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TNF-alpha: a link b...
TNF-alpha: a link between hypertriglyceridaemia and inflammation in SLE patients with cardiovascular disease
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- Svenungsson, E (författare)
- Karolinska Institutet
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Fei, GZ (författare)
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- Jensen-Urstad, K (författare)
- Karolinska Institutet
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- de Faire, U (författare)
- Karolinska Institutet
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- Hamsten, A (författare)
- Karolinska Institutet
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- Frostegard, J (författare)
- Karolinska Institutet
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(creator_code:org_t)
- 2016-07-02
- 2003
- Engelska.
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Ingår i: Lupus. - : SAGE Publications. - 0961-2033 .- 1477-0962. ; 12:6, s. 454-461
- Relaterad länk:
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http://kipublication...
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https://doi.org/10.1...
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Abstract
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- 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.
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