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Impaired Arterial Stiffness in Systemic Lupus Ertythematosus - Correlations with Inflammation Markers
Background: Systemic lupus erythematosus (SLE) is an inflammatory disease caused by autoimmune dysregulation, which mainly affects young women, usually free from atherosclerosis. Accelerated atherosclerosis is a well established complication of SLE and it cannot be explained by Framingham risk facto...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medical University Publishing House Craiova
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3994677/ https://www.ncbi.nlm.nih.gov/pubmed/24778842 |
Sumario: | Background: Systemic lupus erythematosus (SLE) is an inflammatory disease caused by autoimmune dysregulation, which mainly affects young women, usually free from atherosclerosis. Accelerated atherosclerosis is a well established complication of SLE and it cannot be explained by Framingham risk factors alone, and has been attributed to complex interactions between traditional risk factors and factors associated with the disease per se, or its treatment. Arterial stiffness and endothelium function may serve as a valuable measure to be counted in the follow-up of these patients prior to a potential cardiovascular event. The aim of the study was to evaluate atherosclerosis, inflammatory process, immune mediated, using imaging techniques and to identify the role of molecules known to be involved in inflammation, hsCRP, homocysteine, IL-6, ESR and fibrinogen, in the development and perpetuation of atherosclerosis in patients with systemic lupus erythematosus. Methods Our prospective study included 53 patients diagnosed with systemic lupus erythematosus and fulfilled the revised ACR (American College of Rheumatology) criteria for the classification of SLE. Exclusion criteria were <18 years of age, history of CVD, infections, diabetes mellitus, dyslipidemia. Results: We enrolled 53 patients with SLE, 50 (94%) women and 3 (6%) men, with a mean age of 31,92 years (SD 5,55; limits 22-44) with no significant difference between sex (31,65±3,4 years in women and 37,33±4,05 years in men). The measurement of inflammation markers revealed increased values for all the variables: ESR had a mean value of 69,19± 14,18mm, fibrinogen 445,66 ±4,56mg%; IL-6 had a mean value of 11,209 ±1,56pg/ml; homocysteine 17,721±2,5374 µmol/l and for hs CRP the mean value was 3,493±1,12 mg/l. The assesement of arterial stiffness showed a mean value of 23,32% (SD 5,82; 95%CI 21,716 - 24,925) for AIx and 9,1m/s (SD 0,49; 95%CI 8,971 - 9,244) for cfPWV. There was a positive, significant correlation between AIx and hsCRP (r=0,612; 95%CI 0,4104 - 0,7576; p<0,001), (r=0,526; 95% CI 0,2979 to 0,6971; p=0,0001), for AIx and homocysteine (r=0,526; 95%CI 0,2979 to 0,6971; p=0,0001). The correlation coefficient with AIx was similar for ESR and fibrinogen (r=0,63 and 0,60). IL-6 and AIx correlated correlated positively, (r=0,369; 95%CI 0,1097 - 0,5813), statistically significant (p=0,006), but the correlation was not powerful. hsCRP and cfPWV were related (r=0,652; 95%CI 0,4677-0,7862; p<0,001); cfPWV also correlated with IL-6 (r=0,6552; 95%CI 0,4677- 0,7862; p<0,0001), homocysteine (r=0,9174; 95%CI 0,8606- 0,9517; p<0,0001), ESR (r=0,74) and fibrinogen (r=0,64). Conclusions: In summary, our data suggest that arterial stiffness is related to the level of systemic inflammation, and that inflammation is involved in the early alteration of arterial wall. Increase in arterial stiffness can be detected by applanation tonometry, and may serve as an important predictor of future cardiovascular events, since an early diagnosis may have a significant value in preventing the development of major vascular disease. |
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