支气管哮喘防治全球创议(GINA)将哮喘的严重程度分为三度四级，其中三级和四级属于中度和重度哮喘。在整个哮喘人群当中，中重度哮喘大约只占1／3，但在临床上轻度哮喘患者很少就诊，中重度哮喘大约占就诊患者的2／3甚至更多。中重度哮喘患者由于症状明显，频繁就诊，因为哮喘控制不良，经常出现急性发作，需要住院治疗，虽然人数不是很多，但占用了大部分的医疗资源。无论是从提高哮喘防治的整体水平的角度，还是从减少哮喘疾病负担的角度，都应当将中重度哮喘作为哮喘长期管理的主要的目标人群。
直到10年前，慢性阻塞性肺疾病(COPD)还被认为是一种持续进展、不可逆的疾病，一个疗效堪忧、前景暗淡、回报甚微的疾病[1]，正因为如此，很少开展COPD的治疗性试验。最近l0年以来在世界上的大部分国家和地区COPD已构成主要的疾病负担之一[2,3]，带来的直接和间接成本不断增加，促使各国政府和医药企业增加了对COPD临床试验的投入，一系列大型国际多中心临床试验的结果，使我们对COPD知之不多甚至一无所知的侧面有了新的认识，改变了我们固有的观念，并勾勒出COPD未来的前景。在这一领域，中国呼吸病学T作者贡献不多，自主开展的COPD多中心临床试验寥寥无几。回顾上个世纪70年代以来COPD临床试验的历程，无疑对我们有极大的启示作用。
咳嗽是呼吸专科门诊最常见的症状之一，其中大部分又是所谓不明原因的慢性咳嗽(unexplained chronic cough)，即常规影像学检查未发现明确病变者。在此类慢性咳嗽当中，咳嗽变异型哮喘(CVA)是一重要病因，早年Irwin报道，慢性咳嗽的病因包括哮喘和气道高反应(33％)、鼻后滴漏 (28％)、慢性支气管炎(12％)、症状性胃食管反流(10％)、病毒感染后咳嗽(25％)，其他因素包括血管紧张素转换酶抑制剂(ACEI)性咳嗽、精神性咳嗽(10％)以及多因素所致的咳嗽(约占20％) J。在我国尚缺乏CVA发病率的大样本流行病学资料，最近上海同济医院进行了一项调查，在呼吸专科门诊287例由于慢性咳嗽就诊的患者当中，无论是老年人还是中青年患者，CVA均是主要的病因(老年人 34．6％ ，中青年41．5％)，其次为上气道咳嗽综合征(UACS， 19．3％和23．5％)、ACEI相关性咳嗽(16．3％ 和1．7％)、胃食管反流性疾病(GERD，10．6％ 和3．7％) 。由于呼吸科医生以至普通内科医生逐渐熟悉了解这一疾病，在门诊病人当中CVA的比重越来越大，粗略估计CVA大约占不明原因慢性咳嗽病例1／3左右，占哮喘病例1／3左右。另一方面，尽管许多临床医生知晓CVA，但涉及其诊治仍存在不少的问题。
ICS/LABA联合治疗的提出和推广，是近十年来哮喘治疗领域的一个革命性进展。然而，从LABA问世之初，围绕LABA的争议就始终没有平息过。在2010年2月18日，FDA再次发出关于LABA安全性的公告。美国FDA申明LABA绝不应当（should never）单独用于治疗儿童或成人哮喘。制造商须在这类药物产品的标签上加入这一警示，同时采取其他步骤以减少这类药物的过度使用。这些药物包括单独的LABA制剂，如施立稳（Serevent，沙美特罗）和 Foradil（福莫特罗），也包括和ICS的复合制剂如Advair（沙美特罗/氟替卡松）及信必可（布地奈德/福莫特罗）。FDA要求产品标签反映以下信息：●如果没有使用其他哮喘控制性药物，如ICS，则不应当使 用LABA。LABA只能与其他控制性药物联合使用，不应当单独使用。只有对那些其他哮喘控制性药物不能取得充分控制的患者，才能够长期使用 LABA。●使用LABA治疗应当采用取得哮喘症状控制的最短的疗程，一旦哮喘取得控制，只要有可能就应当停用。患者应当用其他的控制性药物维持。●需要使用LABA和ICS治疗的儿童和青少年患者，应当使用一种既含有ICS也含有LABA的复合制剂，以保证治疗的依从性。
根据慢性阻塞性肺疾病全球创议(GOLD)的定义，慢性阻塞性肺疾病急性加重(AECOPD)是“在COPD的自然病程中发生的事件，气紧、咳嗽或／和咳痰等基础症状加重超出正常的日间变异的范围，急性发病，可能需要改变常规的治疗”[1]。AECOPD意味着对医疗卫生资源耗用的增加，如非预约的就医、使用药物增加，使用抗生素或口服皮质激素甚至住院，等等。仅仅依据是否占用卫生资源来定义AECOPD并不适当，这一点还要取决于医疗卫生资源的可获得性，同时有研究提示部分AECOPD可以是自限性的，特别是轻度急性加重。另一方面，占用医疗卫生资源的形式可以大致评估AECOPD的严重程度，如需要增加常规的吸人性药物常常意味着轻度AECOPD，需要短程口服抗生素或糖皮质激素意味着中度AECOPD，而需要住院者多为重度AECOPD。AECOPD是导致COPD患者健康状态降低乃至死亡的主要原因，也是耗用医疗卫生资源从而构成COPD疾病负担的主要部分，需要采用有力的干预措施以降低其发生率[2]。
发生在我国汶川的5·12特大地震为里氏8.0级，造成大量人员伤亡及财产损失。据统计，截至2008年6月2日12时，此次大地震全国共有69 107人遇难，373 577人受伤，18 230人失踪。地震发生后，国家立即动员大量人力搜救受伤人员，使部分被掩埋人员及时从倒塌废墟中挖掘出来。同时，全国卫生系统紧急动员，对这些被抢救出的伤员进行了救治。据卫生部统计，到目前为止，因地震伤病住院治疗合计92,973人，已出院68 565人，仍有11 832人住院，共救治伤员583 891人次（http://scnews.newssc.org/system/2008/06/02/010871823.shtml）。分析既往地震及其他自然灾害中病人的伤害的情况及救治经验，总结此次地震中病人受伤情况及救治过程中的得失，对我们应对以后的地震及其他自然灾害有一定帮助。
ObjectiveTo explore the diagnostic value of fractional exhaled nitric oxide (FeNO) in adult asthma.MethodsPubMed, Embase, Cochrane Library, Wanfang, CNKI and VIP databases were searched for relevant literatures from the time of database establishment to February 2021. Data analysis were made by Revman and Stata.ResultsA total of 44 articles with 47 records and 9654 subjects were included. The diagnosis sensitivity, specificity, positive and negative predictive value of FeNO were 0.71 (95%CI 0.65 - 0.76), 0.80 (95%CI 0.75 - 0.84), 3.47 (95%CI 2.86 - 4.21), and 0.37 (95%CI 0.31 - 0.43), respectively. The diagnostic odds ratio was 9.49 (95%CI 7.13 - 12.61), and the area under the receiver operating characteristic curve was 0.82 (95%CI 0.79 - 0.85).ConclusionsFeNO has certain diagnostic value in diagnosis of asthma. Types of asthma, region and cut-off value all have impact on the diagnostic efficiency of FeNO.
Objective To explore the clinical features and diagnostic procedure of atypical asthma characteristic of chest pain.Methods The patients with unexplained chest pain were screened by lung function test and bronchial provocation test.The diagnosis of asthma was established by therapeutic test and exclusive procedure.The clinical manifestations were analyzed.Results In 56 cases of unexplained chest pain 20 cases were diagnosed as asthma.While all patients referred to clinic with chest pain as chief complaint，a majority of patients (11 cases，85%) showed obscure chest tightness，breath shortness and cough..Some cases reported the same trigger factors as asthma.Chest pain was relieved in all cases after regular antiasthma treatments.Conclusions Chest pain could be a specific presentation of asthma which may be misdiagnosed as other diseases.Bronchial provocation tests and antiasthma therapy should be considered to screen and diagnose this atypical asthma.
Objective To explore the potential roles and mechanism of Wnt5a and its receptors in the pathogenesis of bronchiectasis. Methods From October 2017 to April 2018, outpatients with bronchiectasis who needed bronchoscopy were recruited in the Department of Respiratory and Critical Care Medicine of West China Hospital of Sichuan University. The control group was patients with pulmonary nodules less than 10 mm in diameter by health inspection. Patients who used antibiotics and/or glucocorticoids within the past 4 weeks or had other airway diseases were excluded. Serum and bronchial mucosa were collected for detection of Wnt5a by enzyme-linked immunosorbent assay and real-time polymerase chain reaction (PCR), respectively. The receptor of Wnt5a, Ror2, and the downstream pro-inflammatory cytokines, interleukin (IL)-1β and IL-6, were measured in the bronchial mucosa by real-time PCR. Results From October 2017 to April 2018, 32 outpatients with bronchiectasis were found but only 17 patients finished this study, and simultaneously 18 patients with pulmonary nodules were chosen as control. The level of serum Wnt5a in patients with bronchiectasis were significantly higher than that in the control group (P<0.05). Correlation analyses showed that serum Wnt5a level was positively correlated with the level of serum C reactive protein (r=0.806, P<0.05), but had no relation with the level of white blood cell count, blood neutrophil percentage, pulmonary function or bronchiectasis severe index. The mRNA levels of Wnt5a and its receptor Ror2 in bronchial mucosa of patients with bronchiectasis were significantly higher than those in the control group (P<0.001). The mRNA levels of IL-1β and IL-6 in bronchial mucosa of patients with bronchiectasis were higher than those in the control group (P<0.05). Conclusion Wnt5a may play crucial roles in the development of bronchiectasis through Wnt5a/Ror2 signaling pathways to regulate the release of pro-inflammatory cytokines including IL-1β and IL-6.
Objective To investigate the intervention effect of 3-phosphoinositede dependent protein kinase-1 (PDK1) inhibitor on prostaglandin E2 (PGE2) in smoking-induced chronic obstructive pulmonary disease (COPD) mice. Methods Fifty C57BL/6 male mice were randomly divided into normal control group, smoking group, smoking +low dose PDK1 inhibitor group, smoking + medium dose PDK1 inhibitor group and high dose PDK1 inhibitor group with 10 mice in each group. The mice in the normal control group inhaled phosphate-buffered saline twice a day for 12 weeks, and the mice in the smoking group were fumigated twice a day, 5 days per week for 12 weeks, and the other three groups were given intraperitoneal injection of low-dose PDK1 inhibitor OSU-03012 (0.25 mg/kg), medium-dose PDK1 inhibitor (0.5 mg/kg) and high-dose PDK1 inhibitor (1.0 mg/kg) respectively before smoking. After smoking, lung function was tested, the bronchoalveolar lavage fluid (BALF) of each mouse was taken for cell count, the PGE2 in serum and BALF of mice was determined by enzyme linked immunosorbent assay, and the lung tissue of mice was sectioned with paraffin and stained by hematoxylin-eosin (HE), and pathological changes were observed under microscope. Results Compared with the control group, FEV100/FVC and FEV200/FVC of the mice in each smoking group were significantly decreased (P<0.05); The number of cells in BALF of smoking group was significantly higher than that of normal control group (P<0.05). There was no significant difference in the total number of BALF cells, the proportion of neutrophils and macrophages between the smoking + low-dose PDK1 inhibitor group and the smoking group. However, the total number of BALF cells and the proportion of neutrophils in the smoking + medium dose PDK1 inhibitor group and the high dose PDK1 inhibitor group gradually decreased, while the proportion of macrophages gradually increased, compared with the normal control group, the PGE2 concentrations of serum and BALF in the smoking group and the smoking + PDK1 inhibitor group were significantly higher than those in the control group. Compared with the smoking group, the PGE2 concentrations of serum and BALF in the middle and high dose PDK1 inhibitor groups were significantly lower than those in the smoking group. HE staining of lung tissue showed that there were a large number of inflammatory cell infiltration, alveolar cavity dilatation, alveolar wall rupture and fusion, alveolar formation, significant decrease in the number of alveoli and other pathological changes in the smoking group, which were consistent with the pathological changes of COPD. The inflammatory cell infiltration, mucus obstruction and alveolar dilatation were slightly alleviated in the smoking + low-dose PDK1 inhibitor group, while the inflammatory cell infiltration, alveolar wall thinning and alveolar dilatation were improved in both the medium-dose inhibitor group and the high-dose inhibitor group, and the improvement was more obvious in the high-dose inhibitor group. Conclusion The lung function of the smoked COPD mouse decreases, the airway inflammation is obvious, and the secretion of PGE2 is also increased, while the use of PDK1 inhibitor could reduce the secretion of PGE2, reduce airway inflammation and pathological changes, and improve lung function in a dose-dependent manner.