Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From summer to mid-autumn for four consecutive years (1974 to 1977), a 50-year-old woman barber experienced cough and exertional dyspnea with sputum production. Rales were audible at the posterior lung bases bilaterally. Her chest x-ray film showed diffuse nodular shadows, and pulmonary function studies revealed markedly decreased DCO. Open chest lung biopsy was performed and granulomatous lesions with multinucleated giant cells without central necrosis were observed. Having experienced multiple episodes for four years, she ceased to show symptoms after demolishing and reorganizing her house. This case is thought to represent the typical summer-type hypersensitivity pneumonitis, which we have subsequently found to be the most prevalent form of hypersensitivity pneumonitis in Japan.
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PMID:Clinical episodes of granulomatous pneumonitis. Repetition during four consecutive summers. 669 11

A unique form of hypersensitivity pneumonitis in which clinical symptoms appear in the summer and subside spontaneously in the mid-autumn was found in Japan. This disease was named summer-type hypersensitivity pneumonitis and was found the most prevalent form in Japan. This disease has the following characteristic features: 1) initiation in the summer; 2) repeated episodes during subsequent seasons for many years; 3) familial occurrence; 4) no occupational relationship; 5) positive returning-home provocation test; 6) cough, dyspnea and remittent fever as a clinical triad; 7) diffuse nodular shadows on chest x-ray film; 8) leukocytosis with neutrophilia; 9) moderately decreased % VC and markedly decreased Dco and PaO2; 10) skin reactivity to PPD is negative while symptomatic; 11) pulmonary lesions of biopsied specimens show epithelioid cell granulomas without central necrosis (63.3 percent), plus alveolitis and/or pneumonitis; 12) isolation of patients from their home environment diminishes symptoms; 13) corticosteroid is effective; 14) seasonal atmospheric microbiological pollution is speculated upon, but the offending antigen is not defined yet.
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PMID:Summer-type hypersensitivity pneumonitis. A unique disease in Japan. 669 85

Sixty-six patients, diagnosed as Japanese summer-type hypersensitivity pneumonitis at Osaka Prefectural Habikino hospital between 1973 and 1980, were studied. The diagnosis was based on the clinical features and summer-seasonal nature of the disease. The presence of an aetiological agent within patients' home environment was suggested by the recurrence of acute symptoms of high fever, cough and dyspnoea 5-8 hr after coming home from hospital, and by spontaneous improvement on leaving home. Immunological studies revealed the presence of anti-Cryptococcus antibody in sixty-four of sixty-five patients' sera, by indirect immunofluorescence against Cryptococcus neoformans. Precipitating antibody against culture supernatant protein-antigen of Cr. neoformans was detected in more than 80% of sera obtained from patients during the active stage of the disease. The positive result on inhalation provocation-challenge, using culture supernatant protein-antigen, suggested that Cr. neoformans or antigenically related Cryptococcus species may cause Japanese summer-type hypersensitivity pneumonitis.
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PMID:Japanese summer-type hypersensitivity pneumonitis: studies using Cryptococcus antigen. 674 30

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

Symptoms consistent with hypersensitivity pneumonitis (HP) occurred in 26 of 50 employees working in a localized area of a large factory. This area was served by a single heating-cooling unit utilizing a water humidification system. The illness consisted of flu-like symptoms with fever, chills, headache, cough, dyspnea. Most of the subjects affected demonstrated precipitating antibodies to a variety of organisms associated with HP, and inhalation challenge with water from the humidification system resulted in the reproduction of symptoms in one employee with a history suggestive of HP. Removal of the humidification system has resulted in a "cure" in that symptoms have not recurred during a one year followup period since the removal.
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PMID:Humidifier lung. An outbreak in office workers. 676 70

A patient employed in a plant where blue cheese was manufactured developed hypersensitivity pneumonitis to Pencillium roqueforti. Symptoms of cough, dyspnea, and malaise, and findings of bibasilar crackles, reduced lung volumes, hypoxemia, and bilateral infiltrates on chest roentgenogram, resolved after she left the workplace. Bronchoalveolar lavage revealed a high percentage of lymphocytes. Antibody to P. roqueforti was demonstrated in serum and lavage fluid. To our knowledge this case represents a new occurrence of hypersensitivity lung disease in the cheese manufacturing industry in the United States.
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PMID:Cheese worker's hypersensitivity pneumonitis. 683 56

To study the clinical and physiologic manifestations of the grain fever syndrome and the potentially pathogenic role of complement activation, 12 subjects (six grain workers and six healthy non-grain workers) underwent inhalation provocations with airborne grain dust. The clinical response was characterized by facial warmth, headache, malaise, myalgias, feverish sensation, chilliness, throat and tracheal burning sensation, chest tightness, dyspnea, cough, and expectoration. Fever developed in four grain workers and two controls. Leukocytosis, ranging between 11,700 and 24,300 leukocytes/mm3 with left shift, developed in five grain workers and five controls. There was no evidence of complement activation by the classical or alternate pathway. None of the subjects had serum precipitins to grain dust. The pulmonary response was characterized by a decrease in FEV1, FVC, MMF, Vmax50, and Vmax75, with significant rise in pulmonary resistance and consistent change in dynamic compliance but without changes in static compliance or diffusing capacity. Hence, grain dust inhalation induced diffuse airways obstruction without detectable parenchymal reaction. The airways response to high concentrations of grain dust inhalation were unrelated to the presence of immediate skin hypersensitivity. Although we cannot exclude the etiopathogenetic role of an immunologic reaction to grain dust, our data do not support the hypothesis that the grain fever syndrome is a precipitin-mediated allergic pneumonitis. More likely, the manifestations of grain fever probably reflect the host reaction to grain dust bacterial endotoxins and/or nonallergic mediator release by grain or grain dust constituents.
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PMID:Grain fever syndrome induced by inhalation of airborne grain dust. 707 83

Fifteen children, 6-14 years old, who were heavily exposed to pigeon droppings, presented with cough, chills and breathlessnes on mild exertion. Twelve gave immediate positive skin test reactions to pigeon droppings. Ten of the fifteen also gave a late (Arthus) reaction, and seven gave a positive delayed reaction which was maximal at 24--72 hr. Nine children had precipitins against avian droppings. In ten patients who were tested for lymphocyte transformation, five gave positive responses to both serum and pigeon droppings. Radiological findings of the chest showed parenchymatous infiltrations and diffuse interstitial reticulations, suggestive of extrinsic allergic alveolitis. In a control group of fifteen heavily-exposed children who had no symptoms, immediate and late skin reactions occurred respectively in five and two. One only had a positive precipitin test, and one of five tested had a positive lymphoblastic transformation. In a non-exposed comparable group of children, all tests were negative except for one immediate positive skin response. Children heavily exposed to the inhalation of avian antigens can develop extrinsic allergic bronchiolo-alveolitis.
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PMID:Extrinsic allergic bronchiolo-alveolitis in children. 719 99

Breathing air from a humidifier or an air conditioning unit contaminated by various microorganisms can cause an acute lung disease involving fever, cough and dyspnea, termed "humidifier fever". This type of hypersensitivity pneumonitis was first described in 1959 by PESTALOZZI in the Swiss literature and subsequently by BANASZAK et al. in the Anglo-American. Here a chronic form of this disease which led to pulmonary fibrosis is described: A 37-year-old woman who works in a cheese shop presented with dyspnea which had been progressive over two years, weight loss, a diffuse reticular pattern radiographically and a severe restrictive defect in lung function tests. Open lung biopsy revealed chronic interstitial and alveolar inflammation with non-caseating granulomas and fibrotic changes. Circulating immune complexes and precipitins against the contaminated humidifier water and cheese mites were found, but no antibodies suggesting legionnaires' disease. Two out of five otherwise healthy employees of this cheese shop, where a new humidifying system had been installed 7 years earlier, also had precipitins against the contaminated water from the humidifier and the cheese mites. Despite ending of exposure and longterm steroid and immunosuppressive therapy, the signs and symptoms of pulmonary fibrosis persisted. Contrary to the acute disease, this chronic form is termed "humidifier lung". The importance is stressed of investigating the possibility of exposure to contaminated humidifiers or air conditioning units in all cases of newly detected pulmonary fibrosis.
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PMID:[Humidifier lung]. 722 22

Since August, 1978, an epidemic characterised by respiratory symptoms and fever spread rapidly in a restricted area near Tampere, Finland. Four months later over half of the adult population reported intermittent or constant symptoms. The most frequent symptoms were cough, dyspnoea, chills, fever, headaches, muscle pain and aching of joints. The symptoms appeared to be associated with exposure to water vapour derived from tap water. Consequently this disease, which resembled extrinsic allergic alveolitis, was given the name 'bathing fever' for lack of any prevailing diagnosis. In clinical provocation tests lung diffusion capacity usually decreased, the leucocyte count increased, and a slight rise in body temperature was observed. Despite many efforts the specific causative agent in the tap water has not been identified. Neither massive chlorination of the water nor changing the sand filter of the water-works had any significant effect on the quality of the water. Therefore the source of water supply was changed in April, 1979. The symptoms have subsequently disappeared. Present knowledge about bathing fever suggests that, though rare, it may be typical of the Scandinavian type of climate.
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PMID:Bathing fever epidemic of unknown aetiology in Finland. 744 43


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