The apolipoprotein E2 isoform is associated with accelerated onset of coronary artery disease in systemic lupus erythematosus

Background: Systemic lupus erythematosus (SLE) is a highly prevalent autoimmune disease and coronary artery disease (CAD) is a complication of SLE which is often crucial for the patient’s prognosis. It is hypothesized that apolipoprotein E (Apo E), which is involved in cholesterol metabolism, might play a role in this process. Material/Methods: Patients with SLE registered at the University of Toronto Lupus Clinic who had DNA available for study had their Apo E genotype determined. Each case was assessed for the presence of CAD, and Apo E allele frequencies in patients with SLE were compared with data from the general population. Age at onset and disease duration of CAD were also recorded and compared between groups. Results: DNA was stored from 152 patients, of whom 38 (25%) had CAD. There was no difference in the frequencies of the Apo E isoforms between SLE patients and the general population. Patients with the E2 allele developed CAD after a mean ±SD of 6.0±1.9 yrs compared with 14.5±5.4 yrs in those with E3/3 (p<0.01). Conclusions: The distribution of Apo E genotypes in SLE is not significantly different from that of the North American population. In SLE, Apo E2 was associated with a more rapid development of CAD. Therefore, Apo E2 might interact with other disease-related factors to accelerate the onset of CAD in some patients with SLE and as such might be an additional marker of risk in this population.