pulmicort and Bronchitis

The efficacy of montelukast (MONT), a cysteinyl leukotriene receptor antagonist, in nonasthmatic eosinophilic bronchitis (NAEB), especially its influence on cough associated life quality is still indefinite. We evaluated the efficacy of MONT combined with budesonide (BUD) as compared to BUD monotherapy in improving life quality, suppressing airway eosinophilia and cough remission in NAEB.. A prospective, open-labeled, multicenter, randomized controlled trial was conducted. Patients with NAEB (aged 18-75 years) were randomized to inhaled BUD (200 μg, bid) or BUD plus oral MONT (10 μg, qn) for 4 weeks. Leicester cough questionnaire (LCQ) life quality scores, cough visual analog scale (CVAS) scores, eosinophil differential ratio (Eos), and eosinophil cationic protein (ECP) in induced sputum were monitored and compared.. The control and MONT groups contained 33 and 32 patients, respectively, with similar baseline characteristics. Significant with-in group improvement in CVAS, LCQ scores, Eos, and ECP was observed in both groups during treatment. After 2-week treatment, add-on treatment of MONT was significantly more effective than BUD monotherapy for CVAS decrease and LCQ scores improvement (both P < 0.05). Similar results were seen at 4-week assessment (both P < 0.05). 4-week add-on therapy of MONT also resulted in a higher percentage of patients with normal sputum Eos (<2.5%) and greater decrease of ECP (both P < 0.05).. MONT combined with BUD was demonstrated cooperative effects in improvement of life quality, suppression of eosinophilic inflammation, and cough remission in patients with NAEB.

Topics: Acetates; Adolescent; Adult; Aged; Aged, 80 and over; Bronchitis; Budesonide; Cough; Cyclopropanes; Female; Humans; Inflammation; Male; Middle Aged; Quality of Life; Quinolines; Sulfides; Young Adult

Budesonide at 800 μg/d is generally suggested for treatment of nonasthmatic eosinophilic bronchitis (NAEB). In asthma, adjunctive therapy with montelukast has been shown to confer addictive anti-inflammatory effects to inhaled corticosteroid (ICS). However, whether such effects could be extrapolated to NAEB is not known.. To study the efficacy and tolerability of add-on therapy with montelukast as compared to double-dose ICS in suppressing airway eosinophilia and decreasing cough severity in NAEB.. In a randomized controlled trial, 26 nonsmoking, steroid-naïve NAEB patients presenting with chronic cough were treated with 800 μg/d budesonide or 400 μg/d budesonide plus montelukast 10 mg/d for 4 weeks. Cough visual analogue scale (CVAS) and eosinophil differential ratio in induced sputum (Eos) were monitored at baseline, Week 1, 2 and 4. Adverse events during treatment were recorded.. The two groups were comparable in age, gender distribution, cough duration, FEV(1)% predicted, FEV(1)/FEV ratio, baseline CVAS and geometric mean of Eos. Both regimens significantly reduced Eos and CVAS throughout the treatment course, with abrogation of sputum eosinophilia at end of therapy. There was no significant difference between the two groups in reduction of Eos and CVAS at all time points. Both regimens were well tolerated.. This preliminary study demonstrated that add-on montelukast might be an effective and well tolerated alternative to the generally suggested dose of ICS in treating steroid-naive NAEB, with suppression of eosinophilic inflammation, reduction of cough severity and sparing of ICS doses. (NCT01121016).

Topics: Acetates; Adult; Aged; Bronchitis; Bronchodilator Agents; Budesonide; Chronic Disease; Cough; Cyclopropanes; Drug Therapy, Combination; Female; Forced Expiratory Volume; Humans; Leukotriene Antagonists; Male; Middle Aged; Pilot Projects; Pulmonary Eosinophilia; Quinolines; Sulfides; Treatment Outcome; Young Adult

To determine induced sputum cell counts and interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-alpha) and leukotriene B4 (LTB4) levels as markers of neutrophilic inflammation in moderate persistent asthma, and to evaluate the response to inhaled steroid therapy.. Forty-five moderate asthmatic patients and 10 non-smoker controls were included in this study. All patients received inhaled corticosteroid (800 microg of budesonide) for 12 weeks. Before and after treatment pulmonary function tests were performed, and symptom scores were determined. Blood was drawn for analysis of serum inflammatory markers, and sputum was induced.. Induced sputum cell counts and inflammatory markers were significantly higher in patients with asthma than in the control group. The induced sputum eosinophil counts of 12 patients (26%) were found to be less than 5%, the non-eosinophilic group, and sputum neutrophil counts, IL-8 and TNF-alpha levels were significantly higher than the eosinophilic group (neutrophil, 50+/-14% versus 19+/-10%, p<0.01). In both groups, there was a significant decrease in sputum total cell counts and serum and sputum IL-8, TNF-alpha and LTB4 levels after the treatment. There was no change in sputum neutrophil counts. Although the sputum eosinophil count decreased only in the eosinophilic subjects, there was no significant difference in inflammatory markers between the groups. The symptom scores were significantly improved after treatment, while the improvement did not reach statistical significance on pulmonary function test parameters.. Notably, in chronic asthma there is a subgroup of patients whose predominant inflammatory cells are not eosinophils. Sputum neutrophil counts and neutrophilic inflammatory markers are significantly higher in these patients. In the non-eosinophilic group, inhaled steroid caused an important decrease in inflammatory markers; however, there was no change in the sputum eosinophil and neutrophil counts.

Topics: Administration, Inhalation; Adult; Aged; Anti-Inflammatory Agents; Asthma; Biomarkers; Bronchitis; Budesonide; Eosinophilia; Female; Forced Expiratory Volume; Humans; Male; Middle Aged; Sputum

Previous studies involving adults have demonstrated that airway glucocorticosteroids inhibit plasma exudation and eosinophil activity in allergic rhinitis. This study explores the possibility that plasma exudation, exudative responsiveness, and the occurrence of eosinophil activity-related proteins are glucocorticosteroid-sensitive nasal mucosal indices in allergic children. Using a placebo-controlled, parallel-group design effects of nasal budesonide (64 microg per nasal cavity b.i.d) were determined in children with seasonal allergic rhinitis. Nasal lavage fluid levels of eotaxin, eosinophil cationic protein (ECP), and alpha2-macroglobulin, indicating plasma exudation, were determined, the latter with and without challenge with topical histamine. Nasal lavage fluid levels of alpha2-macroglobulin and ECP increased significantly during the pollen season, and the acute plasma exudation response to histamine was significantly greater during than outside the season. There was a trend towards a seasonal increase in nasal lavage fluid levels of eotaxin. Budesonide significantly inhibited the seasonal increase in alpha2-macroglobulin as well as the exudative hyperresponsiveness to histamine. Any tendency of increases in mucosal output of eotaxin and ECP was abolished by the glucocorticosteroid treatment. We conclude that mucosal exudation of plasma, as a global sign of active inflammatory processes, is a glucocorticosteroid-sensitive facet of allergic rhinitis in children. Exudative hyperresponsiveness, potentially caused by several weeks of mucosal inflammation, emerges as a significant feature of allergic rhinitis in children, and its development is prevented by local treatment with a glucocorticosteroid drug. The seasonal increase in ECP and the trend for an increase in eotaxin were absent in the glucocorticosteroid-treated subjects.

Topics: Administration, Topical; Adolescent; Allergens; alpha-Macroglobulins; Anti-Inflammatory Agents; Betula; Blood Proteins; Bronchitis; Budesonide; Chemokine CCL11; Chemokines, CC; Child; Child Welfare; Double-Blind Method; Eosinophil Granule Proteins; Female; Glucocorticoids; Histamine; Humans; Inflammation Mediators; Male; Nasal Lavage Fluid; Nasal Mucosa; Nasal Provocation Tests; Pollen; Rhinitis, Allergic, Seasonal; Ribonucleases; Seasons; Severity of Illness Index; Treatment Outcome

Eosinophilic bronchitis is a common cause of chronic cough, characterized by sputum eosinophilia similar to that seen in asthma, but unlike asthma the patients have no objective evidence of variable airflow obstruction or airway hyperresponsiveness. The reason for the different functional associations is unclear. The authors have tested the hypothesis that in eosinophilic bronchitis the inflammation is mainly localized in the upper airway. In an open study the authors measured the lower (provocative concentration causing a 20% fall in forced expiratory volume in one second (PC20)) and upper (PC25 MIF50) airway responsiveness to histamine, lower and upper airway inflammation using induced sputum and nasal lavage, in II patients with eosinophilic bronchitis. The authors assessed changes in these measures and in cough reflex sensitivity to capsaicin and cough severity after 400 microg of inhaled budesonide for 4 weeks. A nasal eosinophilia was present in only three patients with one having upper airway hyperresponsiveness. Following treatment with inhaled corticosteroids the geometric mean sputum eosinophil count decreased from 12.8% to 2.9% (mean difference 4.4-fold, 95% confidence interval (CI) 2.14-10.02), the mean +/- sem cough visual analogue score on a 100 mm scale decreased from 27.2 +/- 6.6 mm to 12.6 +/- 5.7 mm (mean difference 14.6, 95% CI 9.1-20.1) and the cough sensitivity assessed as the capsaicin concentration required to cause two coughs (C2) and five coughs (C5) improved (C2 mean difference 0.75 doubling concentrations, 95% CI 0.36-1.1; C5 mean difference 1.3 doubling concentration, 95% CI 0.6-2.1). There was a significant positive correlation between the fold change in sputum eosinophil count and doubling dose change in C5 after inhaled budesonide (r=0.61). It is concluded that upper airway inflammation is not prominent in eosinophilic bronchitis and that inhaled budesonide improves the sputum eosinophilia, cough severity and sensitivity suggesting a causal link between the inflammation and cough.

Topics: Administration, Inhalation; Administration, Topical; Adult; Aged; Anti-Inflammatory Agents; Bronchial Hyperreactivity; Bronchitis; Budesonide; Confidence Intervals; Cough; Dose-Response Relationship, Drug; Eosinophilia; Female; Glucocorticoids; Humans; Male; Middle Aged; Nasal Lavage Fluid; Reference Values; Treatment Outcome

Asthma-like symptoms, methacholine hyperresponsiveness, use of inhaled steroids, airway inflammation, and increased tenascin expression in the reticular basement membrane have been reported in competitive cross-country skiers.. To investigate the effect of inhaled budesonide, 400 mug twice daily, on indices of airway inflammation in 'ski asthma', defined as asthma-like symptoms within the previous year and bronchial hyperresponsiveness to methacholine.. A randomised double-blind placebo-controlled parallel-group bronchial biopsy and bronchoalveolar lavage (BAL) study of 25 (19 male) competitive cross-country skiers (mean age 18 (16-20) years for a mean (range) treatment period of 22 (10-32) weeks over the competitive season.. No changes were seen regarding cellular inflammation in the bronchial mucosa or tenascin expression. In the BAL fluid, both groups had a significant decrease in activated T-suppressor (CD8) lymphocytes and an increase in macrophages, with no differences across the groups. Within the budesonide group, there was a decrease in IL2 receptor-activated T-helper lymphocytes and an improvement in FEV(1). Asthma-like symptoms were unchanged in 17 (68%) skiers. Methacholine provocation test was negative in 15 subjects, and remained positive in 5 subjects in each group. The improvement in bronchial responsiveness occurred in both groups and was not accompanied by a decrease in cellular inflammation.. We were unable to show any clear beneficial effect of budesonide in 'ski asthma'. As changes in training intensity probably accounted for the spontaneous improvement in bronchial responsiveness, more attention should be directed at reducing environmental stress to the airways than at attempting pharmacological modulation of induced inflammatory changes.

Topics: Administration, Inhalation; Administration, Topical; Adolescent; Adult; Anti-Inflammatory Agents; Biopsy; Bronchi; Bronchitis; Bronchoalveolar Lavage Fluid; Budesonide; Double-Blind Method; Female; Glucocorticoids; Humans; Male; Skiing

In a double-blind, cross-over study, we examined the effect of inhaled budesonide (800 microgram twice daily via Turbohaler) on lung function and various markers of airway inflammation including airway responsiveness to methacholine (PC20), exhaled nitric oxide (NO), eosinophils in induced sputum, bronchoalveolar lavage (BAL), and airway biopsies from 14 patients with mild asthma needing beta2- agonist therapy only. After inhaled steroids, there was a significant increase in FEV1 and PC20, and reduction in exhaled NO. Eosinophils in induced sputum and airway biopsy sections were also significantly decreased, although BAL eosinophil counts remained unchanged. At baseline, significant correlations were observed between exhaled NO and PC20 methacholine (r = 0.64, p < 0.05), exhaled NO and peak expiratory flow rate (PEFR) variability (r = 0. 65, p < 0.05), sputum eosinophils and FEV1 (r = -0.63, p = 0.05), and sputum eosinophils and log PC20 methacholine (r = -0.67, p < 0. 05). After treatment with inhaled steroids, there was a significant correlation between eosinophils in biopsy sections, and BAL, with log PC20 methacholine. It is likely that these parameters represent different aspects of the inflammatory process, which are all inhibited by inhaled steroids.

Topics: Administration, Inhalation; Adult; Asthma; Bronchi; Bronchitis; Bronchoconstrictor Agents; Bronchodilator Agents; Budesonide; Cross-Over Studies; Double-Blind Method; Eosinophils; Female; Forced Expiratory Volume; Humans; Lung; Male; Methacholine Chloride; Peak Expiratory Flow Rate

We hypothesized that regular use of long-acting beta-agonists could delay recognition of ("mask") increasing airway inflammation. We studied steroid-sparing and "masking" effects of salmeterol versus placebo in 13 asthmatic individuals requiring >= 1,500 microgram inhaled corticosteroid daily. Corticosteroid doses were reduced weekly until criteria were met for an exacerbation or the corticosteroid was fully withdrawn. Subjects were restabilized on their original dose of inhaled corticosteroid for 4 wk before crossover to the alternative treatment. Subjects maintained symptom and peak expiratory flow (PEF) diaries, and underwent weekly spirometric, methacholine challenge, sputum eosinophil, and serum eosinophil cationic protein (ECP) measurements. Mean corticosteroid dose was reduced by 87% during salmeterol treatment, versus 69% with placebo (p = 0.04). Sputum eosinophils increased before exacerbation despite stable symptoms, FEV1, and PEF. In the week before clinical exacerbation, sputum eosinophil counts were higher in the salmeterol-treatment arm (19.9 +/- 29.8% [mean +/- SD], versus placebo 9.3 +/- 17.6%; p = 0.006). Five subjects showed > 10% sputum eosinophilia before exacerbation during salmeterol treatment, as compared with two receiving placebo. In this model, salmeterol controlled symptoms and lung function until inflammation became significantly more advanced. We conclude that the bronchodilating and symptom-relieving effects of salmeterol can mask increasing inflammation and delay awareness of worsening asthma.

Topics: Administration, Inhalation; Adrenergic beta-Agonists; Adult; Albuterol; Anti-Asthmatic Agents; Asthma; Beclomethasone; Blood Proteins; Bronchial Provocation Tests; Bronchitis; Bronchoconstrictor Agents; Bronchodilator Agents; Budesonide; Cross-Over Studies; Disease Progression; Eosinophil Granule Proteins; Eosinophils; Female; Glucocorticoids; Humans; Inflammation Mediators; Leukocyte Count; Male; Methacholine Chloride; Middle Aged; Peak Expiratory Flow Rate; Placebos; Ribonucleases; Salmeterol Xinafoate; Spirometry; Sputum

11 patients with severe bronchial asthma entered a randomized trial of glucocorticosteroid budesonide of Russian produce. Of them 6 patients received inhalations of budesonide (800 micrograms/day for 6 months), 5 control patients did not receive the drug. As shown by investigations of external respiration and bronchoalveolar lavage with estimation of cytogram, metacholine provocative tests, fiber bronchoscopy, budesonide inhalations relieved clinical symptoms of asthma, bronchial hyperreactivity and inflammation.

Topics: Administration, Inhalation; Adult; Aerosols; Aged; Asthma; Bronchial Hyperreactivity; Bronchial Provocation Tests; Bronchitis; Bronchodilator Agents; Bronchoscopy; Budesonide; Female; Glucocorticoids; Humans; Male; Middle Aged; Pregnenediones

A placebo-controlled, double blind, cross-over study of inhaled budesonide was carried out to examine its effectiveness in the treatment of chronic airflow limitation (CAL). Fourteen patients (11 males, mean age 66 years) with stable CAL received placebo treatment for four weeks followed by inhaled budesonide 400 micrograms BD for eight weeks. Response was assessed by measuring forced expiratory volume in one second (FEV1). There was no significant improvement in the overall spirometric measurements and symptom scores except a reduction in daily peak expiratory flow rate fluctuation (p < 0.05). However, individual patients showed significant increase in FEV1. Two patients (14%) had greater than 30% increase in FEV1 in response to inhaled corticosteroids. This response could not be predicted from history of allergy, skin test, bronchial challenge test, peripheral blood or sputum eosinophilia. We conclude that only a minority of patients with stable CAL may respond to inhaled budesonide. Nonetheless, patients who are symptomatic despite treatment with maximum doses of bronchodilators may have a trial of inhaled corticosteroids in order to demonstrate any additional benefit.

Topics: Administration, Inhalation; Administration, Topical; Aerosols; Aged; Anti-Inflammatory Agents; Bronchial Provocation Tests; Bronchitis; Bronchodilator Agents; Budesonide; Chronic Disease; Double-Blind Method; Emphysema; Glucocorticoids; Humans; Male; Middle Aged; Pregnenediones; Respiratory Mechanics

We compared the effect of an inhaled corticosteroid, budesonide, and an inhaled beta 2-agonist, terbutaline, on clinical symptoms, lung function, and airway inflammation in 14 adult patients with newly diagnosed asthma. The study was conducted as a randomized, double-blind, parallel-group trial. Seven patients inhaled 600 micrograms, twice daily, of budesonide, the other seven patients inhaled 375 micrograms, twice daily, of terbutaline via identical metered-dose inhalers with a spacer. Bronchial biopsy specimens, obtained before randomization and after 3 months of treatment, were analyzed by electron microscopy. Both groups improved clinically budesonide was more effective than terbutaline in improving morning and evening peak expiratory flow rates, as well as bronchial responsiveness to inhaled histamine. Treatment with budesonide was accompanied by increased numbers of ciliated airway cells and intraepithelial nerves and fewer inflammatory cells, including eosinophils, especially in the epithelium, these changes were not observed in specimens from terbutaline-treated patients. We conclude that, in contrast to inhaled terbutaline, inhaled budesonide improved lung function and bronchial hyperreactivity in adult subjects with asthma treated for 3 months and that this corticosteroid was more effective in ameliorating abnormalities of the bronchial epithelium and decreasing inflammation in the airways.

Topics: Administration, Inhalation; Adult; Asthma; Biopsy; Bronchi; Bronchitis; Bronchodilator Agents; Budesonide; Double-Blind Method; Drug Evaluation; Female; Glucocorticoids; Humans; Male; Middle Aged; Pregnenediones; Respiratory Function Tests; Terbutaline

In a placebo controlled study the effects of 6 weeks' treatment with inhaled budesonide (1.6 mg daily) on the impedance of the respiratory system, spirometry and symptom scores were evaluated in 35 patients with chronic bronchitis with forced expiratory volume in one second (FEV1) greater than or equal to 70% predicted. Thirty patients completed the study. No statistically significant differences in the changes in morning peak expiratory flow rate (PEFR), symptom scores, use of terbutaline rescue medication and FEV1 were found between the placebo and the active treatment group. Budesonide treatment was found to result in a small decrease in resonant frequency and a less negative frequency dependence of resistance compared with the placebo group.

Topics: Aerosols; Airway Resistance; Bronchitis; Bronchodilator Agents; Budesonide; Double-Blind Method; Female; Humans; Male; Middle Aged; Pregnenediones; Respiratory Mechanics; Spirometry

The aim of the present randomized, double-blind study was to evaluate the effect of inhaled budesonide on daily symptoms, ventilatory capacity, and airway responsiveness in smokers with chronic bronchitis. Twenty-five subjects with a provocative concentration producing a 20% fall in forced expiratory volume in one second PC20(FEV1) less than 2.0 mg.ml-1, by bronchial histamine challenge, were included. Eighteen subjects accomplished the entire 12 week study, eight receiving inhaled budesonide 400 micrograms b.i.d. and ten receiving placebo. Cough decreased significantly in the actively treated group during the treatment period, but no change could be demonstrated in expectoration, dyspnoea, or sleep disturbances. No changes in any of these symptoms were found in the placebo group, and no differences in symptoms scores were found between the groups. No significant differences in ventilatory capacity or bronchial responsiveness could be demonstrated. In conclusion, a moderately high dose of inhaled steroid in eight subjects with chronic bronchitis did not improve the symptom scores, ventilatory capacity, or airway responsiveness to any clinically relevant degree.

Topics: Administration, Inhalation; Bronchial Provocation Tests; Bronchitis; Bronchodilator Agents; Budesonide; Double-Blind Method; Female; Forced Expiratory Volume; Glucocorticoids; Humans; Male; Middle Aged; Pregnenediones; Randomized Controlled Trials as Topic; Smoking

This study aims to explore the potential of. Using flow cytometry, we enumerated sputum and blood HPCs and EoPs in patients with NAEB (n=15), EA (n=15), and HC (n=14) at baseline. Patients with NAEB and EA were then treated for 1 month with budesonide (200 μg, bid) or budesonide and formoterol (200/6 μg, bid), respectively. HPCs and EoPs in both compartments were re-evaluated.. At baseline, NAEB and EA both had significantly greater numbers of sputum but not blood HPCs and EoPs (. NAEB patients have increased airway levels of HPCs and EoPs. One-month treatment with ICS did not fully suppress the level of EoPs in NAEB. Controlling

Topics: Adrenal Cortex Hormones; Asthma; Bronchitis; Budesonide; Eosinophils; Humans; Pulmonary Eosinophilia

BACKGROUND This study was conducted to evaluate the effects of astragaloside IV and budesonide on bronchitis in rats and to explore the mechanism involved. MATERIAL AND METHODS Eighty Sprague-Dawley (SD) rats were randomly divided into 5 groups, including a Bronchitis model group (BM), a Budesonide group (BG), an Astragaloside IV group (AG), an Astragaloside IV combined with Budesonide group (CG), and a blank control group (BC). Lung tissue was stained with hematoxylin and eosin (H&E). The activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). The nuclear factor erythroid 2 [NF-E2]-related factor 2 (Nrf2), Kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (Keap1), BTB and CNC homology 1 (Bach1), B-cell lymphoma-2(Bcl-2), and BCl-2-associated X protein (Bax) mRNA and protein were examined by RT-PCR and Western blot, respectively. RESULTS Compared with the Bronchitis model group, the lung tissue lesions in the Budesonide group, Astragaloside IV group, and Astragaloside IV combined with Budesonide group were effectively ameliorated and the airway resistance was significantly decreased. The activities of SOD, GSH-Px, and CAT were increased after treatment with drugs, while the content of MDA was decreased. The levels of Nrf2, Keap1, and Bcl-2 proteins were increased and the levels of Bach1 and Bax were decreased after treatment with Budesonide and Astragaloside IV. CONCLUSIONS Astragaloside IV combined with budesonide can ameliorate the lesions caused by bronchitis in rats through activating the Nrf2/Keap1 pathway, which plays a protective role on anti-oxidative stress injury.

Topics: Animals; Bronchitis; Budesonide; Drug Combinations; Female; Glutathione Peroxidase; Kelch-Like ECH-Associated Protein 1; Lung; Male; Malondialdehyde; NF-E2-Related Factor 2; Oxidative Stress; Rats; Rats, Sprague-Dawley; Saponins; Signal Transduction; Superoxide Dismutase; Triterpenes

To describe the long term use of inhaled budesonide in cats with naturally occurring asthma and chronic bronchitis and to measure its effects.. Owners of 43 cats diagnosed with asthma or chronic bronchitis, which had been prescribed 400 µg of inhaled budesonide twice daily, were contacted and information was retrieved by a questionnaire. Nineteen cats still receiving inhaled budesonide after more than 2 months were re-evaluated clinically and underwent barometric whole body plethysmography and adrenocorticotropic hormone-stimulation testing.. In 20 of the cats, therapy had been withdrawn by the owners. Cats (n=23) still receiving inhaled budesonide improved clinically and 19 cats that were reevaluated had significantly lower basal PENH (P=0·048) and higher PCPenh300 (P=0·049) values than before treatment. Corticosteroid-induced side effects were not observed in any cats but hypothalamic-pituitary-adrenal axis suppression was detected in 3 of 15 cases.. Treatment with inhaled budesonide was well tolerated, resulting in improvement of clinical signs and barometric whole body plethysmography parameters. Although inhaled budesonide therapy was found to cause suppression of the hypothalamic-pituitary-adrenal axis in some cats, no cats showed clinical signs attributable to corticosteroid side effects.

Topics: Administration, Inhalation; Animals; Asthma; Bronchitis; Bronchodilator Agents; Budesonide; Cat Diseases; Cats; Chronic Disease; Female; Male; Plethysmography, Whole Body; Treatment Outcome

Topics: Adult; Breath Tests; Bronchial Provocation Tests; Bronchitis; Budesonide; Cupressus; Female; Humans; Immunoglobulin E; Male; Nitric Oxide; Pulmonary Eosinophilia; Rhinitis, Allergic, Seasonal; Skin Tests; Sputum

Eosinophilic bronchitis is an important cause of chronic cough. Treatment with inhaled corticosteroids is associated with a short-term improvement in cough and reduced sputum eosinophil count but the long-term outcome is uncertain.. To determine the long-term outcome in patients diagnosed with and treated for eosinophilic bronchitis.. We have performed a longitudinal study of symptoms, eosinophilic airway inflammation, spirometry and airway hyper-responsiveness in all patients diagnosed with eosinophilic bronchitis over 7 years.. We identified 52 patients with eosinophilic bronchitis and longitudinal data of greater than 1 year (mean 3.1 years) was available in 32 patients, all of whom were treated with inhaled steroids. Three (9%) patients developed symptoms consistent with asthma and a methacholine PC20<8 mg/mL on one or more occasion. Five (16%) patients developed fixed airflow obstruction defined by a persistent post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity<70%. One (3%) patient had complete resolution of symptoms and eosinophilic airway inflammation off treatment. The remaining patients had ongoing eosinophilic airway inflammation and/or continuing symptoms. Multiple linear regression identified smoking, female gender and area under the curve of sputum eosinophil count over time as the most important predictors of decline in FEV1.. The most common outcome in eosinophilic bronchitis is continuing disease and complete resolution is rare. Asthma and fixed airflow obstruction developed in relatively few patients. The most important factors associated with a more rapid decline in FEV1 were female gender, smoking and prolonged eosinophilic airway inflammation.

Topics: Administration, Inhalation; Adolescent; Adrenal Cortex Hormones; Adult; Aged; Aged, 80 and over; Airway Obstruction; Asthma; Bronchitis; Bronchodilator Agents; Budesonide; Cough; Eosinophilia; Female; Forced Expiratory Volume; Humans; Longitudinal Studies; Male; Middle Aged; Prognosis; Sex Factors; Smoking; Time Factors; Treatment Outcome

A case is discussed of eosinophilic bronchial inflammation without asthma due to chloramine T (CLT) exposure in a nurse. She reported a non-productive chronic cough on contact with CLT during workshifts. She had negative results of skin prick testing to CLT. However, sensitisation to CLT was confirmed by the presence of specific anti-chloramine IgE. Airway responsiveness to histamine was normal before and after CLT challenge. Eosinophil proportion in sputum was increased at 6 and 24 h after CLT challenge.

Topics: Anti-Inflammatory Agents; Bronchitis; Budesonide; Chloramines; Chronic Disease; Cough; Disinfectants; Eosinophilia; Female; Humans; Middle Aged; Occupational Exposure; Tosyl Compounds

Eosinophilic inflammation of the airway is usually associated with airway hyper-responsiveness in bronchial asthma. However, there is a small group of patients which has the eosinophilic inflammation in the bronchial tree with normal spirometry and no evidence of airway hyper-responsiveness, which was named eosinophilic bronchitis. The objectives of this study are 1) to investigate the incidence of eosinophilic bronchitis in the chronic cough syndrome and 2) to evaluate the clinical features and course of eosinophilic bronchitis.. We evaluated 92 patients who had persistent cough for 3 weeks or longer. In addition to routine diagnostic protocol, we performed differential cell count of sputum. Eosinophilic bronchitis was diagnosed when the patient had normal spirometric values, normal peak expiratory flow variability, no airway hyper-responsiveness and sputum eosinophilia (> 3%).. The causes of chronic cough were post-nasal drip in 33%, cough variant asthma in 16%, chronic bronchitis in 15% and eosinophilic bronchitis in 12% of the study subjects. Initial eosinophil percentage in the sputum of patients with eosinophilic bronchitis was 26.8 +/- 6.1% (3.8-63.7%). Treatment with inhaled steroid is related with a subjective improvement of cough severity and a significant decrease of sputum eosinophil percentage (from 29.1 +/- 8.3% to 7.4 +/- 3.3%). During the follow-up period, increase in sputum eosinophil percentage with aggravation of symptoms were found.. Eosinophilic bronchitis is one of the important cause of chronic cough. Assessment of airway inflammation by sputum examination is important in investigating the cause of chronic cough. Cough in eosinophilic bronchitis is effectively controlled by inhaled corticosteroid, but may follow a chronic course.

Topics: Adult; Aged; Anti-Inflammatory Agents; Asthma; Bronchitis; Budesonide; Chronic Disease; Cough; Eosinophilia; Female; Gastroesophageal Reflux; Humans; Male; Middle Aged; Respiratory Function Tests; Severity of Illness Index; Sputum

In non-smokers the underlying causes for chronic persistent cough (CPC) e.g. chronic cough without diagnostic chest X-ray or pulmonary function test--are usually as follows: several common upper airways diseases, bronchial (cough type) asthma, gastrooesophageal reflux or treatment with an ACE (angiotensin converting enzyme)--inhibitor. In 10% of CPC however the cause remains uncertain. We report a 30 year old non-smoker with severe coughing and repeated vomiting for two months. No laboratory or technical data could be collected suggestive of a common cause of CPC: Upper airways disease, bronchial flow limitation or hyperresponsiveness, ACE inhibitor medication, B. pertussis infection, gastrooesophageal reflux disease (by 24 hours pH-probe) were ruled out. Fiberbronchoscopic findings remained unremarkable, except for the bronchial biopsy specimen, which showed moderate eosinophilic inflammation of the mucosa and marked thickening of the subepithelial layer. Since the cough was non-productive, sputum induction with 3 ml nebulised 3% NaCl solution was performed. 28% of the granulocytes were eosinophil stained. A low quality morning sputum (< 1 ml) showed 21% eosinophilia. Thus, the diagnosis of eosinophilic bronchitis was established. 400 micrograms budesonide dry powder inhalations b.i.d. for one week resolved the cough, treatment was stopped after three weeks. No recurrence was seen two months later. Both the cough type asthma and the eosinophilic bronchitis could represent a form fruste of classical bronchial asthma beyond wheezing or dyspnoea, but with the common main symptom: cough. Since hyperresponsiveness and cough are phenotypic hallmarks of cough variant asthma, in eosinophilic bronchitis--beside cough--another two features of asthma are present: eosinophilic inflammation of the mucosa along with sputum eosinophilia and subepithelial layer thickening. Not surprisingly, eosinophilic bronchial inflammation could be shown in patients with cough variant asthma as well, who--up to 56% during a four year-period--develop classic asthma. The long-term outcome of eosinophilic bronchitis is not known, however. Thus, asthma, cough variant asthma and cough due to eosinophilic bronchitis can mirror different phenotypes or phases of the same entity. CPC due to either the cough type asthma or the eosinophilic bronchitis is like asthma fast responding to inhalative steroids. (Induced) sputum staining should be added to the diagnostic armamentarium of CPC.

Topics: Adult; Asthma; Bronchial Hyperreactivity; Bronchitis; Bronchodilator Agents; Budesonide; Chronic Disease; Cough; Diagnosis, Differential; Eosinophilia; Humans; Male

Although anti-inflammatory potency of inhaled corticosteroids is well established, little is known about their role in the acute phase. The aim of this study was to compare the acute anti-inflammatory effect of inhaled budesonide with systemic dexamethasone on allergen-induced inflammatory changes in asthmatic rats. Eighty-four Sprague Dawley rats were divided into four groups; group I (control, n = 24), group II (ovalbumin sensitized, n = 24), group III (systemic dexamethasone, n = 24), and group IV (budesonide, n = 12). All groups except group I were given ovalbumin aerosol challenges 14 days after sensitization with ovalbumin. The same procedure was applied to the control group using 0.9% saline. Group III received dexamethasone 0.3 mg/kg intraperitoneally and group IV received inhaled budesonide 10mL (0.5mg/mL) twice before the challenge. Eight hours after the challenge, bronchi of all the rats were evaluated for the degree of peribronchial inflammation. The most severe inflammation was seen in 8 of 24 rats (33%) in the second group, in 1 of 24 rats (4%) in the third group, and in 1 of 24 rats (4%) in the control group. None of the rats in group IV showed severe inflammation. No statistically significant difference was detected with respect to the presence of 3+ inflammation between the control vs. dexamethasone-, control vs. budesonide-, and dexamethasone vs. budesonide-receiving groups. Budesonide administration via nebulizer prior to exposure to an allergen may attenuate bronchial inflammation as effectively as systemic dexamethasone in rats.

Topics: Acute Disease; Administration, Inhalation; Animals; Asthma; Bronchitis; Budesonide; Dexamethasone; Rats; Rats, Sprague-Dawley

The bronchitis index (BI) is a scoring system for the visual quantification of airway inflammation by flexible bronchoscopy. A prospective study was carried out to determine whether patients with intermittent asthma present a considerable visible airway inflammation. Ten steroid-naive patients with intermittent asthma taking only inhaled beta2-agonists were enrolled and received budesonide (800 microg/day) over a period of 4 weeks. The airway inflammation was assessed by flexible electronic videobronchoscopy before and after the steroid treatment phase and quantified using the BI. Despite normal pulmonary function, all patients with intermittent asthma showed a marked visible airway inflammation that was reversed by a 4-week treatment with the inhaled steroid budesonide. The present study demonstrates that the BI may be useful as a clinical research tool for the assessment and quantification of airway inflammation in asthma. Furthermore, our results support the widely recognized theory that airway inflammation is present even in patients with mild asthma, and emphasize the necessity of an early therapy with inhaled steroids.

Topics: Administration, Inhalation; Asthma; Bronchi; Bronchitis; Bronchodilator Agents; Bronchoscopy; Budesonide; Female; Humans; Male; Middle Aged; Prospective Studies; Severity of Illness Index

Eosinophilic bronchitis presents with chronic cough and sputum eosinophilia, but without the abnormalities of airway function seen in asthma. It is important to know how commonly eosinophilic bronchitis causes cough, since in contrast to cough in patients without sputum eosinophilia, the cough responds to inhaled corticosteroids. We investigated patients referred over a 2-yr period with chronic cough, using a well-established protocol with the addition of induced sputum in selected cases. Eosinophilic bronchitis was diagnosed if patients had no symptoms suggesting variable airflow obstruction, and had normal spirometric values, normal peak expiratory flow variability, no airway hyperresponsiveness (provocative concentration of methacholine producing a 20% decrease in FEV(1) ([PC(20)] > 8 mg/ml), and sputum eosinophilia (> 3%). Ninety-one patients with chronic cough were identified among 856 referrals. The primary diagnosis was eosinophilic bronchitis in 12 patients, rhinitis in 20, asthma in 16, post-viral-infection status in 12, and gastroesophageal reflux in seven. In a further 18 patients a diagnosis was established. The cause of chronic cough remained unexplained in six patients. In all 12 patients with eosinophilic bronchitis, the cough improved after treatment with inhaled budesonide 400 micrograms twice daily, and in eight of these patients who had a follow-up sputum analysis, the eosinophil count decreased significantly, from 16.8% to 1.6%. We conclude that eosinophilic bronchitis is a common cause of chronic cough, and that sputum induction is important in the investigation of cough.

Topics: Administration, Inhalation; Adult; Aged; Algorithms; Anti-Inflammatory Agents; Bronchitis; Bronchodilator Agents; Budesonide; Chronic Disease; Cough; Dose-Response Relationship, Drug; Drug Administration Schedule; Eosinophilia; Female; Humans; Male; Middle Aged; Sputum

The expression of the glucocorticoid receptor (GR) in untreated or in steroid-dependent asthmatic patients is poorly understood. We therefore studied GR mRNA and protein levels in bronchial biopsies obtained from seven untreated asthmatic patients, seven control volunteers, and seven patients with chronic bronchitis. We also studied in bronchial epithelial cells obtained by brushing from 13 untreated asthmatics, 18 steroid-dependent asthmatics, 11 control volunteers, and 12 patients with chronic bronchitis, GR and heat shock protein 90 kD (hsp90) mRNA as well as the immunoreactivity of GR, intercellular adhesion molecule (ICAM-1), and granulocyte macrophage-colony-stimulating factor (GM-CSF). GR mRNA and protein level was similar in all subject groups in both biopsies and bronchial epithelial cells. Hsp90 mRNA level was also similar in all subject groups. ICAM-1 expression was significantly increased in bronchial epithelial cells from untreated asthmatics, but ICAM-1 was not expressed in those from steroid-dependent asthmatic patients. GM-CSF expression was significantly increased in bronchial epithelial cells from untreated and steroid-dependent asthmatic patients. GR expression within the airways is unaltered by oral long-term steroid treatment in asthma, but the expression of some but not all specific markers for asthma is modified by oral steroid.

Topics: Administration, Oral; Adult; Aged; Albuterol; Anti-Inflammatory Agents; Asthma; Biopsy; Bronchi; Bronchitis; Bronchodilator Agents; Budesonide; Chronic Disease; Epithelial Cells; Gene Expression Regulation; Glucocorticoids; Granulocyte-Macrophage Colony-Stimulating Factor; HSP90 Heat-Shock Proteins; Humans; Intercellular Adhesion Molecule-1; Middle Aged; Prednisone; Proteins; Receptors, Glucocorticoid; RNA, Messenger; Salmeterol Xinafoate; Theophylline

In the case reported, serial evaluation of sputum inflammatory cell counts made it possible to identify an unusual series of events in a man with eosinophilic bronchitis. The patient initially presented with a productive cough, which did not respond to treatment with antibiotics or high-dose inhaled corticosteroids. A diagnosis of eosinophilic bronchitis was made after demonstration of intense sputum eosinophilia. When inhaled corticosteroids were stopped, symptoms and sputum eosinophilia became worse and airway hyperresponsiveness developed. Both abnormalities were reversed by a course of prednisone. When the prednisone was stopped the productive cough recurred but on this occasion sputum examination suggested a different disease process and the symptoms resolved after a course of co-trimoxazole. The patient has subsequently remained well on no treatment with little or no sputum eosinophilia.

Topics: Anti-Infective Agents; Anti-Inflammatory Agents; Asthma; Bronchial Hyperreactivity; Bronchitis; Budesonide; Cough; Diagnosis, Differential; Eosinophilia; Eosinophils; Glucocorticoids; Humans; Leukocyte Count; Male; Middle Aged; Neutrophils; Prednisone; Pregnenediones; Sputum; Trimethoprim, Sulfamethoxazole Drug Combination

The transcription factor Fos is involved in cell proliferation and differentiation. Its expression in normal and pathological adult human tissues and cells has rarely been studied. We therefore studied bronchial biopsies obtained from 14 normal subjects (NS), 18 non-steroid-treated asthmatics, 10 corticosteroid-treated asthmatics and 10 patients with chronic bronchitis (CB), in addition to 34 patients with lung cancer (LC), by immunofluorescence for Fos immunoreactivity, using a highly specific polyclonal antibody. Bronchial tissue of 0/10 NS, 11/18 non-steroid-treated asthmatics, 1/10 steroid-treated asthmatics, 0/10 CB and 1/34 LC expressed Fos. In asthmatic patients, the expression was heterogeneous, localized to epithelial cells and correlated with the epithelium shedding (tau = 0.45, P = 0.0001). Corticosteroid-treated patients rarely expressed Fos, suggesting a role for this proto-oncogene in asthmatic bronchial inflammation. Fos was rarely expressed in the normal and pathological (CB, LC) proliferative compartment of the human bronchi, suggesting its low role in cell proliferation of the large airways.

Topics: Adenocarcinoma; Adolescent; Adult; Aged; Aged, 80 and over; Asthma; Beclomethasone; Bronchi; Bronchitis; Budesonide; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Chronic Disease; Female; Fluorescent Antibody Technique; Humans; Lung Neoplasms; Male; Middle Aged; Pregnenediones; Proto-Oncogene Mas; Proto-Oncogene Proteins c-fos

Topics: Administration, Inhalation; Aerosols; Asthma; Bronchitis; Bronchodilator Agents; Budesonide; Humans; Infant; Pregnenediones

Topics: Administration, Topical; Adult; Aged; Anti-Inflammatory Agents; Bronchitis; Budesonide; Chronic Disease; Erythrocyte Count; Hematocrit; Hemoglobinometry; Humans; Hydrocortisone; Male; Middle Aged; Pregnenediones; Respiratory Therapy