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)

Multiple scattered foci of bullous emphysema were detected in the lungs of two aged Afghan Hounds. The affected parenchyma contained bronchi with rudimentary cartilage and small smooth muscle bundles. The bronchi were generally lined by cuboidal epithelium. The animals were generally asymptomatic throughout their entire lives. One, the female, developed dyspnoea and tachypnoea terminally, following the rupture of two bullae.
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PMID:Multifocal bullous emphysema with concurrent bronchial hypoplasia in two aged Afghan hounds. 276 Feb 80

Two characteristics, volatility and biotransformation, make mercury somewhat unique as environmental toxicant, and make mercury poisoning as one of occupational diseases in the industry. Acute mercury vapor poisoning is a rare event. It often occurs during industrial accident or ignorant experiment. We report a case, a 28-year-old male waterworks technician, who developed dyspnea, cough, chest pain, metallic taste and ache in the whole body three hours after heating approximately 30 ml of liquid mercury during an experiment. Diarrhea with tarry stool occurred the next day. Chest roentgenogram revealed diffuse pulmonary infiltrates similar to pulmonary edema in both lungs, and was complicated by pneumomediastinum and subcutaneous emphysema later. The concentration of mercury in the plasma was over the toxic level. The urinary excretion of mercury greatly exceeded normal value. During hospitalization, the patient's liver and renal function tests were both normal. He was treated with penicillamine, 300 mg every six hours orally for 10 days in addition to a support treatment and oxygen therapy. He was discharged on the 15th hospital day with partial resolution of pulmonary infiltrates and was free of symptom.
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PMID:[Acute pneumonitis caused by inhalation of mercury vapor--report of a case]. 276 70

Serum levels of alpha 1-antitrypsin were studied in 80 patients with chronic bronchitis. As a manifestation of the inflammatory response, nonsignificant increase was recorded compared to the group of healthy subjects. In discordance with literary data, no significant differences were found between bronchitics smokers and non-smokers. In 5 patients (6.2%), alpha 1-antitrypsin serum levels were below the lower limit of the reference range. The patients complained of cough, expectoration, and dyspnea. As a preventive measure, it is recommended to determine serum alpha 1-antitrypsin levels in smokers before they take up a job in a dusty environment and in bronchitics before inhalation treatment with proteolytic enzymes is administered. In alpha 1-antitrypsin deficit the value of substitution therapy in patients with emphysema is being emphasized.
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PMID:[Levels of alpha 1-antitrypsin in the blood of patients with chronic bronchitis]. 278 79

The aim of this paper is to report a very rare case of bronchobronchiolitis obliterans accompanied by mesenteric Castleman's lymphoma. A 45-year-old woman was admitted to our hospital with progressive exertional dyspnea. Chest radiography showed overinflated lungs suggesting emphysema and pulmonary function tests revealed severely restrictive as well as obstructive impairments. Selective alveolobronchogram and endoscopy using a thin fiberoptic bronchoscope (3 mm in diameter) demonstrated multiple obstructions of small bronchi. Using a biopsy forceps, a small piece of tissue of bronchial wall was obtained from the focus of obstructive change, which showed histologically nonspecific inflammatory change including granulation. Therefore, we diagnosed her disease as bronchobronchiolitis obliterans (BBO). In addition, she had a large abdominal mass. On operation, it was found to be located in the mesenterium. It was then removed and the histological examination revealed Castleman's lymphoma, hyaline-vascular type. After operation, the blood IgM level, which was high on admission decreased rapidly and her dyspnea was reduced, suggesting that Castleman's lymphoma was related to the pathogenesis of her respiratory disease.
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PMID:[A case of bronchobronchiolitis obliterans with Castleman's lymphoma]. 279 67

Thirteen newborns with congenital cystic adenomatoid malformation and six with congenital lobar emphysema were operated on between 1970 en 1988. Eighteen children had more or less severe dyspnoea and (or) tachypnoea, one child presented with respiratory tract infection. The diagnosis could be made on the chest X-ray in most instances. However, diagnostic problems arose in the differentiation between congenital cystic adenomatoid malformation and congenital diaphragmatic hernia. Four times a laparotomy was done for presumed diaphragmatic hernia followed by thoracic surgery in the same session. In two children barium contrast studies of the gastrointestinal tract were done to exclude diaphragmatic hernia. Treatment consisted of lobectomy in 15 cases and segmental resection in four. Histological examination confirmed the clinical diagnosis in all instances. The results of the operations were excellent in all patients. No short- or long-term complications occurred.
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PMID:[Lung operations in dyspneic newborn infants]. 281 85

From 1970 to 1983, 69 individuals (aged from infancy to 87 years) with homozygous alpha 1-antitrypsin deficiency (ZZ) were followed up. 12 had liver disease. Amongst the 33 patients with emphysema mean age of onset of dyspnoea in smokers (32 years) was significantly lower than that in non-smokers (51 years). Mean age at death (excluding that from liver disease) was 48 years in smokers and 67 in non-smokers. In non-smokers mean FEV1 was 77% of that predicted, but in smokers it was only 38% of that predicted. In non-smokers, FEV1 declined with age, but there was considerable individual variation. In smokers, the decline correlated with the extent of cigarette smoking in pack years. Mean decrease in FEV1 in non-smokers was abnormally high (80 ml/year), but significantly less than the massive mean decline of 317 ml/year in smokers. In ex-smokers the mean rate of decrease was 61 ml/year.
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PMID:Smoking, lung function, and alpha 1-antitrypsin deficiency. 285 24

Synchronous laryngeal injury should be considered and diagnosed in patients presenting with maxillo-facial injuries who develop progressive dyspnoea. Surgical emphysema, a cardinal sign, may develop later. Clinical awareness of the problem and prompt referral, will lead to confirmation of the diagnosis. Early management may minimise long term morbidity.
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PMID:Progressive dyspnoea following facial injury. 293 80

The term obstructive lung disease is applied to a group of diseases of different nosology and pathogenesis with the common feature of a characteristic disturbance of the respiratory function consisting in increased resistance of air flow with dyspnoea as the leading clinical symptom. With regard to a differentiated therapy, it is necessary to distinguish precisely between the entities chronic bronchitis, bronchial asthma, emphysema. Meticulous anamnesis, careful clinical examination, basic lung function tests, x-ray examination, electrocardiographic and laboratory examinations, and eventually bronchologic and allergologic methods are sufficient in outpatient and general internal hospital care for a reliable classification and differentiation from a broad spectrum of causes of obstructive symptomatology located outside from the airways.
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PMID:[Differential diagnosis of obstruction--clinical aspects of obstructive lung diseases]. 304 40

Chronic obstructive pulmonary disease (COPD) is equated with chronic bronchitis and emphysema as one disease entity. In COPD airflow limitation is relatively persistent--unlike asthma. Tests for "small-airways disease" form no part of routine practice, for their accuracy in detecting pathological change is debatable. The proteolytic theory of the pathogenesis of emphysema highlights the role of neutrophil elastase, antielastases, oxidants, antioxidants, and thus of potential new treatments. Clinical features of COPD include breathlessness, cough, and sputum, with airflow obstruction and lung hyperinflation. The differential diagnosis includes bronchiectasis, cystic fibrosis, and pulmonary hypertension, but pulmonary fibrosis, etc., is distinguished by radiological infiltrates. Plain chest radiography cannot reliably diagnose emphysema in life, but a new method measuring lung density from the computed tomographic (CT) scan allows location, quantitation, and diagnosis of emphysema (defined by enlargement of distal air spaces) in humans in life. "Pink puffers" with breathlessness, hyperinflation, mild hypoxemia, and a low PCO2 are contrasted with "blue bloaters" with hypoxemia, secondary polycythemia, CO2 retention, and pulmonary hypertension and cor pulmonale. Antismoking measures are a major aim in management. A bronchodilator regimen combining a slow-release oral theophylline with an inhaled beta 2-agonist, ipratropium, and high-dose inhaled steroids is proposed because even modest improvement in obstruction can help these patients. In acute exacerbations with purulent sputum, antimicrobials against Streptococcus pneumoniae and Hemophilus influenzae are used with controlled oxygen therapy aiming to keep the arterial PO2 over 50 mm Hg without the pH falling below 7.25. Influenza prophylaxis is recommended, but pneumococcal vaccination remains debatable. Chronic under-nutrition in "emphysema" implies controlled trials of feeding regimens--but these remain to be assessed. Long-term oxygen therapy is the only treatment known to prolong life in blue bloaters, and oxygen concentrators and transtracheal oxygen delivery are discussed. Pulmonary vasodilators (e.g., beta 2-agonists, hydralazine, nifedipine, angiotensin-converting enzyme [ACE] inhibitors, etc.) have not yet been proved to provide long-term reduction in pulmonary arterial pressure. Blue bloaters have severe nocturnal hypoxemia in rapid eye movement (REM) sleep that is corrected by oxygen or the investigational drug almitrine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic obstructive pulmonary disease. 304 40

Dry Crotalaria saltiana shoots were fed to strain ASL mice at 50, 10 and 1% of the diet. Feeding of Crotalaria shoots at 50 and 10% produced toxicity and death after 7 to 29 days. The signs of Crotalaria poisoning were inappetence, dullness, dyspnea and recumbency. The main lesions were necrosis, portal fibroplasia and hemorrhage in the liver, pulmonary congestion and emphysema, focal catarrhal enteritis, and degeneration of the cells of the renal tubules.
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PMID:Toxic effects of Crotalaria saltiana in mice. 318 63


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