Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 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

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

We reported a 51-yr-old female with radiation-induced chronic constrictive pericarditis. At age 29, she had received a mastectomy and postoperative irradiation because of left breast cancer. At age 45, she had syncope and was diagnosed with complete atrioventricular block and a pacemaker was implanted. At that time, pericardial thickening with effusion was noted. The following year, tricuspid regurgitation was noted. On catheter study, a dip and plateau pattern of the right ventricular pressure curve appeared. At age 50, tricuspid regurgitation worsened due to the lead wire of the pacemaker compressing the leaflet, and the pacemaker was reimplanted. However, the following year, she complained of general fatigue and dyspnea and was admitted to our hospital. On 67Ga study, diffuse accumulation in the cardiac region appeared. There was no perfusion defect detected in the left myocardium, but right myocardial damage was suspected by thallium study. In 99mTc-HSA RI angiography, right atrium dilatation appeared and a pericardial halo around the ventricles was seen. She underwent pericardectomy, tricuspid replacement and pacemaker reimplanted, but she died. On autopsy, pericardial thickening and adhesion, right myocardial fibrosis, the fibrotic change of the bundle branches were seen. We reported a case of radiation-induced constrictive pericarditis. Radionuclide studies were useful in diagnosing and following the patient.
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PMID:[A case of radiation-induced chronic constrictive pericarditis developing 16 years after irradiation]. 823 Aug 30

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