Plasminogen activator inhibitor-1 polymorphisms (−844 G>A and HindIII C>G) in systemic lupus erythematosus: association with clinical variables

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of autoantibodies against nuclear autoantigens as well as cytoplasmic and circulating proteins. Recent studies have demonstrated mechanisms responsible for modulation of the immune response by the plasminogen activator inhibitor-1 (PAI-1). Furthermore, the endogenous PAI-1 has shown to promote a Th2 immune response. We assessed the −844 G>A and Hin dIII C>G PAI - 1 polymorphisms in SLE. In a case–control study of 71 SLE patients classified according to ACR criteria and 71 healthy subjects (HS). The A allele of −844 PAI - 1 polymorphism showed a significant difference in SLE patients (41%) when compared with HS (27%) [ P = 0.01; OR = 1.8, 95%, CI = 1.1–3.0]. In addition, the −844 G>A PAI - 1 polymorphism was associated with increased risk for SLE in a dominant genetic model (G/G vs. G/A + A/A; OR = 2.3, 95% CI = 1.14–4.44). Also, anti-RNP positive antibodies in SLE were associated with G/G −844 PAI - 1 genotype. The Hin dIII polymorphism did not show any differences. The haplotype analysis showed that the AC haplotype confers susceptibility to SLE (OR = 3.1, 95% CI, 1.45–6.52; P = 0.003). The AC haplotype of the −844 and Hin dIII PAI - 1 polymorphism might be an additional susceptibility factor to SLE in Mexicans.