α1-抗胰蛋白酶在稳定期慢性阻塞性肺疾病合并支气管扩张患者血清中的表达及其临床意义

doi:10.3969/j.issn.1671-7171.2020.02.010

摘要
图/表
参考文献(13)
相关文章 (15)

全文: PDF (0 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要 【目的】探究α1-抗胰蛋白酶(α1-AT)在稳定期慢性阻塞性肺疾病(COPD)合并支气管扩张患者血清中的表达及其临床意义。【方法】选取2017年1月至2018年12月在本院呼吸内科就诊的稳定期COPD合并支气管扩张患者64例(合并组),另外选取同期在本院诊治的稳定期COPD患者50例作为COPD组和本院健康体检者50例作为对照组。检测三组血清中α1-AT的表达水平,采用Sequenom方法检测α1-AT基因rs1243166单核苷酸多态性并比较。【结果】三组年龄、性别、吸烟史、饮酒史、收缩压、舒张压比较差异均无统计学意义(P>0.05)。对照组、COPD组、合并组α1-AT水平分别为(1.79±0.56)mg/L、(1.45±0.45)mg/L、(0.81±0.31)mg/L,依次降低,组间比较差异有统计学意义(P<0.05)。ROC曲线显示:α1-AT水平诊断COPD联合支气管扩张最佳临界点为3.21 mg/L,此时α1-AT水平诊断COPD联合支气管扩张的灵敏度为71.5%,特异度为79.4%;AUC曲线下面积为0.79。三组rs1243166单核苷酸多态性比较差异有统计学意义(P<0.05),合并组GG、GA基因型频率显著高于COPD组、对照组。相比AA型,GG型、GA型出现COPD合并支气管扩张的风险为1.154、1.697。【结论】α1-AT水平诊断COPD合并支气管扩张灵敏度及特异性较高,α1-AT基因rs1243166 GG型、GA型COPD合并支气管扩张发病率高。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	张力
	刘璇
	陆沈栋
	徐翼

关键词 ：肺疾病,慢性阻塞性, 支气管扩张药, 胰蛋白酶/血液

Abstract：【Objective】To investigate the level and significance of serum α1-antitrypsin (α1-AT) in patients with chronic obstructive pulmonary disease (COPD) complicated with bronchiectasis.【Methods】From January 2017 to December 2018, 64 stable COPD patients with bronchiectasis (combined group) were selected from the respiratory department of our hospital. In addition, 50 stable COPD patients who were treated in our hospital at the same time were selected as the COPD group and 50 healthy people in our hospital as the control group. The expression level ofα1-AT in serum of three groups was detected. The rs1243166 single nucleotide polymorphism of α 1-AT gene was detected by sequenom method and compared.【Results】There was no significant difference in age, gender, smoking history, drinking history, systolic blood pressure and diastolic blood pressure among the three groups (P>0.05). The levels ofα1-AT in the control group, COPD group and combined group were (1.79±0.56) mg / L, (1.45±0.45) mg / L, (0.81±0.31) mg / L, respectively, which decreased in turn, and there was a significant difference between the two groups (P<0.05). ROC curve showed that the best critical point ofα1-AT level diagnosis of COPD combined with bronchiectasis was 3.21 mg / L. at this time, the sensitivity ofα1-AT level diagnosis of COPD combined with bronchiectasis was 71.5%, the specificity was 79.4%; the area under AUC curve was 0.79. There was significant difference in rs1243166 single nucleotide polymorphism among the three groups (P<0.05). The frequencies of GG and GA genotype in the combined group were significantly higher than those in the COPD group and the control group. Compared with AA, the risk of COPD with bronchiectasis in GG and GA was 1.154 and 1.697.【Conclusion】 Alpha 1-AT level is more sensitive and specific in diagnosing COPD combined with bronchiectasis, and incidence rate ofα1-AT gene rs1243166 GG type and GA type COPD combined with bronchiectasis is high.

Key words： Pulmonary Disease,Chronic Obstructive Bronchodilator Agents Trypsin/BL

收稿日期: 2019-05-21

PACS:

R563

引用本文:

张力, 刘璇, 陆沈栋, 徐翼. α1-抗胰蛋白酶在稳定期慢性阻塞性肺疾病合并支气管扩张患者血清中的表达及其临床意义[J]. 医学临床研究, 2020, 37(2): 193-195.
ZHANG Li, LIU Xuan, LU Shen-dong,et al. Expression and Clinical Significance ofα1-antitrypsin in Serum of Patients with Stable Chronic Obstructive Pulmonary Disease Complicated with Bronchiectasis. JOURNAL OF CLINICAL RESEARCH, 2020, 37(2): 193-195.

链接本文:

http://journal07.magtech.org.cn/yxlcyj/CN/10.3969/j.issn.1671-7171.2020.02.010 或 http://journal07.magtech.org.cn/yxlcyj/CN/Y2020/V37/I2/193

[1] Seyama K, Hirai T, Mishima M,et al. A nationwide epidemiological survey of alpha1-antitrypsin deficiency in Japan[J].Respir Investig,2016,54(3):201-206.
[2] Edgar RG, Patel M, Bayliss S, et al. Treatment of lung disease in alpha-1 antitrypsin deficiency: a systematic review[J].Int J Chron Obstruct Pulmon Dis,2017,12:1295-1308.
[3] Turino GM, Ma S, Cantor JO, et al. Biomarkers in alpha-1 antitrypsin deficiency chronic obstructive pulmonary disease[J].Ann Am Thorac Soc,2016,13(Suppl 4):S336-S340.
[4] 王婧雯,王秋颖,徐建国.慢性阻塞性肺病稳定期合并2型糖尿病患者血清α1-抗胰蛋白酶、中性粒细胞弹力蛋白酶水平[J].中国老年学杂志,2013,33(3):510-511.
[5] 2016 GOLD.COPD 诊断、治疗与预防全球策略(更新版)[J].中国全科医学,2016,19(5):524.
[6] Rahaghi FF, Miravitlles M. Long-term clinical outcomes following treatment with alpha 1-proteinase inhibitor for COPD associated with alpha-1 antitrypsin deficiency: a look at the evidence[J].Respir Res,2017,18(1):105.
[7] Jouhadi Z, Odou MF, Zerimech F, et al. Alpha1 antitrypsin deficiency due to an homozygous PI* Null Q0Cairo mutation: Early onset of pulmonary manifestations and variability of clinical expression[J].Respir Med Case Rep,2018,24:58-62.
[8] 钟雪梅,李黎,米热班·热夏提, 等.α1-抗胰蛋白酶与维吾尔族慢性阻塞性肺疾病的相关性分析[J].医学信息,2018,31(2):67-70.
[9] 王林升,张国玉,周孟恩.支气管扩张患者α1-AT的基因多态性和血清α1-AT水平及其临床意义的研究[J].临床肺科杂志,2010,15(10):1414-1416.
[10] 邱洁,张雅囡,陈娟, 等.宁夏地区慢性阻塞性肺疾病血清α1-抗胰蛋白酶检测分析[J].中国现代医学杂志,2012,22(17):58-61.
[11] 宋帅.α1-抗胰蛋白酶最新研究进展[J].国际检验医学杂志,2018,39(11):1356-1360.
[12] Mueller C, Gernoux G, Gruntman AM, et al. 5 year expression and neutrophil defect repair after gene therapy in alpha-1 antitrypsin deficiency[J].Mol Ther,2017,25(6):1387-1394.
[13] Hazari YM, Bashir A, Habib M, et al. Alpha-1-antitrypsin deficiency: Genetic variations, clinical manifestations and therapeutic interventions[J].Mutat Res,2017,773:14-25.