TNF-α: a link between hypertriglyceridaemia and inflammation in SLE patients with cardiovascular disease
Identifieur interne : 002057 ( Main/Exploration ); précédent : 002056; suivant : 002058TNF-α: a link between hypertriglyceridaemia and inflammation in SLE patients with cardiovascular disease
Auteurs : E. Svenungsson [Suède] ; G-Z Fei [Suède] ; K. Jensen-Urstad [Suède] ; U. De Faire [Suède] ; A. Hamsten [Suède] ; J. Frosteg Rd [Suède]Source :
- Lupus [ 0961-2033 ] ; 2003-06.
English descriptors
- Teeft :
- Acute phase reactants, Ammation, Ammatory, Ammatory cells, Anticardiolipin antibodies, Arterioscler thromb vasc biol, Arthritis rheum, Atherosclerosis, Atherosclerotic plaques, Ation, Basic characteristics, Blood pressure, Bold font marks signi cance, Cance, Cant, Cantly, Cardiovascular, Cardiovascular disease, Carotid arteries, Case group, Classi cation, Clinical evidence, Clinical manifestations, Continuous variables, Correlation analysis, Cytokine, Density lipoprotein, Detection range, Diabetic patients, Disease activity, Ertrigl yceridaem, Erythematosus, High risk, Higher levels, Homeostasis model assessment, Homocysteine, Homocysteine levels, Human stnf kits, Hypertrigl yceridaem, Important factor, Incidence rates, Independent predictor, Insulin, Insulin resistance, Karolinska hospital, Karolinska institutet, Lipid metabolism, Lipoprotein, Lipoprotein disturbances, Lipoprotein fractions, Lupus, Metabolic characteristics, Metabolic risk factors, Methods section, Myocardial infarction, Necrosis, Nephrotic syndrome, Nity receptors, Plaque, Plaque occurrence, Plasma concentrations, Plasma homocysteine, Plasma insulin, Population controls, Proin ammatory cytokine, Receptor, Rheumatoid arthritis, Risk factor, Risk factors, Sedimentation rate, Signi, Signi cance, Signi cant, Signi cant difference, Signi cantly, Similar lipoprotein changes, Soluble receptors, Soluble tumour necrosis factor receptor, Spearman rank correlation coef cients, Stnfr1, Stnfr2, Svenungsson, Systemic, Systemic lupus, Systemic lupus erythematosus, Triglyceride, Tumor necrosis, Tumor necrosis factor, Vldl, Vldl cholesterol, Yceridaem.
Abstract
Patients with systemic lupus erythematosus (SLE) are at high risk of cardiovascular disease (CVD). Tumour necrosisfactor-a (TNF-α) has been implicatedin the pathophysiologicalprocessesof both SLE and CVD. This study focuses on the role of TNF-α and its soluble receptors in SLE-related CVD. In summary, 26 women (52 + 8.2 years) with SLE and a history of CVD (SLE cases)were compared with 26 age-matched women with SLE and no clinical manifestations of CVD (SLE controls) and 26 age-matched population-based control women (population controls). Plasma concentrations of circulating TNF-α, TNF-α receptor 1 (sTNFR1) and TNF-α receptor 2 (sTNFR2) were determined by ELISA. TNF-α, sTNFR1 and sTNFR2 were raised in SLE cases as compared to SLE controls (P = 0.009; P = 0.001; P = 0.001, respectively), and SLE controls had higher levels than population controls (P = 0.001; P = 0.02; P = 0.001, respectively). Exclusively in the SLE case group there was a striking positivecorrelationbetweenTNF-α and plasma triglycerides(r = 0.57, P < 0.002), VLDL triglycerides (r = 0.54, P = 0.004) and VLDL cholesterol (r = 0.58, P = 0.002). Furthermore, TNF-α correlated with the waist-hip ratio but not with estimated insulin resistance. TNF-α may thus be a major factor in SLE-related CVD acting both by contributing to hypertriglyceridaemia and by promoting atherosclerosis-relatedinflammation. sTNFR1 and sTNFR2 are strongly associated with CVD in SLE but their exact roles in disease development remain to be elucidated.
Url:
DOI: 10.1191/0961203303lu412oa
Affiliations:
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<term>Ammation</term>
<term>Ammatory</term>
<term>Ammatory cells</term>
<term>Anticardiolipin antibodies</term>
<term>Arterioscler thromb vasc biol</term>
<term>Arthritis rheum</term>
<term>Atherosclerosis</term>
<term>Atherosclerotic plaques</term>
<term>Ation</term>
<term>Basic characteristics</term>
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<term>Bold font marks signi cance</term>
<term>Cance</term>
<term>Cant</term>
<term>Cantly</term>
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<term>Cardiovascular disease</term>
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<term>Case group</term>
<term>Classi cation</term>
<term>Clinical evidence</term>
<term>Clinical manifestations</term>
<term>Continuous variables</term>
<term>Correlation analysis</term>
<term>Cytokine</term>
<term>Density lipoprotein</term>
<term>Detection range</term>
<term>Diabetic patients</term>
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<term>Ertrigl yceridaem</term>
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<term>Plasma concentrations</term>
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<term>Signi</term>
<term>Signi cance</term>
<term>Signi cant</term>
<term>Signi cant difference</term>
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<term>Tumor necrosis</term>
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<front><div type="abstract" xml:lang="en">Patients with systemic lupus erythematosus (SLE) are at high risk of cardiovascular disease (CVD). Tumour necrosisfactor-a (TNF-α) has been implicatedin the pathophysiologicalprocessesof both SLE and CVD. This study focuses on the role of TNF-α and its soluble receptors in SLE-related CVD. In summary, 26 women (52 + 8.2 years) with SLE and a history of CVD (SLE cases)were compared with 26 age-matched women with SLE and no clinical manifestations of CVD (SLE controls) and 26 age-matched population-based control women (population controls). Plasma concentrations of circulating TNF-α, TNF-α receptor 1 (sTNFR1) and TNF-α receptor 2 (sTNFR2) were determined by ELISA. TNF-α, sTNFR1 and sTNFR2 were raised in SLE cases as compared to SLE controls (P = 0.009; P = 0.001; P = 0.001, respectively), and SLE controls had higher levels than population controls (P = 0.001; P = 0.02; P = 0.001, respectively). Exclusively in the SLE case group there was a striking positivecorrelationbetweenTNF-α and plasma triglycerides(r = 0.57, P < 0.002), VLDL triglycerides (r = 0.54, P = 0.004) and VLDL cholesterol (r = 0.58, P = 0.002). Furthermore, TNF-α correlated with the waist-hip ratio but not with estimated insulin resistance. TNF-α may thus be a major factor in SLE-related CVD acting both by contributing to hypertriglyceridaemia and by promoting atherosclerosis-relatedinflammation. sTNFR1 and sTNFR2 are strongly associated with CVD in SLE but their exact roles in disease development remain to be elucidated.</div>
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