补中益气汤治疗慢性阻塞性肺疾病临床疗效分析

目的探讨补中益气汤加减联合西医常规疗法治疗稳定期慢性阻塞性肺疾病(COPD)患者的临床疗效及其对患者呼吸肌和肺功能的影响。方法纳入2015年8月至2016年8月在本院治疗的120例稳定期COPD患者,根据治疗方法不同分为补中益气组(补中益气汤加减+舒利迭)和常规组(舒利迭)各60例,连续用药8周。采用第1秒用力呼气容积占预计值的百分比(FEV1%预计值)、第1秒用力呼气容积/用力肺活量(FEV1/FVC)评价各组患者治疗前后的肺功能指标。采用辅助呼吸肌动用评分、医学研究委员会呼吸困难刻度尺(MRC)评分对患者的呼吸肌力进行评估。采用SPSS 16.0对数据进行统计分析。结果治疗后,补中益气组患者的咳嗽、咳痰、喘息、自汗、易感冒、气短、哮鸣音等评分均低于常规组(P0.05);补中益气组的第1秒用力呼气容积占预计值的百分比(FEV1%预计值)和第1秒用力呼气容积/用力肺活量(FEV1/FVC)均高于常规组[FEV1%:(57.92±6.09)(52.84±6.64);FEV1/FVC:(67.34±7.11)vs(63.01±6.95);P0.05],且均较治疗前显著增高(P0.05);补中益气组的呼吸肌动用评分和MRC评分均低于常规组[(1.41±0.41)(1.79±0.50);(1.38±0.39)(1.61±0.49);P0.05],且均较治疗前显著下降(P0.05);补中益气组的治疗总有效率高于常规组(95.00%vs 81.67%;P0.05)。结论补中益气汤加减联合西医常规疗法治疗稳定期COPD患者能改善肺功能、缓解呼吸肌疲劳症状,提高临床疗效。     

慢性阻塞性肺疾病稳定期的肺康复治疗

<正>慢性阻塞性肺病(COPD)是发达国家五大死亡原因之一,在其他大多数国家也是死亡率上升的原因[1]。COPD被定义为一种常见的,可预防和治疗的疾病,其特征为持续的呼吸症状和由气道和(或)肺泡异常引起的慢性气流受限,通常是由于暴露于有毒颗粒或气体造成的[2]。吸烟是COPD发展的主要原因,但其他环境因素,如生物质燃料暴露和空气污染也有助于COPD的形成[3]。除了暴露因素外,宿主的个体因素也是导致COPD的原因[2]。COPD不仅导致肺功能     

慢性阻塞性肺疾病稳定期的治疗

慢性阻塞性肺疾病（chronic obstructive pulmonary diseases,COPD）稳定期指患者咳嗽、咳痰、气短等症状稳定或症状轻微。沈阳部分社区40岁以上人群调查表明稳定期患者占COPD的86．62％,稳定期患者平均每人每年急性加重1～2次,     

康复治疗在老年慢性阻塞性肺疾病稳定期的应用

<正>慢性阻塞性肺疾病(COPD)发病率和死亡率均较高〔1〕,COPD急性期的治疗以药物为主,缓解期主要通过肺康复治疗联合药物治疗以延缓病情、减轻症状,但药物治疗有其适应证与禁忌证,且不良反应、副作用常见,因而康复治疗在COPD稳定期的作用尤为重要〔2,3〕。临床上采用的治疗方法很多,现将近年来老年COPD稳定期患者的康复治疗手段作一综述。1肺康复锻炼COPD患者气流受限不完全可逆,且呈进行性发展,药物治     

中医肺康复法治疗慢性阻塞性肺疾病稳定期患者的疗效

目的评价中医肺病康复疗法对慢性阻塞性肺疾病(COPD)稳定期患者的疗效。方法选取COPD稳定期患者60例,随机分为治疗组30例和对照组30例,对照组给予多索茶碱片口服,治疗组由专门的肺病康复师给予一整套中医肺病康复指导及治疗,疗程2个月。观察治疗前、后两组患者中医证候评分变化、6 min步行距离、BODE指数、生存质量评分(SGRQ)、肺功能及不良反应。结果两组患者治疗后中医证候评分与本组治疗前比较,差异有统计学意义(P<0.01),且治疗组中医证候疗效优于对照组(P<0.01);治疗组6 min步行距离、生存质量评分(SGRQ)、肺功能在治疗后比治疗前明显增加(P<0.01),且在治疗后两组间比较差异有统计学意义(P<0.05,P<0.01);两组患者BODE指数、安全性指标差异无统计学意义(P>0.05)。结论中医肺康复法治疗COPD稳定期患者疗效确切,可明显改善患者症状,提高生存质量,增加运动耐量,且安全性好、未发现任何不良反应。     

稳定期慢性阻塞性肺疾病的抗生素治疗进展

慢性阻塞性肺疾病(COPD)是一种呼吸系统常见的慢性疾病,炎症反应在其发生、发展过程中是导致一系列病理生理改变的重要机制.根据病程可分为稳定期和急性加重期,目前的研究表明对于易出现急性加重的患者,一年内长期使用阿奇霉素或红霉素可减少急性加重风险(A级证据),至于长期使用抗生素的安全性和有效性仍待更多的研究.现针对稳定期COPD的抗生素治疗作一综述,探讨不同给药方式及抗生素种类对COPD患者的益处、不良反应以及耐药性的影响,旨在为临床工作提供参考.     

三拗片辅助治疗慢性阻塞性肺疾病稳定期患者的临床疗效

目的 通过三拗片联合西药辅助治疗慢性阻塞性肺疾病(COPD)稳定期患者,探讨其临床治疗效果.方法 将我院收治190例确诊为慢性阻塞性肺疾病稳定期的患者随机分为实验组102例和对照组88例,试验组选择三拗片联合西药进行治疗,对照组仅用西药治疗,比较两组患者的临床疗效,包括有效率、肺功能指标、血气分析指标,评估测试问卷评分和不良反应发生率等.结果 治疗1个月后,试验组临床总有效率为93.1％,对照组临床总有效率为81.8％,两组比较差异有统计学意义(P＜0.05);两组治疗后1秒用力呼气量(FEV1)、最大肺活量(FVC)、FEV1/FVC、PaO2、PaCO2差异有统计学意义(P＜0.05);实验组患者COPD评估测试问卷(CAT)评分下降更为明显(P＜0.05).结论 三拗片联合西药治疗在治疗慢性阻塞性肺疾病稳定期方面比单用西药疗效更为显著,且安全性良好,值得临床推广应用.     

慢性阻塞性肺疾病稳定期药物治疗的研究进展

慢性阻塞性肺疾病(COPD)是一种具有气流受限特征的可以预防和治疗的疾病,气流受限不完全可逆、呈进行性发展,与肺部对香烟烟雾等有害气体或有害颗粒的异常炎症反应有关.COPD主要累及肺脏,但也可引起全身(或称肺外)的不良效应.本文将近年来COPD稳定期的药物治疗进展综述如下.     

稳定期慢性阻塞性肺疾病与血清炎性因子的相关性临床治疗分析

目的：分析稳定期 COPD 与血清炎性因子的相关性。方法搜集2012年12月至2014年11月我院稳定期 COPD 43例作为研究组,对照组选取同期健康吸烟者43例。分别采集研究组与对照组外周静脉血,取标本上清液,采用酶联免疫法进行检测,观察研究组与对照组的单核细胞趋化蛋白1(MCP-1)、C 反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)、脑钠肽(BNP)水平,并对两组人员的检测结果进行对比。分析研究组不同圣乔治呼吸问卷(SGRQ)评分、BODE 指数分级患者检测水平,对检测指标与疾病相关性进行研究。结果研究组与对照组血清炎性因子对比,研究组各项指标较高,差异有统计学意义(P <0.05)。检测结果显示疾病与 MCP-1、CRP、TNF-α、BNP 密切相关。结论稳定期 COPD 患者 MCP-1、CRP、TNF-α、BNP 等血清炎性因子明显升高,与疾病有一定相关性。因此,对于此种疾病的治疗,应当充分考虑血清炎性因子的影响,并明确影响程度,确保疾病诊断的准确性,为后续治疗奠定基础。     

无创正压通气治疗稳定期慢性阻塞性肺疾病的疗效

无创正压通气(noninvasive positive pressure ventilation,NPPV)在慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)急性加重期和稳定期患者中都有广泛应用.对于急性加重期患者,NPPV可显著降低气管插管率、病死率、住重症监护病房(ICU)时间及住院时间等.对于稳定期患者,NPPV能显著改善呼吸困难症状及部分肺功能指标、提高PaO2水平、缓解呼吸肌疲劳、增强活动耐力以及改善睡眠和生活质量,但对于NPPV能否显著降低PaCO2水平,降低住院率、病死率、住ICU时间以及住院时间等,尚存在较大争议.充分了解NPPV在稳定期COPD患者中的疗效,对于提高NPPV的临床应用水平具有重要意义.     

老年人慢性阻塞性肺疾病的诊断与治疗

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）是危害人类健康的最常见呼吸系统疾病之一。据世界卫生组织（World Health Organization,WHO）调查,1990年全球COPD病死率位居各类疾病病死率的第6位,预测2020年将上升至第3位,并且成为世界疾病经济负担的第5位。     

慢性阻塞性肺疾病稳定期门诊治疗的临床研究

目的研究COPD稳定期的不同治疗方案。方法将90例COPD患者随机分为3组：舒利迭组（吸入沙美特罗氟替卡松50／250μg每天2次）、联合用药组（口服茶碱缓释片0．1g每天2次＋吸入丙酸氟替昔松125μg每天2次）及对照组（按需使用硫酸沙丁胺醇气雾剂）,随访1年,观察1年后的肺功能（FEV1、FVC、FEV1％pred、FEV1/FVC和FEF25—75％）,6分钟步行距离（6 minuteswalkingdistance,6MWD）和1年中急性加重的次数。结果治疗后舒利迭组和联合用药组的FEV1、FVC、FEV1％pred、FEV1／FVC、FEF25—75％和6MWD分别与对照组及治疗前比较均有改善（P值均〈0．05）;治疗后舒利迭组比联合用药组FVC和FEF2575％改善更明显（分别为2．41±0．61和2．11±0．47,44．9±10．1和35．4±8．8。P值均〈0．05）。结论舒利迭（50／250μg）、联合用药（口服茶碱缓释片＋丙酸氟替卡松气雾剂）对稳定期COPD患者疗效肯定,前者对FVC和FEF25—75％的改善较后者强。     

从循证医学看呼吸系统疾病康复的有效性和进展

呼吸系统疾病是现代医学界受到重视的高患病率、高致残率和高死亡率的重要疾病之一,临床上最早开展肺康复的是慢性塞性肺部疾病（COPD）和肺结核患者,但它同样成功地应用于其他肺疾病以及肺外科手术如肺移植,肺段、肺叶切除等术前准备或术后康复治疗。肺康复适用于所有呼吸系统疾病或病变趋向稳定的患者,即使患者病情严重,只要选择方法合适,制定恰当的目标,均能从康复中受益。     

Corticosteroids in stable chronic obstructive pulmonary disease

Although systemic corticosteroids are widely used in treating stable chronic obstructive pulmonary disease (COPD), the evidence for their efficacy is still disputed. To reappraise this evidence, the authors used a new analytic strategy in which the 14 available randomized clinical trials were evaluated according to a methodologic "review of systems" and an examination of the statistical precision of the outcome results. Although none of the trials satisfied all of the methodologic criteria for both validity and clinical pertinence, the trials finding steroids efficacious were generally better designed and more statistically precise than trials failing to show efficacy. The authors propose a set of five main methodologic guidelines that require a stable baseline state, a crossover design with suitable washout, adequate doses of corticosteroids, pragmatic designs, and comprehensive choices of outcome events. Attention to these guidelines can help improve both design and evaluation for future trials of systemic steroids for stable COPD.     

老年COPD合并肺心病急性发作期的抗凝治疗

目的探讨低分子肝素在治疗老年COPD合并肺心病急性发作期的疗效。方法收集50例老年肺心病急性加重期患者,随机分为低分子肝素治疗组和常规组各25例,治疗前和用药后第7 d分别采血测定凝血功能;纤维蛋白原;D-二聚体;血液流变学指标,包括红细胞压积、全血粘度、血浆粘度（高切、低切）;以及肺动脉收缩压（SPAP）、氧分压、二氧化碳分压等指标。结果治疗组及常规组病人经治疗后病情均有明显好转,治疗组临床疗效明显优于常规组且不良反应少。结论老年COPD合并肺心病患者,了解其血栓前状态,并通过低分子肝素抗凝治疗,降低肺动脉栓塞的发病率,降低高死亡率,且不良反应少。     

Treatment of stable chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a readily diagnosable disorder that responds to treatment. Smoking cessation can reduce symptoms and prevent progression of disease. Bronchodilator therapy is key in improvement of lung function. Three classes of bronchodilators-beta agonists, anticholinergics, and theophylline-are available and can be used individually or in combination. Inhaled glucocorticoids can also improve airflow and can be combined with bronchodilators. Inhaled glucocorticoids, in addition, might reduce exacerbation frequency and severity as might some bronchodilators. Effective use of pharmacotherapy in COPD needs integration with a rehabilitation programme and successful treatment of co-morbidities, including depression and anxiety. Treatment for stable COPD can improve the function and quality of life of many patients, could reduce admissions to hospital, and has been suggested to improve survival.     

Cerebral bioenergetics in stable chronic obstructive pulmonary disease

Cerebral intracellular energy production (cerebral bioenergetics) via oxidative phosphorylation and the production of adenosine triphosphate (ATP) is critical to cerebral function. To test the hypothesis that patients with chronic stable hypoxia also generate neuronal ATP via an anaerobic metabolism, we studied the changes in cerebral (31)P magnetic resonance spectra ((31)P MRS) in patients with stable chronic obstructive pulmonary disease (COPD), and compared the results with MR spectra from similar areas of the brain in control subjects. Ten patients with stable COPD (age: 65 +/- 9 yr [mean +/- SD]; Pa(O(2)): 8.8 +/- 1.2 kPa; Pa(CO(2)): 6.1 +/- 0.8 kPa; pH 7.42 +/- 0.03, and FEV(1): 41 +/- 20% predicted) and five healthy volunteers underwent cerebral (31)P MRS (TR-5,000 ms) at 1.5 T. When COPD patients were compared with controls, the percentage MR signal with respect to total MR-detectable phosphorus-containing metabolites was increased from inorganic phosphate (Pi) (7.1 +/- 1. 3% versus 3.9 +/- 0.7%, p = 0.0001) and phosphomonoesters (PMEs) (9. 4 +/- 1.2% versus 6.9 +/- 0.3%, p = 0.0001), whereas the signal from phosphodiesters was reduced (34.8 +/- 3.2 versus 40.4 +/- 3.3%, p = 0.015). The ratios of Pi to betaATP (0.8 +/- 0.2 versus 0.4 +/- 0.1, p = 0.001) and of PME to betaATP (1.0 +/- 0.2 versus 0.7 +/- 0.1, p = 0.015) were increased, but the phosphocreatine-to-Pi ratio (2.1 +/- 0.6 versus 3.2 +/- 0.6, p = 0.01) was reduced in patients as compared with controls. This alteration in phosphorus-containing metabolites within cerebral cells provides evidence of extensive use of anaerobic metabolism in hypoxic COPD patients.     

Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.