Racial and ethnic determinants of psoriatic arthritis phenotypes and disease activity

Abstract

Objective

Individuals of racially and ethnically diverse backgrounds are underrepresented in PsA research/clinical trials, despite evidence that their disease presentation, severity and course may be distinct. Here we aim to describe how race, ethnicity and other socioeconomic factors inform disease characteristics in PsA.

Methods

A total of 817 consecutive patients with PsA from a large, diverse metropolitan area were enrolled in an observational, longitudinal registry. Demographics, medical history, medication use and psoriatic disease phenotype and activity were all recorded and analysed.

Results

The population was 77.4% non-Hispanic White, 2.2% Black, 7.1% Asian and 9.9% identified as other races or multiracial, and 11.8% identified as Hispanic. Hispanic and non-white individuals had higher tender joint counts (P = 0.033), with similar swollen joint counts (P = 0.308) and medication use (P = 0.171). They also had high rates of radiographic axial disease. Hispanic individuals were significantly more likely to have higher tender joint counts (P = 0.029), higher RAPID3 (Routine Assessment of Patient Index Data 3) scores (P = 0.004) and moderate–severe psoriasis (P = 0.010) compared with non-Hispanic White individuals.

Conclusion

In this diverse cohort, 22.6% of patients identified as underrepresented racial and/or ethnic groups, mostly Asian or Hispanic. Despite similar swollen joint counts and medication use, non-white individuals have higher tender joint counts compared with White individuals. Phenotypically, they also were more likely to have radiographic axial involvement. These findings may reflect differences in PsA presentation, experience and outcomes in individuals of various racial and ethnic groups, which need to be taken into consideration in clinical care and research design.

psoriasis, psoriatic arthritis, race, ethnicity, disparities

Rheumatology key messages

• Most studies of psoriatic disease cohorts are overwhelmingly comprised of White participants.

• This study utilizes a cohort unique in its diversity of race, ethnicity and socioeconomic status.

• Individuals of non-white backgrounds report higher tender joint counts compared with White individuals.

Introduction

PsA is an immune-mediated inflammatory arthritis associated with skin psoriasis and can take various forms, including arthritis, enthesitis, dactylitis and axial disease. Untreated, PsA can lead to erosive and deforming disease, yet it remains underdiagnosed and undertreated. Despite recent advances in therapy, many patients do not achieve clinically meaningful improvement [1]. At an individual level, this also translates into reduced quality of life, substantial psychosocial morbidity, high stress levels and feelings of stigmatization, and high rates of unemployment.

One remaining gap in care is understanding how race and ethnicity influence clinical presentation, treatment response and quality of life among patients with PsA. Originally thought to be a ‘Caucasian’ disease, the accumulated body of evidence suggests otherwise. Recent studies using large national cohorts and databases have found a significant burden of psoriatic disease in Asian, Black and Hispanic populations [2, 3]. Yet, few studies have looked at racial and ethnic differences in patients with PsA, and clinical trials are made up of an overwhelmingly White population [4].

In the present study, we assessed the racial and ethnic differences that stem from clinical features, comorbidities and treatment of PsA in a highly diverse, metropolitan patient population.

Patients and methods

Study design and population

A total of 817 consecutive adult patients meeting CASPAR (ClASsification criteria for Psoriatic ARthritis) criteria for PsA were enrolled from the New York University (NYU) Psoriatic Arthritis Center (PAC) and associated outpatient clinics and practices, including Bellevue Hospital from 7 January 2015 to 30 November 2022 into an observational, prospective cohort registry. Baseline visit was defined as the first clinical interaction at the NYU Langone Health System, regardless of timepoint in disease duration or treatment. The study was approved by the NYU Institutional Review Board (s20-00084) with waived written consent from individual participants as all data were collected in a deidentified manner.

Data and outcomes

Demographics, comorbidities, disease outcomes and medication use was recorded. Race and ethnicity were self-reported using a fixed set of categories. Participants were divided into groups of White individuals and non-white individuals (including Hispanic individuals). All data were extracted from the electronic medical record and entered into a REDCap database. Given the specifications of each clinical site, individuals seen at the NYU PAC were classified as having commercial insurance/Medicare and individuals seen at other NYU sites and Bellevue were classified as Medicaid/uninsured. Disease activity measures included physical exam findings [tender and swollen joint counts, as well as body surface area affected by psoriasis (BSA)] and patient-reported outcomes (Routine Assessment of Patient Index Data 3, RAPID3). Mild psoriasis was defined as BSA <3%, moderate 3–10% and severe >10%.

Statistical analysis

Baseline characteristics of study participants during the first visit were summarized using frequency and proportion for categorical variables and mean and s.d. for continuous variables. Statistical comparisons between groups were performed using independent two-sample t-tests and χ² tests as appropriate to test for group differences. Regression models were adjusted for age, sex and medication use. Count outcome variables were analysed using negative binomial regression to account for overdispersion, and continuous variables were analysed using linear regression and marginal means were used to predict mean differences for each outcome. Data were analysed using statistical software R.

Results

The NYU cohort consisted of 817 unique individuals. The cohort was 48.6% female with a mean age of 46.5 (s.d. 14.4, Table 1). The population was 77.3% non-Hispanic White, 7.1% Asian, 2.2% Black and 9.9% identified as other races (including one American Indian as well as multiracial individuals and multiethnic individuals). Overall, 11.8% identified as Hispanic. In terms of comorbidities, 182 (22.4%) had depression, 166 (20.3%) anxiety, 181 (22.2%) hypertension, 176 (21.5%) hyperlipidemia, 132 (16.2%) metabolic disease and 69 (8.5%) diabetes, with an average BMI of 27.8. As a group, and at first visit, participants had an average of 3.2 (s.d. 4.8) tender joints, 1.9 (s.d. 3.3) swollen joints, 3.2% (s.d. 9.0) BSA and 610 (74.7%) were on any medication for PsA including 354 (43.3%) on biologics.

Table 1.

Baseline characteristics of New York University PsA centre

Characteristics	All (n = 817)	Non-Hispanic, White (n = 632)	White Hispanic + non-white (n = 185)	P-value
Age, mean (s.d.)	46.47 (14.42)	47.16 (14.73)	44.1 (13.06)	0.007
Female, n (%)	398 (48.71)	307 (48.58)	91 (49.19)	0.883
Race/ethnicity, n (%)a				0.000
White	632 (77.4)	632 (100.00)
Asian	58 (7.10)		58 (31.35)
Black	15 (1.84)		15 (8.11)
Other	81 (9.92)		81 (43.78)
Hispanic	93 (11.38)		93 (50.27)
BMI, mean (s.d.)	27.75 (6.69)	27.61 (6.59)	28.28 (7.05)
Comorbidities, n (%)
Depressionb	182 (22.36)	150 (23.73)	32 (17.30)	0.072
Anxietyb	166 (20.32)	141 (22.31)	25 (13.51)	0.009
ADHDb	35 (4.28)	31 (4.91)	4 (2.16)	0.105
Hypertension	181 (22.15)	141 (22.31)	40 (21.62)	0.843
Hyperlipidemia	176 (21.54)	140 (22.15)	26 (19.46)	0.433
Myocardial infarction	11 (1.35)	9 (1.42)	2 (1.08)	0.722
Coronary artery disease	32 (3.92)	26 (4.11)	6 (3.24)	0.591
Stroke	11 (1.35)	9 (1.42)	2 (1.08)	0.722
Metabolic disease	132 (16.16)	90 (14.24)	42 (22.70)	0.006
Diabetes	69 (8.45)	45 (7.12)	24 (12.97)	0.012
Current smoker	63 (7.71)	43 (6.80)	20 (10.81)	0.072
Medication use, n (%)
Any	610 (74.66)	479 (75.79)	131 (70.81)	0.171
Biologic	354 (43.33)	273 (43.20)	81 (43.78)	0.968
Disease involvement, n (%)
Axial diseasec	179 (21.91)	129 (20.41)	50 (27.03)	0.056
Axial (radiographic)	150 (18.36)	103 (16.30)	47 (25.41)	0.005
Axial (non-radiographic)	29 (3.55)	26 (4.11)	3 (1.62)	0.107
Enthesitis	274 (33.54)	211 (33.39)	63 (34.05)	0.866
Dactylitis	263 (32.19)	208 (32.91)	55 (29.73)	0.415
Nail disease	467 (57.16)	360 (56.96)	107 (57.84)	0.832
Skin disease	807 (98.78)	622 (98.42)	185 (100.00)	0.085
Scalp PsO	490 (59.98)	375 (59.34)	115 (62.16)	0.490
Inverse PsO	135 (16.52)	105 (16.61)	30 (16.22)	0.898
Radiographic erosion	227 (27.78)	171 (27.06)	56 (30.27)	0.391
Disease severity
Tender joint count, mean (s.d.)	3.23 (4.78)	3.00 (4.5)	4 0.00(5.59)	0.033
Swollen joint count, mean (s.d.)	1.91 (3.25)	1.84 (3.03)	2.17 (3.90)	0.308
Active enthesitis, n (%)	274 (33.54)	211 (33.39)	63 (34.05)	0.866
BSA, mean (s.d.)	3.17 (8.97)	2.79 (8.30)	4.56 (11.00)	0.062
Moderate–severe BSA, n (%)	138 (18.98)	100 (17.51)	38 (24.36)	0.069
RAPID3, mean (s.d.)	10.54 (6.54)	10.26 (6.21)	11.83 (7.80)	0.107
Active nail disease, n (%)	436 (53.37)	339 (53.64)	97 (52.43)	0.772
Nail disease NRS, mean (s.d.)d	1.20 (1.80)	1.15 (1.77)	1.41 (1.95)	0.212
Diagnosis, mean (s.d.)
Age at PsA diagnosis	39.39 (13.98)	39.97 (14.39)	37.62 (12.51)	0.054
PsA duration	7.19 (9.63)	7.42 (10.10)	6.48 (8.04)	0.243
PsO duration	18.01 (14.73)	19.46 (15.27)	13.37 (11.76)	0.000

a

Patients may identify as more than one race/ethnicity. Other includes one patient who identified as American Indian as well as those who identify as multiracial or multiethnic.

b

Mental health conditions defined by established diagnosis (patient report and/or International Classification of Diseases code) and/or use of psychiatric medication.

c

Axial disease was defined by imaging findings regardless of symptomatology, radiographic indicating evidence of disease on radiographs of the sacroiliac joints or spine and non-radiographic indicating evidence of disease on MRI only.

d

Nail NRS scored from 0–10, with 0 indicating no involvement and 10 indicating severe involvement. ADHD: attention deficit hyperactivity disorder; PsO: psoriasis; BSA: body surface area covered by psoriasis; RAPID3: Routine Assessment of Patient Index Data 3; NRS: numeric rating scale.

We first compared non-Hispanic White individuals (n = 632) with non-white (n = 185) participants (including those identifying as Hispanic regardless of race). White individuals were older (P = 0.01), had higher rates of anxiety (P = 0.01), and lower rates of metabolic disease (P = 0.01) and diabetes (P = 0.01). Disease characteristics were generally similar although the presence of radiographic axial disease was more common in non-white individuals (25.4% vs 16.3%, P = 0.005). Non-white individuals had a higher tender joint count [4.0 (s.d. 5.6) vs 3.0 (s.d. 4.5), P = 0.03] and a numerically higher BSA [4.6% (s.d. 11.0) vs 2.8 (s.d. 8.3), P = 0.06] despite similar systemic medication use (Fig. 1A). When adjusting for age, sex and medication use, non-white individuals had a tender joint count that was 1.03 joints higher (95% CI 0.05–2.01) than the count of White individuals (Fig. 2A), while there was no difference in swollen joint count. Non-white individuals also had 1.8% (95% CI 0.2–3.4) more BSA involved and scored 1.7 (95% CI 0.1–3.3) points higher on the RAPID 3 instrument. Further modelling found that the difference in tender joints remained significant when adjusting for PsA disease duration, but not when adding both PsA disease duration and comorbidities (Supplementary Fig. S1, available at Rheumatology online).

Figure 1.

Disease activity measures by race and ethnicity for (A) all participants at the baseline encounter (n = 817, left) and for participants at the baseline encounter who were not taking any medication for PsA (n = 207, right). Disease activity measures at baseline and year 1 (B) are demonstrated for a subset of patients who were followed for a period of at least 1 year (n = 309). Blue indicates non-Hispanic White individuals, pink indicates non-white individuals. RAPID3: Routine Assessment of Patient Index Data 3

Figure 2.

Estimated mean differences based on regression model analysis. (A) Mean differences for race and ethnicity adjusted for age, sex and medication use. Mean difference represents non-white individuals (including Hispanic individuals) as compared with White individuals as the reference. (B) Mean difference for sex adjusted for age, race and ethnicity, and medication use. Mean difference represents female participants as compared with male participants as the reference. *P < 0.05. TJC: tender joint count; SJC: swollen joint count; BSA: body surface area affected by psoriasis; RAPID3: Routine Assessment of Patient Index Data 3

In a subgroup of patients who were not on any medication (n = 207) at the time of first visit, non-white individuals had a significantly higher tender joint count [5.8 (s.d. 6.7) vs 3.6 (s.d. 4.4), P = 0.04], BSA [5.4% (s.d. 8.2) vs 2.2% (s.d. 3.0), P = 0.02] and RAPID3 score [13.5 (s.d. 7.5) vs 9.9 (s.d. 5.5), P = 0.02], with a similar swollen joint count [3.6 (s.d. 4.7) vs 2.6 (s.d. 3.5), P = 0.17] compared with White participants (Fig. 1A and Supplementary Table S1, available at Rheumatology online). A second subgroup of patients was followed longitudinally for at least 1 year (n = 309, 230 White and 79 non-white individuals). At this timepoint, 96.1% of White individuals and 98% of non-white individuals were on medication for PsA. Within this sample, while tender/swollen joint counts, %BSA affected with psoriasis and RAPID3 had improved in all patients, at year 1, non-White individuals exhibited numerically fewer tender and swollen joints than White individuals (Fig. 1B).

Hispanic participants (n = 93) had similar rates of psychiatric disorders to White individuals, but significantly higher rates of current smoking (12.9% vs 6.8%, P = 0.04) and metabolic disease (24.7% vs 14.2%, P = 0.01), and a higher average BMI [30.2 (s.d. 8.0) vs 27.6 (s.d. 6.7), P = 0.01] (Supplementary Table S2, available at Rheumatology online). Hispanic individuals were more likely to have radiographic axial disease (25.8% vs 16.3%, P = 0.03), higher tender joint counts [4.4 (s.d. 5.5) vs 3.0 (s.d. 4.5), P = 0.03], higher RAPID3 scores [14.6 (s.d. 7.7) vs 10.3 (s.d. 6.2), P = 0.004] and moderate–severe psoriasis (30.7% vs 17.5%, P = 0.01), despite similar swollen joint counts and medication use, compared with White individuals. Asian patients (n = 58) were generally younger, had significantly lower rates of depression (8.6% vs 23.7%, P = 0.01) and anxiety (5.2% vs 22.3%, P = 0.002), as well as lower average BMI [25.4 (s.d. 4.4) vs 27.6 (s.d. 6.6), P = 0.002] than White individuals (Supplementary Table S3, available at Rheumatology online). All disease outcomes and medication use were similar between the two groups.

Analyses were also performed based on insurance status (commercial insurance/Medicare, n = 750 vs Medicaid coverage/uninsured, n = 67). Those with Medicaid coverage/uninsured were older (P = 0.004), and had more hypertension (37.3% vs 20.8%, P = 0.002), metabolic disease (35.8% vs 14.4%, P < 0.001) and diabetes (25.4% vs 6.9%, P = <0.001) (Supplementary Table S4, available at Rheumatology online). They were also more likely to be current smokers (14.9% vs 7.1%, P = 0.021). In terms of disease outcomes, a greater proportion of those with Medicaid coverage/uninsured had erosions on imaging (26.5% vs 41.8%, P = 0.008), but had a lower number of swollen joints [1.08 (s.d. 2.2) vs 1.98 (s.d. 3.3), P = 0.005] and were more likely to be on biologics (60.7% vs 44.9%, P = 0.018).

When comparing phenotypes based on sex, female participants (n = 398) had higher rates of depression (28.9% vs 15.8%, P = <0.001) and anxiety (23.8% vs 16.6%) compared with male participants (n = 419) (Supplementary Table S5, available at Rheumatology online). Female participants were also less likely to have nail involvement (49.5% vs 64.4%, P < 0.001) and inverse psoriasis (13.6% vs 19.3%, P = 0.027). Despite having similar tender and swollen joint counts, %BSA and medication use, female participants had higher RAPID3 scores [11.5 (s.d. 6.6) vs 9.8 (s.d. 6.4), P = 0.007] compared with male participants. This was also seen when adjusting for age, medication use and race (Fig. 2B).

Discussion

Here we describe a large racially and ethnically diverse cohort of patients with PsA. To our knowledge, this is the largest US-based study not only to look at comorbidities and phenotype, but also to capture PsA disease activity measures. Although psoriasis and PsA are more common in the White population compared with the non-white population, it affects people of all races and ethnicities. Using the 2011–14 the National Health and Nutrition Examination Survey (NHANES), Armstrong et al. found an overall psoriasis prevalence of 3% in the USA, with a prevalence of 3.6% in White individuals, 2.5% in Asian individuals, 1.9% Hispanic individuals and 1.5% Black individuals [2]. A similar prevalence pattern was seen among US individuals with insurance for PsA (0.19–0.34%, 0.04–0.19%, 0.13–0.19% and 0.09–0.3% in White, Black, Asian and Hispanic individuals, respectively) [3]. These differences are likely to be smaller than what is reported when adjusting for access to care and other socioeconomic factors [5].

Data on ethnically and racially diverse individuals with psoriatic disease remains sparce. In a psoriasis cohort, Abrouk et al. found that Asian and Hispanic individuals were more likely to present with severe disease than White individuals [6]. At one Veterans Affairs medical centre site, Kerr et al. found that Black individuals with psoriasis, compared with White individuals, had a trend towards higher Psoriasis Area and Severity Index (PASI) scores and had a lower quality of life, but were also less likely to be on systemic therapy [7]. In line with these psoriasis studies, we found that Hispanic individuals had higher rates of moderate–severe skin psoriasis and that non-white individuals, as well as Asian individuals, had a numerically higher %BSA affected with psoriasis. Importantly, these differences were observed despite similar use of systemic therapies, although Hispanic individuals in particular did have higher average BMIs which may contribute to higher skin activity. Furthermore, in the subset of patients not on PsA treatment, non-white individuals had a significantly higher %BSA. This implies that non-white individuals may have different therapy responses, underlying the importance of including these populations in psoriasis skin trials, where they have traditionally been poorly represented.

Studies focusing on patients exclusively with PsA are even more limited. Aslam et al. looked at patients with PsA in Northern England who were of South Asian or Northern European ancestries [8]. They found that those with South Asian ancestry had more tender and swollen joints, more severe enthesitis and dactylitis, more skin involvement and worse quality of life compared with those of Northern European ancestry, all with similar medication use and time from symptom onset to medication initiation. Ahmed et al. examined a cohort of US patients with PsA using RAPID3 as a measure of disease activity, and found differences across racial and ethnic groups, with Black and Hispanic patients having higher scores compared with White patients [9]. However, no objective measures of skin or musculoskeletal disease activity were recorded. In terms of disease activity, we found that, in addition to higher %BSA, non-white individuals had a higher rate of tender joints without any difference in swollen joints or medication use. Although the clinical relevance of one additional tender joint may be open to debate, this illustrates that while musculoskeletal disease activity is similar, the way disease is experienced varies. Of note, in the subgroup followed prospectively, the gap in tender joint count closed, suggesting the presence of variables that were not accounted for fully, such as access to care.

Phenotypically, and of high relevance to the field, we observed a significantly increased rate of radiographic axial disease in non-white individuals. This is of particular interest as axial SpA is thought to be more common in White individuals (given its established association with HLA-B27) and may challenge the notion that axial domain is not frequently observed in non-white patients with PsA. Studies in AS have demonstrated higher rates of disease in White populations compared with Black populations [10] in the USA. However, Jamalyaria et al. looked at 925 patients with AS (87% White), and found that Black individuals (and to a less extent Hispanic individuals) had worse disease activity and baseline radiographic severity [11]. Additionally, while Black individuals had the lowest prevalence of HLA-B27 positivity (62.4%), White individuals and Hispanic individuals had similarly high positivity rates (85.3% and 86.7%). Therefore, it may be that our findings are driven by our predominantly Hispanic population. Importantly, not all patients underwent axial imaging, which was determined at the discretion of the treating physician. Lastly, we found that Asian individuals were diagnosed with PsA at a younger age, a phenomenon also seen in other studies [12].

Given the cross-sectional nature of our study, we were limited by the fact that patients present at different timepoints in their disease course. Although we found similar results when accounting for medication use and in a subgroup of untreated patient, this does not fully reflect the effects of disease burden and symptom duration. Furthermore, our dataset lacks complete information on HLA-B27 status to investigate increased rates of radiographic axial disease in non-white individuals, although further efforts are currently being pursued to obtain HLA genotyping. Most importantly, despite the relatively large, diverse population of our study compared with other cohorts, we acknowledge that our sample size is still limited. To achieve the most robust sample size, we grouped our population into White individuals and Hispanic and non-white individuals, which is an artificial divide, and is likely not a biologically accurate reflection of individual racial and ethnic groups. Furthermore, the majority of the non-White individuals were Hispanic and findings may have been driven predominantly by this particular group of patients. Although we look at insurance type, we also lack detailed information on socioeconomic status and other economic and environmental factors that may be associated with race and ethnicity differences such as access to care, employment and health literacy.

As previously described, our cohort demonstrated a high rate of psychiatric disorders associated with PsA with an overall depression prevalence of 22.3% [13] (in contrast to the Centers for Disease Control and Prevention’s reported prevalence of self-reported depression in New York in 2021 of 17%). We also found high rates of cardiovascular and metabolic disease, which were relatively higher in non-white individuals with PsA, although with variability across different racial and ethnic groups. While Hispanic patients were more likely to have cardiovascular disease and metabolic disease, and to be current smokers compared with White patients, Asian patients were less likely to present with comorbidities compared with White patients.

The clinical presentation of PsA is also influenced by gender and sex differences. In our cohort, women were more likely to have entheseal involvement, which was seen in some previous studies [14]. They also had lower prevalence of psoriatic nail disease in line with current literature demonstrating that men generally have 11–12% higher prevalence of nail involvement [14]. However, some of this difference may be due to women presenting with painted nails, limiting the clinical examination of this domain. While women had similar tender and swollen joint counts compared with men, they had higher RAPID3 scores. This was not unexpected as previous studies showed that women experience more pain and worse quality of life than men, as well as have higher rates of depression and anxiety which have been associated with worse PsA outcomes [15]. It follows that composite measures that include patient-reported pain and tender joint count may be higher in women than men despite relatively similar inflammatory states, and this may account for some of the differences in the ability of women to achieve remission endpoints in clinical trials.

It remains unclear through what mechanism(s) race and ethnicity may impact PsA phenotype and activity, although genetic predisposition, differences in the immune system and/or environmental exposures (including access to care and socioeconomic factors) may all be implicated. Ultimately, larger population-based studies with representation of all racial and ethnic groups coupled with molecular endotyping as well as more detailed socioeconomic phenotyping are needed to better understand the commonalties and differentiating features of demographic and biologic drivers of disease for each patient group population with PsA.

Data availability

Data will be made available upon request to the authors.

Funding

This study was funded by NIH/NIAMS (1UC2AR081029 to Scher, T32-AR-069515 to R.H.H., J.U.S.), NYU Colton Center for Autoimmunity, Rheumatology Research Foundation, the National Psoriasis Foundation, The Beatrice Snyder Foundation and The Riley Family Foundation.

Disclosure statement: R.H.H. has served as a consultant for Janssen and UCB. A.L.N. has served as a consultant for Sun Pharma and UCB. S.M.R. has served as a consultant for UCB, Novartis, Amgen, Fresenius Kabi and Abbvie, and has received clinical research support from Pfizer, Janssen and Eli Lilly. J.U.S. has served as a consultant for Janssen, Novartis, Pfizer, Sanofi, Amgen, UCB, BMS and AbbVie, and has received funding for investigator-initiated studies from Janssen and Pfizer. E.L. has served as a consultant for UCB, GSK and Aurinia.