OBJECTIVE: To assess a possible relation between proinflammatory mediators (IL-1R1, IL-12, IL-18, TLR-2, and TLR-4) gene polymorphisms and preeclampsia (PE). METHODS: Genotyping was performed on 109 preeclamptic patients and 174 healthy fertile women with at least two previous successful pregnancies (controls). χ(2) or Fisher's exact test were used to compare genotype frequencies. The control group included 174 pregnant women matched by race to the study group. RESULTS: Genotypic and allelic distributions for all six polymorphisms were similar between the study and control groups. IL-1R1 (PstI, rs2234650): p = 0.82 ; IL-12 (+1188, rs3212227): p = 0.93; IL-18 (-137, rs187238): p = 0.74 ; IL-18 (-607, rs1946519): p = 0.22; TLR-2 (+2258, rs5743708): p = 0.97; and TLR-4 (+896, rs4986790): p = 0.23. CONCLUSION: The analyzed gene polymorphisms are not associated with PE.
OBJECTIVE: To assess a possible relation between proinflammatory mediators (IL-1R1, IL-12, IL-18, TLR-2, and TLR-4) gene polymorphisms and preeclampsia (PE). METHODS: Genotyping was performed on 109 preeclamptic patients and 174 healthy fertile women with at least two previous successful pregnancies (controls). χ(2) or Fisher's exact test were used to compare genotype frequencies. The control group included 174 pregnant women matched by race to the study group. RESULTS: Genotypic and allelic distributions for all six polymorphisms were similar between the study and control groups. IL-1R1 (PstI, rs2234650): p = 0.82 ; IL-12 (+1188, rs3212227): p = 0.93; IL-18 (-137, rs187238): p = 0.74 ; IL-18 (-607, rs1946519): p = 0.22; TLR-2 (+2258, rs5743708): p = 0.97; and TLR-4 (+896, rs4986790): p = 0.23. CONCLUSION: The analyzed gene polymorphisms are not associated with PE.