الفهرس 
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Abstract
RA patients have high prevalence of subclinical carotid atherosclerosis, which can be recognized by ultrasound, thus help to identify patients with increased CVD risk. Traditional CV risk factors still not fully explain the higher incidence of CVD in RA and this risk may be associated with other features specific for RA, such as the systemic inflammation, disease duration and specific RA therapies. Sixty percent of the risk for RA is due to genetic causes which also account for 30%–60% of the risk in CVD. The human OPG gene (TNFRSF11B) can be affected by genetic polymorphisms which could have functional consequences on CVD and bone homeostasis. Also tissue samples of the synovium from the joints of RA patients expressed OPG, suggesting that OPG could have a possible role in the pathogenesis of both atherosclerosis and RA.
This study aimed to assess the association between serum OPG level and the OPG gene polymorphism (rs2073618) with RA and markers of subclinical atherosclerosis in a group of RA Egyptian patients and to find their relation to the demographic, clinical, laboratory and disease activity parameters in RA patients. This study was performed on 80 RA patients diagnosed according to the 2010 (ACR/EULAR) classification criteria for RA. RA patients were divided into, 38 RA patients with atherosclerosis (group I), 42 RA patients without atherosclerosis (group II) based on carotid ultrasound findings. Forty age and sex healthy volunteers were selected to serve as control group. All patients subjected to complete history taking , thorough clinical examination, Laboratory assessment, activity of RA was defined by DAS 28 and ability to perform daily living activities was measured using the (m-HAQ).
Carotid atherosclerosis was evaluated by high resolution ultrasound, rs2073618 OPG genotyping was performed by PCR, and serum OPG concentrations were measured by ELISA after which comparisons were performed between RA patients and control group.
The mean CIMT was significantly higher in RA patients in comparison to control group and it was significantly higher in RA patients with moderate to severe disease activity in comparison to those with low disease activity or in remission. Serum OPG levels were significantly higher in RA patients compared to controls and was higher in RA patients with atherosclerosis compared to those without atherosclerosis, also OPG’s titre was significantly higher in RA patients with carotid atheromatous plaque in comparison to those without atheromatous plaque.
Serum OPG level had positive significant correlation with RA disease duration; SBP; hs-CRP; Anti CCP; DAS 28 ESR; DAS 28 CRP; m-HAQ and Mean CIMT. There was no statistically significant difference among neither CC, CG, GG genotypes nor C, G alleles of the studied OPG gene among all of the studied groups.