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 68-year-old male developed dry cough and exertional dyspnea after handling paint spray containing isocyanates (TDI, MDI) for three months. Initially, the symptoms fluctuated according to whether he was at work or not. He was admitted to our hospital on February 7, 1990, because of progressive worsening of symptoms. In spite of admission to hospital and cessation of exposure to isocyanates, there was no improvement of symptoms. His chest X-ray film showed diffuse small nodular and reticular shadows. Transbronchial lung biopsy revealed thickening of the alveolar walls and formation of Masson's bodies associated with mononuclear cell infiltration in alveolar spaces. High titers of TDI-HSA and MDI-HSA specific IgG antibodies were detected by ELISA, and a high level of serum soluble IL2 receptor was also detected. From these results, we diagnosed hypersensitivity pneumonitis due to exposure to isocyanates. One week administration of prednisolone caused dramatic improvement of his symptoms, chest X-ray findings, and laboratory data. His clinical course and response to prednisolone therapy indicated that long-term steroid administration could not be avoided. The prolonged symptoms and the necessity for long-term steroid therapy are discussed.
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PMID:[A case of hypersensitivity pneumonitis due to isocyanate exposure showing progression even two months after removal of the antigen]. 131 20

A 41-year-old paint sprayer, who had worked with polyurethane paint since the spring of 1989, developed exertional dyspnea and dry cough and entered hospital on December 4, 1989. Plain chest X-ray film and a computed tomogram of the lung revealed diffuse micronodular shadows in both lower lung fields. DLco was shown to be significantly decreased in a pulmonary function test. A sample of bronchoalveolar lavage fluid showed increased T lymphocytes and a decreased CD4/8 ratio. A lung biopsy specimen revealed alveolitis, but neither Masson body nor granulomas were seen. Serum antibody specific to TDI-HSA was detected, and an environmental provocation test was positive. From these results, the patient was diagnosed as having isocyanate-induced hypersensitivity pneumonitis. We advised him to wear a compression-air mask when he worked, because he did not want to quit his job. Respiratory symptoms have not been seen since then, but careful observation was thought to be necessary. The involvement of type III humoral and type IV cellular immunity was suspected in this case.
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PMID:[A case of isocyanate-induced hypersensitivity pneumonitis and a compression-air mask thought to be effective in its prevention]. 165 22

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

A case of allergic oculorhinitis induced by toluene diisocyanate (TDI) exposure in a subject who two years later developed bronchial asthma due to TDI is described. A 55-year-old nonatopic spray painter developed symptoms of oculorhinitis two or three hours after direct occupational exposure to polyurethane varnish; at the first examination neither specific nor nonspecific bronchial hyperresponsiveness was present. Two years later the patient, who had remained in his job, developed episodic dyspnea, wheezing, and cough immediately after TDI exposure, with persistence of oculorhinitis; at this time a slight immediate-type response to a specific bronchial provocative test with polyurethane varnish and TDI was observed. Nonspecific bronchial hyperresponsiveness was mild. Specific IgE to TDI-HSA conjugate was present at both the first and second examinations. We conclude that, in some cases, TDI may cause "allergic" oculorhinitis and bronchial asthma, probably with an immunological IgE-mediated mechanism.
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PMID:TDI-induced oculorhinitis and bronchial asthma. 298 3

This study aimed at investigating sensitizing and hazardous effects of a new acid anhydride, pyromellitic dianhydride (PMDA), in addition to those of phthalic anhydride, maleic anhydride and trimellitic anhydride, in a group of 92 exposed workers in two German chemical plants. Of the 92 workers, 56 reported work-related complaints with a predominance of phlegm and dyspnoea in those exposed to anhydride dust for less than 1 year. Haemorrhagic rhinitis occurred only after a prolonged exposure of more than 15 years. Specific IgE antibodies to anhydride-HSA conjugates could be detected in 15 exposed subjects, 12 of whom had work-related symptoms. The IgE-positive group had significantly more impaired lung function parameters than the IgE-negative group. The proportion of IgE-positive subjects was highest in the groups with dyspnoea (5/18), cough (6/24) and rhinitis (11/44) whereas only 1 of 11 workers with haemorrhagic rhinitis had such antibodies. A follow-up study of 23 affected workers was performed after 10 months to assess clinical symptoms, lung function and IgE antibody levels. This follow-up study showed the absence of obstructive ventilation patterns in three out of six subjects in addition to cessation of symptoms in most initially affected workers who were no longer exposed. On the other hand, 14 workers under continuous exposure had comparable pathological findings on re-examination. Our results confirm that anhydrides including the lesser known PMDA, behave as respiratory irritants and as immediate-type sensitizers. They predominantly induced reversible symptoms in workers whose exposure stopped after a working period of about 0.7 years. Abnormal lung function parameters normalized in nearly 50% of these subjects.
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PMID:A clinical and immunological study on 92 workers occupationally exposed to anhydrides. 856 89

We report the case of a 55-year-old male who experienced cough, dyspnea, wheezing, and nasal congestion immediately upon exposure to FD&C Blue Dye No. 2 (Indigotine) at work. The patient had worked for 10 years mixing and grinding powdered synthetic red, yellow, and blue dyes for use in foods; symptoms had occurred for 2 years and only with exposure to Indigotine (C16H8N2Na2O8S2), a free flowing blue powder. Prick testing to Indigotine (20 mg/mL) was negative. ELISA failed to detect specific IgE, IgA, IgM, or IgG to Indigotine-HSA conjugates. Bronchial challenge was done according to the method of Pepys et al. beginning with 4 x 10(-4) lactose dilution of Indigotine powder. After 5 minutes of exposure to 4 gm Indigotine/100 gm lactose, the patient developed dyspnea and audible wheezing. At 20 minutes postexposure, there was a 20% decline in FEV1 from prechallenge baseline; no late phase response was observed. A second bronchial challenge with sodium sulfate, the major nondye product additive was negative. To our knowledge, this is the first documented case of occupational asthma due to FD&C Blue Dye No. 2. The pathogenesis is uncertain but does not appear to be IgE mediated.
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PMID:Occupational asthma caused by FD&C blue dye no. 2. 881 38

Since type I allergy caused by specific IgE antibodies may play principal roles and IgG antibody-mediated reactions have been thought to be involved in some parts of the pathogenesis, this study was performed to investigate the role of IgE- or IgG-mediated hypersensitivity reactions in development of toluene diisocyanate (TDI) asthma in Korean workers. For 81 TDI spray painters, self-administrative questionnaires and direct interviews on respiratory symptoms, chest auscultation, and measurements of forced vital capacity (FVC) and forced expiratory volume in 1 sec (FEV1.0) were performed. The TDI concentration in their working environments was measured. Levels of serum IgE and IgG specific to TDI were estimated by radioallergosorbent test (RAST) and ELISA using p-tolyl isocyanate-human serum albumin (TMI-HSA) as the antigen. When sputum, cough, and dyspnea aggravated by work or wheezing existed, when FVC or FEV1.0 was less than 80% of the normal reference value, or when IgE RAST for TDI was positive, the peak expiratory flow rate (PEFR) was recorded four times per day for over 2 weeks. If decrease of PEFR was over 20% of baseline PEFR and changing pattern of PEFR was closely related to workshift in time, then a diagnosis of TDI asthma was made. Changing patterns of PEFR of 8 (9.9%) workers corresponded to the diagnostic criteria of TDI-related occupational asthma. Levels of the specific IgE were increased in 9 (11.1%) of the 81 subject workers and in 3 (37.5%) of the 8 PEFR-positive workers. Levels of the specific IgG were increased in 9 (11.1%) workers, and in only 1 (12.5%) of the asthmatics sensitive to TDI. Neither elevated TDI-specific IgE levels nor PEFR test positivities were associated with increased IgG levels. The mean titer of the PEFR-test-positive workers was slightly lower than that of the PEFR-negative workers and that of the IgE RAST-positive workers lower than that of the test-negative workers, but there was no statistical significance. These results suggest that IgG is not deeply involved in the pathogenesis of TDI-induced occupational asthma in Korean workers.
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PMID:Seroimmunological characteristics of Korean workers exposed to toluene diisocyanate. 935 88