Objective. To make individualised decisions regarding treatment is one of the most important challenges in clinical practise, and identification of sensitive and specific markers of prognosis is an important research question. The main objective of this study was to evaluate relationships between the level of autoantibodies, radiographic changes and laboratory markers of bone, and cartilage destruction. Methods. A total of 114 RA patients were examined. The serum concentration of IgM RF, antibodies to cyclic citrullinated peptide (anti-CCP), modified citrullinated vimentin (anti-MCV), matrix metalloproteinase 3 (MMP-3), and cartilage oligomeric matrix protein (COMP, ng/mL) were measured. The van der Heijde-modified Sharp Score was used to quantify the radiologic changes. Results. Among the patients who were high-positive for anti-MCV, the value of total modified Sharp score (mTSS) (96.5; 66–120) was higher as well as the joint space narrowing (82; 60.5–105.5), and a higher level of MMP-3 was recorded more frequently (56%) in comparison with negative/low-positive patients (57; 31–88, 50; 29–82, 31% resp., ). The level of COMP was also higher among patients high-positive for anti-MCV (9.7; 8.1–13.1 and 6.8; 5.4–10.7, resp., ). Conclusion. A high positive level of anti-MCV as contrasted with anti-CCP and IgM RF is associated with more pronounced destructive changes in the joints. 1. Introduction Rheumatoid arthritis (RA) is one of the most prevailing inflammatory arthropathies that affects primarily able-to-work persons what attributes a high social significance to the disease. Destruction of bone and cartilage is one of the key manifestations of RA [1]. The development of RA is associated with the formation of a wide spectrum of autoantibodies, including rheumatoid factors (RFs) and anti-citrullinated protein antibodies (ACPAs) (antiperinuclear factor, antikeratin antibodies, antibodies to cyclic citrullinated peptide (anti-CCP), modified citrullinated vimentin, anti-MCV, citrullinated fibrinogen, etc.), the presence of which contributes substantially to the course and prognosis of disease [2, 3]. At present, ACPA-positive and ACPA-negative RA subtypes are identified, which differ in molecular mechanisms of pathogenesis, severity course and approaches to the treatment administered [4–6]. ACPA-positive RA is characterized by accelerated radiologic progression, a severe course of the disease with higher total mortality [6, 7]. Hyperproduction of proinflammatory cytokines (interleukins (IL)-1, 6, 17, tumor necrosis factor α— TNF-α) and growth factors in RA
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