THU0321 Acute phase markers in psoriatic arthritis identify patients with a more severe phenotype. (12th June 2018)

• Record Type: Journal Article
• Authors: Haroon, M.; Ahmad, M.; Mason, O.; FitzGerald, O.
• Is Part Of: Annals of the rheumatic diseases. Volume 77(2018)Supplement 2
• Page Start: 378
• Page End: 379
• Publication Date: 2018-06-12
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2018-eular.3834
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: CRP and ESR are the most commonly and probably the most studied inflammatory markers among patients with inflammatory arthritis. In contrast to rheumatoid arthritis, however, these markers are raised in less than 50% of people with psoriatic arthritis (PsA). Little is known about the long term significance of elevated inflammatory markers during the course of PsA disease. Objectives: In a well characterised PsA cohort with a long term follow up, we examined the association of CRP and ESR over the disease course with demographics, clinical and radiographic features, patient reported outcome measures and the number of comorbid conditions. Methods: A cohort of 283 PsA patients all meeting CASPAR criteria and attending rheumatology clinics were evaluated. All underwent detailed skin and rheumatologic assessments, along with cardiovascular risk factor evaluation. Moreover, we documented the presence/absence of comorbidities using the Charlson Comorbidity Index (CCI). All of these patients had CRP and ESR laboratory values assessed along with the other routine laboratory parameters during the disease course. For each patient, we documented CRP and ESR values at 3 different time points: firstly, at the time of the initial diagnosis; secondly, the highest value of CRP and ESR recorded during the disease course; and thirdly at the time of full assessment for this study. Cumulative inflammation over time was represented by the cumulative averages of CRP (ca-CRP) and ESR (ca-ESR) which were calculated from the AUC (Area Under the Curve) of the 3 documented measurements divided by the total number of months of follow-up. Variables significantly associated at a Bonferroni-corrected p-value were included in the multiple linear regression modelling CRP and ESR. Results: A total of 283 PsA patients [mean age 54.6±12 years; 52% female; mean PsA duration of 19±9 years; 25% with sacroiliitis; 44.5% with peripheral joint erosions; 60% of patients requiring TNFi for PsA] attended for detailed assessments. The median (IQR) and mean (SD) Ca-CRP was 8.8 (4.6–14.8) and 11.72 (10.52), respectively. The median (IQR) and mean (SD) Ca-ESR was 13.8 (7.8–20.1) and 15.78 (10.46). The variables were also checked for multicollinearity. On multiple linear regression, erosions, sacroileitis, and the CCI were most significantly associated with Ca-CRP (unstandardised coefficient B=6.4, 2.9, 1.05, respectively, p<0.01), when controlled for all other variables in the model [(F=77.6, p<0.001), 72% (R-square)]. There was borderline significant association with the higher number of DMARDs and TNFi used (p=0.09, 0.08, respectively). Moreover, on multiple linear regression analysis, the erosions, extent of joint involvement (oligoarthritis/polyarthritis), number of TNFi used and the CCI were most significantly associated with Ca-ESR (unstandarised coefficient B=3.8, 1.8, 1.8, 0.76, respectively) when controlled for all other variables in the model [(F=130, p<0.001), 77% (R-square)]. Conclusions: PsA is a heterogeneous disease with <50% of patients developing radiographic damage. Elevated inflammatory markers, CRP and ESR, can help identify patients with a severe PsA phenotype. Such patients experience more radiographic damage, they have more comorbidities and their disease is more resistant to DMARDs and TNFi. Disclosure of Interest: M. Haroon Grant/research support from: Abbvie, Pfizer, Speakers bureau: Abbvie, Pfizer, UCB, M. Ahmad: None declared, O. Mason: None declared, O. FitzGerald Grant/research support from: Pfizer, Abbvie, MSD, Roche, UCB, Janssen and Cellgene