Background: SLE is a chronic autoimmune disease of unknown etiology. pNL is the most frequent complication with the worst prognosis. A chronic systemic inflammatory cascade with high atherogenic and procoagulant potential occurs in SLE. Atheromatosis is a multifactorial inflammatory subclinical process, which is the basis of the plaques that lead to cardiovascular disease in pSLE. Adipokines play a role in atherosclerosis and it is a risk for stroke associated with SLE. The aim of this study was to evaluate the association of serum Leptin and Adiponectin and SNP polymorphisms of the MTHFR (A1298C) and FGG (C10034T) genes, which are associated with metabolic pathways of Atheromatosis in pLN.
Methodology: This was a cross-sectional analytical observational study of pLN. Cases (n = 98) and controls (n = 100), chosen by simple random sampling from a nested cohort of one our previous pLN project. Serum concentrations of Leptin and Adiponectin were performed by ELISA. Polymorphisms of the MTHFR (A1298C) and FGG (C10034T) genes were performed by qPCR. The statistical significance was interpreted as p<0.05.
Results and conclusions: In the present study, a statistically significant difference was found between the serum Leptin and Adiponectin pNL subjects levels when those were compared with the controls (p = 0.00). No association was found between the SNPs polymorphisms of the FGG and MTHFR genes with NLp subjects, however, when analyzing the influence of these polymorphisms on the serum adipokines, a relationship was found between the genotypes of the MTHFR gene and FGG with these adipokines.