Patients with systemic lupus erythematosus (SLE) have increased risk of atherosclerosis and cardiovascular disease (CVD) that cannot be explained by traditional risk factors. Several studies indicate that mannose-binding lectin (MBL) may modify the development of atherosclerosis. The study was designed to investigate association of MBL gene polymorphism with occurrence of preclinical atherosclerosis in systemic lupus erythematosus patients. The study was carried out on 46 patients with SLE and 17 age and sex matched healthy volunteers as control group. MBL2 genotypes were assessed in patients and controls by polymerase chain reaction restriction fragment length polymorphism methods and intima-media thickness of the common carotid artery (ccIMT) was determined by means of ultrasonography. In addition, lipogram profile, ESR, CRP, anti-ds DNA antibodies and C3, C4 were measured and disease activity index (SLEDAI) was estimated. Frequency of A/B + B/B genotypes of MBL was significantly higher in SLE patients (47.8%) compared to controls (29.4%). ccIMT was significantly increased 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 significant increase in serum LDL, TG, ESRI, CRP and SLEDAI score, and significant decrease in HDL, C3, and C4 compared to wild genotype. ccIMT of mutant SLE subgroup was significantly correlated with SLE related risk factors for atherosclerosis.

In conclusion: The mutant genotypes of MBL may be atherogenic and their SLE patients had a higher IMT which correlated significantly with SLE related risk factors for atherosclerosis. Further studies should focus on the mechanisms by which MBL and MBL genotypes affect atherosclerosis development.