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Airway Reactivity (airway + reactivity)
Selected AbstractsAirway reactivity in children before and after stem cell transplantationPEDIATRIC PULMONOLOGY, Issue 9 2009Lea Bentur MD Abstract Stem cell transplantation (SCT) is associated with pulmonary complications. We encountered several children post-SCT with a clinical picture suggestive of airway hyper-reactivity (AHR) and evidence of reversible airway obstruction that was not reported pre-transplant. We evaluated the possibility of increased AHR as assessed by methacholine challenge test (MCT) following the course of SCT, and assessed a possible correlation between AHR and pulmonary complications. This was a prospective study evaluating consecutive patients referred for SCT to the Department of Pediatric Hemato-Oncology. Evaluation included pulmonary function test and MCT before and after SCT, and assessment of pulmonary complications. Twenty-one of 33 patients completed the study. The mean PC20 was 14.3,±,4.1 mg/ml prior to SCT; afterward the mean PC20 decreased to 11.2,±,5.6 mg/ml (P,=,0.018). The number of patients with airway reactivity (PC20,,,8 mg/ml) increased from 2/21 patients before SCT to 8/21 patients after SCT (P,=,0.043; McNemar test with Yates correction). Pulmonary complications and hospitalization were recorded in 33.3% of the patients (7/21 patients): 62.5% of the patients (5 patients) with AHR compared to 15.4% (2 patients) in the group without AHR (P,=,0.041; Fisher exact test). There were 10 hospitalizations among the 8 patients with positive MCT compared to 2 hospitalizations in 13 patients with negative MCT (median 1 vs. 0, P,=,0.045; Mann,Whitney U -test). Increased airway reactivity was observed in our study following the course of SCT. Positive MCT after SCT may be associated with increased risk of pulmonary complications. Larger prospective studies are needed to evaluate the possible mechanisms responsible for increased AHR and the clinical importance of these findings. Pediatr Pulmonol. 2009; 44:845,850. © 2009 Wiley-Liss, Inc. [source] Clinical and inflammatory features of occupational asthma caused by persulphate salts in comparison with asthma associated with occupational rhinitisALLERGY, Issue 6 2010G. Moscato To cite this article: Moscato G, Pala G, Perfetti L, Frascaroli M, Pignatti P. Clinical and inflammatory features of occupational asthma caused by persulphate salts in comparison with asthma associated with occupational rhinitis. Allergy 2010; 65: 784,790. Abstract Background:, The relationships between asthma and rhinitis are still a crucial point in respiratory allergy and have scarcely been analysed in occupational setting. We aimed to compare the clinical and inflammatory features of subjects with occupational asthma only (OA) to subjects with OA associated to occupational rhinitis (OAR) caused by persulphate salts. Methods:, The clinical charts of 26 subjects diagnosed in our Unit as respiratory allergy caused by ammonium persulphate (AP), confirmed by specific inhalation challenge (SIC), were reviewed. Twenty-two out of twenty-six patients underwent pre-SIC-induced sputum challenge test (IS) and 24/26 underwent nasal secretion collection and processing. Results:, Twelve out of twenty-six patients received a diagnosis of OA-only and 14/26 of OAR. Duration of exposure before diagnosis, latency period between the beginning of exposure and asthma symptom onset, basal FEV1, airway reactivity to methacholine and asthma severity did not differ in the two groups. Eosinophilic inflammation of upper and lower airways characterized both groups. Eosinophil percentage in IS tended to be higher in OAR [11.9 (5.575,13.925)%] than in OA-only [2.95 (0.225,12.5)%] (P = 0.31). Eosinophilia in nasal secretions was present both in subjects with OAR [55 (46,71)%] and in subjects with OA-only [38 (15,73.5)%], without any significant difference. Discussion:, Our results indicate that OA because of ammonium persulphate coexists with occupational rhinitis in half of the patients. Unexpectedly, rhinitis did not seem to have an impact on the natural history of asthma. The finding of nasal inflammation in subjects with OA-only without clinical manifestations of rhinitis supports the united airway disease concept in occupational respiratory allergy as a result of persulphates. [source] Dysregulation of the stress response in asthmatic childrenALLERGY, Issue 1 2009K. N. Priftis The stress system co-ordinates the adaptive responses of the organism to stressors of any kind. Inappropriate responsiveness may account for increased susceptibility to a variety of disorders, including asthma. Accumulated evidence from animal models suggests that exogenously applied stress enhances airway reactivity and increases allergen-induced airway inflammation. This is in agreement with the clinical observation that stressful life events increase the risk of a new asthma attack. Activation of the hypothalamic,pituitary,adrenal (HPA) axis by specific cytokines increases the release of cortisol, which in turn feeds back and suppresses the immune reaction. Data from animal models suggest that inability to increase glucocorticoid production in response to stress is associated with increased airway inflammation with mechanical dysfunction of the lungs. Recently, a growing body of evidence shows that asthmatic subjects who are not treated with inhaled corticosteroids (ICS) are likely to have an attenuated activity and/or responsiveness of their HPA axis. In line with this concept, most asthmatic children demonstrate improved HPA axis responsiveness on conventional doses of ICS, as their airway inflammation subsides. Few patients may experience further deterioration of adrenal function, a phenomenon which may be genetically determined. [source] Airway reactivity in children before and after stem cell transplantationPEDIATRIC PULMONOLOGY, Issue 9 2009Lea Bentur MD Abstract Stem cell transplantation (SCT) is associated with pulmonary complications. We encountered several children post-SCT with a clinical picture suggestive of airway hyper-reactivity (AHR) and evidence of reversible airway obstruction that was not reported pre-transplant. We evaluated the possibility of increased AHR as assessed by methacholine challenge test (MCT) following the course of SCT, and assessed a possible correlation between AHR and pulmonary complications. This was a prospective study evaluating consecutive patients referred for SCT to the Department of Pediatric Hemato-Oncology. Evaluation included pulmonary function test and MCT before and after SCT, and assessment of pulmonary complications. Twenty-one of 33 patients completed the study. The mean PC20 was 14.3,±,4.1 mg/ml prior to SCT; afterward the mean PC20 decreased to 11.2,±,5.6 mg/ml (P,=,0.018). The number of patients with airway reactivity (PC20,,,8 mg/ml) increased from 2/21 patients before SCT to 8/21 patients after SCT (P,=,0.043; McNemar test with Yates correction). Pulmonary complications and hospitalization were recorded in 33.3% of the patients (7/21 patients): 62.5% of the patients (5 patients) with AHR compared to 15.4% (2 patients) in the group without AHR (P,=,0.041; Fisher exact test). There were 10 hospitalizations among the 8 patients with positive MCT compared to 2 hospitalizations in 13 patients with negative MCT (median 1 vs. 0, P,=,0.045; Mann,Whitney U -test). Increased airway reactivity was observed in our study following the course of SCT. Positive MCT after SCT may be associated with increased risk of pulmonary complications. Larger prospective studies are needed to evaluate the possible mechanisms responsible for increased AHR and the clinical importance of these findings. Pediatr Pulmonol. 2009; 44:845,850. © 2009 Wiley-Liss, Inc. [source] Nitric oxide evaluation in upper and lower respiratory tracts in nasal polyposisCLINICAL & EXPERIMENTAL ALLERGY, Issue 7 2008C. Delclaux Summary Background A decrease in nasal nitric oxide (NO) and an increase in exhaled NO have been demonstrated in patients with nasal polyposis (NP). Objectives The aims were to evaluate the flux of NO from the three compartments of the respiratory tract, namely, upper nasal, lower conducting and distal airways, and to search for relationships between NO parameters and indexes of upper and lower disease activity (bronchial reactivity and obstruction). The effect of medical treatment of polyposis was also evaluated. Methods Seventy patients with polyposis were recruited. At baseline, pulmonary function tests (spirometry, plethysmography, bronchomotor response to deep inspiration using forced oscillation measurement of resistance of respiratory system, methacholine challenge, multiple flow rates of exhaled NO and nasal NO measurements) were performed together with an assessment of polyposis [clinical, endoscopic and computed tomography (CT) scores]. Results Statistical relationships were demonstrated between nasal NO flux and severity scores (clinical: ,=,0.31, P=0.015; endoscopic: ,=,0.57, P<0.0001; CT: ,=,0.46, P=0.0005), and between alveolar NO concentration and distal airflow limitation (FEF25,75, ,=,0.32, P=0.011). Thirty-six patients were assessed after 11 [7,13] (median [interquartile]) months of medical treatment, demonstrating an improvement in clinical and endoscopic scores, an increase in nasal NO flux, a decrease in NO flux from conducting airways, an improvement in the mild airflow limitation (forced expiratory volume in 1 s, FEF25,75, even in non-asthmatic patients) and a decrease in the bronchoconstrictor effect of deep inspiration. Conclusions The medical treatment of NP improves both airway reactivity and obstruction, whatever the presence of asthma, suggesting a functional link between upper and lower airway functions. [source] Serum immunoglobulin E levels predict human airway reactivity in vitroCLINICAL & EXPERIMENTAL ALLERGY, Issue 2 2000Schmidt Background Airway hyperresponsiveness to non-specific stimuli is one characteristic feature of airway diseases such as bronchial asthma and chronic bronchitis. Until now, studies aiming to demonstrate a relationship between in vivo conditions associated with airway hyperreactivity and in vitro airway responsiveness have been inconclusive. Objective Since serum immunoglobulin (Ig) E is believed to be one determinant of airway reactivity in vivo, we studied whether in vitro airway reactivity in lung resection material from patients with elevated levels of serum IgE was increased as compared with patients with undetectable IgE. By this approach, we aimed to elucidate the role of circulating IgE for bronchial smooth muscle reactivity in vitro. Methods Bronchial rings from nine patients with total serum IgE levels above 200 U/mL and 10 patients with total serum IgE levels below 10 U/mL were passively sensitized, i.e. incubated overnight with buffer or sensitizing serum containing high levels of total IgE (> 250 U/mL). Afterwards, contractile responses to histamine were assessed in the organ bath. Results Histamine responsiveness was significantly increased in airways obtained from patients with IgE levels above 200 U/mL as compared with airways from patients with IgE levels below 10 U/mL (P < 0.05). Passive sensitization of bronchi from patients with low IgE significantly increased histamine responsiveness, as compared with non-sensitized controls from the same patients (P < 0.05). In contrast, passive sensitization of airways from patients with elevated IgE did not further increase responsiveness. There was no difference in histamine reactivity between non-passively sensitized and passively sensitized tissue preparations from patients with IgE above 200 U/mL and passively sensitized tissues from patients with IgE below 10 U/mL. Conclusion Our findings reveal that elevated levels of serum IgE predict airway hyperresponsiveness to histamine in vitro. At the same time, they indicate that the in vitro model of passive sensitization, in addition to its ability to induce allergen responses, also mimics conditions of non-specific airway hyperreactivity, which are relevant under in vivo conditions. [source] Association of tobacco smoke exposure and respiratory syncitial virus infection with airways reactivity in early childhoodPEDIATRIC PULMONOLOGY, Issue 6 2001Alan Adler MD Abstract Exposure to infectious agents and environmental tobacco smoke are thought to induce bronchial hyperresponsiveness (BHR). This study was undertaken to determine the effects of passive exposure to tobacco smoke and respiratory syncitial virus (RSV) lower respiratory infection (LRI) during infancy on the occurrence of BHR in the first 2 years of life. Eighty-six cases of documented RSV (mean age, 188 days) and 78 controls (mean age, 162 days) were enrolled from the clinic and in-patient service of a single hospital. None had a history of prior LRI. Subjects were studied at 6-month intervals up to 19 months of age with a standardized respiratory illness and parental smoking questionnaire, partial expiratory flow-volume curves by the "hug" (rapid thoracic compression) technique, and methacholine challenge. Exposure to maternal and paternal cigarette smoking, maternal history of asthma, and mold exposure were associated with decreased levels of length-corrected maximal flow at functional residual capacity (V,maxFRC). RSV-LRI was not related to V,maxFRC. After adjustment of V,maxFRC for these factors, V,maxFRC was a significantly and positively correlated with a methacholine concentration provoking a 40% fall in V,maxFRC (PC40) and negatively correlated with dose-response slope. After adjustment for V,maxFRC, there were no independent effects of tobacco smoke exposure or RSV-LRI on methacholine responses. These data do not support a role for RSV as a risk factor for airways reactivity in childhood and indicate that exposure to tobacco smoke affects airways reactivity through its effects on airways. Pediatr Pulmonol. 2001; 32:418,427. © 2001 Wiley-Liss, Inc. [source] | ||||||||||