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  • Title: [The investigation of genotype and expression of alpha1-AT in patients with COPD].
    Author: Zhang Y, He B, Zhao MW, Wang XH, Jiang L, Yao WZ.
    Journal: Zhonghua Yi Xue Za Zhi; 2005 May 18; 85(18):1270-3. PubMed ID: 16029614.
    Abstract:
    OBJECTIVE: To detect genotype and expression of alpha1-AT in the patients with COPD to investigate the effect of alpha1-AT on pathogenesis of COPD. METHODS: Detection of PiZ allele in exon V and S allele in exon III were performed by PCR-Amplification of Specific Allele (PASA). The levels of serum alpha1-AT in some of subjects were measured by Enzyme-Linked Immunoadsordent Assay (ELISA). RESULTS: The PCR production of S mutation was 285 base pair fragment. The PCR production of Z-mutation was 250 base pair fragment. The results showed that All subjects were PiMM genotype of alpha1-AT, including COPD and control group. The mean serum alpha1-AT concentration, in patients with COPD, was 2.3 g/L +/- 1.1 g/L. In control group, the mean serum alpha1-AT concentration was 2.7 g/L +/- 0.84 g/L. The levels of alpha1-AT in patients with COPD are significantly lower than that in control group (P = 0.012). RV/TL and degree of pursiness are negative correlation with the levels of alpha1-AT. The r value were -0.208 and -0.262 respectively. CONCLUSION: There was no difference in genetic polymorphism of alpha1-AT between the patients with COPD and controls. However, the levels of serum alpha1-AT were significantly lower in the patients with COPD compared with control subjects. alpha1-AT deficiency may be a factor of the pathogenesis of COPD. The mechanism of alpha1-AT deficiency needs to be addressed.
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