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Tumor necrosis factor α, interleukin‐6 and interleukin‐10 polymorphisms in preeclampsia
Author(s) -
Vural Pervin,
Degirmencioglu Sevgin,
Saral Neslihan Y.,
Demirkan Ayse,
Akgul Cemil,
Yildirim Gokhan,
Issever Halim,
Eroglu Hacer
Publication year - 2010
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/j.1447-0756.2009.01111.x
Subject(s) - genotype , medicine , preeclampsia , single nucleotide polymorphism , allele , tumor necrosis factor alpha , interleukin 6 , interleukin , immunology , pregnancy , allele frequency , cytokine , endocrinology , gene , genetics , biology
Aim: Preeclampsia (PE) is one of the most serious disorders of pregnancy. The imbalance between pro‐ and anti‐inflammatory cytokines may play a role in its etiology. The aim of the present study was to investigate whether cytokine gene polymorphism is associated with PE, and to evaluate the relationship between genotypes and clinical/laboratory manifestation of PE. Methods: We investigated single nucleotide polymorphisms of tumor necrosis factor (TNF)α(‐308 G/A), interleukin (IL)‐6 (‐174 G/C), IL‐10 (‐1082 G/A) genes in DNA from peripheral blood leukocytes of 101 PE patients and 95 healthy control women. Results: In PE, there was a significant increase of the IL‐10 (‐1082) A allele frequency ( P = 0.04). No significant differences were found in genotypes or allele frequencies of TNFα(‐308) and IL‐6 (‐174) genes between PE women and controls. While TNFα(‐308) and IL‐6 (‐174) genotypes did not influence clinical/laboratory parameters in PE, IL‐10 (‐1082) A allele carrying genotypes (AG + AA) were associated with higher glucose and lower HDL‐cholesterol levels. Conclusion: Because women with IL‐10 (‐1082) AA genotype have 3.38‐fold increased risk of developing PE according to GG genotype (95% CI 1.21–9.4, P = 0.01), we suggest that IL‐10 (‐1082) variant A allele is associated with an increased risk of preeclampsia, which is independent from its metabolic effects.