老年AECOPD患者病毒感染的相关临床特征分析

目的 了解患有慢性阻塞性肺疾病急性发作(Acute exacerbations of chronic obstructive pulmonary disease,AECOPD)老年患者相关病毒感染现状,同时探讨其与临床特征的相关性.方法 选取于2012年7月～2014年10月在我院呼吸科进行治疗并经诊断为AECOPD的老年患者90例作为研究对象,均采集鼻咽拭子,利用多重巢式PCR法对相关呼吸道病毒(9种)进行检测,并根据病毒检测结果将患者分为阳性组及阴性组.搜集两组患者临床特征信息,包括基线资料、临床症状、体征、化验结果及病情变化等,经统计学分析与病毒感染的相关性.结果 纳入的90例患者中,病毒检测阳性有23例,阳性率达25.6％,其中,FluB和hCOV双重感染1例(4.3％)、FluB 4例(17.4％)、RSV2例(8.7％)、hPIV 5例(21.7％)、hCOV 3例(13.0％)、hRV 8例(34.8％),鼻病毒感染患者占据比例最高.对组间临床特征差异进行统计学分析,仅死亡率一项阳性组高于阴性组,且差异具有统计学意义,其他资料差异不存在统计学意义.结论 病毒感染在AECOPD老年患者群体中具有较高检测阳性率,且鼻病毒感染最为多见,病毒感染与患者预后具有一定相关性,但目前临床对病毒感染的特异性检测尚存在一定困难.     

陕西省发热呼吸道症候群病原谱和呼吸道合胞病毒基因特征

目的 分析陕西省发热呼吸道症候群患者咽拭子中16种呼吸道病毒病原谱构成和呼吸道合胞病毒基因特征.方法 2010年1月至2011年1月收集符合监测定义患者咽拭子标本208份,采用基于毛细管电泳的多重RT-PCR反应进行病毒核酸检测,包括人鼻病毒(HRV)、冠状病毒(HCOV)、流感病毒(Flu)、副流感病毒(HPIV)、腺病毒(ADV)、呼吸道合胞病毒(HRSV)、人偏肺病毒(HMPV)以及博卡病毒(HBOV),并对其中HRSV检测阳性的标本进行G基因羧基末端测序与种系进化分析,研究流行于陕西的HRSV分子流行病学特征.结果 总病毒检出率为53％(109/208),检测到的阳性病毒病原构成率分别为:HRSV42.2％、Flu24.5％、PIV20％,HRV13.6％,ADV10.9％,HCOV7.3％、HMPV4.6％和3份HBOV2.7％.有20％(22/109)病例为混合病毒感染,其中有14例为PIV与其他病毒混合感染,15 ～ 39岁年龄组混合感染率最高,差异有统计学意义(P＜0.05).总呼吸道病毒的感染率在各年龄组中差别不大,除Flu、HMPV和PIV外,其他病毒(HRV、HBoV、HCoV、ADV、HRSV)的感染人群主要以0～4岁小儿为主.46例多重RT-PCR HRSV阳性病例中,42例为HRSV A血清型的NA1基因型;2例为B血清型,其中1例为BA9基因型,1例为GB2基因型.结论 @@陕西发热呼吸道症候群由多种呼吸道病毒引起,存在2种或以上病毒的混合感染,其中以PIV与其他病毒混合感染为主.HRSV是2010年陕西省发热呼吸道症候群的主要病原,其中A血清型的NA1基因型是陕西2010年流行的绝对优势型别.     

无创正压通气对夜间慢性阻塞性肺疾病患者呼吸力学和睡眠紊乱的影响

目的 探讨无创正压通气(NIPPV)对夜间慢性阻塞性肺疾病(COPD)患者呼吸力学和睡眠紊乱的影响.方法 选择南方医科大学珠江医院呼吸内科自2010年10月至2011年10月收治的COPD急性加重期住院患者16例,常规肺通气功能测定,经过NIPPV治疗病情稳定后,分别在患者自主呼吸和NIPPV时睡眠状态下进行呼吸力学和多导睡眠图的监测,连续采集并计算各项呼吸和睡眠参数.结果 COPD患者睡眠状态下,NIPPV与自主呼吸相比较,呼吸频率(RR)差异无统计学意义(P＞0.05);潮气量(VΥ)由(0.35±0.10)L升高到(0.45±0.12)L、每分钟通气量(VE)由(6.17±1.15) L/min升高到(7.97±2.34) L/min、平均吸气流量(VΥ/Ti)由(0.24±0.09) L/s升高到(0.39±0.11) L/s、动态肺顺应性(CLdyn)由(43.46±12.75) ml/cm H2O(1cm H2O=98 Pa)升高到(60.23±17.31) ml/cm H2O、指脉氧饱和度(SpO2)由(83.55±5.07)％升高到(95.67±5.38)％,差异均有统计学意义(P＜0.05～P＜0.001);吸气时间占呼吸周期比值(Ti/Ttot)由0.43±0.11降低到0.33±0.08、气道阻力(Raw)由(25.64±6.02) cm H2O/L-1·s-1降低到(20.34±3.67) cm H2O/L-1·s-1、压力-时间乘积(PTP)由(423.12±89.06) cm H2O· s-1·min-1降低到(170.44±41.53) cm H2O· s-1· min-1、呼气末二氧化碳分压(PETCO2)由(63.74±8.45) mm Hg(1 mm Hg=0.133 kPa)降低到(45.32±5.74) mm Hg,差异均有统计学意义(P＜0.05～ P＜0.001).睡眠效率(SEF％)由(74.23±12.78)％升高到(84.41±15.11)％、快速动眼睡眠时间占总睡眠时间百分比(REM/TST％)由(12.16±7.38)％升高到(19.35±9.41)％、慢波睡眠占总睡眠时间百分比(SWS/TST％)由(5.38±3.35)％升高到(13.68±7.25)％、夜间基础指脉氧饱和度(SpO2％base)由(84.77±4.97)％升高到(96.46±4.32)％、夜间最低指脉氧饱和度(SpO2％lowest)由(75.03±6.32)％升高到(85.78±4.84)％,差异均有统计学意义(P＜0.05);睡眠潜伏期(SLT)由(63.32±25.26) min降低到(30.57±8.02) min、微觉醒指数由(38.24± 17.57)次/h降低到(25.66±15.78)次/h、呼吸暂停低通气指数(AHI)由(3.63±0.76)次/h降低到(2.51±0.67)次/h、呼吸紊乱最长时间(BDLon)由(40.02±8.83)s降低到(21.37±5.66)s、指脉氧饱和度低于90％时间占总睡眠时间百分比(SpO2％＜90％/TST％)由(29.36±9.74)％降低到(17.72±5.27)％,差异均有统计学意义(P＜0.05).结论 NIPPV可显著改善睡眠状态下COPD患者的呼吸力学异常,降低了气道阻力和呼吸做功,改善了COPD患者夜间低氧和低通气状态,一定程度上改变了COPD患者的异常睡眠结构,纠正了睡眠紊乱,睡眠质量显著提高.     

同步悬空俯卧位对稳定期慢性阻塞性肺疾病患者肺通气功能的影响

探讨同步悬空俯卧位对稳定期慢性阻塞性肺疾病(COPD)患者肺通气功能情况的影响。方法 2009年6月至10月本院门诊就诊的12例稳定期COPD患者,在人工呼吸床上随机采用仰卧位、悬空俯卧位、托平俯卧位、同步悬空俯卧位4种不同体位,每个体位观察10 min,通过NICO无创心肺功能监测系统连续测定患者在不同体位时的心率、动脉血氧饱和度、呼气末二氧化碳分压等一般生命体征和呼吸频率、潮气量、肺泡潮气量、生理无效腔(Vd/Vt)、吸气峰流速(PIF)、呼气峰流速(PEF)等呼吸动力学指标。根据患者的肺功能按美国胸科协会(ATS)和欧洲呼吸学会(ERS)制定的肺功能共同指南标准划分不同阻塞程度,并分析存在通气功能障碍患者的潮气量和呼吸频率等肺功能变化情况。结果 4种体位对心率、动脉血氧饱和度、呼气末二氧化碳分压无明显的影响。呼吸频率在4种体位中由慢至快呈现同步悬空俯卧位＜仰卧位＜托平俯卧位＜悬空俯卧位的趋势[(14.8±3.2)次/min＜(17.6±4.5)次/min ＜(18.4±3.4)次/min＜(19.5±3.4)次/min,均P＜0.05],潮气量和肺泡潮气量由高至低呈现同步悬空俯卧位＞仰卧位＞托平俯卧位＞悬空俯卧位的趋势。生理无效腔、PIF、PEF各组差异无统计学意义。3例重度和5例极重度阻塞通气功能障碍的患者潮气量在各体位间差异均无统计学意义,呼吸频率则在同步悬空俯卧位时最低,分别为(15.3±1.8)次/min、(16.6±1.8)次/min,且与悬空俯卧位时的呼吸频率差异有统计学意义[(19.4±3.4)次/min、(21.4±3.6)次/min,均P＜0.05]。结论 同步悬空俯卧位与其他两种俯卧呼吸体位一样,经短时间观察是安全稳定的,同步悬空俯卧位显著降低患者的呼吸频率、增加潮气量。在阻塞性通气功能障碍的情况下,对潮气量的影响不明显,但仍能降低患者的呼吸频率。     

Detection of multiple viral and bacterial infections in acute exacerbation of chronic obstructive pulmonary disease: A pilot prospective study

Few studies have evaluated the contribution of multiple virus and bacterial infections in acute exacerbation of chronic obstructive pulmonary disease. This study estimated the burden of multiple viral and bacterial respiratory infections in moderate to very severe chronic obstructive pulmonary disease patients that were prospectively followed‐up during a 12‐month pilot study. Clinical data were collected monthly and sputum was collected at the time of each acute exacerbation event. Classical culture techniques for bacteria and multiplex polymerase chain reaction (PCR) and microarray detection assays were performed to identify viral and atypical bacterial pathogens in the sputum. Overall, 51 patients were included and 45 acute exacerbation events were investigated clinically and microbiologically. Among the 45 acute exacerbation events, 44% had evidence of viral infection involving human rhinovirus (HRV) and metapneumovirus (hMPV) in 20% and 18%, respectively. Intracellular bacteria were not found in sputum by PCR. Common bacterial pathogens were identified in 42% of acute exacerbation patients, most frequently Branhamella catarrhalis, Streptococcus pneumoniae and Haemophilus influenzae. Viral or virus and bacteria co‐infections were detected in 27% of acute exacerbation events (n = 12) with HRV and hMPV involved in 92% of cases. Patients with co‐infections did not present greater clinical severity scores at exacerbation and more recurrence of acute exacerbation events at 3 and 6 months than those with single infections (P > 0.4). These results suggest that HRV and hMPV may be contributors or cofactors of AECOPD. These findings indicate that viral or virus and bacterial co‐infections do not impact significantly on the clinical severity of acute exacerbation of chronic obstructive pulmonary disease and recurrence at 3 and 6 months. J. Med. Virol. 85:866–873, 2013. © 2013 Wiley Periodicals, Inc.     

沙丁胺醇、丙酸倍氯米松和溴化异丙托品联合雾化吸入治疗慢性阻塞性肺疾病急性加重

目的 探讨沙丁胺醇、丙酸倍氯米松和溴化异丙托品三者联合雾化吸入对慢性阻塞性肺疾病急性加重(AECOPD)患者肺功能及动脉血气的影响.方法 以本院2011年1月至2014年1月收治的AECOPD患者108例为研究对象,随机数字表分为对照组(n=54)和联合治疗组(n=54).对照组采用常规治疗,联合治疗组加用沙丁胺醇、丙酸倍氯米松和溴化异丙托品雾化吸入治疗.治疗前及治疗后第7天进行两组患者动脉血气分析,记录动脉血pH值、动脉血氧分压(PaO2)和动脉血二氧化碳分压(PaCO2);并测定肺功能,记录第1秒用力呼气容积(FEV1)、FEV1占预计值％(FEV1％pred)和用力肺活量(FVC).结果 血气分析显示,治疗前两组患者动脉血pH值、PaO2和PaCO2差异均无统计学意义(均P＞0.05).治疗后两组患者动脉血pH值、PaO2和PaCO2均较治疗前显著改善(均P＜0.05).与对照组比较,治疗后联合治疗组患者PaO2明显增加[(79.5±9.4) mmHg比(64.0±7.7) mmHg,P＜0.05;1mmHg=0.133 kPa],PaCO2明显降低[(49.3±11.5)mmHg比(61.0±12.2)mmHg,P＜0.05].治疗后两组患者动脉血pH值差异无统计学意义(P＞0.05).治疗前两组患者FEV1、FEV1 ％pred、FVC差异均无统计学意义(均P＞0.05).治疗后两组患者FEV1、FEV1％pred、FVC均较治疗前有显著改善(均P＜0.05).与对照组比较,治疗后联合治疗组患者FEV1、FEV1％ pred、FVC均显著升高[(1.35±0.14)L比(1.18±0.11)L,(61.15±9.51)％比(54.55±8.71)％,(2.49±0.16)L比(2.19±0.17)L,均P＜0.05].结论 沙丁胺醇、丙酸倍氯米松和溴化异丙托品三者联合雾化吸入治疗AECOPD疗效较好.     

重症慢性阻塞性肺疾病急性加重期下呼吸道感染病原菌及其耐药性分析

目的:了解重症慢性阻塞性肺疾病急性加重期(AECOPD)患者下呼吸道感染病原菌的特点及耐药情况,指导临床合理用药。方法:取我院2007年10月~2010年9月住院的189例重症AECOPD患者合格痰标本及防污染毛刷刷取的气管内分泌物标本进行细菌培养、鉴定及药敏试验。结果:共分离病原菌147株,其中以革兰阴性杆菌占首位,达64.6%,依次为铜绿假单胞菌、不动杆菌、大肠埃希菌和阴沟肠杆菌。其次是革兰阳性球菌,占21.8%。真菌占13.6%,以白念珠菌检出率最高。药敏结果显示革兰阴性杆菌对第三代头孢菌素耐药严重,对哌拉西林-他唑巴坦、碳青霉烯类抗生素较敏感;革兰阳性球菌对青霉素、克林霉素、红霉素耐药率高,未发现对万古霉素耐药。结论:重症AECOPD患者下呼吸道感染病原菌以革兰阴性杆菌为主,且耐药现象明显,二重感染逐年增加,且占有较大比重。临床AECOPD患者选用抗生素治疗时应重视细菌培养及药敏试验,减少不合理用药,减少耐药菌株与二重感染产生。     

慢性阻塞性肺病患者心理状况及影响因素

调查慢性阻塞性肺疾病（COPD）患者心理状况和影响因素，对60例患者和60例健康者对照，应用焦虑和抑郁情绪表（HAO）对两组进行问卷调查，结果显示，患者评分显著差于健康者，年龄、病程和通气功能与患者抑郁症状和总分呈显著性相关，提示患者伴有心理障碍，重视和兼顾心理症状诊治颇有必要。     

Immune response in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a major public health problem because of its high prevalence, rising incidence and associated socio-economic cost. The inhalation of toxic particles and gases, mostly tobacco smoke, is the main risk factor for COPD. Yet, not all smokers are equally susceptible to these toxic effects and only a percentage of them develop the disease (so-called ‘susceptible smokers’). This, in combination with the observation that COPD shows familial aggregation, suggests that the genetic background of the smoker is a key element in the pathogenesis of the disease. On the other hand, it is well established that ‘susceptible’ smokers exhibit an enhanced inflammatory response of the lung parenchyma as compared with ‘resistant’ smokers (i.e., those who manage to maintain lung function within the normal age range despite their habit). Importantly, in COPD patients this inflammatory response does not resolve after quitting smoking, again at variance with resistant smokers. All in all, these observations suggest that the pathogenesis of COPD may involve, in some patients, an autoimmune component which contributes to the enhanced and persistent inflammatory response that characterizes the disease. Here we: i) review briefly the pathobiology of COPD; ii) present the available scientific evidence supporting a potential role for autoimmunity in COPD; iii) propose a three-step pathogenic hypothesis in the transition from smoking to COPD; and iv) discuss potential implications for the diagnosis and treatment of this frequent, growing, devastating and costly disease.     

慢性阻塞性肺疾病急性加重患者呼吸道病毒的检测分析

目的 探讨呼吸道病毒感染与慢性阻塞性肺疾病急性加重(AECOPD)的相关性.方法 随机选择140例慢性阻塞性肺疾病急性加重(AECOPD)患者,60例健康老年志愿者为对照组,分别检测呼吸道合胞病毒(RSV)、单纯疱疹病毒(HSV)、腺病毒(ADV)、巨细胞病毒(CMV)、副流感病毒(PIV)、流感病毒A/B(FluA/B)特异性抗体IgM水平,对组间阳性率进行比较.结果 AECOPD组患者中IgM阳性率依次为RSV＞PIV＞ FluA/B＞CMV＞ADV＞ HSV.AECOPD组与对照组各病毒抗体阳性率比较差异有统计学意义(P＜0.05).结论 病毒感染是AECOPD重要因素,病毒感染参与了AECOPD病情的进展过程,在呼吸道病毒流行的季节应做好预防工作.     

内源性硫化氢调节慢性阻塞性肺疾病大鼠氧化/抗氧化平衡

目的: 探讨硫化氢(H₂S)在吸烟(CS)联合脂多糖(LPS)建立的大鼠慢性阻塞性肺疾病(COPD)模型中的抗氧化作用。方法: 32只清洁级健康雄性SD (Sprague-Dawley)大鼠,随机分为4组:对照组(control)、CS+LPS组、CS+LPS+硫氢化钠(NaHS,H₂S供体)组、CS+LPS+炔丙基甘氨酸(PPG,胱硫醚-γ-裂解酶抑制剂)组。30 d后测定大鼠肺功能,光镜观察肺组织病理变化并予评分;测定血浆中H₂S含量及肺组织中胱硫醚-γ-裂解酶(CSE)蛋白表达;检测肺组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)及过氧化氢酶(CAT)活性以反映氧化应激。结果: 与对照组相比,CS+LPS组大鼠呼气峰流速(PEF)下降24%(P<0.01),气道内压(IP)升高66%(P<0.01),肺组织病理评分升高(P<0.01);NaHS或PPG干预后,与CS+LPS组比较,肺功能无改变;NaHS干预后,病理评分下降(P<0.05)。在第16 d时,CS+LPS组血浆中H₂S含量较对照组升高26%(P<0.05);30 d后,CS+LPS+PPG组较CS+LPS组H₂S含量降低22%(P<0.01)。CS+LPS组中CSE蛋白表达较对照组升高(P<0.01);与CS+LPS组比较,CS+LPS+NaHS组和CS+LPS+PPG组无显著差异。与对照组相比,CS+LPS组肺组织中MDA含量升高24%(P<0.05),总SOD活性升高47%(P<0.01),CAT活性升高52%(P<0.01);与CS+LPS组相比,NaHS干预后, MDA含量降低21%(P<0.05),总SOD活性及CAT活性无显著差异;而PPG干预后,总SOD活性下降33%(P<0.05)。结论: H₂S在COPD大鼠中起到抗氧化作用,CSE/H₂S途径可能参与COPD疾病的发展。     

谷氨酰半胱氨酸连接酶催化亚单位基因甲基化而非多态性与慢性阻塞性肺疾病相关

目的 探讨谷氨酰半胱氨酸连接酶催化亚单位(GCLC)基因多态性和甲基化与慢性阻塞性肺疾病(COPD)易感的相关性.方法 收集166例COPD患者为COPD组,同期与上述COPD患者相似的非COPD人群166例为对照组.使用基因测序法检测两组人群GCLC基因启动子区域的单核苷酸多态性(SNP),分析各SNP位点的单倍体型与COPD发病的关系.使用甲基化DNA免疫共沉淀芯片(MeDIP-chip)检测两组人群GCLC启动子区域甲基化水平,进行两组人群GCLC mRNA表达水平和血谷胱甘肽(GSH)浓度的比较.结果 通过直接测序法在GCLC启动子区域鉴定出12个SNP,其中4个SNP,即-2137MT、-129C/T、+27591C/G和+37764MG在COPD组和对照组人群中的发生率超过10％.-129C/T与-2137MT、+27591C/G、+37764MG均处于连锁不平衡.COPD组和对照组人群上述4个SNP的等位基因频率和基因型频率差异均无统计学意义(均P＞0.05).MeDIP-chip检测显示COPD组GCLC启动子区域甲基化水平明显高于对照组(P＜0.001).COPD组肺组织标本GCLC mRNA表达水平明显低于对照组(3.71±0.48比5.16±0.39,P＜0.05),血谷胱甘肽(GSH)水平也低于对照组[109.72±32.38)mg/L比(179.87±46.23) mg/L,P＜0.05].结论 中国人群GCLC启动子区域甲基化而非GCLC基因多态性与COPD相关.     

慢性阻塞性肺疾病动物模型研究概况

慢性阻塞性肺病(chronic obstructive pulmonary disease,COPD)由基因-环境交互作用而致病,目前COPD拟临床研究大多是采用诱发性动物模型。动物选择根据实际需要以鼠、猪和灵长类动物为主。造模方法主要是将可诱发COPD的危险因素,强加于动物以诱导COPD的发生。造模时间的长短则与诱因的性质和暴露量密切相关。模型建成后主要从肺功能、肺部病理改变等方面,并采用血清炎症因子、细胞因子检测等手段对模型进行评价,但在实际操作中尚有待进一步的评估。     

通光散对慢性阻塞性肺疾病模型大鼠气道阻力和气道炎症的影响

目的 建立慢性阻塞性肺疾病(COPD)大鼠模型,观察通光散对COPD模型大鼠气道阻力和气道炎症的影响.方法 60只雄性SD大鼠按随机数字表法分为正常对照组、模型组、阳性对照组和通光散组,每组15只.模型组、阳性对照组和通光散组采用熏烟和气管给予内毒素脂多糖的复合方法建立COPD大鼠模型.第15天开始各组大鼠给予每周5次药物干预,通光散组给予通光散汤3 ml灌胃;阳性对照组给予羧甲司坦150 mg/kg灌胃;正常对照组和模型组给予生理盐水3ml灌胃.第90天实验结束,进行大鼠有创气道阻力测定和肺组织病理检测.结果 正常对照组、模型组、阳性对照组和通光散组大鼠有创气道阻力分别为(0.227±0.027) cm H2O· ml-1·s-1、(0.425±0.117)cm H2O·ml-1·s-1、(0.263±0.043) cm H2O· m l-1·s-1、(0.269±0.050)cm H2O·ml-1· s-1(1 cm H2O=0.098 kPa).模型组大鼠气道阻力高于其他3组(均P＜0.05),而其余3组之间差异均无统计学意义(均P＞0.05).病理检测显示,模型组大鼠肺组织有严重的支气管组织和肺泡组织病理改变,而通光散组和阳性对照组的病变程度均较轻.结论 通光散可以降低COPD模型大鼠的气道阻力,抑制气道炎性反应.     

Leukotriene pathway inhibitors in asthma and chronic obstructive pulmonary disease

Leukotrienes can be generated from a wide variety of cells including mast cells and eosinophils. The biological properties of these products include bronchial smooth muscle contraction, stimulation of mucous production, enhancement of vascular permeability, and recruitment of eosinophils. These properties can contribute significantly to the pathobiology of asthma. Recently, zafirlukast and montelukast, and zileuton, leukotriene D₄ receptor antagonists and 5-lipoxygenase inhibitors, respectively, have been developed and are available for treating asthma. Studies have found these compounds modify bronchospasm with exercise, the pulmonary reaction to aspirin in sensitive subjects, and the airway response to inhaled antigen. Furthermore, in patients with chronic asthma, leukotriene modifiers improve airflow obstruction, decrease the need for rescue medication, and diminish symptoms. Moreover, these drugs can prevent asthma exacerbations. However, there is little evidence that these medications have potent anti-inflammatory activity. Nonetheless, leukotriene modifiers represent new, and effective, therapeutics in the treatment of asthma; at present, the positioning of these products in relationship to inhaled corticosteroids, for example, in the treatment of asthma has not been fully defined but will emerge with further study and use in the clinic setting.     

Severe chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) exacts a heavy toll on society, yet its prevention, diagnosis and treatment receives inadequate attention from both the medical community and from society at large. Guidelines released in 2001 from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) are aimed at redressing this inequity. In this review, we integrate information from the GOLD guidelines with recent updates on the prevention, treatment and management as related specifically to the most severe form of this disease. In order to help distinguish COPD from other disorders that may mimic or confound its treatment, we place particular emphasis on the definition, underlying pathophysiology and diagnosis of COPD. In addition, we discuss future directions in pharmacotherapy.     

Potential drug-drug interactions in hospitalized patients with chronic heart failure and chronic obstructive pulmonary disease

Introduction

Polypharmacy is common in patients with chronic heart failure (HF) and/or chronic obstructive pulmonary disease (COPD), but little is known about the prevalence and significance of drug-drug interactions (DDIs). This study evaluates DDIs in hospitalized patients.

Material and methods

We retrospectively screened medical charts over a 6-month period for diagnosis of chronic HF and/or COPD. Potential DDIs were evaluated using Lexi-Interact software.

Results

Seven hundred and seventy-eight patients were included in the study (median age 75 years, 61% men). The median number of drugs on admission and discharge was 6 (interquartile range (IQR) 4–9) and 7 (IQR 5–), respectively (p = 0.10). We recorded 6.5 ±5.7 potential DDIs per patient on admission and 7.2 ±5.6 on discharge (p = 0.2). From admission to discharge, type-C and type-X potential DDIs increased (p < 0.05 for both). Type X interactions were rare (< 1%), with the combination of a β-blocker and a β₂ agonist being the most common (64%). There were significantly more type-C and type-D potential DDIs in patients with chronic HF as compared to patients with COPD (p < 0.001). Patients with concomitant chronic HF and COPD had more type-C and type-X potential DDIs when compared to those with individual disease (p < 0.005). An aldosterone antagonist and ACE inhibitor/ARB were prescribed to 3% of chronic HF patients with estimated glomerular filtration rate < 30 ml/(min × 1.73 m²).

Conclusions

The DDIs are common in patients with chronic HF and/or COPD, but only a few appear to be of clinical significance. The increase in potential DDIs from admission to discharge may reflect better guideline implementation rather than poor clinical practice.     

慢性阻塞性肺疾病骨骼肌萎缩的治疗现状

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)不仅是一种局限于呼吸道和肺部的疾病,还是一种可以累及肺外各器官的全身疾病,其肺外效应包括心血管疾病、焦虑和抑郁及骨骼肌萎缩等疾病,其中骨骼肌萎缩严重影响患者的生活质量及预后,造成巨大的社会和经济负担.然而,肌肉组织固有的适应性为骨骼肌萎缩提供了治疗机会.适当的干预措施可逆转或延迟骨骼肌萎缩的发展进程.     

冬虫夏草对慢性阻塞性肺疾病模型鼠还原型谷胱甘肽-氧化型谷胱甘肽平衡和Thl—Th2型细胞因子的影响

目的探讨冬虫夏草对大鼠慢性阻塞性肺疾病（COPD）模型还原型谷胱甘肽（GSH）-氧化型谷胱甘肽（GSSG）失衡的干预作用及对Thl．Th2型细胞因子的影响。方法18只sD大鼠完全随机分为COPD对照组、冬虫夏草干预组和N-乙酰半胱氨酸（NAC）干预组（每组各6只）,分别在COPD模型制作中胃饲生理盐水、冬虫夏草和NAC,观察大鼠肺组织病理改变。检测冬虫夏草和NAC干预后支气管肺泡灌洗液（BALF）中Thl．Th2型细胞因子和巨噬细胞中GSH和GSH／GSSG变化。结果与COPD对照组（32＋13）相比,冬虫夏草干预组和NAC干预组的平均肺泡计数增加（49＋10,52＋14,P〈O．05）。冬虫夏草干预组和NAC干预组BALF中巨噬细胞GSH水平和GSH-GSSG较COPD对照组升高（t=3．06,t=3．24;t=2．36,t=2．82;均P〈0．05）。冬虫夏草干预组和NAC干预组BALF上清液中Thl型细胞因子IFN-y水平较COPD对照组升高（f=2．34,t=2．32,P〈0．05）。结论冬虫夏草可能通过提高COPD模型巨噬细胞内GSH水平,补充抗氧化水平而达到纠正Thl—Th2失衡的免疫调节。