AB0782 Serum pentraxin 3 as a biomarker in patients with spondyloarthritis.

Abstract

BackgroundA proper evaluation and management of patients with spondyloarthritis (SpA) requires the use of biomarkers, facilitating early diagnosis, reflecting disease activity and clinical response to therapies. The chronic, systemic inflammatory process is responsible for increased CV risk in SpA patients. Pentraxin 3 (PTX3) is an inflammatory marker, a member of long pentraxin superfamily, argued to be involved in pathogenesis of both inflammation and atherosclerosis. PTX3 is produced locally in the inflamed tissue, by different cell types including macrophages, endothelial cells, synoviocytes, but not hepatocytes. PTX3 is produced in walls of blood vessels, in atherosclerotic plaques, as a response to pro-inflammatory cytokines.ObjectivesThe aim of the study was to assess the role of PTX3 as a biomarker in patients with SpA and to evaluate the relationship between PTX3 and CV risk markers (carotid intima-media thickness (cIMT), lipid profile).MethodsThe study group consisted of 40 consecutive patients with SpA: 29 patients with psoriatic arthritis (PsA) and 11 patients with ankylosing spondylitis (AS). The group consisted of 16 (40%) women and 24 (60%) men, with the mean (SD) age 43.9 (12.0) (range 25–68) and disease duration 7,8 (7,6) years (range 1–32). An assessment of the disease activity included: laboratory inflammatory parameters (erythrocyte sedimentation rate (ESR), C-reactive protein, CRP) and clinical assessment (in patients with peripheral SpA (pSpA) joints counts and disease activity score in 28 joints (DAS28); in patients with axial SpA (axSpA) Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI) and pain of the spine according to the patient in visual analogue scale (VAS). A measurement of carotid intima-media thickness (cIMT) was performed using high-resolution B-mode ultrasonography to estimate features of atherosclerosis (cIMT> 0.9 mm and/or presence of atherosclerotic plaques).ResultsThe median (IQR) PTX3 concentration in SpA patients was 3.39 (2.22-3.88) ng/ml. The mean (SD) value of ESR was 27.7 (28.3) mm/h and CRP concentration 13.6 (19.9) mg/l.The mean values of clinical indices were as follows: DAS28 3.8 (1.1), BASDAI 4.02 (2.1), BASFI 4.22 (2.2), VAS spine pain 41.4 (24.0).The mean (SD) cIMT value was 0.77 (0.23) mm (range 0.48-1.33). The features of atherosclerosis were detected in 7 (17.5%) patients.No significant correlations were found between PTX3 and other inflammatory markers (ESR, CRP). There were no correlations between PTX3 concentration the clinical indices of the disease activity (DAS28, BASDAI, BASFI, VAS spine pain). No differences of PTX3 concentrations were detected between pSpA and axSpA patients.The PTX3 concentrations were significantly higher in patients with definite atherosclerosis (cIMT > 0.9 mm) than in patients with subclinical or no atherosclerosis (cIMT=< 0.9) (5.79 (3.84-8.59) vs 3.06 (2.0-3.52) ng/ml, p=0.01), as well as in patients with atherosclerotic plaques in comparison with no plaques (6.79 (4.86-8.59) vs 3.26 (2.0-3.71) ng/ml, p=0.02) (Figure 1).ConclusionThe results of our study suggest that in patients with SpA, PTX3 could be regarded as a biomarker indicating intensity of atherosclerosis. However PTX3 was not associated with parameters of disease activity in patients with SpA.