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Increased cardiovascular morbidity and mortality has been documented in several chronic inflammatory rheumatic diseases. In addition to the traditional cardiovascular risk factors, disease activity itself may contribute to this increase.
Tumour necrosis factor (TNF)-α, a pivotal cytokine in chronic inflammation, also affects lipid metabolism, insulin resistance and endothelial function. Therapeutic use of TNF-α blockers reduces inflammation and modifies the lipoprotein spectrum of patients. A significant increase in high-density lipoprotein (HDL) cholesterol levels has been documented after short-term infliximab therapy.1–5 However, this beneficial effect seems to be transient and more prolonged use of TNF-α blockers may lead to an increase in total cholesterol and low-density lipoprotein (LDL) cholesterol, inducing a more “atherogenic” phenotype.6 7
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