Mannose binding lectin gene polymorphism and preclinical carotid atherosclerosis in patients with systemic lupus erythematosus.

Patients with systemic lupus erythematosus (SLE) have increased risk of atherosclerosis and CVD that cannot be explained by traditional risk factors. Previous studies indicated that mannose binding lectin (MBL) may modify the development of atherosclerosis. This study was designed to investigate association of MBL gene polymorphism with occurrence of preclinical atherosclerosis in SLE. The study included 46 patients with SLE and 17 age and sex matched controls. MBL2 genotypes were assessed in patients and controls by the PCR-RFLP method and intima-media thickness of the common carotid artery (cclMT) was determined by means of ultrasonography. Also, serological markers were measured and the disease activity index (SLEDAI) was estimated. SLE patients had higher frequency of MBL A/B + B/B genotypes (47.8%) than controls (29.4%). ccIMT was higher in patients having A/B, B/B, A/B+B/B genotypes when compared with wild genotype (A/A). Patients with A/B+B/B genotypes showed high serum level of LDL, TG, ESRI, CRP and SLEDAI score, but low level of HDL, C3, and C4 compared to wild genotype. ccIMT of mutant SLE subgroup correlated well with SLE risk factors for atherosclerosis. In conclusion, mutant genotypes of MBL may be atherogenic as SLE patients had a higher IMT, which correlated significantly with SLE risk factors for atherosclerosis.