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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Environmental lung injury may take the form of acute tracheobronchitis, asthma, pulmonary edema, chronic bronchitis, emphysema, allergic pneumonitis, fibrosing alveolitis, pleurisy, and neoplastic disease. Environmental factors eliciting these responses include irritant gases and fumes, oxidants, organic allergens, inorganic dust, bacterial enzymes, and high partial pressures of oxygen. The basic pulmonary reactions to these toxic agents--bronchoconstriction, vasoconstriction, increased vascular permeability, inflammation, carcinogenesis--may be mediated, aggravated, or modulated by biologically active substances. These humoral agents include biogenic amines (e.g. histamine): peptides (e.g., bradykinin, vasoactive intestinal peptide, and spasmogenic lung peptide); enzymes (e.g., proteases, superoxide dismutase, and mixed function oxidases); and acidic lipids (e.g., prostaglandins, prostaglandin endoperoxides, and thromboxanes).
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PMID:Environmental injury of the lung: role of humoral mediators. 35 83

Case histories are analyzed of 1565 hay fever patients first attending an allergy unit. The mean age of the test persons was 19.5 years. 40% were in the age group 5 to 15 years. The sex distribution showed a slight but statistically significant prevalence of males (56.6%). 56.8% had a positive family history of allergies and 44.2% had other allergic conditions such as atopic dermatitis (31.6%), perennial rhinitis and perennial asthma (19% each), urticaria, food allergy and drug allergy (5% each) and insect sting allergy (3%). A clear cut peak both for rhinitis and for asthmatic symptoms %30.5% and 20.2% respectively) was found in the age group 5--9 years. Up to the 14th year the symptoms of pollen allergy were already exhibited by 68.5% of the patients. 97% of the pollen allergics suffered from rhinitis, 95% from conjunctivitis, 40% from bronchial asthma and another 20% from tracheobronchitis or asthmatic bronchitis. As additional symptoms of pollen allergy due to haematogenous spread of the pollen antigens we observed a seasonal form of atopic dermatitis in 3%, a seasonal urticaria or angioedema in 3.5%, migraine in 6.3% and arthralgia, gastro-intestinal troubles and fever in fewer than 1% each. Almost 98% of the patients were sensitized to grass or cereal pollens. However, only 18% suffered from an isolated grass pollinosis (summer hay fever). The other patients were additionally clinically sensitized by other pollens with different blossoming periods, i.e. 35% by three pollens responsible for the so-called spring pollinosis, and 50% by weeds (plantain, nettle, mugwort) the cause of late summer pollinosis. Only 13 patients suffered from an isolated spring pollinosis (hazel, alder, birch, willow). In 14 patients (not quite 1%) with a clear-cut history and clinical symptoms of pollinosis, all the skin tests were negative. In these cases the sensitization was probably restricted to the respiratory tract. Despite the new in-vitro methods such as the RAST, carefully performed skin tests linked to a knowledge of the pollen calendars of the region and the allergological history remain the most reliable and cheapest procedure for the specific diagnosis of pollen allergy.
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PMID:[Pollionosis: I. Findings on the clinical aspects and the pollen spectrum in 1565 pollen-sensitive patients]. 49 10

A series of 16 patients with tracheal compression by the innominate artery is presented. In more than half of the patients the symptoms began during the first few days of life with stridor varying severity, recurrent tracheobronchitis and apneic spells. In six cases requiring surgical treatment the immediate result was good. In ten mild cases treatment consisted of medical management and follow-up. The present study confirms that the great arteries can exert compression on the trachea, which can always be relieved by means of an operation which moves the arteries forward. Bronchoscopy is considered to be the only reliable means of diagnosis. This entity should be considered more often in the differential diagnosis in children less than 3 years of age with stridor, breathing difficulties, recurrent infections, apneic spells, and asthma.
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PMID:Innominate artery compression syndrome. Presentation of 16 cases. 78 80

The increased cultivation and sales of Euphorbia fulgens Karw., originating in Mexico, has in the last few years led to occupational allergy, type I, in three growers manifesting itself as nasal disease, tracheobronchitis or bronchial asthma. Intracutaneous tests with pollen extracts were positive in all cases, even at high dilution. A specific hyposensitisation regimen, conducted over five months, gave highly promising results in one patient who had no symptoms in the following season, despite similar exposure. Such sensitisation by pollens of Euphorbia fulgens Karw. is probably widespread among growers and florists. The allergen is found only in the pollen, not in other parts of the plant. There is no relation to the toxic substances in the milk-sap of this plant family (Euphorbiaceae).
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PMID:[Occupational allergy due to inhalation of pollen from Euphorbia fulgens Karw (author's transl)]. 126 72

A retrospective study was performed in order to compare the clinical evolution of chronic bronchial asthma with onset in childhood with that of bronchial asthma registered at adult age. The group included 150 cases (87 females and 63 males) out of which 108 (72%) asthma with late onset and 42 (28%) asthma symptoms registered in childhood and adolescence. The symptoms were: allergic rhinitis and spastic tracheobronchitis in 18 (42.8%), dyspneic recurrent bronchitis in 16 (38%), nasal polyposis in 4 (9.5%) and atopic dermatitis in 4 (9.5%) cases. A possible allergic etiology was not taken into consideration in these cases. According to the data obtained, it results that the evolution and the prognosis of bronchial asthma are more severe in patients with its onset in childhood, where there were noted: more severe clinical forms of the disease, higher ventilation dysfunction, more numerous social (family) consequences of the disease, and a higher necessity of long term, systemic corticotherapy than in cases of bronchial asthma with late onset. The delay in the preventive treatment or an incorrect application of it in childhood will condition to a great extent the unfavourable evolution of the disease.
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PMID:[The late evolution of bronchial asthma appearing in children]. 129 96

One prediction of the protease-antiprotease hypothesis of chronic obstructive pulmonary disease (COPD) pathogenesis is the appearance of elastin-derived degradation products in the plasmas of affected patients that are due to the breakdown of alveolar interstitial elastin by an excess of elastolytic activity in the lung. We previously demonstrated a significant elevation of plasma elastin-derived peptides (EDP) in subjects with COPD in comparison with asymptomatic smokers with normal spirometry or normal nonsmokers. To better determine the selectivity of the assay for EDP as a marker of COPD, we measured plasma EDP levels in different patient populations. These included subjects with COPD, subjects with diseases that may involve accelerated elastolysis (pneumonia, atherosclerotic vascular disease, and inflammatory arthritis), subjects with diseases hypothesized to involve pulmonary inflammation without elastolysis (asthma and acute tracheobronchitis), asymptomatic smokers with normal spirometry, and healthy, nonsmoking subjects. Mean plasma EDP levels in subjects with COPD were elevated above those in all other subjects (p less than 0.01). The prospective analyses of specificity and sensitivity of plasma EDP levels as markers of COPD gave values of 91 and 65%, respectively. Utilizing receiver operating characteristic curve analysis to assess the diagnostic and screening performance of plasma EDP as a test for COPD (perfect test equals an area under the curve of 1.0), the area under the curve was 0.87, which compares favorably with many widely used clinical tests. These data demonstrate that the assay for plasma EDP is a quantitative, easily measured, and highly specific marker for subjects with COPD.
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PMID:Specificity and sensitivity of the assay for elastin-derived peptides in chronic obstructive pulmonary disease. 846 8

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

The variant forms of bronchial asthma were studied. It was established that in 66.4% of the patients examined the bronchial obstructive syndrome was caused by bronchial asthma. In 50.30% of the patients bronchial asthma had an atypical course--variant (forme fruste) forms. Three types of variant forms of bronchial asthma are differentiated: allergic tracheobronchitis (47.23%), the so called "wet" asthma (3.27%) and the so called "dry" bronchial asthma (0.8%). The therapeutic conduct should take into consideration the presence of variant forms of bronchial asthma.
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PMID:[Variant (forme fruste) forms of bronchial asthma]. 341 7

In order to address the role that the ambient air pollution mix, comprised of gaseous pollutants and various physical and chemical measures of particulate matter, plays in exacerbating cardiorespiratory disease, daily measures of fine and coarse particulate mass, aerosol chemistry (sulfates and acidity), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Toronto, Ontario, Canada, in the summers of 1992, 1993, and 1994. These time series were then compared with concurrent data on the number of daily admissions to hospitals for either cardiac diseases (ischemic heart disease, heart failure, and dysthymias) or respiratory diseases (tracheobronchitis, chronic obstructive long disease, asthma, and pneumonia). After adjusting the admission time series for long-term temporal trends, seasonal variations, the effects of short-term epidemics, day of the week effects, and ambient temperature and dew point temperature, positive associations were observed for all ambient air pollutants for both respiratory and cardiac diseases. Ozone was least sensitive to adjustment for the gaseous and particulate pollution measures. However, the association between the health outcomes and carbon monoxide, fine and coarse mass, sulfate levels and aerosol acidity could be explained by adjustment for exposure to gaseous pollutants. Increases in ozone, nitrogen dioxide, and sulfur dioxide equivalent to their interquartile ranges corresponded to an 11% and 13% increase in daily hospitalizations for respiratory and cardiac diseases, respectively. The inclusion of any one of the particulate air pollutants in multiple regression models did not increase these percentages. Particle mass and chemistry could not be identified as an independent risk factor for the exacerbation of cardiorespiratory diseases in this study beyond that attributable to climate and gaseous air pollution. We recommend that effects of particulate matter on health be assessed in conjunction with temporally covarying gaseous air pollutants.
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PMID:The role of particulate size and chemistry in the association between summertime ambient air pollution and hospitalization for cardiorespiratory diseases. 928 96

Exacerbations of chronic obstructive pulmonary disease (COPD) are usually treated with bronchodilator therapy, glucocorticoids and antibiotics. However, there are few experimental data on the effects of these agents in patients with acute COPD. A beta(2)-adrenoceptor agonist is usually given first because it can be expected to produce a rapid response. An anticholinergic agent should also be given when the patient is severely ill or responds inadequately to the beta(2) agonist. These agents can be administered via a nebuliser or using a metered-dose inhaler in conjunction with a spacer device. Glucocorticoids can accelerate recovery if the standard empirical regimens for acute exacerbations of asthma are used, although a longer treatment duration appears to be required. Theophylline provides little additional benefit in patients who receive frequent doses of inhaled bronchodilators and an adequate dosage of a glucocorticoid. Although the role of bacterial infections is not completely understood, the use of antibiotics is justified in patients with severe airflow limitation who have febrile tracheobronchitis.
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PMID:Pharmacological treatment in acute exacerbations of chronic obstructive pulmonary disease. 950 91


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