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  • Title: Blood serum levels of amino-terminal pro-C-type natriuretic peptide in patients with rheumatoid arthritis.
    Author: Olewicz-Gawlik A, Trzybulska D, Grala P, Hrycaj P.
    Journal: Adv Med Sci; 2010; 55(2):261-5. PubMed ID: 20934962.
    Abstract:
    PURPOSE: Angiogenesis is a prominent feature of rheumatoid synovitis and contributes to perpetuation of joint disease. The aim of presented study was to evaluate the association of inflammatory response and endothelial dysfunction parameters with serum levels of amino-terminal pro-C-type natriuretic peptide (NT-proCNP), a surrogate measure for a potent regulator of vascular tone and angiogenesis, CNP. MATERIAL/METHODS: We included in this study 40 rheumatoid arthritis (RA) patients (36 female, four male) and 30 healthy controls (28 female, two male). Disease activity score (DAS28), Health Assessment Questionnaire Disability Index (HAQDI), Rheumatoid Arthritis Disease Activity Index (RADAI) and visual analogue scales (VAS) for pain and arthritis were determined. The concentrations of the following laboratory parameters (serum C-reactive protein (CRP), soluble (s) L-, sP-, sE-selectin, NT-proCNP, IgM rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibodies) were measured using sandwich enzyme-linked immunosorbent assay (ELISA). RESULTS: The concentrations of NT-proCNP in RA patients were significantly increased when compared to healthy controls (p<0.001). In RA patients we found significant correlations only between sE-selectin and NT-proCNP levels (p=0.02). No significant associations were found between serum NT-proCNP and soluble selectin levels and patients' age and sex. Also, the parameters of clinical profile in the RA group (HAQ, RADAI, DAS28, VAS-pain, VAS-arthritis, swollen and tender joint counts) showed no association with serum NT-proCNP, sE-, sP- and sL-selectin. CONCLUSIONS: Serum concentration of NT-proCNP reflecting serum CNP level is likely secondary to the activation of endothelium. Nevertheless, the results of our study encourage to further studies over the role of CNP in the pathogenesis of RA, preferably on tissue level.
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