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)

Chronic obstructive lung disease (COLD) includes chronic bronchitis, chronic obstructive bronchitis and pulmonary emphysema. Bronchial obstruction can be caused by intraluminal processes (mucous secretion) as well as alterations of the bronchial wall (i.e. spasm of bronchial smooth muscle, hypertrophy of mucous glands, cellular infiltrates) or of the lung parenchyma (destruction of pulmonary structures). The development of pulmonary emphysema may be related to an imbalance of oxidants and antioxidants as well as that of elastases and anti-elastases. Smoking appears to play the most important role in this process.
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PMID:[Pathophysiology of chronic obstructive lung diseases]. 278 82

A study was made of the content of protease alpha 1-inhibitor and of the phenotyping of protease alpha 1-inhibitor subtypes in 666 patients with different chronic non-specific pulmonary diseases. It is concluded that pronounced deficiency of protease alpha 1-inhibitor is of importance in the formation of primary emphysema, chronic obstructive bronchitis and bronchial asthma. The clinical characteristics of obstructive pulmonary diseases marked by protease alpha 1-inhibitor deficiency have been investigated.
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PMID:[Etiologic significance of hereditary deficiency of proteinase alpha1-inhibitor in the formation of respiratory diseases]. 278 64

The paper is concerned with the results of roentgenofunctional investigation of 293 miners, among them there were 63 patients with dust bronchitis and 230 patients with the main types of dust disease (anthracosis, silicosis and anthracosilicosis). Two-stage roentgenopneumopolygraphy (RPPG) with a chess grid and spiral pneumoroentgenography (SPRG) with a spiral grid were employed. Respiratory dysfunction in patients with pneumoconiosis depended on an x-ray and morphological type of fibrosis and stage of disease rather than on its type. The formation of zones of emphysematous inflation in the apical area, in the upper and middle regions of the lungs was revealed, however signs of basal emphysema were ++undetectable. Analysis of RPPG and SPRG findings has shown that unlike pneumoconiosis, dust bronchitis is characterized by earlier development of respiratory dysfunction of more noticeable type, particularly in early signs of disease.
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PMID:[Experience with the roentgenodiagnosis of disturbances of respiratory function in coal miners]. 280 Mar 15

In Canada, USA and 9 Western European Countries, 121 respiratory physicians responded to an English language questionnaire asking them to state how they would investigate, treat and label four model patients, chosen to represent well-recognized patterns of clinical features of chronic airflow obstruction. Selection of further investigations appeared to be determined more by the probable diagnostic label than by the need to define selected characteristics in the whole range of such patients. Differences in recommended treatment between countries were less than others have reported for the treatment of asthma. Analysis of the diagnostic labels showed: the classic terms asthma, chronic bronchitis, emphysema still predominated in clinical practice and were considered to be better defined entities than any of the many terms introduced to describe chronic airflow obstruction in the last 30 yrs; the term chronic bronchitis was a source of confusion unless qualified to indicate presence or absence of obstruction; the use of combination terms such as chronic asthmatic bronchitis and chronic obstructive bronchitis showed large differences between countries; there were few differences related to national language. The implications of these findings are discussed.
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PMID:Diagnostic labels applied to model case histories of chronic airflow obstruction. Responses to a questionnaire in 11 North American and Western European countries. 280 91

Twenty one patients with bronchial adenoma, treated surgically in our hospital, include three different neoplasms: carcinoid, cylindroma and mucoepidermoid adenoma. In this series, clinical characteristics were: bronchial obstruction when the tumor protrudes into the lumen and infection, first in the bronchus (bronchitis or bronchiectasis) then in the parenchyma (acute, recurrent or chronic pneumonia, tension abscess). Ball-valve action of the tumor may result in lobar or segmental emphysema. Preoperatively, most of the patients had been misdiagnosed as bronchitis, carcinoma of lung, bronchiectasis or acute tension abscess. In our series, all the patients were alive in a follow up of 2-8 years. Yet one patient is living with local recurrence and distant metastasis. To our experience, pneumonia recurring in the same area of the lung, localized wheezing, with or without endocrine symptoms, lobar or segmental emphysema may suggest bronchial adenoma. Tomography and endoscopy are important for diagnosis. For the treatment, sleeve resection of the main bronchus was done in 2, bronchoplastic lobectomy in 7, lobectomy in 10, and pneumonectomy in 2. Sleeve resection of the main bronchus or bronchoplastic lobectomy is recommended as a reliable procedure for this disease.
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PMID:[Diagnosis and surgical treatment of bronchial adenoma]. 282 Jun 82

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

The survival of 354 claimants for compensation for pulmonary asbestosis among former workers of the Wittenoom crocidolite mine and mill in Western Australia has been examined. There were 118 deaths up to December 1982. The median time between start of work and claim for compensation was 17 years. The standardised mortality ratio (SMR) for deaths from all causes was 2.65 (p less than 0.0001). The SMR for pneumoconiosis was 177.2 (p less than 0.0001), bronchitis and emphysema 2.6 (p = 0.04), tuberculosis 44.6 (p less than 0.0001), respiratory cancer (including five deaths from malignant pleural mesothelioma) 6.4 (p less than 0.0001), gastrointestinal cancer 1.6 (p = 0.22), all other cancers 1.6 (p = 0.17), heart disease 1.4 (p = 0.07), and all other causes 2.18 (p = 0.004). Plain chest radiographs taken within two years of claiming compensation were found for 238 subjects and were categorised independently by two observers according to the International Labour Organisation criteria without knowledge of exposure or compensation details. Profusion of radiographic opacities, age at claiming compensation, work in the Wittenoom mill, and degree of disability awarded by the pneumoconiosis medical board were significant predictors of survival, but total estimated exposure to asbestos was not. Radiographic profusion and degree of disability were, however, predictable by total exposure. The median survival from claim for compensation was 17 years in subjects with ILO category 1 pneumoconiosis, 12 years in category 2, and three years in category 3.
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PMID:Compensation, radiographic changes, and survival in applicants for asbestosis compensation. 299 May 24

I found the recent increase during the past eight years of the incidence of respiratory infections caused by Branhamella catarrhalis. Namely, I experienced 74 cases (93 episodes) of the respiratory infections; 5 pneumonia, 14 acute bronchitis, 1 lung abscess, 36 chronic bronchitis, 7 chronic bronchiolitis, 21 bronchiectasis and 9 chronic pulmonary emphysema with infection. In 65 of 93 infectious episodes, Branhamella catarrhalis was isolated as a pure culture and in 28 episodes it was associated with other organisms, 13 Haemophilus influenzae etc. In all the cases, a positive correlation was found between beneficial clinical results and disappearance of the organism from the sputum. Minimum inhibitory concentrations of the representative beta-lactam and other antibiotics against 104 strains were determined. All of these strains were obtained during last four years from 1980 to 1983 from the purulent sputa as the main pathogen. Annually, this organism has significantly acquired resistance to beta-lactams. By 1983, 74% of Branhamella catarrhalis isolated from the purulent sputa became a beta-lactamase producers. And the failure cases of Branhamella catarrhalis infections treated with beta-lactams have increased during the last two years. These results have clearly showed also the importance of Branhamella catarrhalis as the common pathogen for respiratory organ.
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PMID:Clinical significance of respiratory infection caused by Branhamella catarrhalis with special reference to beta-lactamase producing strains. 300 26

The activity of the renin-angiotensin (RA) system and the ability of the lungs to generate angiotensin II (AII) were studied in 11 patients with stable cor pulmonale and respiratory failure caused by chronic obstructive bronchitis and emphysema. Angiotensin I concentrations (18.7 +/- 8.3 pmol/L) were normal, and transpulmonary AII formation rates (TRAIIFR) (14.2 +/- 18.1 pmol/min) were not significantly different from those recorded in nonedematous cardiac subjects (19.9 +/- 20.1 pmol/min), matched for sex, age, and diuretic therapy. The main determinant of TPAIIFR was the mixed venous AI concentration. Administration of oxygen for 30 min led to a small increase in TPAIIFR in the majority of patients. This increase could not be accounted for by changes in mixed venous AI. There was no correlation between serum angiotensin-converting enzyme levels and either the TPAIIFR or the systemic arterial AII concentrations.
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PMID:Transpulmonary angiotensin II formation in patients with chronic stable cor pulmonale. 303 31

Protease-antiprotease imbalance in the lung is considered to be a likely pathogenetic mechanism in the development of lung injury--particularly emphysema. Aminophylline is often used in bronchitis, bronchial asthma and emphysema. To assess, whether aminophylline indeed affects this mechanism we evaluated in vitro its influence at therapeutical concentrations (12 and 20 micrograms/ml) on phagocytosis, release of total protein and lysosomal enzymes after phagocytosis, spontaneous migration and chemotaxis of human neutrophils to zymosan-activated serum. There were no significant differences in phagocytosis, release of leukoprotease and acid phosphatase between neutrophils with and without aminophylline at both concentrations. However, the release of total protein was different (p less than 0.02, 12 micrograms/ml) and lower (p less than 0.02, 20 micrograms/ml) than the control. The mean decrease in protein release was 13.5 +/- 6% of the control and aminophylline inhibited the release of the protein with molecular weight below 35.000 daltons. Significant migration inhibition was found in 22% cases (12 micrograms/ml, n = 9) and in 53% (20 micrograms cm-3, n = 13). Neutrophil chemotaxis was different (p less than 0.02, 12 micrograms/ml) and lower (p less than 0.05, 20 micrograms/ml) than the control. The obtained results suggest that high doses, of aminophylline may diminish inflammatory recruitment of neutrophils--a rich source of elastase to the lung, and thus diminish proteolytic pulmonary injury.
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PMID:The influence of aminophylline on human neutrophils--possible protection of lung from proteolytic injury. 307 41


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