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慢性阻塞性肺疾病(COPD)是一种可预防、可治疗的疾病,其肺部病变的特征为持续存在的气流受限,气流受限通常呈进行性发展,与气道和肺脏对有害颗粒或气体的炎症反应增强有关[1].COPD常常与其他疾病如心血管疾病、骨质疏松、焦虑和抑郁等合并存在,这些疾病可对其进展产生显著影响,而且COPD患者无论病情轻重,都可以出现合并症.焦虑、抑郁是COPD最常见的心理合并症,其中COPD患者合并焦虑可达10% ~33%,合并抑郁可达7% ~ 42%[2-5],焦虑抑郁可导致COPD患者治疗依从性下降,急性加重的次数及急诊就医、住院的次数增加,严重影响了COPD患者的生活质量,影响疾病的预后,本文将从焦虑、抑郁对COPD患者疾病急性加重次数、住院时间、呼吸功能、生活质量、用药依从性、疾病的负担、预后等方面的影响进行综述. 相似文献
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慢性阻塞性肺疾病(COPD)是一种以气流受限为特征的疾病,是一种常见病及多发病[1].COPD急性加重期可增加住院率及治疗费用.COPD的发病机制与氧化/抗氧化失衡及免疫失衡等有关.N-乙酰半胱氨酸(NAC)是目前治疗CUPD常用的抗氧化剂,我们采用NAC治疗COPD患者35例.观察其疗效为治疗COPD提供了依据.报告如下. 相似文献
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慢性阻塞性肺疾病(COPD)是一种致残率和死亡率较高的常见病.吸烟是引起COPD的主要病因之一.戒烟可预防COPD和减缓疾病进展,是减少COPD危险因素的有效方法.本文综述戒烟在COPD治疗中的作用及戒烟药物的相关临床疗效评价. 相似文献
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慢性阻塞性肺疾病(COPD)是一种慢性气道阻塞性疾病,早期病情隐匿,症状明显时肺功能已有明显减退,后期出现心、肺功能不全危及生命.但是,COPD是可防可治的疾病,通过长期规范的健康教育,早发现早治疗可延缓COPD的发病进程.现将对COPD患者和家属实施健康教育的效果报告如下. 相似文献
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慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
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慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
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慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
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慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
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慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
10.
慢性阻塞性肺疾病(clIlronic obstructive pulmonary disease,COPD)是常见的呼吸系统疾病,防止与延缓COPD患者病情进一步恶化是治疗目的.在综合治疗的基础上,合理氧疗可以提高患者的生命质量,延长生命期[1].但由于多种原因可影响氧疗效果,我科对COPD患者实施一系列护理干预,以提高COPD患者氧疗的治疗效果,报告如下. 相似文献
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Bone disease in inflammatory bowel disease 总被引:1,自引:0,他引:1
C. M. S. Schulte 《Alimentary pharmacology & therapeutics》2004,20(S4):43-49
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Crohn's disease: monitoring disease activity 总被引:7,自引:1,他引:6
R. Sostegni M. Daperno N. Scaglione A. Lavagna R. Rocca & A. Pera 《Alimentary pharmacology & therapeutics》2003,17(S2):11-17
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目的 探讨不完全川崎病与典型性川崎病的异同以便早诊断、早治疗.方法 回顾分析60例确诊为川崎病患儿的临床和实验室资料.结果 不完全川崎病临床诊断指标中的症状出现率较典型性川崎病低(x2 =16.46、10.10、11.71、34.43,均P<0.01),两者实验室检查指标WBC、Pt、ESR及CRP之间差异无统计学意义(x2 =0.04、0.12、0.04、0.26,均P>0.05),两者冠状动脉病变发生率差异有统计学意义(x2=31.43,P<0.05).结论 川崎病的早期诊断要结合临床特点、实验室检查和超声心动图检查. 相似文献
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Cooke GE 《Vascular pharmacology》2006,44(2):66-74
We now have a greater understanding of the workings of the human genome as well as a wide assortment of pharmacological and mechanical therapies that clearly improve mortality and quality of life for our patients with cardiovascular disease, but these areas of therapeutics and genomics have essentially advanced independently with little interaction up until recently. Pharmacogenetics is the study of the effect of a medication as it relates to single or defined sets of genes. A major goal will be to integrate the two so that true personalized therapy can be delivered. This review explores the clinical implications of the complex interactions in multigenic disease and pharmacology with examples of atherosclerosis and heart failure. The therapies of today are the direct result of understanding the epidemiological, molecular and genetic basis of cardiovascular disease with the application to clinical practice. The complexity of multigenic disease and the promise of pharmacogenetics will require that we improve on the methods of drug evaluation and this includes the need for new statistical methods, bioinformatics, and novel clinical trial design with sufficient power to detect differences in therapy. There must be a continued effort to apply biological and mechanistic plausibility in understanding disease and pharmacology but openness to new ideas and concepts, especially in understanding the workings of the genome. 相似文献
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K Ohara 《Nihon shinkei seishin yakurigaku zasshi》2000,20(5):213-218
Since 1991, about 20 triplet repeat expansion disorders have been reported. They are clinically characterized by anticipation, worsening severity or earlier age at the onset with each succeeding generation, and imprinting, a process whereby specific genes are differentially, marked during parental gametogenesis, resulting in their differential expression. The anticipation in psychoses was pointed out in the 19th century, but it was ignored because no one knew the mechanism at that time. The discovery of triplet repeat expansion diseases has reawakened interest in anticipation in psychiatric diseases. Anticipation has been confirmed in schizophrenia, mood disorders, and anxiety disorders. Molecular approaches have been taken to reveal the involvement of a triplet repeat expansion mechanism in psychoses. Most efforts have been made for CAG-type trinucleotide repeats. So far, most results did not support a trinucleotide repeat expansion mechanism also in psychoses. One plausable explanation for the "false positive" result is the presence of CAG trinucleotide repeats, which are highly polymorphic but not associated with an obvious abnormal phenotype. The screening for triplet repeats besides those of the CAG type remain to be performed. 相似文献