Background: Racial and ethnic differences in rheumatoid arthritis (RA) phenotype, disease activity measures and co-morbidities have been reported. Few studies have analyzed these differences in a population with the same access to healthcare.
Objectives: The purpose is to investigate the association between ethnicity and RA severity within an accessible healthcare system.
Methods: Cross-sectional study of 210 RA patients (ACR 2010 criteria) from 6 Catalonian hospitals (within a universally accessible public system). Latin-American (LA) mestizo and Asiatic (Pakistan and Indian) patients were included consecutively, and compared with a European-White (EW) control group. Sociodemographic variables, disease activity, prognostic markers, serology and treatment were collected and compared between groups. Multivariable linear regression evaluated the association between race groups and disease activity, adjusting for potential confounders, including age, RF, ACPA, smoking habit, symptom duration, and treatment.
Results: A total of 210 patients were included (82.6% female, mean age 59.8 ± 13.5). 82 patients were LA, 23 Asiatic and 105 EW. LA and Asian patients were younger than EW patients, and had a younger age at diagnosis. There were no differences in RA duration between EW and LA, Asian patients had a shorter disease duration than EW and LA. LA and Asian patients were more frequently seropositive, and are less smokers than EW patients. There were no differences between groups in disease activity assessed by DAS-ESR and CDAI, even though LA patients had significantly higher SJC. LA and Asian patients used glucocorticoids more frequently than EW patients. Additionally, LA patients used biologic or JAK inhibitors targeted sintetic DMARDs (b/tsDMARDs) more frequently than EW (60.5% vs 39.4% respectively). Full data in Table 1. A second analysis was performed pairing for age and disease duration, with similar results. Multivariable linear regression adjusted for potential confounders found no association between disease activity measured by DAS28-ESR and ethnicity (B=0.048, p=0.496). Female sex and use of glucocorticoids were significantly associated with higher DAS28-ESR (B=0.245, p=<0.001 and B=0.339, p=<0.001 respectively). The analysis of CDAI as dependant variable showed similar results.
Conclusion: In the context of an accessible public healthcare system, in this RA cohort, we found no differences in disease activity between the three ethnic groups analysed. However LA patients were younge, used more frequently glucocorticoids and b/tsDMARD than EW suggesting a more aggressive disease phenotype.
Demographics and clinical characteristics of RA patients
European White
| Latin American
| p | Asiatic
| p | |
---|---|---|---|---|---|
Demographics | |||||
Age | 66.21 ± 11.6 | 55.03 ± 12.6 | <0.001 | 50.14 ± 11.5 | <0.001 |
Female | 81% | 91.5% | 0.042 | 62.5% | 0.098 |
BMI | 27.86 ± 5.9 | 29.69 ± 19.4 | 0.369 | 27.8 ± 8.8 | 0.493 |
Ever smoker | 49.1% | 26.9% | 0.003 | 12.5% | 0.006 |
RA Characteristics | |||||
RF+ | 72.4% | 80.2% | 0.214 | 100% | 0.004 |
ACPA+ | 70.5% | 90.1% | 0.001 | 95.7% | 0.002 |
Age at diagnosis | 55.52 ± 12.6 | 43.35 ± 12.2 | <0.001 | 43.65 ± 11.4 | <0.001 |
RA duration | 11.06 ± 6.5 | 13.05 ± 14.1 | 0.214 | 6.69 ± 6.0 | 0.002 |
RA characteristics – disease activity | |||||
TJC | 2.31 ±6.7 | 1.82 ± 2.9 | 0.505 | 3.26 ± 6.2 | 0.267 |
SJC | 0.39 ± 1.2 | 0.89 ± 2.0 | 0.047 | 1.0 ± 2.1 | 0.093 |
Pain VAS | 2.72 ±2.6 | 3.44 ± 2.4 | 0.065 | 3.60 ± 2.3 | 0.081 |
PGH | 2.80 ± 2.2 | 3.38 ± 1.9 | 0.060 | 3.65 ± 2.3 | 0.051 |
ESR | 27.21 ± 25.4 | 27.71 ± 23.3 | 0.891 | 28.70 ± 21.9 | 0.398 |
DAS28-ESR | 2.86 ± 1.4 | 3.19 ± 1.2 | 0.087 | 3.35 ± 1.5 | 0.065 |
CDAI | 31.92 ± 28.2 | 33.80 ± 24.8 | 0.636 | 36.61 ± 25.2 | 0.232 |
Erosive disease | 33.3% | 26.8% | 0.295 | 21.7% | 0.254 |
Treatment | |||||
Use of GC | 32.4% | 50.0% | 0.015 | 60.9% | 0.011 |
b/tsDMARDs | 39.4% | 60.5% | 0.004 | 52.2% | 0.262 |
Line of b/tsDMARDs | 2.18 ± 1.8 | 2.50 ± 2.0 | 0.427 | 1.91 ± 0.8 | 0.316 |
D2T-RA (of pax in b/tsDMARD ) | 10.5% | 36% | 0.391 | 27.3% | 0.988 |
Comorbidities | |||||
Charlson Index | 1.91 ± 1.3 | 1.49 ± 1.03 | 0.013 | 2.0 ± 1.2 | 0.387 |
RCDI | 1.69 ± 1.6 | 0.73 ± 1.1 | <0.001 | 1.13 ± 1.3 | 0.061 |
HTA | 42.9% | 22.2% | 0.003 | 34.8% | 0.476 |
DM2 | 13.6% | 8.9% | 0.322 | 34.8% | 0.016 |
DLP | 41% | 22.9% | 0.007 | 21.7% | 0.085 |
Fragility fracture | 9.6% | 2.5% | 0.050 | 0% | 0.121 |
Depression | 17.3% | 12.2% | 0.333 | 4.3% | 0.115 |
Data presented as mean ± 1 standard deviation or n (%). BMI: body mass index, RF: rheumatoid factor, ACPA: anti-citrullinated peptides antibodies, TJC: tender joint count, SJC: swollen joint count, pain VAS: pain visual analog scale, PHS: patient global health, ESR: erythrocyte sedimentation rate, GC: glucocorticoid, b/ts DMARD: biologic or targeted synthetic Disease-Modifying Antirheumatic Drugs, D2T-RA: difficult to treat Rheumatoid Arthritis, RCDI: rheumatic disease co-morbidity index, HTA: hypertension, DM2: diabetes mellitus type 2, DLP: dyslipidemia.
REFERENCES: NIL.
Acknowledgements: NIL.
Disclosure of Interests: None declared.
© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (