Demonstration of dilatation of peripheral airways

Summary. To investigate the ability of various lung-function tests to demonstrate dilatation of peripheral airways, ten asthmatics inhaled increasing doses of a f2-agonist by two different and controlled techniques. Low inspiratory flow with a long post-inspi-ratory pause favoured peripheral deposition, and a high inspiratory flow with a short post-inspiratory pause favoured central deposition of drug in the airways. Ordinary spirometry, maximum expiratory flow rates after breathing air as well as a helium-oxygen mixture, a single breath N₂-test and resistance of the respiratory system were obtained before and after each of five terbutaline doses with both inhalation techniques. By using a double-dummy technique, the study could be performed double blinded. Effects were compared at doses giving equal effects on PEF, assumed to represent equal deposition of bronchodilator and effects on central airways. At such ‘iso A PEF doses’, particularly FVC and the slope of phase III of the N₂-test improved more following the slow inhalation technique. It is concluded that changes in those tests reflect dilatation in peripheral airways in asthmatics.,     

Pronounced bronchial hyper-responsiveness and asthma severity

Summary. Fifty-six asthmatics from an asthma ward or from an asthma out-patient clinic were challenged with two low concentrations (0–03 and 0–012 mg) of metacholine chloride in order to assess the relationship between pronounced hyper-responsiveness and asthma severity in a clinical setting. Only inhaled bronchodilators were stopped before challenge. Asthma severity was assessed retrospectively and prospectively on the basis of treatment, number of days in hospital, intensive care, number of emergency visits and days on sick-leave. The results show that pronounced hyper-responsiveness (n= 28) is not associated with asthma severity. It is concluded that a single simplified test of pronounced bronchial hyper-responsiveness, performed without taking into consideration the actual state of the disease and without stopping all medication, is of no help in identifying the patients with the clinically most severe asthma and worst prognosis.,     

‘You have to learn to live with it’: a qualitative and quantitative study of older people with asthma

Introduction: Asthma mortality has declined overall because of a range of public health initiatives. In western countries, the majority of asthma deaths now occur in people over the age of 50. The reasons for the poorer response of older age groups to public health asthma initiatives are not known. Objectives: We undertook a study to investigate the disease perspectives of older people with asthma and barriers which may exist and prevent optimal asthma care. Methods: Fifty‐five participants (16 male and 39 female) aged over 50 from an inner city, suburban area and a rural region were recruited. Lung function was measured, and questionnaire data on asthma symptoms, knowledge and control, medication use and respiratory health were collected. Participants were also interviewed in‐depth, and the quantitative and qualitative data were triangulated. Results: Participants with a duration of asthma for >30 years reported significantly fewer symptoms and better quality of life irrespective of asthma severity, indicating less appreciation of symptoms in those with a long asthma duration. Interviews revealed this was related to previous asthma management strategies when treatment options were limited. Participants with a recent diagnosis sought understanding of asthma and the reason for their illness. Initiatives to improve asthma care in older people need to reflect these findings. Conclusions: Self‐management strategies for older people need to be tailored according to the time of disease onset and the duration of disease. Please cite this paper as: Goeman DP, O’Hehir RE, Jenkins C, Scharf SL and Douglass JA. ‘You have to learn to live with it’: a qualitative and quantitative study of older people with asthma. The Clinical Respiratory Journal 2007; 1:99–105.     

Longitudinal decline in pulmonary function in atopic cough and cough variant asthma

OBJECTIVE: Cough variant asthma and atopic cough are different clinical manifestations of eosinophilic airway inflammation presenting with isolated chronic non-productive cough. The aim of this study was to examine the longitudinal change in pulmonary function in cough variant asthma and atopic cough. METHODS: Longitudinal change in FEV1 was prospectively examined in 20 patients with cough variant asthma, 14 patients with atopic cough and 271 asymptomatic healthy subjects. All were lifetime non-smokers. Of the 20 cough variant asthma patients, 13 were taking long-term inhaled corticosteroid therapy (ICS) (beclomethasone dipropionate 615 +/- 58 micro g/day) and the other seven were not. Spirometry was taken at first visit, after cough was almost completely relieved on therapy, and at least once every year for 5 or more years afterwards. RESULTS: The slope of longitudinal change in FEV1 was not significantly different among cough variant asthma patients (- 0.029 +/- 0.007/year), atopic cough patients (- 0.021 +/- 0.022/year) and asymptomatic subjects (- 0.028 +/- 0.002 L/year). In patients with cough variant asthma, the slope in patients not taking inhaled corticosteroids (ICS) was 0.032 +/- 0.007 L/year, which was not significantly different from that in patients taking ICS (- 0.027 +/- 0.010 L/year). CONCLUSION: Pulmonary function decline is not greater in cough variant asthma than atopic cough and the normal population, and long-term ICS has no effect on the decline in cough variant asthma.     

变应性鼻炎患者血清一氧化氮水平变化及临床意义

目的 :通过 5 6例变应性鼻炎患者血清一氧化氮 (NO)浓度的观察 ,研究内源性NO水平的变化与变应性鼻炎病理过程的关系及其临床意义。方法 :血清NO水平采用硝酸还原酶比色法测定。结果 :变应性鼻炎组血清NO水平显著高于正常对照组 (q =2 7.2 3,P <0 .0 1)及慢性鼻炎组 (q =15 .2 3,P<0 .0 1)。慢性鼻炎组与正常对照组血清NO浓度差异无显著性 (q =1.89,P >0 .0 5 )。结论 :变应性鼻炎患者血清中NO水平显著高于正常对照组及慢性鼻炎组 ,提示NO在变应性鼻炎的发病过程中可能起重要作用 ,对其机理的研究为变应性鼻炎的治疗提供新的方法。     

可溶性白细胞介素-2受体与支气管哮喘

支气管哮喘是常见病和多发病，多种细胞因子参与了支气管哮喘的发病过程。发作期支气管哮喘患者血清可溶性白细胞介素—2受体(SIL—2R)水平明显增高。本文就这方面的进展作一综述。     

Probiotic-induced suppression of allergic sensitization and airway inflammation is associated with an increase of T regulatory-dependent mechanisms in a murine model of asthma

BACKGROUND: Microbial intestinal colonization in early in life is regarded to play a major role for the maturation of the immune system. Application of non-pathogenic probiotic bacteria during early infancy might protect from allergic disorders but underlying mechanisms have not been analysed so far. OBJECTIVE: The aim of the current study was to investigate the immune effects of oral application of probiotic bacteria on allergen-induced sensitization and development of airway inflammation and airway hyper-reactivity, cardinal features of bronchial asthma. METHODS: Newborn Balb/c mice received orally 10(9) CFU every second day either Lactobacillus rhamnosus GG or Bifidobacterium lactis (Bb-12) starting from birth for consecutive 8 weeks, during systemic sensitization (six intraperitoneal injections, days 29-40) and airway challenge (days 54-56) with ovalbumin. RESULTS: The administration of either Bb-12 or LGG suppressed all aspects of the asthmatic phenotype: airway reactivity, antigen-specific immunoglobulin E production and pulmonary eosinophilia (mean: 137 vs. 17 and 13 cellsx10(3)/mL, respectively). Antigen-specific recall proliferation by spleen cells and T-helper type 2 cytokine production (IL-4, IL-5 and IL-10) by mesenteric lymph node cells also showed significant reduction, while TGF production remained unchanged. Oral LGG administration particularly suppressed allergen-induced proliferative responses and was associated with an increase in numbers of TGF-beta-secreting CD4+/CD3+ T cells in mesenteric lymph nodes (6.5, 16.7%) as well as nearly 2-fold up-regulation of Foxp3-expressing cells in peribronchial lymph nodes. CONCLUSIONS: Neonatal application of probiotic bacteria inhibits subsequent allergic sensitization and airway disease in a murine model of asthma by induction of T regulatory cells associated with increased TGF-beta production.     

IL-12表达障碍与支气管哮喘关系研究进展

支气管哮喘是由Th2介导的Ⅰ型变态反应,与内源性IL-12生成不足有关,该文综述了IL-12的生物学效应、IL-12表达障碍与支气管哮喘的关系以及IL-12、重组IL-12（rIL-12）在支气管哮喘治疗方面的应用前景。IL-12与Ⅰ型变态反应关系密切,内源性IL-12表达不足使支气管哮喘患者免疫系统向Th2方向偏移,在过敏原或病毒等外因的刺激下发生支气管哮喘。用IL-12对支气管哮喘进行免疫治疗已在动物实验中取得了显著效果,将IL-12、rIL-12或IL-12的内源性诱生物应用于人体的方法也在不断探索中并取得了一定效果,基于IL-12的治疗方法可能为支气管哮喘等变应性疾病的免疫治疗开辟新的途径。