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Plasma levels of pentraxin 3 in patients with spondyloarthritis.
Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals 2018 Februrary
CONTEXT: Determining the disease's inflammatory activity in spondyloarthritis (SpA) is difficult although very important as it is this that drives treatment.
OBJECTIVE: To investigate if plasma pentraxin-3 (PTX3) could act as an inflammatory marker in SpA.
METHODS: Eighty one SpA patients (11 with psoriatic arthritis (PsoA) and 70 with ankylosing spondylitis (AS)) and 90 gender and age paired controls were studied for plasma PTX3 levels by ELISA. Patients had determinations of disease activity through C reactive protein (CRP), erythrocyte sedimentation rate (ESR), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score (ASDAS)-CRP. Epidemiological, clinical and treatment data were collected through chart review.
RESULTS: SpA patients had lower concentrations of plasma PTX3 than controls (median of 0.95 ng/mL vs 1.64 ng/mL; p < 0.0001). Correlation of PTX3 levels and BASDAI, ASDAS-CPR, CRP levels and ESR could not be found. No differences in PTX3 levels were detected between PSoA and AS patients (p = 0.42). Uveitis, presence of HLA B27, tobacco exposure, age and disease duration did not influence PTX3 levels.
CONCLUSIONS: PTX3 plasma levels do not reflect disease activity in SpA. However, it probably participates in the ethiopathogenetic process, as it is consumed in these patients.
OBJECTIVE: To investigate if plasma pentraxin-3 (PTX3) could act as an inflammatory marker in SpA.
METHODS: Eighty one SpA patients (11 with psoriatic arthritis (PsoA) and 70 with ankylosing spondylitis (AS)) and 90 gender and age paired controls were studied for plasma PTX3 levels by ELISA. Patients had determinations of disease activity through C reactive protein (CRP), erythrocyte sedimentation rate (ESR), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score (ASDAS)-CRP. Epidemiological, clinical and treatment data were collected through chart review.
RESULTS: SpA patients had lower concentrations of plasma PTX3 than controls (median of 0.95 ng/mL vs 1.64 ng/mL; p < 0.0001). Correlation of PTX3 levels and BASDAI, ASDAS-CPR, CRP levels and ESR could not be found. No differences in PTX3 levels were detected between PSoA and AS patients (p = 0.42). Uveitis, presence of HLA B27, tobacco exposure, age and disease duration did not influence PTX3 levels.
CONCLUSIONS: PTX3 plasma levels do not reflect disease activity in SpA. However, it probably participates in the ethiopathogenetic process, as it is consumed in these patients.
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