Abstract:
Background. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease
characterized by systemic inflammation that affects multiple organs and systems.
Dyslipidemia is common in SLE, contributing to an increased cardiovascular risk, influenced
by inflammatory, immunological, and therapeutic factors.
Objective(s). Analysis and synthesis of recent data regarding the prevalence, mechanisms,
and impact of dyslipidemia in SLE, as well as the evaluation of the role of treatment in
altering the lipid profile.
Materials and methods. Recent scientific studies and data from international literature,
accessed through PubMed, Medscape, and ScienceDirect, were reviewed and integrated,
exploring the correlations between SLE, dyslipidemia, and cardiovascular risk. This analysis
highlights the pathogenic mechanisms and clinical consequences for patients.
Results. Dyslipidemia affects 36% to 60% of patients with SLE and is caused by chronic
inflammation (IL-6, TNF-α, CRP), oxidative stress (activation of Th1/Th17 cells, oxysterols,
anti-LDL autoantibodies), as well as hormonal and metabolic disturbances. These changes
disrupt lipid metabolism, promoting early atherosclerosis characterized by increased
triglycerides, LDL, total cholesterol, and decreased HDL. Glucocorticoids worsen
dyslipidemia, whereas hydroxychloroquine, statins, and certain biologic therapies (e.g.,
rituximab, belimumab) have demonstrated benefits by lowering triglycerides and increasing
HDL levels effectively.
Conclusion(s). The high prevalence of dyslipidemia in SLE significantly increases
cardiovascular risk. The involved mechanisms are complex and include chronic
inflammation, oxidative stress, and immune dysfunction. Effective therapy with statins,
antimalarials, and immunosuppressants improves the lipid profile.
