Association between rheumatoid arthritis activity and atherosclerosis

We assessed atherosclerosis as a risk factor in rheumatoid arthritis [RA] patients who experience excess atherosclerosis and cardiovascular risk. They were compared with osteoarthritis [OA] patients as a control group. The severity of atherosclerosis remains to be determined through carotid intima-media thickness [IMT] as a reflector for systemic atherosclerosis. The study was performed on 30 RA patients without history of cardiovascular accidents. The severity of carotid atherosclerosis was evaluated with the mean max IMT, i.e., mean of the maximal wall thickness at carotid segments. Serum level of IL-18 was measured in both RA and OA groups. Erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP] were used to measure systemic inflammation. The relationship of the carotid artery IMT with inflammatory markers was examined in RA versus OA as a control. IL-18 concentration was higher in RA versus OA and it positively correlated with IMT, p<0.05. Lipid profile was also higher in RA than OA and positively correlated with CRP, ESR and IL -18 serum level hyperlipidemia and body mass index [BMI], p<0, 05, We demonstrated an association between higher serum IL-18 level and atherosclerotic risk factors. Increased liability of atherosclerosis has the link between IL-18 and atherosclerosis. So, inflammation and cardiovascular risk factors interact to enhanced atherosclerosis in RA patients. Our findings need more evaluation in large study groups with cardiovascular risk profiles

Tissue plasminogen and plasminogen activator inhibitor-1 serum level in osteoarthritis and rheumatoid arthritis patients

The activity of tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1 [PAI-1] in the plasma of 40 rheumatoid arthritis [RA] patients [Gl] and 10 osteoarthritis [OA] patients [G2] was measured. Group I mean age was 40.95 +/- 3.57 and the duration of disease was 91.65 +/- 37.93 weeks. Group II mean age was 50.87 +/- 5.39 and the duration of disease was 77.43 +/- 12.75 weeks. Ten apparently healthy subjects were examined as a control group [G3]. Their mean age was 25.44 +/- 10.45. The relationship between plasma t-PA and PAI-1 and their correlation with disease activity were studied in patients with rheumatoid arthritis [RA=G1] and [OA=G2], and control group a comparative study group showed that, RA Gl increased t-PA and PAI-1 activity, in comparison with OA patients and control group. In addition, there was an imbalance between plasminogen activator inhibitor-type 1 [PAI-1] and t-PA in RA than OA patient or control. These results show an alteration of the PAI-1/t-PA system in RA, which increases with disease activity. This alteration may play a role in joint destruction in RA