the topical treatment group developed PsA, as did 3.5% in the conventional DMARD group, 1.9% in the biologics group, and 9.1% overall. Treatment with biologics was associated with a significantly lower odds of developing PsA compared with treatment with conventional DMARDs (3 versus 17.2 per 1,000 patient-years; incidence rate ratio [IRR], 0.17; P = .0177). There was a trend toward reduced odds of developing PsA among those on biologic therapy compared with those on topicals (3 versus 9.8 per 1,000 patient-years; IRR, 0.3; P = .0588).

The researchers confirmed all medical encounters using electronic medical records and the study had a long follow-up time, but was limited by the single center and its retrospective nature. It also could not associate reduced risk with specific biologics.

The findings probably reflect the presence of subclinical PsA that many clinicians don’t see, according to Dr. Thaçi. While a dermatology practice might find PsA in 2% or 3%, or at most, 10% of patients with psoriasis, “in our department it’s about 50 to 60 percent of patients who have psoriatic arthritis, because we diagnose it early,” he said.

He found the results of the study encouraging. “It looks like some of the biologics, for example IL [interleukin]-17 or even IL-23 [blockers] may have an influence on occurrence or delay the occurrence of psoriatic arthritis.”

Dr. Thaçi noted that early treatment of skin lesions can increase the probability of longer remissions, especially with IL-23 blockers. Still, that’s no guarantee the same would hold true for PsA risk. “Skin is skin and joints are joints,” Dr. Thaçi said.

Dr. Thaçi and Dr. Lo Giudice had no relevant financial disclosures.

Pustular psoriasis is a rare condition that presents significant challenges to clinicians, not least because it comes in varied forms that are not well understood.

It has various dermatologic and rheumatologic manifestations and sometimes overlaps with plaque psoriasis. Pustular palmoplantar psoriasis (PPP) affects the palmar and plantar areas of the skin, while generalized pustular psoriasis (GPP) can affect large areas of skin and tends to be more severe, even life threatening. PPP can accompany psoriatic arthritis or can be a side effect of tumor necrosis factor (TNF) inhibitor therapy, or a non–drug-induced component of rheumatologic syndromes, according to Kristina Callis Duffin, MD, an associate professor and chair of dermatology at the University of Utah, Salt Lake City.

“Each phenotype could be considered an orphan disease, and the response to therapy is often unpredictable,” Dr. Duffin said during a session on pustular psoriasis at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

But there is some positive news. A study in 2011 of several people with GPP opened the door to better understanding the pathophysiology of pustular psoriasis. Researchers identified a causal autosomal mutation in the IL36RN gene, which encodes an antagonist to the interleukin-36 receptor (Am J Hum Genet. 2011 Sep 9;89[3]:432-7). “As a result of this paper and others, drug development in this space has recently accelerated,” Dr. Duffin said.

In fact, she added,“it’s my opinion that pustular psoriasis is now where plaque psoriasis was 20 years ago, when accelerated drug development was driving a better understanding of the pathogenesis of psoriatic disease and its comorbidities, and also driving outcome measure development.”

In another presentation at the meeting, Hervé Bachelez, MD, PhD, professor of dermatology and immunologist at the University of Paris and Saint-Louis Hospital, Paris, discussed recent advances in drug development for pustular psoriasis. He noted other recent findings of genetic variants related to the disease, including AP1S3, CARD14, and SERPINA3.

For GPP, he said, the current algorithm for management is based on weak evidence for treatments like acitretin, cyclosporine, methotrexate, and infliximab. The story is similar for other biologics, with evidence in the form of case series; open-label studies; controlled, prospective studies; or retrospective analyses. Most of the evidence has been amassed for TNF inhibitors. A retrospective study of all TNF inhibitors suggested they may be effective as induction and maintenance therapy, he noted.

Among IL-17A inhibitors, a prospective study of 12 patients in Japan found secukinumab showed efficacy against GPP, as did studies of ixekizumab and brodalumab. A small phase 3 study in Japan demonstrated efficacy for the IL-23 inhibitor guselkumab in patients with erythrodermic psoriasis and GPP (J Dermatol. 2018 May;45[5]:529-39).

The limited data are a reflection in part of the difficulty in studying GPP, since its flares tend to be more self-remitting than with psoriasis vulgaris or PPP.

There are two monoclonal antibodies against the IL-36 receptor currently being developed. A proof-of-concept study of one of them, spesolimab, showed promise against GPP, with five of seven patients reaching “clear” or “almost clear” scores on the Generalized Pustular Psoriasis Physician Global Assessment within a week after infusion and in all seven by the fourth week (N Engl J Med. 2019 Mar 7;380[10]:981-3).

With respect to PPP, the strongest evidence for conventional therapies comes from two randomized, controlled trials of cyclosporine, with response rates of 48% and 89%, compared with 19% and 21%, respectively, in the placebo groups, although the primary endpoint was poorly designed, according to Dr. Bachelez. Retinoids like etretinate and acitretin, combined with psoralen and UVA, also have some supporting evidence regarding efficacy.

Among biologics, secukinumab did not fare well in a phase 3 study of patients with PPP. A subset of patients may benefit from it, but there are no biomarkers available to identify them, Dr. Bachelez said. A phase 2 study of guselkumab in Japan told a similar story, with only weak signs of efficacy. While there are many more ongoing clinical trials evaluating treatments for PPP, which is encouraging, PPP seems to be more challenging at this stage to tackle than GPP, Dr. Bachelez added. “The genetically inherited IL-36 antagonist abnormalities are clearly driving the advances regarding the pathogenesis of the disease, mainly for GPP rather than PPP.”

Part of the efforts to develop therapies for pustular psoriasis relies on the development of new outcome measures, or adaptation of existing ones. “We have a need to adapt or develop new investigator-reported measures, we need to adapt or develop new patient-reported outcomes,” Dr. Duffin said.

Many existing measures use inconsistent language and anchoring definitions, and some may be proprietary, she added. “The language varies by sponsor and is sometimes tweaked or modified by the agencies. Often synonyms are being used … it raises questions, does it change the validity of the instrument?”

Dr. Duffin called for the research community to use the pause in clinical research during the COVID-19 pandemic to reassess the research agenda, develop consensus on performing and training for GPP and PPP assessments, develop patient-reported outcomes, and strengthen connections to industry.

Dr. Duffin and Dr. Bachelez have consulted, served on the advisory board, been a speaker for, and/or received research support from a wide range of pharmaceutical companies, including those that manufacture and develop psoriasis treatments.
 

Pustular psoriasis is a rare condition that presents significant challenges to clinicians, not least because it comes in varied forms that are not well understood.

It has various dermatologic and rheumatologic manifestations and sometimes overlaps with plaque psoriasis. Pustular palmoplantar psoriasis (PPP) affects the palmar and plantar areas of the skin, while generalized pustular psoriasis (GPP) can affect large areas of skin and tends to be more severe, even life threatening. PPP can accompany psoriatic arthritis or can be a side effect of tumor necrosis factor (TNF) inhibitor therapy, or a non–drug-induced component of rheumatologic syndromes, according to Kristina Callis Duffin, MD, an associate professor and chair of dermatology at the University of Utah, Salt Lake City.

“Each phenotype could be considered an orphan disease, and the response to therapy is often unpredictable,” Dr. Duffin said during a session on pustular psoriasis at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

But there is some positive news. A study in 2011 of several people with GPP opened the door to better understanding the pathophysiology of pustular psoriasis. Researchers identified a causal autosomal mutation in the IL36RN gene, which encodes an antagonist to the interleukin-36 receptor (Am J Hum Genet. 2011 Sep 9;89[3]:432-7). “As a result of this paper and others, drug development in this space has recently accelerated,” Dr. Duffin said.

In fact, she added,“it’s my opinion that pustular psoriasis is now where plaque psoriasis was 20 years ago, when accelerated drug development was driving a better understanding of the pathogenesis of psoriatic disease and its comorbidities, and also driving outcome measure development.”

In another presentation at the meeting, Hervé Bachelez, MD, PhD, professor of dermatology and immunologist at the University of Paris and Saint-Louis Hospital, Paris, discussed recent advances in drug development for pustular psoriasis. He noted other recent findings of genetic variants related to the disease, including AP1S3, CARD14, and SERPINA3.

For GPP, he said, the current algorithm for management is based on weak evidence for treatments like acitretin, cyclosporine, methotrexate, and infliximab. The story is similar for other biologics, with evidence in the form of case series; open-label studies; controlled, prospective studies; or retrospective analyses. Most of the evidence has been amassed for TNF inhibitors. A retrospective study of all TNF inhibitors suggested they may be effective as induction and maintenance therapy, he noted.

Among IL-17A inhibitors, a prospective study of 12 patients in Japan found secukinumab showed efficacy against GPP, as did studies of ixekizumab and brodalumab. A small phase 3 study in Japan demonstrated efficacy for the IL-23 inhibitor guselkumab in patients with erythrodermic psoriasis and GPP (J Dermatol. 2018 May;45[5]:529-39).

The limited data are a reflection in part of the difficulty in studying GPP, since its flares tend to be more self-remitting than with psoriasis vulgaris or PPP.

There are two monoclonal antibodies against the IL-36 receptor currently being developed. A proof-of-concept study of one of them, spesolimab, showed promise against GPP, with five of seven patients reaching “clear” or “almost clear” scores on the Generalized Pustular Psoriasis Physician Global Assessment within a week after infusion and in all seven by the fourth week (N Engl J Med. 2019 Mar 7;380[10]:981-3).

With respect to PPP, the strongest evidence for conventional therapies comes from two randomized, controlled trials of cyclosporine, with response rates of 48% and 89%, compared with 19% and 21%, respectively, in the placebo groups, although the primary endpoint was poorly designed, according to Dr. Bachelez. Retinoids like etretinate and acitretin, combined with psoralen and UVA, also have some supporting evidence regarding efficacy.

Among biologics, secukinumab did not fare well in a phase 3 study of patients with PPP. A subset of patients may benefit from it, but there are no biomarkers available to identify them, Dr. Bachelez said. A phase 2 study of guselkumab in Japan told a similar story, with only weak signs of efficacy. While there are many more ongoing clinical trials evaluating treatments for PPP, which is encouraging, PPP seems to be more challenging at this stage to tackle than GPP, Dr. Bachelez added. “The genetically inherited IL-36 antagonist abnormalities are clearly driving the advances regarding the pathogenesis of the disease, mainly for GPP rather than PPP.”

Part of the efforts to develop therapies for pustular psoriasis relies on the development of new outcome measures, or adaptation of existing ones. “We have a need to adapt or develop new investigator-reported measures, we need to adapt or develop new patient-reported outcomes,” Dr. Duffin said.

Many existing measures use inconsistent language and anchoring definitions, and some may be proprietary, she added. “The language varies by sponsor and is sometimes tweaked or modified by the agencies. Often synonyms are being used … it raises questions, does it change the validity of the instrument?”

Dr. Duffin called for the research community to use the pause in clinical research during the COVID-19 pandemic to reassess the research agenda, develop consensus on performing and training for GPP and PPP assessments, develop patient-reported outcomes, and strengthen connections to industry.

Dr. Duffin and Dr. Bachelez have consulted, served on the advisory board, been a speaker for, and/or received research support from a wide range of pharmaceutical companies, including those that manufacture and develop psoriasis treatments.
 

Pustular psoriasis is a rare condition that presents significant challenges to clinicians, not least because it comes in varied forms that are not well understood.

It has various dermatologic and rheumatologic manifestations and sometimes overlaps with plaque psoriasis. Pustular palmoplantar psoriasis (PPP) affects the palmar and plantar areas of the skin, while generalized pustular psoriasis (GPP) can affect large areas of skin and tends to be more severe, even life threatening. PPP can accompany psoriatic arthritis or can be a side effect of tumor necrosis factor (TNF) inhibitor therapy, or a non–drug-induced component of rheumatologic syndromes, according to Kristina Callis Duffin, MD, an associate professor and chair of dermatology at the University of Utah, Salt Lake City.

“Each phenotype could be considered an orphan disease, and the response to therapy is often unpredictable,” Dr. Duffin said during a session on pustular psoriasis at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

But there is some positive news. A study in 2011 of several people with GPP opened the door to better understanding the pathophysiology of pustular psoriasis. Researchers identified a causal autosomal mutation in the IL36RN gene, which encodes an antagonist to the interleukin-36 receptor (Am J Hum Genet. 2011 Sep 9;89[3]:432-7). “As a result of this paper and others, drug development in this space has recently accelerated,” Dr. Duffin said.

In fact, she added,“it’s my opinion that pustular psoriasis is now where plaque psoriasis was 20 years ago, when accelerated drug development was driving a better understanding of the pathogenesis of psoriatic disease and its comorbidities, and also driving outcome measure development.”

In another presentation at the meeting, Hervé Bachelez, MD, PhD, professor of dermatology and immunologist at the University of Paris and Saint-Louis Hospital, Paris, discussed recent advances in drug development for pustular psoriasis. He noted other recent findings of genetic variants related to the disease, including AP1S3, CARD14, and SERPINA3.

For GPP, he said, the current algorithm for management is based on weak evidence for treatments like acitretin, cyclosporine, methotrexate, and infliximab. The story is similar for other biologics, with evidence in the form of case series; open-label studies; controlled, prospective studies; or retrospective analyses. Most of the evidence has been amassed for TNF inhibitors. A retrospective study of all TNF inhibitors suggested they may be effective as induction and maintenance therapy, he noted.

Among IL-17A inhibitors, a prospective study of 12 patients in Japan found secukinumab showed efficacy against GPP, as did studies of ixekizumab and brodalumab. A small phase 3 study in Japan demonstrated efficacy for the IL-23 inhibitor guselkumab in patients with erythrodermic psoriasis and GPP (J Dermatol. 2018 May;45[5]:529-39).

The limited data are a reflection in part of the difficulty in studying GPP, since its flares tend to be more self-remitting than with psoriasis vulgaris or PPP.

There are two monoclonal antibodies against the IL-36 receptor currently being developed. A proof-of-concept study of one of them, spesolimab, showed promise against GPP, with five of seven patients reaching “clear” or “almost clear” scores on the Generalized Pustular Psoriasis Physician Global Assessment within a week after infusion and in all seven by the fourth week (N Engl J Med. 2019 Mar 7;380[10]:981-3).

With respect to PPP, the strongest evidence for conventional therapies comes from two randomized, controlled trials of cyclosporine, with response rates of 48% and 89%, compared with 19% and 21%, respectively, in the placebo groups, although the primary endpoint was poorly designed, according to Dr. Bachelez. Retinoids like etretinate and acitretin, combined with psoralen and UVA, also have some supporting evidence regarding efficacy.

Among biologics, secukinumab did not fare well in a phase 3 study of patients with PPP. A subset of patients may benefit from it, but there are no biomarkers available to identify them, Dr. Bachelez said. A phase 2 study of guselkumab in Japan told a similar story, with only weak signs of efficacy. While there are many more ongoing clinical trials evaluating treatments for PPP, which is encouraging, PPP seems to be more challenging at this stage to tackle than GPP, Dr. Bachelez added. “The genetically inherited IL-36 antagonist abnormalities are clearly driving the advances regarding the pathogenesis of the disease, mainly for GPP rather than PPP.”

Part of the efforts to develop therapies for pustular psoriasis relies on the development of new outcome measures, or adaptation of existing ones. “We have a need to adapt or develop new investigator-reported measures, we need to adapt or develop new patient-reported outcomes,” Dr. Duffin said.

Many existing measures use inconsistent language and anchoring definitions, and some may be proprietary, she added. “The language varies by sponsor and is sometimes tweaked or modified by the agencies. Often synonyms are being used … it raises questions, does it change the validity of the instrument?”

Dr. Duffin called for the research community to use the pause in clinical research during the COVID-19 pandemic to reassess the research agenda, develop consensus on performing and training for GPP and PPP assessments, develop patient-reported outcomes, and strengthen connections to industry.

Dr. Duffin and Dr. Bachelez have consulted, served on the advisory board, been a speaker for, and/or received research support from a wide range of pharmaceutical companies, including those that manufacture and develop psoriasis treatments.
 

Patients with psoriatic disease are known to be at increased risk of heart failure. A new cohort study suggests that part of the risk may be attributable to the disease itself, not just traditional cardiovascular risk factors like obesity and metabolic abnormalities that are common comorbidities in psoriatic disease. There may also be differences in the risk profiles of patients with ischemic and nonischemic heart failure.

Courtesy Dr. Sahil Koppikar

Previous studies have shown that heart failure risk in patients with psoriatic arthritis is 32% higher than in the general population, and with psoriasis, it is 22%-53% higher. However, those studies were based on administrative databases with no clinical information to back up the accuracy of diagnoses, Sahil Koppikar, MD, from the University of Toronto, said during a presentation of the research at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

The finding that psoriatic disease inflammation may be a direct risk factor for heart failure might be good news for patients. “By controlling inflammation, we may be able to reduce the risk of heart failure in these patients,” Dr. Koppikar said.

During a question and answer session, discussant Deepak Jadon, MBChB, PhD, director of the rheumatology research unit and lead for psoriatic arthritis at Addenbrooke’s Hospital, Cambridge (England), noted that patients with conditions like lupus and systemic sclerosis may undergo regular echocardiograms, chest CTs, or other surveillance, and asked if Dr. Koppikar could recommend a framework for similar surveillance in psoriatic arthritis.

“With the current data we have, I don’t know if we can make recommendations. What we learned from our study is that patients that have elevated inflammatory disease, with elevated inflammatory markers for a prolonged period of time, were at higher risk than [if they had elevated markers only] just before the event. So poorly controlled patients might be something you should be more aware of, and maybe get cardiology involved. But I don’t think it’s something we should be doing right now for all patients,” Dr. Koppikar said.

The researchers analyzed data from a psoriasis cohort at the University of Toronto that began in 2006. Every 6-12 months, they were assessed by a rheumatologist and underwent imaging assessment and laboratory tests. The primary outcome of the study was the first heart failure event, which the researchers identified by linking the cohort database with provincial hospitalization and mortality databases. They verified all events by examining medical records. They also assessed the association between heart failure and disease activity over time rather than just before the event.

The analysis included 1,994 patients. A total of 64 new heart failure events occurred during a mean follow-up of 11.3 years (2.85 per 1,000 person-years), including 38 ischemic and 26 nonischemic events. A multivariate analysis found that heart failure was associated with adjusted mean (AM) tender joint count (hazard ratio, 1.51; P = .02), AM swollen joint count (HR, 1.82; P = .04), AM erythrocyte sedimentation rate (HR, 1.26; P = .009), AM C-reactive protein (HR, 1.27; P = .001), Health Assessment Questionnaire (HR, 1.95; P = .001), and minimum disease activity state (HR, 0.40; P = .04). The multivariate analysis was adjusted for sex, hypertension, diabetes mellitus, body mass index, ischemic heart disease, lipids, and smoking status.

When the researchers separated the analysis into ischemic and nonischemic heart failure, some interesting associations popped out. Nonischemic heart failure was associated with AM tender joint count (HR, 1.83; P = .004), but ischemic heart failure was not. Other factors associated with nonischemic but not ischemic heart failure included AM swollen joint count (HR, 3.56; P = .0003), damaged joint count (HR, 1.29; P = .04), and pain score (HR, 1.22; P = .047). Minimum disease activity had the opposite result: It was associated with only ischemic heart failure (HR, 0.40; P = .04).

The study cohort more closely resembles a rheumatology cohort than a dermatology cohort, and it suggests that patients with psoriatic arthritis have different cardiovascular comorbidities than those with pure psoriasis, according to Diamant Thaçi, MD, PhD, professor and chairman of the department of dermatology at the University of Lübeck (Germany). “It shows how it important it is to look for comorbidity in the rheumatologic setting,” Dr. Thaçi said in an interview.

The study was supported by the Arthritis Society. Dr. Koppikar and Dr. Thaçi have no relevant financial disclosures.

SOURCE: Koppikar S et al. GRAPPA 2020 Virtual Annual Meeting.

Patients with psoriatic disease are known to be at increased risk of heart failure. A new cohort study suggests that part of the risk may be attributable to the disease itself, not just traditional cardiovascular risk factors like obesity and metabolic abnormalities that are common comorbidities in psoriatic disease. There may also be differences in the risk profiles of patients with ischemic and nonischemic heart failure.

Courtesy Dr. Sahil Koppikar

Previous studies have shown that heart failure risk in patients with psoriatic arthritis is 32% higher than in the general population, and with psoriasis, it is 22%-53% higher. However, those studies were based on administrative databases with no clinical information to back up the accuracy of diagnoses, Sahil Koppikar, MD, from the University of Toronto, said during a presentation of the research at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

The finding that psoriatic disease inflammation may be a direct risk factor for heart failure might be good news for patients. “By controlling inflammation, we may be able to reduce the risk of heart failure in these patients,” Dr. Koppikar said.

During a question and answer session, discussant Deepak Jadon, MBChB, PhD, director of the rheumatology research unit and lead for psoriatic arthritis at Addenbrooke’s Hospital, Cambridge (England), noted that patients with conditions like lupus and systemic sclerosis may undergo regular echocardiograms, chest CTs, or other surveillance, and asked if Dr. Koppikar could recommend a framework for similar surveillance in psoriatic arthritis.

“With the current data we have, I don’t know if we can make recommendations. What we learned from our study is that patients that have elevated inflammatory disease, with elevated inflammatory markers for a prolonged period of time, were at higher risk than [if they had elevated markers only] just before the event. So poorly controlled patients might be something you should be more aware of, and maybe get cardiology involved. But I don’t think it’s something we should be doing right now for all patients,” Dr. Koppikar said.

The researchers analyzed data from a psoriasis cohort at the University of Toronto that began in 2006. Every 6-12 months, they were assessed by a rheumatologist and underwent imaging assessment and laboratory tests. The primary outcome of the study was the first heart failure event, which the researchers identified by linking the cohort database with provincial hospitalization and mortality databases. They verified all events by examining medical records. They also assessed the association between heart failure and disease activity over time rather than just before the event.

The analysis included 1,994 patients. A total of 64 new heart failure events occurred during a mean follow-up of 11.3 years (2.85 per 1,000 person-years), including 38 ischemic and 26 nonischemic events. A multivariate analysis found that heart failure was associated with adjusted mean (AM) tender joint count (hazard ratio, 1.51; P = .02), AM swollen joint count (HR, 1.82; P = .04), AM erythrocyte sedimentation rate (HR, 1.26; P = .009), AM C-reactive protein (HR, 1.27; P = .001), Health Assessment Questionnaire (HR, 1.95; P = .001), and minimum disease activity state (HR, 0.40; P = .04). The multivariate analysis was adjusted for sex, hypertension, diabetes mellitus, body mass index, ischemic heart disease, lipids, and smoking status.

When the researchers separated the analysis into ischemic and nonischemic heart failure, some interesting associations popped out. Nonischemic heart failure was associated with AM tender joint count (HR, 1.83; P = .004), but ischemic heart failure was not. Other factors associated with nonischemic but not ischemic heart failure included AM swollen joint count (HR, 3.56; P = .0003), damaged joint count (HR, 1.29; P = .04), and pain score (HR, 1.22; P = .047). Minimum disease activity had the opposite result: It was associated with only ischemic heart failure (HR, 0.40; P = .04).

The study cohort more closely resembles a rheumatology cohort than a dermatology cohort, and it suggests that patients with psoriatic arthritis have different cardiovascular comorbidities than those with pure psoriasis, according to Diamant Thaçi, MD, PhD, professor and chairman of the department of dermatology at the University of Lübeck (Germany). “It shows how it important it is to look for comorbidity in the rheumatologic setting,” Dr. Thaçi said in an interview.

The study was supported by the Arthritis Society. Dr. Koppikar and Dr. Thaçi have no relevant financial disclosures.

SOURCE: Koppikar S et al. GRAPPA 2020 Virtual Annual Meeting.

Patients with psoriatic disease are known to be at increased risk of heart failure. A new cohort study suggests that part of the risk may be attributable to the disease itself, not just traditional cardiovascular risk factors like obesity and metabolic abnormalities that are common comorbidities in psoriatic disease. There may also be differences in the risk profiles of patients with ischemic and nonischemic heart failure.

Courtesy Dr. Sahil Koppikar

Previous studies have shown that heart failure risk in patients with psoriatic arthritis is 32% higher than in the general population, and with psoriasis, it is 22%-53% higher. However, those studies were based on administrative databases with no clinical information to back up the accuracy of diagnoses, Sahil Koppikar, MD, from the University of Toronto, said during a presentation of the research at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

The finding that psoriatic disease inflammation may be a direct risk factor for heart failure might be good news for patients. “By controlling inflammation, we may be able to reduce the risk of heart failure in these patients,” Dr. Koppikar said.

During a question and answer session, discussant Deepak Jadon, MBChB, PhD, director of the rheumatology research unit and lead for psoriatic arthritis at Addenbrooke’s Hospital, Cambridge (England), noted that patients with conditions like lupus and systemic sclerosis may undergo regular echocardiograms, chest CTs, or other surveillance, and asked if Dr. Koppikar could recommend a framework for similar surveillance in psoriatic arthritis.

“With the current data we have, I don’t know if we can make recommendations. What we learned from our study is that patients that have elevated inflammatory disease, with elevated inflammatory markers for a prolonged period of time, were at higher risk than [if they had elevated markers only] just before the event. So poorly controlled patients might be something you should be more aware of, and maybe get cardiology involved. But I don’t think it’s something we should be doing right now for all patients,” Dr. Koppikar said.

The researchers analyzed data from a psoriasis cohort at the University of Toronto that began in 2006. Every 6-12 months, they were assessed by a rheumatologist and underwent imaging assessment and laboratory tests. The primary outcome of the study was the first heart failure event, which the researchers identified by linking the cohort database with provincial hospitalization and mortality databases. They verified all events by examining medical records. They also assessed the association between heart failure and disease activity over time rather than just before the event.

The analysis included 1,994 patients. A total of 64 new heart failure events occurred during a mean follow-up of 11.3 years (2.85 per 1,000 person-years), including 38 ischemic and 26 nonischemic events. A multivariate analysis found that heart failure was associated with adjusted mean (AM) tender joint count (hazard ratio, 1.51; P = .02), AM swollen joint count (HR, 1.82; P = .04), AM erythrocyte sedimentation rate (HR, 1.26; P = .009), AM C-reactive protein (HR, 1.27; P = .001), Health Assessment Questionnaire (HR, 1.95; P = .001), and minimum disease activity state (HR, 0.40; P = .04). The multivariate analysis was adjusted for sex, hypertension, diabetes mellitus, body mass index, ischemic heart disease, lipids, and smoking status.

When the researchers separated the analysis into ischemic and nonischemic heart failure, some interesting associations popped out. Nonischemic heart failure was associated with AM tender joint count (HR, 1.83; P = .004), but ischemic heart failure was not. Other factors associated with nonischemic but not ischemic heart failure included AM swollen joint count (HR, 3.56; P = .0003), damaged joint count (HR, 1.29; P = .04), and pain score (HR, 1.22; P = .047). Minimum disease activity had the opposite result: It was associated with only ischemic heart failure (HR, 0.40; P = .04).

The study cohort more closely resembles a rheumatology cohort than a dermatology cohort, and it suggests that patients with psoriatic arthritis have different cardiovascular comorbidities than those with pure psoriasis, according to Diamant Thaçi, MD, PhD, professor and chairman of the department of dermatology at the University of Lübeck (Germany). “It shows how it important it is to look for comorbidity in the rheumatologic setting,” Dr. Thaçi said in an interview.

The study was supported by the Arthritis Society. Dr. Koppikar and Dr. Thaçi have no relevant financial disclosures.

SOURCE: Koppikar S et al. GRAPPA 2020 Virtual Annual Meeting.

COVID-19 has posed serious questions for patients with psoriatic disease and the clinicians who treat them. Both have serious concerns over whether psoriasis or the medications used to treat it pose additional risk for contracting COVID-19 or experiencing worse outcomes with illness.

At the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, experts gathered to discuss these concerns and what is known about the special risk factors for psoriatic disease patients.

Studies from a few registries have been done already among patients with autoimmune disease, and the results so far suggest that patients may be able to breathe a little easier. “I don’t see any data that suggests that use of immunosuppressives or having autoimmune disease increases your risk of acquiring it. I think most of the risk is driven by risk of exposure,” said Kevin Winthrop, MD, MPH, a professor of public health, infectious diseases, ophthalmology at Oregon Health & Science University, Portland, during a presentation.

That assertion was reinforced by data presented by Rebecca Haberman, MD, a rheumatologist at New York University Langone Health. Her group created the Web-Based Assessment of Autoimmune, Immune-Mediated, and Rheumatic Patients during the COVID-19 Pandemic (WARCOV) cohort study to address the question of whether patients with immune-mediated inflammatory disease (IMID), including inflammatory arthritis, psoriasis, or inflammatory bowel disease, should discontinue or modify their immunotherapy regimens in the face of potential exposure to COVID-19.

To date, the study has data on 1,122 patients; 604 with inflammatory arthritis, 128 of whom have tested positive for COVID-19. The team established a cohort using the first 86 IMID patients confirmed to have contracted COVID-19. The hospitalization rate was 16% overall, and use of corticosteroids was associated with increased hospitalization risk. A follow-up analysis looking at the first 103 inflammatory arthritis patients who contracted COVID-19 showed a hospitalization rate of 26% and a mortality of 4%. That hospitalization rate is similar to the general hospitalization rate estimated by the New York Department of Health, Dr. Haberman said in her presentation.

Risk factors associated with hospitalization included being older and having asthma or COPD, which is similar to the general population. Use of oral glucocorticoids was linked to a big increase in risk for hospitalization, even with doses less than 10 mg prednisone daily (odds ratio, 14.31; 95% confidence interval, 3.55-57.70). There were no links between use of any cytokine therapy and risk, but use of TNF inhibitors was associated with a reduced risk (OR, 0.35; 95% CI, 0.13-0.97), while use of JAK inhibitors was associated with greater risk (OR, 6.30; 95% CI, 1.68-23.69). The latter result is tentative because of a small sample size, and it was driven largely by the experiences of patients with psoriatic arthritis.

Another study, run by the COVID-19 Global Rheumatology Alliance, looked at 600 patients with rheumatic disease from 40 countries, and “found no smoking gun,” said Leonard Calabrese, DO, who leads the Cleveland Clinic’s section of clinical immunology, during his presentation. “People can develop this when they’re on hydroxychloroquine. They seem to do not remarkably bad or remarkably good. There is no adverse signal for biologics, but being on prednisone [at a dose of] more than 10 mg is not great,” said Dr. Calabrese, who also noted that other publications have supported these conclusions.

So given these findings, how should clinicians address patient concerns? In the absence of probable exposure, “we say it’s better to have a well-controlled IMID on therapy than a poorly-controlled IMID on submaximal therapy. We say stick to therapy and try to wean the prednisone down as low as possible,” Dr. Calabrese said.

More controversially, what should patients do if they have had a significant exposure, such as a close proximity, prolonged exposure encounter with an individual with documented COVID-19, or at high-risk of disease? Dr. Calabrese noted that the American College of Rheumatology (ACR) guidelines recommend that low-level immunomodulation can be continued, “with an asterisk if it’s hydroxychloroquine, and it is in most of our minds now that we know that it is not effective, and the toxicity in the COVID setting is still being worked out,” he said.

With respect to other immunosuppressants, the ACR recommends stopping them temporarily, although IL-6 inhibitors may be continued in select circumstances. Resumption of the therapeutics can resume after a negative COVID test or completion of a 2-week observation period.

When patients contract COVID-19, antimalarial medications can be continued because they have been studied. “But medium-level immunomodulators, in particular methotrexate, I have grave concerns about because it can inhibit the adaptive immune response and antibody formation,” he said. COVID-19 is a serious infection, and all serious biologics have a package insert saying to stop them in a serious infection. Again, IL-6 inhibitors may be considered an exception in the right circumstances. When to resume these medications remains unknown. “I think that’s a work in progress. Test-based versus clinic-based strategies are a matter of controversy,” Dr. Calabrese said.

Ultimately, the question of what to do with immunosuppressive therapies in this population will continue to be a challenge. “The only good answer is to follow the rules of social distancing and to wear a mask,” said Kristina Callis Duffin, MD, a cochair of the department of dermatology and associate professor of dermatology at the University of Utah, Salt Lake City.

COVID-19 has posed serious questions for patients with psoriatic disease and the clinicians who treat them. Both have serious concerns over whether psoriasis or the medications used to treat it pose additional risk for contracting COVID-19 or experiencing worse outcomes with illness.

At the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, experts gathered to discuss these concerns and what is known about the special risk factors for psoriatic disease patients.

Studies from a few registries have been done already among patients with autoimmune disease, and the results so far suggest that patients may be able to breathe a little easier. “I don’t see any data that suggests that use of immunosuppressives or having autoimmune disease increases your risk of acquiring it. I think most of the risk is driven by risk of exposure,” said Kevin Winthrop, MD, MPH, a professor of public health, infectious diseases, ophthalmology at Oregon Health & Science University, Portland, during a presentation.

That assertion was reinforced by data presented by Rebecca Haberman, MD, a rheumatologist at New York University Langone Health. Her group created the Web-Based Assessment of Autoimmune, Immune-Mediated, and Rheumatic Patients during the COVID-19 Pandemic (WARCOV) cohort study to address the question of whether patients with immune-mediated inflammatory disease (IMID), including inflammatory arthritis, psoriasis, or inflammatory bowel disease, should discontinue or modify their immunotherapy regimens in the face of potential exposure to COVID-19.

To date, the study has data on 1,122 patients; 604 with inflammatory arthritis, 128 of whom have tested positive for COVID-19. The team established a cohort using the first 86 IMID patients confirmed to have contracted COVID-19. The hospitalization rate was 16% overall, and use of corticosteroids was associated with increased hospitalization risk. A follow-up analysis looking at the first 103 inflammatory arthritis patients who contracted COVID-19 showed a hospitalization rate of 26% and a mortality of 4%. That hospitalization rate is similar to the general hospitalization rate estimated by the New York Department of Health, Dr. Haberman said in her presentation.

Risk factors associated with hospitalization included being older and having asthma or COPD, which is similar to the general population. Use of oral glucocorticoids was linked to a big increase in risk for hospitalization, even with doses less than 10 mg prednisone daily (odds ratio, 14.31; 95% confidence interval, 3.55-57.70). There were no links between use of any cytokine therapy and risk, but use of TNF inhibitors was associated with a reduced risk (OR, 0.35; 95% CI, 0.13-0.97), while use of JAK inhibitors was associated with greater risk (OR, 6.30; 95% CI, 1.68-23.69). The latter result is tentative because of a small sample size, and it was driven largely by the experiences of patients with psoriatic arthritis.

Another study, run by the COVID-19 Global Rheumatology Alliance, looked at 600 patients with rheumatic disease from 40 countries, and “found no smoking gun,” said Leonard Calabrese, DO, who leads the Cleveland Clinic’s section of clinical immunology, during his presentation. “People can develop this when they’re on hydroxychloroquine. They seem to do not remarkably bad or remarkably good. There is no adverse signal for biologics, but being on prednisone [at a dose of] more than 10 mg is not great,” said Dr. Calabrese, who also noted that other publications have supported these conclusions.

So given these findings, how should clinicians address patient concerns? In the absence of probable exposure, “we say it’s better to have a well-controlled IMID on therapy than a poorly-controlled IMID on submaximal therapy. We say stick to therapy and try to wean the prednisone down as low as possible,” Dr. Calabrese said.

More controversially, what should patients do if they have had a significant exposure, such as a close proximity, prolonged exposure encounter with an individual with documented COVID-19, or at high-risk of disease? Dr. Calabrese noted that the American College of Rheumatology (ACR) guidelines recommend that low-level immunomodulation can be continued, “with an asterisk if it’s hydroxychloroquine, and it is in most of our minds now that we know that it is not effective, and the toxicity in the COVID setting is still being worked out,” he said.

With respect to other immunosuppressants, the ACR recommends stopping them temporarily, although IL-6 inhibitors may be continued in select circumstances. Resumption of the therapeutics can resume after a negative COVID test or completion of a 2-week observation period.

When patients contract COVID-19, antimalarial medications can be continued because they have been studied. “But medium-level immunomodulators, in particular methotrexate, I have grave concerns about because it can inhibit the adaptive immune response and antibody formation,” he said. COVID-19 is a serious infection, and all serious biologics have a package insert saying to stop them in a serious infection. Again, IL-6 inhibitors may be considered an exception in the right circumstances. When to resume these medications remains unknown. “I think that’s a work in progress. Test-based versus clinic-based strategies are a matter of controversy,” Dr. Calabrese said.

Ultimately, the question of what to do with immunosuppressive therapies in this population will continue to be a challenge. “The only good answer is to follow the rules of social distancing and to wear a mask,” said Kristina Callis Duffin, MD, a cochair of the department of dermatology and associate professor of dermatology at the University of Utah, Salt Lake City.

COVID-19 has posed serious questions for patients with psoriatic disease and the clinicians who treat them. Both have serious concerns over whether psoriasis or the medications used to treat it pose additional risk for contracting COVID-19 or experiencing worse outcomes with illness.

At the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, experts gathered to discuss these concerns and what is known about the special risk factors for psoriatic disease patients.

Studies from a few registries have been done already among patients with autoimmune disease, and the results so far suggest that patients may be able to breathe a little easier. “I don’t see any data that suggests that use of immunosuppressives or having autoimmune disease increases your risk of acquiring it. I think most of the risk is driven by risk of exposure,” said Kevin Winthrop, MD, MPH, a professor of public health, infectious diseases, ophthalmology at Oregon Health & Science University, Portland, during a presentation.

That assertion was reinforced by data presented by Rebecca Haberman, MD, a rheumatologist at New York University Langone Health. Her group created the Web-Based Assessment of Autoimmune, Immune-Mediated, and Rheumatic Patients during the COVID-19 Pandemic (WARCOV) cohort study to address the question of whether patients with immune-mediated inflammatory disease (IMID), including inflammatory arthritis, psoriasis, or inflammatory bowel disease, should discontinue or modify their immunotherapy regimens in the face of potential exposure to COVID-19.

To date, the study has data on 1,122 patients; 604 with inflammatory arthritis, 128 of whom have tested positive for COVID-19. The team established a cohort using the first 86 IMID patients confirmed to have contracted COVID-19. The hospitalization rate was 16% overall, and use of corticosteroids was associated with increased hospitalization risk. A follow-up analysis looking at the first 103 inflammatory arthritis patients who contracted COVID-19 showed a hospitalization rate of 26% and a mortality of 4%. That hospitalization rate is similar to the general hospitalization rate estimated by the New York Department of Health, Dr. Haberman said in her presentation.

Risk factors associated with hospitalization included being older and having asthma or COPD, which is similar to the general population. Use of oral glucocorticoids was linked to a big increase in risk for hospitalization, even with doses less than 10 mg prednisone daily (odds ratio, 14.31; 95% confidence interval, 3.55-57.70). There were no links between use of any cytokine therapy and risk, but use of TNF inhibitors was associated with a reduced risk (OR, 0.35; 95% CI, 0.13-0.97), while use of JAK inhibitors was associated with greater risk (OR, 6.30; 95% CI, 1.68-23.69). The latter result is tentative because of a small sample size, and it was driven largely by the experiences of patients with psoriatic arthritis.

Another study, run by the COVID-19 Global Rheumatology Alliance, looked at 600 patients with rheumatic disease from 40 countries, and “found no smoking gun,” said Leonard Calabrese, DO, who leads the Cleveland Clinic’s section of clinical immunology, during his presentation. “People can develop this when they’re on hydroxychloroquine. They seem to do not remarkably bad or remarkably good. There is no adverse signal for biologics, but being on prednisone [at a dose of] more than 10 mg is not great,” said Dr. Calabrese, who also noted that other publications have supported these conclusions.

So given these findings, how should clinicians address patient concerns? In the absence of probable exposure, “we say it’s better to have a well-controlled IMID on therapy than a poorly-controlled IMID on submaximal therapy. We say stick to therapy and try to wean the prednisone down as low as possible,” Dr. Calabrese said.

More controversially, what should patients do if they have had a significant exposure, such as a close proximity, prolonged exposure encounter with an individual with documented COVID-19, or at high-risk of disease? Dr. Calabrese noted that the American College of Rheumatology (ACR) guidelines recommend that low-level immunomodulation can be continued, “with an asterisk if it’s hydroxychloroquine, and it is in most of our minds now that we know that it is not effective, and the toxicity in the COVID setting is still being worked out,” he said.

With respect to other immunosuppressants, the ACR recommends stopping them temporarily, although IL-6 inhibitors may be continued in select circumstances. Resumption of the therapeutics can resume after a negative COVID test or completion of a 2-week observation period.

When patients contract COVID-19, antimalarial medications can be continued because they have been studied. “But medium-level immunomodulators, in particular methotrexate, I have grave concerns about because it can inhibit the adaptive immune response and antibody formation,” he said. COVID-19 is a serious infection, and all serious biologics have a package insert saying to stop them in a serious infection. Again, IL-6 inhibitors may be considered an exception in the right circumstances. When to resume these medications remains unknown. “I think that’s a work in progress. Test-based versus clinic-based strategies are a matter of controversy,” Dr. Calabrese said.

Ultimately, the question of what to do with immunosuppressive therapies in this population will continue to be a challenge. “The only good answer is to follow the rules of social distancing and to wear a mask,” said Kristina Callis Duffin, MD, a cochair of the department of dermatology and associate professor of dermatology at the University of Utah, Salt Lake City.

Measuring success with a treat-to-target strategy in psoriatic arthritis patients proved to be more comprehensive with the Psoriatic Arthritis Disease Activity Score (PASDAS) than it was with the Disease Activity Score in 28 joints (DAS28), according to findings from a prospective cohort study.

Fewer patients had a low disease activity score according to DAS28, and a higher percentage of patients deemed adequately treated according to DAS28 were found to have residual disease activity, compared with the number of patients so categorized according to PASDAS, researcher Michelle Mulder reported in her presentation of the study at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

“PASDAS implementation in a tightly monitored PsA [psoriatic arthritis] cohort suggests relevant residual disease burden, even though DAS28 was measured at every visit previously,” said Ms. Mulder, an MD/PhD student at Sint Maartenskliniek in Nijmegen, The Netherlands.

The presentation was convincing to Philip Helliwell, MD, PhD, who is a professor of clinical rheumatology at Leeds (England) University, and was also one of the developers of PASDAS. “We know it can be used in clinical practice with a certain amount of organization and clinical staff to help you,” he said during another presentation at GRAPPA.

Treat to target is a widely accepted therapeutic strategy. It’s particularly common in rheumatoid arthritis, but increasing evidence suggests that it improves patient outcomes in psoriatic arthritis. DAS28 is frequently used in treat-to-target approaches in rheumatoid arthritis, and often gets applied to psoriatic arthritis since rheumatologists are already comfortable with it, according to Ms. Mulder. “However, DAS28 has shown some limitations when used in psoriatic arthritis. For example, its joint count is limited to only 28 joints, and it does not take all PsA domains into account,” she said.

DAS28 was previously used at Sint Maartenskliniek in combination with psoriatic arthritis–specific assessment recommendations, but the institution opted in 2019 to switch to PASDAS, which was developed by GRAPPA and the European League Against Rheumatism. “To better adhere to international PsA guidelines, we chose to implement PASDAS in our cohort with the assumption that it might improve patient care,” Ms. Mulder said.

With DAS28, clinicians measured the C-reactive protein (CRP) and Patient Global Visual Analog Scale (VAS) domains and were advised to examine 28 joints for tender and swollen joint count domains. Under the PASDAS guidance, clinicians examined 68 joints for tenderness, 66 joints for swelling, CRP, Patient Global VAS, Physician Global VAS, Leeds Enthesitis Index, dactylitis, and the 12-item Short Form Physical Composite Scale. They also examined the skin, nails, and axial disease.

To examine the effects of the switch from DAS28 to PASDAS, the researchers compared outcomes in 855 patients before and after the change during March to December 2019. The mean age of patients was 55 years, and 46% were female. The mean disease duration was 10 years, and the mean PASDAS score was 3.1. A total of 96% of participants were negative for anti-cyclic citrullinated peptide. Overall, 30% had arthritis, 9% had axial disease, 3% had dactylitis, 21% had enthesitis, 51% had skin disease, and 42% had nail disease.

About three-quarters (77.4%) of patients reached the threshold of low disease activity (LDA) according to the DAS28 measure, while 53.1% did so using the PASDAS. High disease activity occurred in 7.8% of patients according to DAS28, compared with 2.7% as measured by PASDAS. Patients who reached only the DAS28 LDA target but not the PASDAS target, compared with patients who reached the LDA target in both measures, had significantly worse counts for swelling in 66 joints (0.7 vs. 0.2; P < .001) and tenderness in 68 joints (2.1 vs. 0.7; P < .001), as well as worse scores for enthesitis (0.5 vs. 0.1; P < .001), dactylitis (4% vs. 1%; P = .005), patient global VAS (44.0 vs. 14.4; P < .001), Health Assessment Questionnaire (0.8 vs. 0.4; P < .001) and Patient Acceptable Symptom State (unacceptable score in 17% vs. 3%; P < .001).

Ms. Mulder acknowledged that PASDAS imposes a significant burden on clinicians, and noted that Sint Maartenskliniek created patient infrastructure to handle the load. “It’s very important that you set up your clinic in a specific way. When the patient comes in, we draw blood immediately and we ask them to fill in the questionnaires, and then they go to a specialized nurse who measures all the different components of the PASDAS. It took a lot of time to train the specialized nurses and to implement the PASDAS score in our electronic health records. After we did those things, it was quite easy because we have this whole setup. It takes time and it is difficult, but it is definitely possible to do it,” Ms. Mulder said during a live Q&A following her prerecorded presentation.

The study received no funding. Ms. Mulder had no relevant financial disclosures. Dr. Helliwell has financial ties to AbbVie, Amgen, Celgen, Galapagos, Janssen, Novartis, Pfizer, and UCB.

SOURCE: Mulder M et al. GRAPPA 2020 Virtual Annual Meeting.

Measuring success with a treat-to-target strategy in psoriatic arthritis patients proved to be more comprehensive with the Psoriatic Arthritis Disease Activity Score (PASDAS) than it was with the Disease Activity Score in 28 joints (DAS28), according to findings from a prospective cohort study.

Fewer patients had a low disease activity score according to DAS28, and a higher percentage of patients deemed adequately treated according to DAS28 were found to have residual disease activity, compared with the number of patients so categorized according to PASDAS, researcher Michelle Mulder reported in her presentation of the study at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

“PASDAS implementation in a tightly monitored PsA [psoriatic arthritis] cohort suggests relevant residual disease burden, even though DAS28 was measured at every visit previously,” said Ms. Mulder, an MD/PhD student at Sint Maartenskliniek in Nijmegen, The Netherlands.

The presentation was convincing to Philip Helliwell, MD, PhD, who is a professor of clinical rheumatology at Leeds (England) University, and was also one of the developers of PASDAS. “We know it can be used in clinical practice with a certain amount of organization and clinical staff to help you,” he said during another presentation at GRAPPA.

Treat to target is a widely accepted therapeutic strategy. It’s particularly common in rheumatoid arthritis, but increasing evidence suggests that it improves patient outcomes in psoriatic arthritis. DAS28 is frequently used in treat-to-target approaches in rheumatoid arthritis, and often gets applied to psoriatic arthritis since rheumatologists are already comfortable with it, according to Ms. Mulder. “However, DAS28 has shown some limitations when used in psoriatic arthritis. For example, its joint count is limited to only 28 joints, and it does not take all PsA domains into account,” she said.

DAS28 was previously used at Sint Maartenskliniek in combination with psoriatic arthritis–specific assessment recommendations, but the institution opted in 2019 to switch to PASDAS, which was developed by GRAPPA and the European League Against Rheumatism. “To better adhere to international PsA guidelines, we chose to implement PASDAS in our cohort with the assumption that it might improve patient care,” Ms. Mulder said.

With DAS28, clinicians measured the C-reactive protein (CRP) and Patient Global Visual Analog Scale (VAS) domains and were advised to examine 28 joints for tender and swollen joint count domains. Under the PASDAS guidance, clinicians examined 68 joints for tenderness, 66 joints for swelling, CRP, Patient Global VAS, Physician Global VAS, Leeds Enthesitis Index, dactylitis, and the 12-item Short Form Physical Composite Scale. They also examined the skin, nails, and axial disease.

To examine the effects of the switch from DAS28 to PASDAS, the researchers compared outcomes in 855 patients before and after the change during March to December 2019. The mean age of patients was 55 years, and 46% were female. The mean disease duration was 10 years, and the mean PASDAS score was 3.1. A total of 96% of participants were negative for anti-cyclic citrullinated peptide. Overall, 30% had arthritis, 9% had axial disease, 3% had dactylitis, 21% had enthesitis, 51% had skin disease, and 42% had nail disease.

About three-quarters (77.4%) of patients reached the threshold of low disease activity (LDA) according to the DAS28 measure, while 53.1% did so using the PASDAS. High disease activity occurred in 7.8% of patients according to DAS28, compared with 2.7% as measured by PASDAS. Patients who reached only the DAS28 LDA target but not the PASDAS target, compared with patients who reached the LDA target in both measures, had significantly worse counts for swelling in 66 joints (0.7 vs. 0.2; P < .001) and tenderness in 68 joints (2.1 vs. 0.7; P < .001), as well as worse scores for enthesitis (0.5 vs. 0.1; P < .001), dactylitis (4% vs. 1%; P = .005), patient global VAS (44.0 vs. 14.4; P < .001), Health Assessment Questionnaire (0.8 vs. 0.4; P < .001) and Patient Acceptable Symptom State (unacceptable score in 17% vs. 3%; P < .001).

Ms. Mulder acknowledged that PASDAS imposes a significant burden on clinicians, and noted that Sint Maartenskliniek created patient infrastructure to handle the load. “It’s very important that you set up your clinic in a specific way. When the patient comes in, we draw blood immediately and we ask them to fill in the questionnaires, and then they go to a specialized nurse who measures all the different components of the PASDAS. It took a lot of time to train the specialized nurses and to implement the PASDAS score in our electronic health records. After we did those things, it was quite easy because we have this whole setup. It takes time and it is difficult, but it is definitely possible to do it,” Ms. Mulder said during a live Q&A following her prerecorded presentation.

The study received no funding. Ms. Mulder had no relevant financial disclosures. Dr. Helliwell has financial ties to AbbVie, Amgen, Celgen, Galapagos, Janssen, Novartis, Pfizer, and UCB.

SOURCE: Mulder M et al. GRAPPA 2020 Virtual Annual Meeting.

Measuring success with a treat-to-target strategy in psoriatic arthritis patients proved to be more comprehensive with the Psoriatic Arthritis Disease Activity Score (PASDAS) than it was with the Disease Activity Score in 28 joints (DAS28), according to findings from a prospective cohort study.

Fewer patients had a low disease activity score according to DAS28, and a higher percentage of patients deemed adequately treated according to DAS28 were found to have residual disease activity, compared with the number of patients so categorized according to PASDAS, researcher Michelle Mulder reported in her presentation of the study at the virtual annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA).

“PASDAS implementation in a tightly monitored PsA [psoriatic arthritis] cohort suggests relevant residual disease burden, even though DAS28 was measured at every visit previously,” said Ms. Mulder, an MD/PhD student at Sint Maartenskliniek in Nijmegen, The Netherlands.

The presentation was convincing to Philip Helliwell, MD, PhD, who is a professor of clinical rheumatology at Leeds (England) University, and was also one of the developers of PASDAS. “We know it can be used in clinical practice with a certain amount of organization and clinical staff to help you,” he said during another presentation at GRAPPA.

Treat to target is a widely accepted therapeutic strategy. It’s particularly common in rheumatoid arthritis, but increasing evidence suggests that it improves patient outcomes in psoriatic arthritis. DAS28 is frequently used in treat-to-target approaches in rheumatoid arthritis, and often gets applied to psoriatic arthritis since rheumatologists are already comfortable with it, according to Ms. Mulder. “However, DAS28 has shown some limitations when used in psoriatic arthritis. For example, its joint count is limited to only 28 joints, and it does not take all PsA domains into account,” she said.

DAS28 was previously used at Sint Maartenskliniek in combination with psoriatic arthritis–specific assessment recommendations, but the institution opted in 2019 to switch to PASDAS, which was developed by GRAPPA and the European League Against Rheumatism. “To better adhere to international PsA guidelines, we chose to implement PASDAS in our cohort with the assumption that it might improve patient care,” Ms. Mulder said.

With DAS28, clinicians measured the C-reactive protein (CRP) and Patient Global Visual Analog Scale (VAS) domains and were advised to examine 28 joints for tender and swollen joint count domains. Under the PASDAS guidance, clinicians examined 68 joints for tenderness, 66 joints for swelling, CRP, Patient Global VAS, Physician Global VAS, Leeds Enthesitis Index, dactylitis, and the 12-item Short Form Physical Composite Scale. They also examined the skin, nails, and axial disease.

To examine the effects of the switch from DAS28 to PASDAS, the researchers compared outcomes in 855 patients before and after the change during March to December 2019. The mean age of patients was 55 years, and 46% were female. The mean disease duration was 10 years, and the mean PASDAS score was 3.1. A total of 96% of participants were negative for anti-cyclic citrullinated peptide. Overall, 30% had arthritis, 9% had axial disease, 3% had dactylitis, 21% had enthesitis, 51% had skin disease, and 42% had nail disease.

About three-quarters (77.4%) of patients reached the threshold of low disease activity (LDA) according to the DAS28 measure, while 53.1% did so using the PASDAS. High disease activity occurred in 7.8% of patients according to DAS28, compared with 2.7% as measured by PASDAS. Patients who reached only the DAS28 LDA target but not the PASDAS target, compared with patients who reached the LDA target in both measures, had significantly worse counts for swelling in 66 joints (0.7 vs. 0.2; P < .001) and tenderness in 68 joints (2.1 vs. 0.7; P < .001), as well as worse scores for enthesitis (0.5 vs. 0.1; P < .001), dactylitis (4% vs. 1%; P = .005), patient global VAS (44.0 vs. 14.4; P < .001), Health Assessment Questionnaire (0.8 vs. 0.4; P < .001) and Patient Acceptable Symptom State (unacceptable score in 17% vs. 3%; P < .001).

Ms. Mulder acknowledged that PASDAS imposes a significant burden on clinicians, and noted that Sint Maartenskliniek created patient infrastructure to handle the load. “It’s very important that you set up your clinic in a specific way. When the patient comes in, we draw blood immediately and we ask them to fill in the questionnaires, and then they go to a specialized nurse who measures all the different components of the PASDAS. It took a lot of time to train the specialized nurses and to implement the PASDAS score in our electronic health records. After we did those things, it was quite easy because we have this whole setup. It takes time and it is difficult, but it is definitely possible to do it,” Ms. Mulder said during a live Q&A following her prerecorded presentation.

The study received no funding. Ms. Mulder had no relevant financial disclosures. Dr. Helliwell has financial ties to AbbVie, Amgen, Celgen, Galapagos, Janssen, Novartis, Pfizer, and UCB.

SOURCE: Mulder M et al. GRAPPA 2020 Virtual Annual Meeting.