ELEVATED LIPOPROTEIN(a) IN SYSTEMIC LUPUS ERYTHEMATOSUS

Background – The underlying mechanism(s) for the development of premature atherosclerosis in patients with systemic lupus erythematosus (SLE) is not precisely understood. In recent years, lipoprotein(a) [Lp(a)] has emerged as a valuable predictor as well as an independent risk factor for premature atherosclerosis. The objective of this study was to determine blood Lp(a) levels in SLE patients, and to determine whether increased levels are a contributing factor to the development of atherosclerotic complications of SLE. Methods – Serum Lp(a) levels were measured by enzyme immunoassay in 37 SLE patients, nine of their apparently healthy siblings and 35 healthy controls. Student.s t test was used for statistical comparisons. Results – Our data showed a higher frequency of enhanced Lp(a) levels (> 30 mg/dL) in SLE patients as compared with that observed in healthy controls (51.4% vs 25.7%). Analysis of lipid profiles in SLE patients also revealed significantly higher levels of triglycerides as compared with controls (165 ± 16 vs 100 ± 6 mg/dL, p = 0.001). Serum Lp(a) levels were not different between patients with or without glucocorticoids, hospitalization and disease exacerbation (p values equal to 0.9, 0.7 and 0.6, respectively. Moreover, there was no significant difference in serum Lp(a) concentration between nine SLE patients and their siblings (34 ± 11.8 vs 37.3 ± 12.8 mg/dL; p = 0.8). Conclusion – Increased Lp(a) levels are more likely to be encountered in patients with SLE than in healthy subjects. Lp(a) blood levels in SLE, as in healthy individuals, seem to represent a genetically predetermined trait.