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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The application of sputum induction and refined methods of sputum examination has provided the opportunity to examine cell and molecular markers of airway inflammation in asthma, COPD, and other airway diseases. The measurements are relatively noninvasive and can be applied safely, with care, even in more severe exacerbations of asthma and severe COPD. Induced sputum examination can be applied at random and repeatedly and gives results that are reproducible, valid, and responsive to changes in treatment. An eosinophilic bronchitis, defined as sputum eosinophilia, is typical of asthma but can also occur in patients with a chronic cough without asthma, and in some patients with COPD in whom the classic inflammatory response is neutrophilic without eosinophilia. When eosinophilia occurs in COPD, it has been considered to be the result of cigarette smoking but it may be due to other causes. The clinical importance of eosinophilic bronchitis is that it responds to treatment with corticosteroid. In contrast, there is increasing evidence that an absence of sputum eosinophilia is associated with steroid resistance. Hargreave FE, Leigh R. Induced sputum, eosinophilic bronchitis, and chronic obstructive pulmonary disease.
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PMID:Induced sputum, eosinophilic bronchitis, and chronic obstructive pulmonary disease. 1055 71

Eosinophilic bronchitis is a recently described condition presenting with chronic cough and sputum eosinophilia without the abnormalities of airway function seen in asthma. The patient, a 48-yr-old male who had never smoked, presented with an isolated chronic cough. He had normal spirometric values, peak flow variability and airway responsiveness, but an induced sputum eosinophil count of 33% (normal <1%). Although his cough improved with inhaled corticosteroids the sputum eosinophilia persisted. Over 2 yrs he developed airflow obstruction, which did not improve following nebulized bronchodilators and a 2-week course of prednisolone 30 mg once daily sufficient to return the sputum eosinophilia to normal (0.5%). It is suggested that the progressive irreversible airflow obstruction was due to persistent structural change to the airway secondary to eosinophilic airway inflammation, and it is further speculated that eosinophilic bronchitis may be a prelude to chronic obstructive pulmonary disease in some patients.
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PMID:Development of irreversible airflow obstruction in a patient with eosinophilic bronchitis without asthma. 1059 16

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.
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PMID:Airway inflammation, airway responsiveness and cough before and after inhaled budesonide in patients with eosinophilic bronchitis. 1078 Jul 59

Cough is probably the most frequent symptom in chest diseases. Hence, a rational and economical diagnostic procedure is essential to prevent unnecessary costs to the health services, i.e. acute bronchitis, a self-limiting disease, which is the most frequent cause for cough should not involve extensive per case costs. History, physical examination, chest X-ray and lung function testing--which constitute both the first and second, i.e. the basic level of a stepwise approach--allows to diagnose causes in most patients with cough. Without evidence of the cause after completing this basic diagnostic procedure patients with acute cough may require blood gases analysis, electrocardiography, echocardiography, lung perfusion study, spiral CT angiography, bronchoscopy or laboratory examinations for diagnosis of pulmonary embolism, aspiration or (seldom) pleuritis sicca. Chronic persistent cough (CPC) is diagnosed if the basic standard approach to chronic cough fails to lead to final diagnosis. Patients will then need further subtle diagnostic management, i.e. bronchial provocation testing, 24 hour pH probe, ENT- or neurological examination, high resolution CT of the thorax and bronchoscopy. We present two algorithms for the rational diagnostic approach to acute (figure 1) and chronic (figure 2) cough. Each algorithm considers spectrum and frequency of causes on the one hand, the positive predictive value, costs and patient discomfort due to the examination on the other. Nonetheless, despite extensive examination up to 20% of patients suffering from CPC the cause remains unclear [11]. Frequently, the capsaicin cough challenge test can reveal an idiopathic upregulation of the cough reflex as the hypothesised underlying condition. Psychogenic cough however, a rare condition in adults should not coincide with hypersensitivity of the cough reflex. Inconsistency and low reproducibility of results of the capsaicin challenge in patients with psychogenic cough preclude his routine clinical use. In conclusion, the very common acute bronchitis and the ACE inhibitor-induced cough do not require any other diagnostic procedure except patient history and physical examination. A simple basic diagnostic approach will usually allow to evaluate acute and chronic cough. In the remaining cases the proposed algorithm should be used for best results and to prevent excessive costs.
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PMID:[Proposals for a rationale and for rational diagnosis of coughs]. 1078 50

In this paper, recent reviews of the World Health Organization, other review papers, and more recent literature on the human health effects of current air pollution trends in urban areas are reviewed and summarized as follows: Sulphur dioxide. Some studies, but not others, found associations between sulphur dioxide (SO2) exposure and daily mortality and morbidity. Single-pollutant correlations sometimes disappeared when other pollutants, especially suspended particulate matter (SPM), were included. Cross-sectional studies with asthmatics revealed significant, non-threshold relations between SO2 and decrements of the forced expiratory volume in 1 second (FEV1). Nitrogen dioxide. Weak associations between short-term nitrogen dioxide (NO2) exposure from gas cooking and respiratory symptoms and a decrement in lung function parameters were found in children, but not consistently in exposed women. With long-term exposure, children, but not adults, exhibit increased respiratory symptoms, decreased lung function, and increased incidences of chronic cough, bronchitis, and conjunctivitis. A causal relationship between NO2 exposure and adverse health effects has not yet been established. Carbon monoxide. Binding of CO in the lungs with hemoglobin in the blood forms carboxyhemoglobin (COHb), which impairs the transport of oxygen. The health effects of CO include hypoxia, neurological deficits and neurobehavioral changes, and increases in daily mortality and hospital admissions for cardiovascular diseases. The latter persists even at very low CO levels, indicating no threshold for the onset of these effects. Whether the relation between daily mortality and exposure to CO are causal or whether CO might act as a proxy for SPM is still an open question. Ambient CO may have even more serious health consequences than does COHb formation and at lower levels than that mediated through elevated COHb levels. Ozone. Short-term acute effects of O3 include pulmonary function decrements, increased airway responsiveness and airway inflammation, aggravation of pre-existing respiratory diseases like asthma, increases in daily hospital admissions and emergency department visits for respiratory causes, and excess mortality. Exposure-response relations are non-linear for the respective associations between O3 and FEV1, inflammatory changes, and changes in hospital admissions, whereas the relation between percent change in symptom exacerbation among adults and asthmatics is linear. Single-pollutant associations between O3 exposure and daily mortality and hospital admissions for respiratory diseases is statistically significant, even in multi-pollutant models. Suspended particulate matter. Associations between SPM concentrations and mortality and morbidity rates are significant. The acute health effects of SPM, even at short-term low levels of exposure, include increased daily mortality and hospital admission rates for exacerbation of respiratory disease, fluctuations in the prevalence of bronchodilator use, and cough and peak flow reductions, as well as long-term effects with respect to mortality and respiratory morbidity. Such effects depend on particle size and concentration and can fluctuate with daily fluctuations in PM10 or PM2.5 levels. The relation between PM10 or PM2.5 exposure and acute health effects is linear at concentrations below 100 micrograms/m3. Currently no threshold has been reported below which no effects occur. The influence of co-polluting gaseous pollutants could explain part of the observed variance in short-term health effects and reduce the contribution of SPM. Lead. The biological effects of lead can be related to blood lead levels, the best indicator of internal exposure. The potential effects of lead in adults and children include encephalopathic signs and symptoms, central nervous system symptoms, cognitive effects, increased blood pressure, and reduced measures of child intelligence. (ABSTRACT TRUNCATED)
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PMID:Air pollution and health in urban areas. 1093 84

Eosinophilic bronchitis is a common cause of chronic cough, which like asthma is characterized by sputum eosinophilia, but in contrast to asthma there is no variable airflow obstruction or airway hyperresponsiveness. Our hypothesis was that the differences in airway pathophysiology maybe due to less active airway inflammation in eosinophilic bronchitis, with reduced release of important effector mediators. We measured the concentration of various proinflammatory mediators in induced sputum cell-free supernatant in eight patients with eosinophilic bronchitis, 17 patients with asthma matched for sputum eosinophil count, and 10 normal subjects. Cysteinyl-leukotrienes (cys-LT) were measured by enzyme immunoassay, eosinophilic cationic protein (ECP) by fluoroimmunoassay, prostanoids (PGE(2), PGD(2), TXB(2), and PGF(2alpha)) by gas chromatography-negative ion chemical ionization-mass spectroscopy, and histamine by radioenzymic assay. The geometric mean sputum eosinophil count was similar in asthma (13.4%) and eosinophilic bronchitis (12.5%). Sputum cys-LT and ECP were a mean (95% CI) 1.6-fold (1.1, 2.5) and 6.4-fold (1.4, 28) higher in eosinophilic bronchitis and 1.9-fold (1.3, 2.9) and 7.7-fold (1.2, 46) higher in asthma compared with that in control subjects (geometric mean, 5.9 and 95 ng/ml, respectively). In eosinophilic bronchitis the mean concentration of sputum PGD(2) (0.79 ng/ml) and histamine (168 ng/ml) were significantly higher than in asthma (mean absolute difference in PGD(2) concentration, 0.47 ng/ml [95% CI, 0.19 to 0. 74] and mean-fold difference in histamine concentration, 6.7 [95% CI 1.7 to 26]) and normal subjects (0.64 ng/ml [0.36 to 0.90] and 11-fold [3.3 to 36]), respectively. In conclusion, eosinophilic bronchitis is associated with active airway inflammation with increased release of vasoactive and bronchoconstrictor mediators.
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PMID:Induced sputum inflammatory mediator concentrations in eosinophilic bronchitis and asthma. 1098 99

The recent development of noninvasive techniques to measure airway inflammation has led to the recognition of eosinophilic bronchitis, a condition characterized by a sputum eosinophilia identical to that seen in asthma, but without any of the functional abnormalities associated with asthma. The condition is interesting for a number of reasons. Firstly, eosinophilic bronchitis is a common cause of chronic cough, which is important to recognize as it responds well to corticosteroids. However, recognition is not straightforward because it requires assessment of airway inflammation. Secondly, the natural history of eosinophilic bronchitis is uncertain. Some patients with chronic obstructive pulmonary disease without a history of previous asthma have sputum eosinophilia, thus one possibility is that eosinophilic bronchitis may develop into fixed airflow obstruction. Finally, the difference in the association of eosinophilic airway inflammation to airway dysfunction between eosinophilic bronchitis and asthma is of interest as it is possible that it reflects important differences in the nature or site of the airway inflammation. Further study of this interesting condition may shed light on the relationship between airway inflammation and airway responsiveness, leading to a greater understanding of both eosinophilic bronchitis and asthma.
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PMID:Eosinophilic bronchitis: an important cause of prolonged cough. 1108 64

Carbocysteine is a mucoactive drug and is being used for both acute and chronic infectious airway diseases. Although carbocysteine can repair the damage of epithelial cells caused by exposure to various agents, the effects of this agent on allergic airway diseases such as asthma and eosinophilic bronchitis with an isolated chronic cough, in both of which epithelial damage may be characteristic, is not clear. We investigated the effects of carbocysteine on antigen-induced cough hypersensitivity to inhaled capsaicin at 48 h and bronchial hyperresponsiveness to inhaled methacholine at 72 h after challenge with an aerosolized antigen in actively sensitized guinea pigs. After measuring bronchial responsiveness, we examined neutral endopeptidase (NEP) activity in the tracheal tissue. Carbocysteine (10, 30, or 100 mg/kg) was given intraperitoneally every 12 h for 3 days after antigen challenge. The number of coughs elicited by an aerosol of capsaicin (10(-4) M) was significantly (p < 0.01) decreased in carbocysteine groups (6.13 +/- 0.59 at 10 mg/kg, 4.88 +/- 0.67 at 30 mg/kg, and 4.50 +/- 0.33 at 100 mg/kg during 3 min measurement) compared with the control group (9.75 +/- 0.53). Furthermore, carbocysteine dose dependently repaired the antigen-induced decrease of NEP activity in the tracheal tissue, but it did not influence the bronchial hyperresponsiveness or bronchoalveolar lavage cell component. These findings suggest that carbocysteine promotes the repair of damaged epithelium by allergic reaction and may be useful in allergic airway diseases accompanied by isolated chronic coughing, especially eosinophilic bronchitis without asthma and tracheobronchitis with cough hypersensitivity.
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PMID:Effects of carbocysteine on antigen-induced increases in cough sensitivity and bronchial responsiveness in guinea pigs. 1135 19

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.
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PMID:[Eosinophilic bronchitis without asthma--an additional rare cause for chronic persistent cough (CPC)? A 30-year old patient with severe CPC due to eosinophilic bronchitis without asthma or hyperreactivity]. 1144 11

Cough variant asthma (CVA), atopic cough (AC) and eosinophilic bronchitis without asthma (EB) are eosinophilic airway diseases presenting with isolated chronic cough. Among them, bronchodilators are effective only in CVA. Bronchial responsiveness, diurnal variation of pulmonary function and bronchomotor tone are mildly increased to intermediate levels between mild asthma and normal in CVA, but not in AC or EB. Cough sensitivity is heightened in atopic cough and probably in EB, but not in CVA. Bronchoalveolar lavage eosinophilia is present in CVA and EB, but absent in AC. As asthma onset has been recognized in nearly 30% patients with CVA, but not in AC, long-term inhaled corticosteroid therapy is recommended only in CVA.
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PMID:[Eosinophilic airway diseases presenting with isolated cough except for asthma]. 1167 50


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