Atherogenesis in Systemic Lupus Erythematosus: The Role of Production of Autoantibodies to Apolipoprotein A-1 and High-Density Lipoproteins

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease associated with production of many autoantibodies. Patients with systemic lupus erythematosus (SLE) are at increased risk for the development of premature atherosclerosis which could be related to production of au-toantibodies against the anti atherogenic lipoproteins, independent from the traditional risk factors. Objective: The present study aims at determination of whether antibodies against high-density lipoprotein (aHDL) and apolipoprotein A-I (aApo A-I) interfere with the anti-atherogenic anti-inflammatory functions of high-density lipoprotein (HDL) and relate to disease activity in SLE, which may play role in premature atherosclerosis in those patients. Patients and Methods: This work included 75 subjects, composed of 50 female patients justyfing the diagnostic ACR criteria and 25 control subjects. Certain exclusion criteria were established to minimize the multiplicity of factors affecting the atherogenesis process including; DM, anti-phospholipid, renal disease, liver disease, familial dyslipidemia, acute infection and finally hypothyroidism. The subjects enrolled in this study were subjected to full detailed-taking history and clinical examination and activity assessment by using SLEADI. Laboratory testing involved measurement of CBC, ESR, C-RP, LKF tests, FBS, Lipid profile, uric acid, ANA, AdNA, C3, C4, Anticardiolipin lupus anticoagulant. Also anti-HDL anti-Apo A1 antibodies, PON, MDA as well as TAC were measured in the study groups. All subjects were underwent ultrasonographic assessment for measuring Carotid intima media thickness (CIMT). Results: In the present study, it was found that there was elevated levels of total cholesterol, LDL with decreased HDL in patients compared to controls (p-value 0.001). The current study revealed that the level of anti-HDL anti-Apo A1 antibodies were significantly higher in patients than control group (p-value 0.001). Also PON and TAC measurements were decreased in patients relative to controls (p-value 0.001). CIMT in patients was higher relative to controls with statistical significance (p-value 0.05). In this study, there was a statistically significant positive correlation between IMT versus anti-HDL and anti-Apo A1 with (p-value 0.001); however there was no relation between the levels of anti-HDL anti-Apo A1 either with disease duration or SLEADI (p-valu 0.05). Anti-HDL is considered better positive than negative test with higher sensitivity and more validity than anti-Apo A1 (sensitivity 99% specificity 88%). Conclusion: The results of our study support the recent concept of atherosclerosis pathogenesis as an immune mediated disease and supported the role of autoantibodies to the protective lipoproteins in SLE as a cause of premature atherosclerosis in those patients.