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)

A 46-year-old man who had worked in a paint processing plast for over 29 years was admitted to our hospital with complaints of nocturnal dyspnea and dry cough. A chest X-ray film showed diffuse granular shadows in bilateral lungs. Pulmonary function tests revealed reduction of diffusing capacity and restrictive impairments. Hypersensitivity pneumonitis (HP) due to isocyanates was speculated from his occupational history and clinical course. Positive skin tests against TDI-HSA and MDI-HSA, precipitating antibody against TDI-HSA, and negative lymphocyte stimulating tests of peripheral blood and bronchoalveolar lavage fluid were also noticed. Environmental provocation test was positive. Histological findings of transbronchial lung biopsy specimens showed diffuse alveolitis and Masson body, but no granulomas. According to these results, the patient was diagnosed as HP due to TDI. Type III allergy of Gell-Coombs seems to participate in this case. The granulomatous lesion is seen less frequently in isocyanate-related HP than in HP induced by organic dusts, which suggests the difference in immunological and histological reactions between both types of HP.
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PMID:[A case of hypersensitivity pneumonitis due to isocyanate (TDI)]. 256 May 2

The purpose of this study was to ascertain the immunological abnormality of hypersensitivity pneumonitis. The relationship between T cell subsets of lymphocytes in transbronchial lung biopsy (TBLB) specimens and in bronchoalveolar lavage fluid (BALF) were studied in 3 cases of farmer's lung disease (FLD). The lung specimens were examined by immunoperoxidase staining (ABC method) and the cells in BALF by the immunofluorescence method on the flowcytometry. All cases of FLD were diagnosed according to the following criteria: 1) history of exposure to FLD antigen, 2) clinical symptoms (cough, fever, breathlessness), 3) radiologic feature (diffuse small nodular pattern) and functional pattern of interstitial lung disease and 4) evidence of antibodies against Micropolyspora faeni. Histologically, granulomatous interstitial pneumonitis was revealed in all cases. Immunohistochemically, the number of positive lymphocytes was as follows: for Leu 4 (pan T cell) 8.6 cells/15.6 x 10(-3) mm2; Leu 3a (helper/inducer T cell) 5.1 cells; Leu 2a(suppressor/cytotoxic T cell) 1.2 cells on average, respectively. The Leu 3a+ cells were larger in number than the Leu 2a+ cells and the Leu 3a+/Leu 2a+ ratio was 4.76. In the BALF, the percentage of OKT3+ cells (pan T cell) was increased. The percentage of OKT4+ cells (helper/inducer T cell) was higher than that of OKT8+ cells (suppressor/cytotoxic T cell). The OKT4+/OKT8+ ratio was 6.65 in the BALF. The result of this study revealed the close relationship between the numerical distribution of T cell subsets in the lung tissue and in the BALF. It is suggested that the immuno-reaction in the lung tissue of patients with FLD is a type of helper-T cell alveolitis.
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PMID:[Immunohistochemical study of T cell subsets in lung tissue and in BALF of patients with farmer's lung disease]. 258 84

Allergic alveolitis due to mold dust inhalation in farmers is a severe but rare disease in Scandinavia. In this report 38 cases of the disease are presented. There were 31 men and 7 women, with mean ages of 46 and 38 years respectively. Strict diagnostic criteria were used, resulting in 21 definite, 12 probable and 5 possible cases. None of the patients were current smokers, but 10 of the men were ex-smokers. The great majority of the patients fell ill between October and April. The symptoms were dyspnea, cough, fatigue, episodes of fever, and in some cases loss of weight. The average duration of the disease was 6 months. The moldy material most commonly associated with the disease was straw, followed by hay, grain, and wood chips. For those tested serum lactate dehydrogenase was raised in 80% and the mean value for PaO2 was 7.8 kPa. Precipitating antibodies to mold antigens were positive in 68%. In general, pulmonary function tests showed a restrictive pattern. Over half of the patients still had dyspnea on exercise after recovery. Three fourths of the patients were treated with antibiotics and thus clearly had been misjudged as having an infection.
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PMID:Allergic alveolitis in Swedish farmers. 260 70

We reported a case of pneumonitis due to Sho-saiko-to. A 71-year-old woman was admitted to our hospital because of pneumonia. She complained of dry cough, pyrexia and severe dyspnea. Fine crepitation was heard on physical examination of the chest and a chest X-ray film revealed diffuse reticulo-nodular shadow in both lung fields. We suspected summer-type hypersensitivity pneumonitis and followed her up, however her condition deteriorated. Under a suspicion of drug-induced pneumonitis, all drugs were stopped and she was given prednisolone. Consequently her complaints, laboratory data and chest X-ray findings markedly improved. Microscopic examination of a transbronchial lung biopsy specimens showed interstitial pneumonitis. The results of a lymphocyte stimulation test were positive for sho-saiko-to. She gave informed consent after receiving an explanation of the challenge test. She was tested with 2.5 g sho-saiko-to twice and developed high fever and dyspnea with hypoxia, while the chest X-ray film also revealed diffuse infiltrative shadows similar that on admission. Based on these findings, we diagnosed this case as pneumonitis due to sho-saiko-to. To our knowledge, there has been no previous case of pulmonary hypersensitivity due to sho-saiko-to reported in the world.
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PMID:[A case of pneumonitis due to sho-saiko-to]. 263 Jul 77

Hypersensitivity pneumonitis due to the inhalation of spores from the edible mushroom Pholiota nameko was demonstrated. A 52-year-old mushroom worker noticed cough, exertional dyspnea, and high fever several hours after work in the mushroom-cultivating room. His examination revealed bilateral basilar crepitations, fine granular shadows in both lung fields of chest x-ray film, and slight decrease in diffusion capacity. Precipitin and macrophage migration inhibition factor were found against the mushroom spore extract and not other contaminants and molds. Histologic finding by transbronchial lung biopsy showed granulomatous alveolitis. Manifest increase of lymphocytes was found in his bronchoalveolar lavage fluid. Provocative inhalation test with the extract revealed similar symptoms and signs in his workplace eight hours after inhalation. It seems to be the first case of hypersensitivity pneumonitis to the Pholiota nameko mushroom spores.
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PMID:Hypersensitivity pneumonitis due to mushroom (Pholiota nameko) spores. 270 72

A 28-year-old man developed multiple episodes of fever, cough, shortness of breath, and leukocytosis several hours after cutting live oak and maple trees. Fungal cultures of wood chips from oak and maple trees were positive for Penicillium (three species), Paecilomyces sp., Aspergillus niger, Aspergillus sp., and Rhizopus sp. Gel-immunodiffusion studies demonstrated serum precipitins to extracts of oak chips, Penicillium sp., and Paecilomyces sp., and suggested that Penicillium sp. and Paecilomyces sp. shared cross-reactive antigens that were the significant antigens in the oak chips. ELISA studies demonstrated elevated serum levels of IgG to an oak chip extract, inhibition of that ELISA by preincubation of serum with Penicillium sp., and absence of elevated IgG levels to an extract of freshly cut oak wood that had been stripped of bark to minimize mold contamination. The case analysis indicates that the patient likely had hypersensitivity pneumonitis on exposure to Penicillium sp., when he was cutting trees, and identifies cutting live trees as another occupational exposure that may cause hypersensitivity pneumonitis.
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PMID:Woodman's disease: hypersensitivity pneumonitis from cutting live trees. 312 41

A 47-year-old housewife presented with nonproductive cough, progressive breathlessness and intermittent fever during gold treatment, originally prescribed for seropositive polyarthritis, which later fulfilled the criteria for systemic lupus erythematosus (SLE). An open lung biopsy showed abundant interstitial edema with mononuclear inflammatory cells and some eosinophils, and slight bronchiolitis. The picture was nonspecific but suggestive of hypersensitivity pneumonitis. Electron microscopy revealed splitting and local disappearance of the basal laminae of the alveolar capillaries, venules and alveolar epithelium. This injury was confirmed by immunohistochemical staining for type IV collagen and laminin, the major components of basal laminae. In most macrophages there was lysosomal electron dense granular material, i.e. aurosomes, which gave the spectrum of gold in electron microprobe analysis. After the gold treatment was stopped the pulmonary symptoms gradually decreased during several months and no permanent lung disease remained. Whereas the pulmonary manifestation could have been due to her underlying disease we discuss in this study the possibility of its being gold induced.
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PMID:Bronchiolo-alveolitis with pulmonary basal lamina injury in a rheumatoid patient during gold treatment. 312 4

Hypersensitivity pneumonitis is an unusual complication of using humidification devices. It is characterized by the acute onset of dyspnea, cough, fever, and chills after exposure to an offending antigen. This report describes a 54-year-old female laryngectomee who had repeated hospitalizations for postoperative dyspnea with normal chest roentgenograms and sputum cultures, but findings and history consistent with acute hypersensitivity pneumonitis. This seems to be the first reported case of hypersensitivity pneumonitis in a laryngectomee using a home mist machine. When repeated episodes of dyspnea occur in such patients, hypersensitivity pneumonitis should be considered in the differential diagnosis.
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PMID:Hypersensitivity pneumonitis from home mist machine after laryngectomy. 356 52

On epidemiologic grounds, respirable particles from chilled-water air-conditioning systems in textile production plants have been implicated as a cause of hypersensitivity pneumonitis. We have purified the antigen from scum growing in this chilled water by antibody-affinity chromatography by use of IgG isolated from a pool of serum obtained from three workers with disease. Two patients with the disease, three coworkers without the disease, and two unexposed control subjects inhaled a dose of the purified antigen approximately equivalent to that amount calculated to be inhaled during an 8-hour work shift. Both workers with disease experienced fever, malaise, cough, and dyspnea 6 to 8 hours after the aerosol challenge. In these two patients the exposure evoked a transient decrease in circulating lymphocytes, predominantly T cells. Before challenge the patients' peripheral blood mononuclear cells demonstrated a blastogenic response to the antigen. The responding cells had disappeared from the circulation 24 hours after the challenge. Seventy-two hours after the challenge, mononuclear cells that were producing large amounts of specific IgG antibody appeared in the circulation. We conclude that the same antigen(s) that react with IgG antibody produced an acute episode of the disease, that specific antigen-recognition cells disappear from the peripheral blood after exposure to the antigen (presumably because they are attracted to the lung), and that antibody-forming cells appear in the peripheral blood approximately 2 days after a challenge. These antigen-specific reactions of circulating mononuclear cells may be specific for the disease, but studies on a larger number of cases are needed to be certain.
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PMID:Immunologic response to aerosols of affinity-purified antigen in hypersensitivity pneumonitis. 376 Apr

Two sisters (6 and 8 years old) fell ill with coughing, fever and dyspnea after playing in the rotten straw in the barn of their parents' farm. Within 2 weeks symptoms changed to the insidious form of Exogen Allergic Alveolitis. In the broad spectrum of antibodies detected, the Thermophile Actinomycetes were probably the relevant antigens. In spite of efforts to avoid contact with the antigens, there was a relapse of the disease, the most probable sources of the antigens being a mattress in the bed-room and a fodderroom. Since consequent avoidance of antigens is practiced, no signs of relapse have been seen. The other three members of the family were exposed too. The mother and the youngest daughter showed neither symptoms nor specific antibodies. The father turned out to be sensibilitized too. By more attentive self-observation he discovered signs of illness. The distribution of the HLA-markers in the family was not concordant with the pattern of disease nor of antibodies. Some HLA-markers have been described as being associated with Exogen Allergic Alveolitis. Among the markers of our family there are none of these.
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PMID:[Simultaneous illness in siblings with exogenous allergic alveolitis of the farmer's lung type--report of a 3-year course, familial sensitization and HLA markers]. 376 8


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