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Objective: Preterm delivery is an important cause of perinatal death, accounting for 5-15% of the total number of deliveries. The etiology and pathogenesis of preterm birth has not yet fully clear, and that its incidence is the result of the interaction of a variety of environmental and genetic factors. In this study, by analyzing environmental exposure factors that affect the risk of premature birth and tumor necrosis factor (TNF-α) gene polymorphic sites, in-depth epidemiological investigate the association of genetic and environmental factors and the premature onset of the study of the etiology of preterm birth Genetics clues, and provide a theoretical basis for the early prediction of preterm delivery and clinical treatment. Methods: A case-control study, select the Maternal and Child Health Hospital of Guangdong Province from June 2009 to June 2010 preterm birth 89 pregnant women and 110 cases of full-term maternal unified epidemiological questionnaire study of selected study questionnaires and medical records excerpt informed consent cases collected each survey peripheral venous blood 3ml, using polymerase chain reaction - high resolution melting curve (PCR-HRM) technology combined with sequencing assay TNF-α in the study gene -238, -308, 488 points polymorphism distribution. Application of chi-square test and multivariate logistic regression analysis, the major risk factors for screening of preterm labor. Univariate and multivariate logistic regression analysis, the strength of the association of the genotype and the risk of preterm birth. Application multivariate unconditional logistic regression model to analyze gene - environment interactions. Results: 1. Maternal premature rupture of membranes, infected with bacterial vaginosis (BV) during pregnancy, placental abnormalities, family history of preterm, previous history of preterm, low level of education and low household income for preterm birth risk factors (P lt; 0.05) . Multivariate Logistic regression analysis of risk factors, the results display the OR value preterm birth: a family history of preterm 18.868 (95% CI: 1.831-194.386), infection during pregnancy BV 5.378 (95% CI: 1.188-24.348), fetal membranes as early as break the 28.732 (95% CI: 7.445-110.880), placental abnormalities 28.021 (95% CI: 2.871-273.506). 2 (1) detected preterm group and the control group, the TNF-α gene -238 points, 308 points, two sets of genotype distribution and allele frequencies of difference had no statistical significance (P gt; 0.05) . 488 points A allele, GA (AA) genotype frequency distribution in the premature group was significantly higher than that in the control group, the differences were statistically significant (χ2 = 10.036, P = 0.002, χ 2 = 11.235, P = 0.004) . The monthly family income, educational level and other demographic characteristics adjusted OR values ??of the individual suffering from premature birth, the results show that the 488 point A to carry TNF-α gene mutation genotype (GA / AA) is carrying wild genotype (GG) individuals 2.911-fold (95% CI = 1.474-5.748), the GA genotype the risk of preterm delivery will be significantly increased (OR = 2.815,95% CI = 1.402-5.654). G-238A, (2) TNF-α gene and the G-308A, there is a strong linkage disequilibrium (D '= 1.000, r2 = 0.513), the the constituting -238G/-308A and -238G/-308G two single haplotype frequencies greater than 0.03, accounting for 98.2% of all haplotypes. The two kinds of haplotype frequency distribution of in Guangzhou Han women crowd were 7.7% and 90.5%, analysis of each haplotype distribution in the premature group and the control group had no significant difference has nothing to do with the incidence of preterm delivery. Application of multivariate unconditional logistic regression model analysis of gene - gene interactions, an interaction between TNF-α gene 488, -238 and -308 points while carrying 488, -238, -308 wild genotype is premature The protective factors carry 488A/-238G/-308G genotype can significantly increase the risk of premature birth, OR = 3.116 (95% CI1.679 5.784). 3. Multivariate logistic regression models to analyze gene - environment interactions, factors to non-exposed and non-mutant genotype as a reference, the results show separate environmental exposure factors OR values ??are higher than the mutant gene alone OR value, BV family history of preterm premature rupture of membranes, placental abnormalities in preterm incidence since the role of the main effects. Combination of environmental exposure analysis of the interaction with the TNF-α gene SNPs, suggesting 238 and GA AA GA AA genotype of 308 points will enlarge BV exposure effect, there is a positive interaction (r gt; 1), carrying 488 points genotype BV existence of negative interactions (r lt; 1) showed decreasing its exposure effects. Carrying the -238, -308, 488 points GA AA genotype are enlarged premature rupture of membranes exposed to the effects of (r gt; 1) carry -308, 488 points GA AA genotype are amplified placental abnormalities exposure effects (r gt; 1), carrying 488 GA AA genotype will enlarge the family history of preterm exposure effect (r gt; 1) positive interaction showed super-multiplicative model. Conclusion: 1. Maternal family history of preterm pregnancy infect BV, premature rupture of membranes, placental abnormalities of the major risk factors for preterm birth. 488 2.TNF-α gene polymorphisms premature susceptibility of polymorphic loci, alone or in combination with other sites to impact the risk of preterm birth. -238, -308 Locus polymorphism has nothing to do with the genetic susceptibility of the premature birth. Between genes that affect the risk of premature birth, between genes and the environment there is a complex interaction BV, a family history of preterm placenta and premature rupture of membranes in preterm incidence from the role of the main effects, when combined with the TNF-α gene -238, -308 and 488 points GA AA genotype will enlarge or diminish its exposure effects.
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