Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-two children (age range, 3 months to 5.5 years) with a clinical diagnosis of obstructive bronchitis (asthmatoid or spastic bronchitis or bronchiolitis) were found to have bronchial casts in the gastric fluid, and in 2 additional cases casts were spontaneously expectorated in the bronchial exudate. Cast bronchitis had a long-term course of 10 to 24 months in 65 of the 74 patients. Common radiologic findings included bronchi presumably filled with secretions, areas of atelectasis, and lung emphysema of varying degrees. Cast bronchitis did not appear to be associated with eosinophilia and elevated serum IgE levels. Therefore, an extrinsic allergic mechanism is not likely involved in the pathogenesis of the condition. Bronchial casts had varying consistencies; although they were usually soft, they were sometimes rather hard. They were hollow, often ramified, and white and measured from 0.5 to 2 cm in length. Histologically, they consisted of metaplastic squamous epithelium with a varying degree of inflammatory cells and noncellular material. Some differences in biochemical composition were observed between bronchial casts and bronchial exudate of acute catarrhal bronchitis. No viruses could be isolated in 11 cast specimens. Our results suggest that cast formation is mainly related to the metaplastic transformation of the bronchial epithelium and that this metaplasia may play an important pathophysiologic role in certain infants and children with obstructive bronchitis.
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PMID:Cast bronchitis in infants and children. 240 84

The history holds the central role in distinguishing among asthma, chronic bronchitis, and emphysema. A personal or family history of atopy, a history of seasonal worsening of disease in response to a known environmental agent, perhaps seasonal, and marked variability in the severity of airflow obstruction, often with dramatic responsiveness to bronchodilator drugs, strongly support the diagnosis of asthma. Exacerbation of wheezing by exposure to cold air or following the ingestion of a drug, and asthma variants, such as nocturnal cough responsive to bronchodilator agents or exercise-induced asthma, all support the diagnosis of asthma. Peripheral blood eosinophilia or sputum eosinophilia support the diagnosis of asthma providing other known causes of eosinophilia can be excluded. Positive skin tests are helpful in establishing the atopic state and indicating its possible etiology. An elevated serum IgE level supports the diagnosis of asthma; a normal one does not exclude it. Cigarette smoking is a common background factor in both chronic bronchitis and emphysema, and both diseases are infrequently observed in the absence of this history. Long-standing mucous hypersecretion preceding airflow obstruction suggests the presence of chronic bronchitis. Progressive dyspnea on effort as the predominant symptom suggests the possibility of emphysema. Reversibility of airflow obstruction suggesting the presence of asthma can be obtained either from physical examination or serial pulmonary function studies. Apart from this, neither of these techniques is very useful in differential diagnosis. Evidence of emphysema in the chest roentgenogram and a low value of the Dco/VA are sensitive tests for the presence of emphysema but are not highly specific. The main value of making the differentiation among these three conditions now lies in establishing a prognosis and guiding the use of corticosteroid therapy. As new information accumulates on the pathogenesis, prevention, and treatment of asthma, chronic bronchitis, and emphysema, precise diagnosis is likely to acquire increased significance.
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PMID:Distinguishing among asthma, chronic bronchitis, and emphysema. 396 40

Using a solid-phase radioimmunoassay, serum IgE level was determined in 46 normal subjects, 53 patients with bronchial asthma, 44 patients with chronic bronchitis and / or emphysema, and 19 patients with restrictive lung disease. Sputum IgE was measured simultaneously in 51 of the subjects. The range of serum IgE concentration in the normal subjects was wide. It varied between 15 and 750 ng/ml with a mean of 135 ng. Asthmatic patients had significantly higher levels of serum IgE with a mean of 579 ng/ml, but only 30% fell outside the normal 95% confidence limits. Patients with chronic bronchitis, emphysema and restrictive lung diseases had normal IgE levels. There was a significant correlation between serum and sputum IgE levels.
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PMID:Symposium on allergic lung diseases. 3. Serum and sputum immunoglobulin E levels in respiratory diseases in adults. 481 34

The relationships of smoking, allergy skin test reactivity, and serum IgE to ventilatory function have been analyzed in 1,182 subjects from a general population sample. The study group consisted of subjects aged 35 or more who deny previous lung surgery, old tuberculosis, or a current diagnosis of heart disease in the absence of chronic bronchitis or emphysema. Impairment of the forced expiratory volume in one second (FEV1) shows a definite relationship to total serum IgE. However, this relationship is significant only for a low FEV1 which is accompanied by symptoms suggesting asthmatic or a chronic bronchitis type disease. Allergy skin test reactivity to a battery of common aeroallergens shows no overall relationship to FEV1. However, after accounting for total serum IgE, positive allergy skin tests tend to be associated with high rather than low FEV1 values. The findings suggest that some type of IgE which is not specific for aeroallergens but which is associated with smoking, may be important in the pathogenesis of the "chronic asthmatic bronchitis" syndrome.
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PMID:Interactions of smoking and immunologic factors in relation to airways obstruction. 664 Dec 98

Of the twenty-three employees at a pharmaceutical plant manufacturing a new product containing papain, twelve had respiratory symptoms of cough, wheezing, dyspnoea, or chest paint. Most were studied with in-depth interviews by a doctor, extensive pulmonary function tests, and immunoserological tests for IgE and precipitating antibodies specific for papain, as well as total IgE antibodies to common natural allergens. There were significant correlates (all P values < 0.05) between the presence of specific IgE antibodies to papain and decreases of FEV1, FEF75--85, TLC, RV, and response to bronchodilators as percentage change from baseline for all spirographic flow rates. Atopic workers developed pulmonary symptoms and antipapain antibodies significantly sooner after papain exposure than did the others. Duration of exposure had no effect on symptomatology, pulmonary function, or immunological response. However, those judged to have the greatest amount of dust exposure per work-day had significantly more pulmonary symptoms (P < 0.005). Papain produced lung diseases by acting as an inhalant allergen rather than a proteolytic enzyme. Papain is a potent sensitizer in humans for the production of respiratory disease. The pulmonary reactions, based on physiological data, seem to involve small airways, alveolar, and interstitial lung tissue in an inflammatory rather than destructive manner, and thus resemble bronchitis and interstitial lung disease rather than pulmonary emphysema or typical bronchial asthma.
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PMID:Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies. 746 Feb 65

Indicies of asthma were measured in smokers with chronic bronchitis (CB) + pulmonary emphysema (PE), smokers with CB only, and non-smokers with CB, to examine whether smoking is involved in the development of asthma-like condition in patients with chronic obstructive pulmonary disease (COPD). Airway hypersensitivity was measured with an Astrograph method, and the reversibility of airway obstruction was measured as improvement in FEV1.0 and as percent change in FEV1.0 after inhalation of a beta-agonist. Both hypersensitivity and reversibility were significantly higher in smokers with CB+PE and in smokers with CB only than in non-smokers with CB. The number of eosinophils in sputum, but not in peripheral blood, was slightly higher in the smokers than in the non-smokers. The serum levels of IgE were significantly higher in the smokers than in the non-smokers. No significant difference in the rate of positive skin tests for common allergens was observed among the three groups, but the rate of positive tests for Broncasma Berna was very high in the smokers, and all such tests were negative in the non-smokers. These results indicate that among patients with COPD an asthmatic component is more frequently found in smokers than in non-smokers, and suggest that smoking plays some part in the development of asthma-like condition in these diseases.
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PMID:[Possible involvement of smoking in the development of asthma-like conditions in patients with chronic obstructive pulmonary disease]. 773 Nov 16

Chronic obstructive pulmonary disease (COPD) is a disease involving either or both of chronic bronchitis and emphysema. In the elderly, bronchial asthma is usually called chronic asthma because of sustained asthma attacks and resistance to therapy. Although the absolute value of IgE is low in the asthma in the elderly, IgE values correlated to the symptoms of asthma in the elderly. Therefore, asthma in the elderly is supposed to be primarily caused by allergic reactions. Airway epithelium products histamine methyl-transferase (HMT) and cholinesterase. Allergic reactions and/or virus infection in the airway epithelium reduce productions of these enzymes, which exacerbate bronchoconstriction. Steroid hormones increase these enzymes and relieve bronchoconstriction. Silent aspiration may exacerbate asthma attack in the night and recurrent cough and sputum in COPD. Macrolide antibiotics relieve chronic infections in the elderly. Plural constriction against bullae using thoracoscopy reduce dyspnea dramatically in emphysema.
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PMID:[Clinical strategy of chronic obstructive pulmonary disease in the elderly]. 811 44

Exposure to airborne endotoxin in infancy may protect against asthma by promoting enhanced T(H)1 response and tolerance to allergens. On the other hand, later in life, it adversely affects patients with asthma. Endotoxin binding to receptors on macrophages and other cells generates IL-12, which inhibits IgE responses. It also generates cytokines like IL-1, TNF-alpha, and IL-8, which cause inflammation. These signal transduction pathways resemble those leading to the generation of cytokines, such as IL-4, IL-13, and IL-5, which are responsible for the inflammation of IgE-mediated allergic disease. The main difference seems to be that endotoxin recruits neutrophils, but IgE recruits eosinophils, and the details of the tissue injury from these granulocytes differ. Sources of airborne endotoxin include many agricultural dusts, aerosols from contaminated water in many industrial plants, contaminated heating and air-conditioning systems, mist-generating humidifiers, and damp or water-damaged homes. Acute inhalation of high concentrations of endotoxin can cause fever, cough, and dyspnea. Chronic inhalation of lesser amounts causes chronic bronchitis and emphysema and is associated with airway hyperresponsiveness. Airborne endotoxin adversely affects patients with asthma in 3 ways: (1) by increasing the severity of the airway inflammation; (2) by increasing the susceptibility to rhinovirus-induced colds; and (3) by causing chronic bronchitis and emphysema with development of irreversible airway obstruction after chronic exposure of adults. The most effective management is mitigating exposure. The potential of drug treatments requires further clinical investigation.
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PMID:Endotoxin-stimulated innate immunity: A contributing factor for asthma. 1149 29

Severe alpha1-anti-trypsin (AAT) deficiency implies a high risk of pulmonary emphysema development. The possible relationship between partial deficiencies of this enzyme and bronchial asthma remains controversial. The objective of this study was to ascertain the distribution of AAT phenotypes in a non-selected asthmatic patient population. Across-sectional study on a sample of 111 patients with asthma was carried out. Demographic and clinical variables were collected with serum IgE concentrations, plasma eosinophil number and serum AAT concentrations determined, together with the Pi phenotype. Asthma was mild in 36 (32.4%) patients, moderate in 45 (40.5%) and severe in 30 (27%). No differences were observed in eosinophil count or serum IgE or AAT concentrations among patients with different degrees of severity. Twenty-two (19.8%) asthmatics with deficient phenotypes for AAT were identified, distributed equally in all severity stages of the disease. No significant differences were found in clinical and functional characteristics, or in asthma morbidity between PiMM and PiMS patients or the heterozygote group (PiMS and PiMZ). Eosinophil count and IgE concentrations did not differ significantly between asthmatics with normal phenotype and heterozygotes. In conclusion, the distribution of AAT phenotypes in asthmatic patients did not differ from that found in the general population. Heterozygote phenotypes for the deficiency do not appear to confer greater severity or different clinical expression of asthma in adults.
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PMID:Influence of deficient alpha1-anti-trypsin phenotypes on clinical characteristics and severity of asthma in adults. 1190 53

A literature review shows that airborne enzymes occurring in the general environment and in purified form in industrial production have a high allergenic potential to the airways, causing rhinitis, conjunctivitis and asthma. It can be assumed that this also applies to the increasing number of enzymes manufactured by the cloning of fast-growing genetically engineered microorganisms. Cross-sectional studies demonstrate exposure-response relations for IgE-mediated sensitisation and airway disorders. Atopic individuals are more susceptible to enzyme allergy than non-atopic individuals. Skin prick testing and measurement of specific IgE antibodies have been shown to be useful diagnostic tools. Very high concentrations of proteases may lead to emphysema. There is also evidence for non-allergic airway inflammation by proteases, probably via protease-activated receptor-2 and intracellular Ca(2+) release. It is recommended that all enzymes be classified with the risk phrase R42 (may cause sensitisation by inhalation) and that their inhalative uptake be totally avoided.
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PMID:Enzymes as occupational and environmental respiratory sensitisers. 1581 3


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