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目的 :研究血管紧张素转换酶 ( ACE)基因的插入 /缺失 ( I/ D)多态性、血管紧张素原 ( AGT)基因 M2 3 5 T变异与高原肺水肿 ( HAPE)的相关性以及二者对 HAPE易感性的预测价值。 方法 :对 5 1例 HAPE患者 (为 HAPE组 )、5 4例正常对照者 (为对照组 )采用多聚酶链式反应方法检测 ACE的 I/ D多态性 ,采用多聚酶链式反应 /限制性长度片段多态性检测 AGT M2 3 5 T变异性。 结果 :ACE基因型 II、ID、DD在 HAPE组和对照组频率分布分别为 12、3 2、7和 8、3 1、15 ,其中 I、D等位基因频率在两组分别为 0 .5 4 9、0 .4 5 1和 0 .4 3 5、0 .5 65 ,两组之间无显著性差异。AGT M2 3 5 T基因型 MM、MT、TT在 HAPE组和对照组中频率分布分别为 7、2 4、2 0和 4、2 3、2 7,其中 M、T等位基因频率在两组分别为 0 .3 73、0 .62 7和 0 .2 87、0 .713 ,两组之间也无显著性差异。 结论 :本研究结果提示 ACE基因 I/ D多态性及 AGT M2 3 5 T变异性不适合作为 HAPE易感性的预测标记 ,并且在HAPE的发生机制中不起主要作用。
AIM: To investigate the association of ACE gene insertion / deletion (I / D) polymorphism, the M235T mutation in angiotensinogen (AGT) gene and HAPE, Predictors of HAPE Susceptibility. Methods: The ACE I / D polymorphism was detected by polymerase chain reaction in 51 HAPE patients and 54 normal controls (control group). The polymerase chain reaction / restriction length Fragment polymorphism detection AGT M2 3 5 T variability. Results: The frequencies of ACE genotypes II, ID and DD in HAPE group and control group were 12, 32, 7 and 8, 31, 15, respectively. The frequencies of I and D alleles were 0.5 4 9,0 .4 5 1 and 0 .4 3 5,0 .5 65, no significant difference between the two groups. The frequencies of AGT M2 3 5 T genotype MM, MT and TT in HAPE group and control group were 7,2 4,2 0 and 4,2 3,2 7, respectively. The frequencies of M and T alleles were in two groups Respectively 0 .3 73,0 .62 7 and 0 .2 87,0 .713, there was no significant difference between the two groups. CONCLUSIONS: The results of this study suggest that ACE gene I / D polymorphism and AGT M235T variability are not suitable predictors of HAPE susceptibility and may not play a major role in the pathogenesis of HAPE.