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Leptin, soluble leptin receptor and leptin gene polymorphism in relation to preeclampsia risk

机译:瘦素,可溶性瘦素受体和瘦素基因多态性与先兆子痫风险的关系

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Few investigators have simultaneously evaluated leptin, soluble leptin receptor (SLR) and leptin gene polymorphisms in preeclampsia cases and controls. We examined these three biomolecular markers in 40 preeclampsia cases and 39 controls. Plasma leptin and SLR concentrations were determined using immunoassays. Genotype for the tetranucleotide repeat (TTTC)(n), polymorphism in the 3'-flanking region of the leptin gene was determined using PCR. Alleles of the polymorphism were characterized by size distributions [short repeats (class 1); and long repeats (class 11)]. Logistic regression was used to calculate odds ratios (OR) and 95 % confidence intervals (Q. Leptin concentrations were higher in our cases than in the controls (53.1 +/- 4.7 vs. 17.7 +/- 2.4 ng/ml, p<0.05). SLR concentrations were slightly lower in our patients than in the controls (25.7 +/- 1.9 vs. 29.1 +/- 1.1 ng/ml, p>0.05). Elevated leptin (>= 14.5 ng/ml) was associated with a 3.8-fold (Cl 1.0-14.4) increased risk; whereas low SLR (< 28.5 ng/ml) was associated with a 6.3-fold (Cl 1.7-23.2) increased risk of preeclampsia. The I/II genotype was associated with a 3.8-fold increased risk of preeclampsia (OR=3.8; 95 % CI 0.8-18.0); and the II/II genotype was not observed among our cases (0 % vs. 33 % p<0.001). Larger studies would be needed to confirm and further clarify the relations between functional variants in the leptin gene and preeclampsia risk.
机译:很少有研究者同时评估先兆子痫病例和对照中的瘦素,可溶性瘦素受体(SLR)和瘦素基因多态性。我们在40例先兆子痫病例和39例对照中检查了这三种生物分子标记。使用免疫测定法测定血浆瘦素和SLR浓度。使用PCR确定了四核苷酸重复(TTTC)(n)的基因型,瘦素基因的3'侧翼区域中的多态性。多态性的等位基因的特征是大小分布[短重复(1类);和长重复(第11类)]。使用Logistic回归来计算比值比(OR)和95%置信区间(Q.本例中的瘦素浓度高于对照组(53.1 +/- 4.7与17.7 +/- 2.4 ng / ml,p <0.05 )。我们患者的SLR浓度略低于对照组(25.7 +/- 1.9 vs. 29.1 +/- 1.1 ng / ml,p> 0.05)。瘦素(> = 14.5 ng / ml)升高与正常人相关。风险增加3.8倍(Cl 1.0-14.4);而低SLR(<28.5 ng / ml)与先兆子痫风险增加6.3倍(Cl 1.7-23.2)相关; I / II基因型与子痫前期风险3.8相关子痫前期的风险增加了两倍(OR = 3.8; 95%CI 0.8-18.0);在我们的病例中未观察到II / II基因型(0%vs. 33%p <0.001)。并进一步阐明瘦素基因功能变异与先兆子痫风险之间的关系。

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