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Atherosclerotic cardiovascular disease (CVD) is the leading cause of death worldwide1. Although many genetic and environmental factors contribute to CVD, lipoproteins remain the pivotal agents in atherosclerosis1. Patients with rheumatoid arthritis (RA) experience a 2- to 3-fold increased risk for atherosclerotic CVD, a phenomenon that is likely attributable to unfavorable effects of cytokine-mediated high-grade inflammation on traditional risk factors such as insulin sensitivity and its direct adverse effects on the vasculature2. The ameliorations in traditional CV risk factor profiles3–5 and interleukin 6-related endothelial dysfunction6 upon disease activity suppression in RA support this paradigm.Considering the fundamental role of dyslipidemia in atherosclerosis in non-RA subjects prompts the question whether RA characteristics alter lipoprotein profiles. Such potential interactions have been the topic of numerous studies performed over the past 3 to 4 decades. As applies to other inflammatory conditions7, high-grade inflammation or disease activity in the context of RA results in a reduction in total and low-density lipoprotein (LDL) cholesterol and a more consistent and marked decrease in high-density lipoprotein (HDL) cholesterol, thereby increasing the atherogenic index, i.e., the total cholesterol/HDL cholesterol ratio3,4. Treatment with traditional disease modifying agents for rheumatic disease (DMARD) and glucocorticoids reverses these changes3,4, an effect that may be less consistent with tumor necrosis factor-α blockade8. The increase in total and LDL cholesterol with traditional DMARD therapy can be prevented by insulin sensitivity-enhancing dietary intervention3.Currently recommended treatment strategies generally comprise aggressive use of DMARD as soon as the disease is diagnosed. As a consequence, the typical RA patients may now no longer experience high-grade inflammation-induced dyslipidemia except during the time prior to seeking medical care. In this new era, then, do lipoprotein profiles … Address correspondence to Dr. P. Dessein, PO Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: dessein{at}telkomsa.net

Which Are the Determinants of Dyslipidemia in Rheumatoid Arthritis and Does Socioeconomic Status Matter in This Context?