Dyslipidemia in rheumatoid arthritis: the possible mechanisms

Area of Science:

• Cardiovascular Science
• Rheumatology
• Immunology

Background:

• Rheumatoid arthritis (RA) is an autoimmune inflammatory disease.
• Cardiovascular disease (CVD) is the leading cause of mortality in RA patients.
• RA is associated with a unique lipid profile, including decreased total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c), particularly under hyperinflammatory conditions, termed the "lipid paradox".

Purpose of the Study:

• To comprehensively review the existing literature on the unique lipid profile in RA.
• To explore the underlying mechanisms driving lipid alterations in RA.
• To investigate the impact of these lipid changes on the increased risk of CVD in RA patients.

Main Methods:

• Literature review integrating the latest research.
• Analysis of systemic inflammation markers, including interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor alpha (TNF-α).
• Examination of the effects of inflammation on HDL particle structure and function, and LDL oxidation.

Main Results:

• Systemic inflammation in RA, driven by proinflammatory cytokines, alters HDL subcomponents and structure, diminishing its anti-atherosclerosis function.
• Inflammation promotes LDL oxidation and plaque formation, contributing to CVD risk.
• Dysfunctional HDL exacerbates LDL metabolism abnormalities, further increasing cardiovascular risk.

Conclusions:

• The "lipid paradox" in RA is explained by systemic inflammation that leads to dysfunctional lipids and increased CVD risk.
• Understanding these mechanisms is crucial for managing cardiovascular complications in RA patients.
• Further research is needed to elucidate the precise molecular pathways linking RA, lipid dysregulation, and atherosclerosis.