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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
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PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

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

A 22-year-old black male presented with progressive dyspnea, a nonproductive cough, and new skin lesions. He was severely hypoxic, and had a severe restrictive defect on pulmonary function testing. A 2-cm lytic defect was noted on skull radiographs. A lung biopsy demonstrated pulmonary fibrosis. A biopsy of a skin lesion was consistent with a diagnosis of multifocal eosinophilic granuloma, or disseminated histiocytosis X. The case presents several unusual features of this uncommon disorder.
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PMID:Multifocal eosinophilic granuloma. 326 19

Respiratory infections of 19 subjects of advanced age and/or with underlying respiratory disease were treated with cefoperazone (CPZ) and its clinical effects were studied. Sixteen subjects suffered from respiratory tract infection and 3 subjects had pneumonia. The age of the subjects ranged from 39 to 77 years with the mean of 63.8, 7 of them being more than 70 years of age. The underlying respiratory diseases included chronic pulmonary emphysema in 6 subjects, diffuse panbronchiolitis in 3, bronchiectasis in 3, silicosis in 2 and one each of chronic bronchitis, pulmonary fibrosis, lung cancer and old pulmonary tuberculosis. One case, 75 years of age, had renal insufficiency. The daily dose of CPZ was 4 grams in 18 of the 19 subjects and the duration of administration ranged 5 to 22 days. The remaining 1 subject received 2 g of CPZ daily for 6 days. Clinical effects were judged from the changes in fever, cough, amount of sputum, dyspnea, rales, cyanosis, chest X-ray, white blood cell counts, CRP, erythrocyte sedimentation rates and results of sputum culture. Clinical effects were good in 16 subjects, fair in 1, and poor in 2. Bacteriological follow-up was carried out in 13 subjects. Infecting bacteria were eliminated from 5 subjects, reduced in 2 and, in 4 subjects, they were replaced by other bacteria. In 1 subject, P. aeruginosa was isolated from sputum even after the treatment with CPZ, and in another subject H. influenzae relapsed immediately after the cessation of the CPZ treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of cefoperazone on respiratory infections of patients of advanced age and/or with underlying respiratory diseases]. 373 62

With the recent development of new potential antibiotics, it has become easier to treat patients with common bacterial infections. However, we find it difficult to handle severe infections due to opportunistic pathogens, developed in the so-called immunocompromised patients. SM-4300 is a newly developed intravenous human gamma-globulin, which is said to be intact without conventional enzyme-treatment and sulfonization. SM-4300 is also free from large molecules of aggregated gamma-globulin. SM-4300 was administered in combination with antibiotics to 2 patients of severe respiratory infections, having refractory underlying diseases. Case No. 1 was a 65-year-old female with bronchopneumonia, who had been suffering from pulmonary fibrosis, chronic bronchitis, chronic congestive heart failure and tricuspid insufficiency for several years. During her hospitalization because of these diseases, she developed cough with slight sputum and exertional dyspnea accompanied by high body temperature of 38 degrees C on January 1983. Chest X-ray revealed infiltration in the right lung field which was compatible with bronchopneumonia. SM-4300 of 5 g was added intravenously on 5th day after 4 day-cefotiam treatment with no improvement. High body temperature subsided and laboratory data became normal around 3 days after single SM-4300 injection. Case No. 2 was a 68-year-old male patient of chronic bronchitis with chronic pulmonary emphysema and bronchial asthma. Around the end of May 1983, he complained of dyspnea on exertion and had mucopurulent sputum, more than 100 ml daily, from which Pseudomonas aeruginosa was cultured in large number. He was afebrile.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies on SM-4300, a new intravenous human gamma-globulin]. 393 26

Mast cells are present in human lung tissue, pulmonary epithelium, and free in the bronchial lumen. By virtue of their location and their possession of specific receptors for IgE and complement fragments, these cells are sentinel cells in host defense. The preformed granular mediators and newly generated lipid mediators liberated upon activation of mast cells by a variety of secretagogues supply potent vasoactive-spasmogenic mediators, chemotactic factors, active enzymes, and proteoglycans to the local environment. These factors acting together induce an immediate response manifest as edema, smooth muscle constriction, mucus production, and cough. Later these mediators and those provided from plasma and leukocytes generate a tissue infiltrate of inflammatory cells and more prolonged vasoactive-bronchospastic responses. Acute and prolonged responses may be homeostatic and provide for defense of the host, but if excessive in degree or duration may provide a chronic inflammatory substrate upon which such disorders as asthma and pulmonary fibrosis may ensue.
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PMID:The human lung mast cell. 642 78

Respiratory symptoms and spirometric pulmonary function data [i.e., first-second forced expiratory volume (FEV1.0) and forced vital capacity (FVC)] for 128 (30%) males who were exposed to alkyl benzene sulphonate in a detergent factory and for 56 (76%) unexposed workers in the same factory are reported herein. Exposed subjects had been employed for 1 month to 15 yr, and they generally complained of cough and mucus secretions, nasal catarrh, chest pain, and breathlessness. Unexposed workers had been employed for 1 month to 13 yr and had a significantly lower (P less than .001) frequency of symptoms, as well as significantly higher (.01 greater than P greater than .001) FEV1.0 and FVC than the exposed workers. The reduction in pulmonary function of exposed subjects from the predicted was significantly higher (.01 greater than P greater than .001) than that experienced by the unexposed subjects. There was a significant 8-hr workshift depression in lung function. There was radiological evidence of pulmonary fibrosis, but lack of pre-employment chest radiographs renders this inconclusive. Respiratory symptoms in exposed subjects decreased with duration of employment, which probably indicates the exodus from the work force of those who could not tolerate the nonsoapy detergent.
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PMID:Pulmonary function of exposed and control workers in a Nigerian nonsoapy detergent factory. 672 84

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) represents a spectrum of granulomatous, interstitial, and alveolar-filling lung disorders of which farmer's lung is a classic example. A major source of offending antigens in these diseases are thermophilic actinomycetes growing in moldy vegetable matter especially Micropolyspora faeni, and members of the Thermoactinomyces genus. Acutely, hypersensitivity pneumonitis presents as cough, dyspnea and fever, with crepitant rales, leucocytosis, diffuse interstitial and alveolar pulmonary infiltrates and a restrictive-type pulmonary functional deficit. Symptoms usually begin 4 to 6 hr after exposure to large quantities of causative organic dust. Chronically, these diseases may present with the gradual onset of cough, dyspnea on exertion, fatigue, anorexia, and weight loss which may progress to pulmonary fibrosis or severe pulmonary insufficiency. While early ideas on the pathogenesis of hypersensitivity pneumonitis support the role of Type III immune complex hypersensitivity, more recent evidence attests to the important and integral role of Type IV or delayed-type hypersensitivity. It is the purpose of this review, therefore, to describe those immune mechanisms relevant to the pathogenesis of hypersensitivity pneumonitis and stress the importance of "local" pulmonary immune responsiveness.
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PMID:Immunology of hypersensitivity pneumonitis. 676 Oct 66

Three patients who developed pulmonary fibrosis following prolonged treatment with nitrofurantoin for chronic urinary tract infections are presented. They had received the drug for 3--4 years; all gave histories of 2--3 years of progressive shortness of breath and an unproductive cough. On examination, all 3 patients had bilateral crackles and 1 had finger clubbing. Chest radiographs showed bilateral shadowing and lung function tests a restrictive defect with reduced gas transfer. Lung biopsies showed extensive fibrosis in 2 patients and advanced honeycomb formation in 1. The response to steroid therapy in 2 patients was excellent, with resolution of symptoms, clearing of the chest radiographs and improvement in lung function. It is proposed that nitrofurantoin has no place in the long-term treatment of chronic urinary tract infections and that its use in acute infections should be questioned.
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PMID:Pulmonary fibrosis following long-term nitrofurantoin therapy. 707 74

Clinical data are presented on 14 patients undergoing BCNU therapy for a primary intracranial glioma (11 biopsied, 3 suspected) in whom pulmonary fibrosis developed as a consequence of the therapy. Pulmonary diffusion abnormalities, dry hacking cough, and chest x-ray changes herald the onset of the process. Microscopic evaluation of lung specimens revealed a wide spectrum of change including hyaline membrane formation, alveolar septal thickening, interstitial fibrosis, and granuloma formation. It is concluded that BCNU causes pulmonary fibrosis that is primarily but not necessarily dose-related and may not be reversible.
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PMID:1,3-Bis(2-chloroethyl)-1-nitrosourea (BCNU)-induced pulmonary fibrosis. 720 51


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