瘦素和瘦素受体多态性与非阑尾性继发性腹膜炎患者的不良结局（死亡）相关。
Leptin and leptin receptor polymorphisms are associated with poor outcome (death) in patients with non-appendicular secondary peritonitis.
机构信息
Instituto de Investigación Científica, Universidad Juárez del Estado de Durango, Calle Constitución 404 sur, Durango, Dgo. CP 34, 000, México.
出版信息
Crit Care. 2011;15(5):R227. doi: 10.1186/cc10467. Epub 2011 Sep 23.
INTRODUCTION
Leptin (LEP) and its receptor (LEPR) participate in the immunological response during infection. LEP serum levels rise during sepsis. In patients with peritonitis, an insufficient elevation in serum LEP is associated with an increased risk of death. As gene variants of LEP and LEPR have been associated with diverse pathologic conditions, we explored the association of genetic polymorphisms of LEP or LEPR with death in patients with secondary peritonitis.
METHODS
A case control study was undertaken. LEP Gene -2548G > A and the LEPR Gene 223A > G polymorphism were determined in 74 patients. The odds ratio of genotype and allele distribution in survival (control) versus death (case) among patients was calculated. Serum LEP, interleukin (IL)-6, tumour necrosis factor alpha, C-reactive protein (C-RP), IL-10 and IL-13 levels were analyzed in 34 patients.
RESULTS
There were significant differences in genotype and allele distribution between survivors and non-survivors for -2548G > A and 223A > G polymorphisms. The presence of the mutant allele A, in -2548, had an odds ratio of 4.64 (95% CI 1.22, 17.67) with significance (P = 0.017) in the risk of death. The presence of mutant allele G, in 223, had an odds ratio of 3.57 (95% CI 1.06, 12.01) with significance in the risk of death (P = 0.033). The presence of allele A in the -2548 polymorphism was associated with differences in serum LEP (P = 0.013), and IL-10 (P = 0.0001). The presence of allele G in 223 polymorphism was likewise correlated with differences in serum LEP (P < 0001), C-RP (P = 0.033), and IL-10 (P = 0.043).
CONCLUSIONS
The polymorphisms studied are associated with death in patients with peritonitis of non-appendicular origin. This association is stronger than many known risk-factors related to peritonitis severity, and is independent of body mass. The physiopathologic mechanism is possibly related to an insufficient increase in the elevation of serum LEP levels, and is unrelated to body mass.
简介
瘦素（LEP）及其受体（LEPR）参与感染期间的免疫反应。败血症期间血清瘦素水平升高。在腹膜炎患者中，血清瘦素升高不足与死亡风险增加相关。由于 LEP 和 LEPR 的基因变异与多种病理状况有关，我们探讨了 LEP 或 LEPR 基因多态性与继发性腹膜炎患者死亡的关系。
方法
进行了病例对照研究。在 74 名患者中确定了 LEP 基因 -2548G > A 和 LEPR 基因 223A > G 多态性。计算了生存（对照）与死亡（病例）患者中基因型和等位基因分布的优势比。分析了 34 名患者的血清瘦素、白细胞介素（IL）-6、肿瘤坏死因子-α、C 反应蛋白（C-RP）、IL-10 和 IL-13 水平。
结果
在 -2548G > A 和 223A > G 多态性中，幸存者和非幸存者之间的基因型和等位基因分布存在显著差异。-2548 中的突变等位基因 A 的存在具有 4.64 的优势比（95%CI 1.22，17.67），具有显著性（P = 0.017），增加了死亡风险。223 中突变等位基因 G 的存在具有 3.57 的优势比（95%CI 1.06，12.01），具有显著性（P = 0.033），增加了死亡风险。-2548 多态性中等位基因 A 的存在与血清瘦素（P = 0.013）和白细胞介素 10（P = 0.0001）的差异相关。223 多态性中等位基因 G 的存在同样与血清瘦素（P < 0001）、C-RP（P = 0.033）和白细胞介素 10（P = 0.043）的差异相关。
结论
研究的多态性与非阑尾来源腹膜炎患者的死亡相关。这种关联强于许多与腹膜炎严重程度相关的已知危险因素，并且与体重无关。病理生理机制可能与血清瘦素水平升高不足有关，与体重无关。
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