Tumor necrosis factor α, interleukin-6 and interleukin-10 polymorphisms in preeclampsia
Journal of Obstetrics and Gynaecology Research, cilt.36, sa.1, ss.64-71, 2010 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 36 Sayı: 1
- Basım Tarihi: 2010
- Doi Numarası: 10.1111/j.1447-0756.2009.01111.x
- Dergi Adı: Journal of Obstetrics and Gynaecology Research
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.64-71
- Anahtar Kelimeler: cytokine, metabolic syndrome, polymorphism, preeclampsia
- Kırklareli Üniversitesi Adresli: Evet
Özet
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. © 2010 Japan Society of Obstetrics and Gynecology.