Intergenotypic Variation of Endothelial Dysfunction and Inflammatory Markers in Eclampsia

Abstract

Background. Cytokine imbalance and endothelial dysfunction are suggested to have a pivotal role in eclampsia. Pathophysiological processes are influenced by genetic factors and nitric oxide (NO) synthases seem to play important roles, although their role is still unclear. Endothelial NO synthase (eNOS) gene polymorphism may affect cytokine production. The aim of this study was to test the hypothesis that inflammatory cytokines impairs endothelium-dependent relaxation and NO production gets vitiated due to eNOs Glu298Asp gene polymorphism causing endothelial dysfunction in eclampsia. Methods. This cross-sectional study included 100 women with eclampsia and 100 healthy pregnant women. Their blood samples were analyzed for NO (indirectly), and inflammatory cytokines and eNOS (Glu298Asp) gene polymorphism were determined by DNA extraction, followed by restriction fragment length polymorphism. Results. Decreased NO metabolites and increased cytokines (tumor necrosis factor-α; interleukin-2, -6; and interferon-γ) levels were found in eclampsia (p < 0.001). Significant differences were found in genotype/allele distribution between the two groups. Occurrence of “T” allele frequency was found to be 0.27 among patients and 0.05 among controls (CI = 95%, OR = 0.7–0.9, p < 0.001). Significant negative correlation was seen between NO and cytokines levels (tumor necrosis factor-α and interferon-γ) in eclamptic women (p = 0.001). Conclusion. This study concluded that eclampsia is associated with decreased levels of NO and increased levels of circulating inflammatory cytokines, which might be contributed due to single-nucleotide polymorphism, pointing toward the role of endothelial and inflammatory components.

• Eclampsia
• Polymorphism
• Cytokines
• eNOS