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Increased intima-media thickness to show relationship between atherosclerosis and inflammation in a human model: patients affected by rheumatoid arthritis and absence of common markers of atherosclerosis Abstract number: P0689 Di Micco* P., Cuomo G., Niglio A., Abbadessa S., Valentini G. Division of Rheumatology, 2nd University of Naples, Italy; Internal Medicine, 2nd University of Naples, Italy *Internal Medicine, Secon University of Naples, Italy; The relationship between inflammation and atherosclerosis (ATS) has often been demonstrated. In particular, cytokines as TNF and IL-1 seem to be involved in atherogenesis. Yet, TNF and IL-1 are involved also in phlogosis induced by rheumatoid arthritis (AR). Morbidity and mortality of patients affected by AR are often related to ATS-related cardiovascular events. We studied intima-media thickness (IMT) and common ATS risk factors in AR patients. We studied 21 patients affected by AR (6 M and 15 F, mean age 55 ± 4 years, 15 with rheumatoid factor, RF, and 6 without RF) and 11 patients 4 M and 7 F (mean age 52 ± 6 years) as control group. We researched erythrosedimentation rate (ESR) and acute phase C reactive protein (CRP), markers of phlogosis, and common ATS risk factors (hypertension, total cholesterol, HDL-ch., LDL-ch., APO-A, APO-B, triglycerides, body mass index). We excluded smokers and patients affected by diabetes. AR activity was investigated by activity index of disease (DAS 28). IMT was investigated by ultrasonography (US) on carotid arteries. Statistical analysis was made by Mann and Whitney test. Total cholesterol (195 ± 31 mg dL-1 vs. 173 ± 26 mg dL-1), LDL-ch. (102 ± 33 mg dL-1 vs. 95 ± 28 mg dL-1), HDL-ch. (65 ± 30 mg dL-1 vs. 58 ± 20 mg dL-1) and triglycerides (160 ± 61 mg dL-1 vs. 122 ± 55 mg dL-1) were higher in control group than in AR patients, but these values did not reach statistical significance. However, APO-A (241 ± 61 mg dL-1 vs. 167 ± 52 mg dL-1) were significantly higher in control group than in AR patients, while APO-B were higher in AR patients than in control group (117 ± 46 mg dL-1 vs. 153 ± 36 mg dL-1). Phlogosis markers were significantly higher in AR patients than in control group (ESR 40 ± 23 mm vs. 10 ± 7 mm; CRP 5 ± 4.0 mg dL-1 vs. 0 ± 1.5 mg dL-1). IMT was significantly higher in AR patients than in control group too (1.0 ± 0.3 mm vs. 0.7 ± 0.3 mm). We found additional carotid plaques in two patients with AR as one of control group. Phlogosis is often investigated as cause of ATS. Our data showed an increased IMT in AR patients during an active phase of the disease and seem to confirm this hypothesis. Common ATS risk factors (exclude diabetes and cigarettes) were similar in both group, while phlogosis markers were high only in AR patients. However, only AR patients showed an increased IMT as markers of ATS, confirming the role of phlogosis in this field. Yet, further studies in experimental and human model and on a large based population are needed to confirm our data. |
To cite this abstract use the following format:
Journal of Thrombosis and Haemostasis 2003; 1 Supplement 1 July: abstract number
Session Details
| Date: | 14/07/2003 |
| Time: | 09:30-11:00 |
| Session name: | TTP/HUS |
| Subject: | Atherogenesis |
| Location: | Hall 3 |
| Presentation type: | Symposium |
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