首页> 外文OA文献 >Serum Levels of Glutamate-Pyruvate Transaminase, Glutamate-Oxaloacetate Transaminase and Gamma-Glutamyl Transferase in 1494 Patients with Various Genotypes for the Alpha-1 Antitrypsin Gene
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Serum Levels of Glutamate-Pyruvate Transaminase, Glutamate-Oxaloacetate Transaminase and Gamma-Glutamyl Transferase in 1494 Patients with Various Genotypes for the Alpha-1 Antitrypsin Gene

机译:1494名α-1抗胰蛋白酶基因的1494例患者谷氨酸 - 丙酮酸转氨酶,谷氨酸 - 草酰胺转移酶和γ-谷氨酸转移酶的血清水平

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摘要

Background: Patients with liver disease associated with alpha-1 antitrypsin deficiency (AATD) are homozygous for the Z mutation, leading to chronic liver damage. Objective: To assess the serum levels of glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), and gamma-glutamyl transpeptidase (GGT) in patients with different genotypes for the alpha-1 antitrypsin (AAT) gene. Methods: Patients (n = 1494) underwent genotyping of the SERPINA1 gene, together with a determination of AAT and GOT and GPT and GGT transaminase levels. Patients with a deficient allele (n = 476) and with a normal genotype were compared. Results: A statistically significant association was found between deficient genotypes and GOT (p < 0.0003), GPT (p < 0.002), and GGT (p < 0.006). Comparing GOT levels in patients with PI*Z deficient variant versus those with normal genotype, an odds ratio (OR) of 2.72 (CI: 1.5–4.87) (p < 0.0005) was obtained. This finding was replicated with the PI*Z allele and the GPT values (OR = 2.31; CI: 1.45–3.67; p < 0.0003). In addition, a statistically significant association was found between liver enzymes and AAT values. Conclusion: The PI*Z allele seemed to be a risk factor for the development of liver damage. AAT deficient genotypes were associated with GOT, GPT, and GGT altered values. Low AAT levels were associated with high GPT and GGT levels.
机译:背景:与α-1抗胰蛋白酶缺乏(AATD)相关的肝病患者是Z突变的纯合,导致慢性肝损伤。目的:评估含有不同基因型(AAT)基因的不同基因型的患者谷氨酸 - 草乙酸酯转氨酶(GOT),谷氨酸 - 丙酮酸转氨酶(GPT)和γ-谷氨酸转氨酶(GGT)的血清水平。方法:患者(n = 1494)的SERPINA1基因的基因分型后行与AAT和GOT和GPT和GGT转氨酶水平的确定一起。患有缺乏等位基因(n = 476)和正常基因型的患者进行了比较。结果:在缺陷的基因型之间发现统计学上显着的关联(P <0.0003),GPT(P <0.002)和GGT(P <0.006)。比较PI * Z缺陷变体与具有正常基因型的患者的患者的水平,获得2.72(CI:1.5-4.87)的差距(或)(或)(P <0.0005)。该发现与PI * Z等位基因和GPT值(或= 2.31; CI:1.45-3.67; P <0.0003)复制。此外,在肝酶和AAT值之间发现了统计学上显着的关联。结论:PI * Z等位基因似乎是肝损伤发展的危险因素。 AAT缺乏基因型与GOT,GPT和GGT改变的值相关。低AAT水平与高GPT和GGT水平相关。

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