慢性阻塞性肺疾病患者的护理管理

<正>慢性阻塞性肺疾病(Chronic obstructive pulmonary disease,COPD)是一种具有气流受限特征的疾病,气流受限不完全可逆,呈进行性发展。据世界卫生组织(WHO)预测,至2020年COPD的死亡率将高居第三位[1]。COPD患者后期大多死于呼吸衰竭或慢性阻塞性肺病的并发症[2]。因此,医务人员不仅要了解患者的病理生理特征,还要从心理和社会的角度为患者提供有效的护理管理及护理措施,从而帮助个     

慢性阻塞性肺疾病全基因组关联研究进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)是一种以不完全可逆的气流受限为主要特征的慢性气道炎症,是一种由遗传因素和环境因素共同作用的复杂疾病,也是世界主要致死疾病之一。近年来,随着全基因组关联研究(genome-wide association study, GWAS)的不断深入,研究者们发现了大量与肺功能或COPD相关的遗传变异或基因位点、药物靶点等。本文综述了2007年以来世界范围内针对肺功能或COPD的GWAS方面的研究工作及其进展综述,分析了可能存在的药物靶点,并探讨了COPD在全基因组关联研究中面临的挑战和困难,为深入研究COPD发病机制提供新思路。     

姜黄素对COPD抗炎抗氧化作用研究进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种以进行性、不完全可逆性气流受限为主要特征的慢性炎症性肺部疾病。该病是有害气体或颗粒导致肺部异常炎症有关[1]。姜黄素是从姜科植物姜黄中提取的一种酚类化合物,有抗氧化、抗炎、抗肿瘤等作用,近年来研究表明姜黄素对香烟诱导COPD大鼠有抗炎抗氧化作用。     

慢性阻塞性肺疾病的研究及护理进展

<正>慢性阻塞性肺疾病(chronic dbstructive pulmonary disease,COPD)是以不完全气流受限呈进行性发展为特征的一种可以预防和治疗的疾病。也是一种与肺部对有害气体或有害颗粒的异常炎症反应有关的慢性疾病,其发病率、致残率及病死率均较高。近年来其发病率呈明显上升的趋势,引起了全世界科学家的高度重视[1],据WHO预测,即使有公共卫生干预措施,至2020年COPD的病死率也将高居第3位[2]。为了加强对COPD的预防、治疗与控制,本文就近年来对COPD的流行病学、危险因素及护理进展作一综述。     

慢性阻塞性肺疾病的研究进展

慢性阻塞性肺疾病（COPD）是一种以不完全可逆性气流受限为特征的、可以预防和治疗的气道慢性炎症性疾病,是呼吸系统常见病之一,主要累及肺脏,但也可引起全身（肺外）的不良效应[1]。在国内外均为常见病,尤其多见于老年人和吸烟者,患病率有逐年上升趋势,     

肺微生物组与慢性阻塞性肺疾病的研究进展

摘要：慢性阻塞性肺疾病（COPD）是一种慢性炎症性呼吸道疾病,其特征是持续气流受限和肺部炎症反应异常。气道内微生物是COPD恶化的主要原因,并且使气道中的炎症反应持续存在而促成COPD进展,这导致肺功能的进一步损害和巨大的医疗保健成本。近年来随着高通量测序技术的发展和运用,人类肺微生物组的研究逐渐成为热点。大量研究表明,COPD患者肺内存在明显不同的微生物群落,而且与COPD的疾病严重程度及恶化状态有关。肺微生物组学的研究有助于人们更全面地理解COPD患者肺内的微生态系统及其在该病恶化和进展中的作用。本文就肺微生物组在COPD中的研究进展作一综述,并探讨未来的研究前景。     

肺微生物组在慢性阻塞性肺疾病中的研究进展CSCD

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）是一种以持续的呼吸道症状和气流受限为主要特征的异质性疾病。新一代基因测序技术已经证明健康肺部存在庞大的微生物群落。越来越多的研究表明,肺微生物群失调与COPD的发生、急性加重次数及病死率有关。肺微生物可能通过调控炎症或免疫过程参与COPD的发病机制。全面了解肺微生物群在COPD不同阶段的动态变化和微生物与宿主的相互作用,有助于进一步揭示其在COPD发病机制中的作用。本文综述了肺微生物组在COPD中的研究进展,探讨其与COPD进展之间的关系及潜在的机制,以期开发有针对性的治疗方法。     

哮喘-慢性阻塞性肺疾病重叠综合征的治疗进展

哮喘-慢性阻塞性肺疾病重叠综合征是一种气流受限型疾病,同时具备哮喘和慢性阻塞性肺疾病特征。治疗哮喘-慢性阻塞性肺疾病重叠综合征具有挑战性,哮喘与COPD病理生理不尽相同,二者合并发生时,病情将变得极为复杂。在治疗过程中,主要使用支气管扩张剂、糖皮质激素等药物。但由于该病病程长、易复发,且治疗较困难,单一用药治疗的效果有限,建议联合用药。     

新疆维吾尔族慢性阻塞性肺病患者疾病严重程度与体重指数的相关性分析

目的:探讨新疆维吾尔族慢性阻塞性肺病(COPD)患者疾病的严重程度(包括临床症状、气流受限严重程度、急性加重风险)与其体重指数(BMI)的相关性。方法:收集2013年1月至2014年6月新疆维吾尔自治区人民医院、石河子大学医学院第一附属医院、喀什地区第一人民医院呼吸科门诊及住院COPD患者110例,分别对其临床症状、气流受限严重程度、急性加重风险进行评估分级,运用Spearman相关分析COPD患者疾病严重程度与体重指数的相关性。结果:COPD患者的肺功能分级越高,体重指数越低,二者呈显著负相关(r=-0.583,P0.05);COPD患者的呼吸困难分级越高,体重指数越低,二者呈显著负相关(r=-0.673,P0.05);不同肺功能分级和呼吸困难分级COPD患者的体重指数比较差异均有统计学意义(P0.05)。COPD患者的急性加重风险越高,其体重指数越低,二者呈显著负相关(r=-0.461,P0.05);高风险组COPD患者的体重指数显著低于低风险组,差异有统计学意义(P0.05)。结论:新疆维吾尔族COPD患者疾病的严重程度与其体重指数之间存在显著相关性,BMI越低,其病情越重。     

miRNA在慢性阻塞性肺疾病发生发展中的作用

随着环境污染严重化以及人口老龄化问题日益突出,肺相关疾病特别是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)已成为发达国家及发展中国家发病和死亡的主要原因。既往研究普遍认为,COPD主要出现不可逆转的气流受限和慢性炎症反应。患者表现为呼吸困难加重,痰量增多,常伴有低氧血症,高碳酸血症等症状。所以,发现新的生物标志物和早期诊断COPD的方法非常必要,这可以减少疾病的发病率和死亡率。近年来,越来越多的研究发现,miRNA通过各种机制在COPD的发生发展中发挥着重要作用。本文主要对近年来miRNA在COPD中的机制研究进展进行简单综述。     

Oxidative,inflammatory, genetic,and epigenetic biomarkers associated with chronic obstructive pulmonary disorder

A large body of evidence indicates that chronic obstructive pulmonary disorder (COPD) is accompanied by oxidative stress and inflammatory and genetic pathways. Epidemiological studies indicate that COPD is a major cause of mortality and morbidity in the world. Recent research development in COPD focuses on accelerated aging and various oxidative stress biomarkers. It involves the clinical manifestation of the disease process and may also contain biochemical, immunological, physiological, morphological, and genetic aspects that add to the progressiveness of the disease. Herein, we summarize findings that highlight the role of dimensions of COPD in the investigation of oxidative stress, inflammatory responses, genetic and epigenetic studies, and pharmacological and dietary antioxidant intervention.     

Integrative genomics of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a complex disease with both environmental and genetic determinants, the most important of which is cigarette smoking. There is marked heterogeneity in the development of COPD among persons with similar cigarette smoking histories, which is likely partially explained by genetic variation. Genomic approaches such as genomewide association studies and gene expression studies have been used to discover genes and molecular pathways involved in COPD pathogenesis; however, these “first generation” omics studies have limitations. Integrative genomic studies are emerging which can combine genomic datasets to further examine the molecular underpinnings of COPD. Future research in COPD genetics will likely use network-based approaches to integrate multiple genomic data types in order to model the complex molecular interactions involved in COPD pathogenesis. This article reviews the genomic research to date and offers a vision for the future of integrative genomic research in COPD.     

The genetics of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a significant cause of global morbidity and mortality. Previous studies have shown that COPD aggregates in families, suggesting a genetic predisposition to airflow obstruction. Many candidate genes have been assessed, but the data are often conflicting. We review the genetic factors that predispose smokers to COPD and highlight the future role of genomic scans in identifying novel susceptibility genes.     

The genetics of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a significant cause of global morbidity and mortality. Previous studies have shown that COPD aggregates in families, suggesting a genetic predisposition to airflow obstruction. Many candidate genes have been assessed, but the data are often conflicting. We review the genetic factors that predispose smokers to COPD and highlight the future role of genomic scans in identifying novel susceptibility genes.     

Association Between Single-Nucleotide Polymorphisms in Interleukin-12A and Risk of Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction due to chronic bronchitis, emphysema, and/or disease of small airways. It has been reported that the genetic variation may play a role in the development and severity of COPD. The purpose of this study was to investigate whether single-nucleotide polymorphisms (SNP) in interleukin (IL)-12A and IL-12B were associated with COPD in a Chinese population. The IL-12A rs2243115 and IL-12B rs3212227 polymorphisms were genotyped by performing polymerase chain reaction-restriction fragment length polymorphism in 298 patients with COPD and 346 healthy controls. We observed that the frequencies of GT and GT+GG of IL-12A rs2243115 were significantly different from TT in the COPD group and the control group (GT vs. TT: odds ratio [OR]=2.35, 95% confidence interval [CI]=1.55-3.57, p<0.001; GT+GG vs. TT: OR=2.46, 95% CI=1.63-3.71, p<0.001). These data suggest that the IL-12A rs2243115 polymorphism may contribute to genetic susceptibility to COPD in a Chinese population.     

人音猬因子相互作用蛋白基因与慢性阻塞性肺疾病

慢性阻塞性肺疾病是呼吸系统常见慢性疾病。该疾病的发病与环境及多基因变异有关。近年的研究显示,人音猬因子相互作用蛋白基因参与多个系统疾病的发生发展,尤其对于呼吸系统该基因与慢性阻塞性肺疾病发病密切相关,该基因上某些单核苷酸多态性与慢性阻塞性肺疾病易感性相关,且在慢性阻塞性肺疾病患者肺组织内存在该基因低表达。另外,该基因与FEV1和FEV1/FVC关系密切,对肺功能有保护作用。目前的研究提示该基因和音猬信号通路在肺胚胎发育、基因表达调控、细胞增殖、细胞凋亡和平滑肌修复等方面发挥着重要调控作用,为慢性阻塞性肺疾病发病机制的研究指明了方向。本文就人音猬因子相互作用蛋白基因与慢性阻塞性肺疾病相关性的研究进展作一综述。     

The CFTR M470V gene variant as a potential modifier of COPD severity: study of Serbian population

Chronic obstructive pulmonary disease (COPD) is a complex disease influenced by genetic and environmental factors. Cystic fibrosis transmembrane conductance regulator (CFTR) protein is an important component of the lung tissue homeostasis, involved in the regulation of the rate of mucociliary clearance. As it is known that certain CFTR variants have consequences on the function of CFTR protein, the aim of this study was to examine the possible role of F508del, M470V, Tn locus, and R75Q variants in COPD development and modulation. Total number of 86 COPD patients and 102 control subjects were included in the study. Possible association between COPD susceptibility, severity, and onset of the disease and allele or genotype of four analyzed CFTR variants was examined. No associations were detected between COPD development, onset of the disease and tested CFTR alleles and genotypes. However, VV470 genotype was associated with mild/moderate COPD stages in comparison to severe/very severe ones (OR = 0.29, 95%CI = 0.11-0.80, p = 0.016). Our study showed that patients with VV470 genotype had a 3.4-fold decreased risk for the appearance of severe/very severe COPD symptoms, and the obtained results indicate that this genotype may have a protective role. These results also suggest the importance of studying CFTR gene as a modifier of this disease.     

A bioinformatics strategy for detecting the complexity of Chronic Obstructive Pulmonary Disease in Northern Chinese Han Population

Chronic Obstructive Pulmonary Disease (COPD) is a complex human disease which is driven not only by genetic factors, but also by various environmental variables, such as gender, age and smoking. Therefore, there is a demand for investigating the complexity among various risk factors involved in COPD. In this study, 44 tagging SNPs from EPHX1, GSTP1, SERPINE2 and TGFB1 were selected and genotyped in 310 COPD cases and 203 controls, all of which belong to the Han from North China. We integrated functional prediction algorithms of nonsynonymous SNPs (nsSNPs) into Bayesian network to explore the complex regulatory relationships among disease traits and various risk factors. The results showed that three basic variables (age, sex and smoking) were risk factors of COPD-related trait and phenotype. Besides these environmental risk factors, deleterious nsSNPs were found to perform better than those of significant synonymous SNPs when used as variables to make risk prediction of disease outcome. This study provides further evidences for detecting the complexity of COPD in Northern Chinese Han Population.     

The SERPINE2 gene is associated with chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a complex human disease likely influenced by multiple genes, cigarette smoking, and gene-by-smoking interactions, but only severe alpha 1-antitrypsin deficiency is a proven genetic risk factor for COPD. Prior linkage analyses in the Boston Early-Onset COPD Study have demonstrated significant linkage to a key intermediate phenotype of COPD on chromosome 2q. We integrated results from murine lung development and human COPD gene-expression microarray studies with human COPD linkage results on chromosome 2q to prioritize candidate-gene selection, thus identifying SERPINE2 as a positional candidate susceptibility gene for COPD. Immunohistochemistry demonstrated expression of serpine2 protein in mouse and human adult lung tissue. In family-based association testing of 127 severe, early-onset COPD pedigrees from the Boston Early-Onset COPD Study, we observed significant association with COPD phenotypes and 18 single-nucleotide polymorphisms (SNPs) in the SERPINE2 gene. Association of five of these SNPs with COPD was replicated in a case-control analysis, with cases from the National Emphysema Treatment Trial and controls from the Normative Aging Study. Family-based and case-control haplotype analyses supported similar regions of association within the SERPINE2 gene. When significantly associated SNPs in these haplotypic regions were included as covariates in linkage models, LOD score attenuation was observed most markedly in a smokers-only linkage model (LOD 4.41, attenuated to 1.74). After the integration of murine and human microarray data to inform candidate-gene selection, we observed significant family-based association and independent replication of association in a case-control study, suggesting that SERPINE2 is a COPD-susceptibility gene and is likely influenced by gene-by-smoking interaction.