Background. Rheumatoid arthritis (RA) is a chronic inflammatory and systemic disease of unknown etiology that primarily affects synovial joints and involves progressive destruction around the joints. Inflammation starting in the joint synovium causes the destruction of cartilage, bone and other adjacent tissues with pannus formation. Objectives. The aim of this study was to evaluate serum matrix metalloproteinase-3 (MMP-3) levels and their clinical and radiological significance in patients with rheumatoid arthritis. Material and methods. The study included 59 patients with RA and 30 healthy controls. Serum MMP-3 levels were measured using the enzyme-linked immunosorbent assay (ELISA) method. Patients with a Disease Activity Score 28 (DAS28) ≤3.2 were categorized as having lower disease activity, while a DAS28 score >3.2 indicated patients with moderate/high disease activity. Additionally, the patients were divided into 2 groups in terms of disease duration: early RA (disease duration ≤2 years) and established RA (disease duration ≥2 years). Functional disability was evaluated using the Health Assessment Questionnaire (HAQ) and Nottingham Health Profile (NHP). Radiographs were scored using modified Larsen scoring. Results. Serum MMP-3 levels in patients with RA were significantly higher than in controls (p = 0.001). Serum MMP-3 levels were correlated with laboratory and clinical parameters of disease activity, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), DAS28, and HAQ score; the exceptions were rheumatoid factor (RF) and cyclic citrullinated peptides (CCP). The serum MMP-3 levels of RA patients with moderate/high disease activity were found to be significantly higher than those of the patients with low disease activity (p < 0.001). However, MMP-3 levels were found to be similar in both established and early RA patients (p = 0.927). Additionally, the modified Larsen scores, which indicate structural damage, correlated significantly with serum MMP-3 levels (p = 0.001). Conclusions. These results indicate that serum MMP-3 levels may be used as an indicator for structural damage such as erosions in the early stages of the disease, and to monitor disease activity.
Paraoxonase 1 (PON 1) is a high-density lipoprotein (HDL)-associated enzyme with antioxidant function protecting low-density lipoprotein (LDL) from oxidation. PON 1 has two amino acid polymorphisms in coding region; L/M 55 and Q/R 192. These polymorphisms modulate paraoxonase activity of the enzyme. PON 1 activity decreases in coronary artery disease (CAD). In the present study, distribution of PON 1 L/M 55 and Q/R 192 polymorphisms and the effect of these polymorphisms on the activities of PON 1, and on the severity of CAD in 277 CAD (+) patient and 92 CAD (-) subjects were examined. PON 1 L/M 55 and Q/R 192 genotypes were determined by PCR, RFLP and agarose gel electrophoresis techniques. Genotype distributions and allele frequencies for PON 1 Q/R 192 polymorphism were not significantly different between controls and CAD (+) patient group (p > 0.05), but in genotype and allele distribution of PON 1 L/M55 polymorphism, there was significantly difference among groups (p < 0.05). Genotype distributions for both polymorphisms were not significantly different between subgroups of single-vessel disease (SVD), double-vessel disease (DVD) and triple-vessel disease (TVD). Serum PON 1 activity was lower in CAD (+) group than in controls and this was also statistically significant (p < 0.001). In both groups, the highest PON activities were detected in LL and RR genotypes. In summary, our results suggest that there is an association between the PON 1 L/M 55 polymorphism of paraoxonase and CAD in Turkish patients but not with PON 1 Q/R 192 polymorphism. However, it is hard to correlate these polymorphisms and severity of CAD.
The cholesteryl ester transfer protein (CETP) plays a crucial role in high-density lipoprotein (HDL) metabolism. Genetic variants that alter CETP concentration may cause significant alterations in HDL-cholesterol (HDL-C) concentration. In this case-control study, we analyzed the genotype frequencies of CETP Taq1B polymorphisms in coronary artery disease patients (CAD; n=210) and controls (n=100). We analyzed the role of the CETP Taq1B variant in severity of CAD, and its association with plasma lipids and CETP concentration. DNA was extracted from 310 patients undergoing coronary angiography. The Taq1B polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism (RFLP) analysis. Lipid concentrations were measured by an auto analyzer and CETP level by a commercial enzyme-linked immunosorbent assay (ELISA) kit. In our study population, the B2 allele frequency was higher in control subjects than patients with single, double or triple vessel disease. B2B2 genotype carriers had a significantly higher high-density lipoprotein cholesterol (HDL-C) concentration than those with the B1B1 genotype in controls (51.93±9.47versus 45.34±9.93; p<0.05) and in CAD patients (45.52±10.81 versus 40.38±9.12; p<0.05). B2B2 genotype carriers had a significantly lower CETP concentration than those with the B1B1 genotype in controls (1.39±0.58 versus 1.88±0.83; p< 0.05) and in CAD patients (2.04±1.39versus 2.81±1.68; p< 0.05). Our data suggest that the B2 allele is associated with higher concentrations of HDL-C and lower concentrations of CETP, which confer a protective effect on coronary artery disease.
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