Cases reported "Bronchial Hyperreactivity"

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1/34. Amalgam allergy associated with exacerbation of aspirin-intolerant asthma.

    BACKGROUND: aspirin-intolerant asthma can be induced not only by acidic analgesics (including acetylsalicylic acid), which effectively inhibit cyclo-oxygenase, but also by cross-reactivity with paraben, and other chemical additives. OBJECTIVE: We examined whether amalgam allergy is involved in the pathogenesis of a aspirin-intolerant asthma. methods: We present the first case of aspirin-intolerant asthma that improved after the removal of dental amalgam. In addition, we performed both the methacholine provocation testing and sulpyrine provocation testing before and after the removal of dental amalgam. RESULTS: In addition, the methacholine concentration causing a 20% fall in FEV1 in provocation tests rose significantly, though hypersensitivity to analgesics evaluated with sulpyrine provocation testing did not decrease. These results suggest that amalgam sensitization is involved in bronchial hyperresponsiveness in aspirin-intolerant asthma. CONCLUSION: Sensitivity to amalgam may cause exacerbation of aspirin-intolerant asthma in some patients. To the best of our knowledge, this is the first case report of amalgam allergy associated with aspirin-intolerant asthma.
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2/34. asthma precipitated by cessation of lithium treatment.

    We report symptomatic asthma, associated with objective and highly significant increases in both airway responsiveness and airflow limitation, presenting de novo in a male patient 6 weeks after suddenly discontinuing lithium carbonate therapy.
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3/34. Case discussions on the pathophysiology and clinical features of near-fatal asthma episodes.

    This article reviews the definition of near-fatal asthma. The slow-onset, late arrival group and the sudden-onset groups of near-fatal asthma patients are discussed. risk factors for near-fatal asthma and the pathologic differences between the two groups are elucidated.
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ranking = 0.7
keywords = asthma
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4/34. Irritant-induced asthma: clinical and functional aspects.

    We report on three patients who experienced persistent asthma symptoms after repetitive irritant exposure which took place over a period from several days to months. Airway inflammation was assessed by induction of sputum and functional follow-up information was obtained from serial lung function tests. All patients had bronchial hyperresponsiveness to methacholine at the time of diagnosis. However, induced sputum samples did not show increased differential count of eosinophils. Treatment with inhaled corticosteroids was started in all of the patients and two of them were removed from work. In the two patients who left the workplace, methacholine inhalation test became negative when symptoms disappeared, whereas the patient who continued working had persistent asthma symptoms and a deterioration of bronchial hyperresponsiveness.
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keywords = asthma
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5/34. Permanent respiratory impairment and upper airway symptoms despite clinical improvement in patients with reactive airways dysfunction syndrome.

    We previously reported clinical findings for 19 patients who developed symptomatic airways hyperactivity following an acute exposure to an inhaled irritant and who were given the diagnosis of reactive airways dysfunction syndrome (RADS). We now report on nine of these patients who have been followed for a mean of 9 years, allowing assessment of function, symptoms, and comorbidity beyond the early phase of acute airway injury and inflammation. None of the patients have resolved their airway hyper-responsiveness and symptoms completely, although only in one subject, who had a premorbid history of asthma, has the condition progressed. A common feature has been sinusitis and other upper-airway symptoms. We conclude that in this group of patients, RADS presented in a consistent pattern regardless of the cause of airway injury, resolved only partially, even in subjects without a premorbid history of respiratory disease, and was associated with significant secondary morbidity, especially affecting the upper airway. This pattern was evident regardless of smoking status or age at time of exposure. We conclude that for these subjects, RADS was a distinct entity with a consistent natural history that conferred permanent impairment, but did generally improve somewhat over time.
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6/34. Occupational asthma and rhinitis caused by multiple herbal agents in a pharmacist.

    BACKGROUND: Herb agents have been widely used for centuries in the Orient and they have been cultivated throughout asia. There have been a few cases of occupational allergy caused by herb materials. We report a case of occupational asthma and rhinitis caused by six herb materials in a pharmacist working at a pharmacy. OBJECTIVE: We sought the role of immediate hypersensitivity in herbal agent-induced asthma in a pharmacist. methods AND RESULTS: The patient had strong positive responses on skin prick test to extracts of six herb materials: Chunkung (Cnidii rhizoma), Banha (pinellia ternata), Sanyak (dioscorea radix), Kangwhal (Ostericum koreanum), Danggui (angelica radix), and Kunkang (Zingiberis rhizoma). Bronchoprovocation tests showed an early asthmatic response to Danggui extract. serum specific IgE antibodies to Chunkung, Banha, and Sanyak were detected by ELISA with no specific IgE bindings to Kangwhal, Danggui, and Kunkang extracts. Twelve percent sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and IgE immunoblotting revealed one IgE binding component (60 kD) within Chunkung extract, two (10, 25 kD) in Banha, and four (33, 34, 65, 98 kD) in Sanyak. Basophil histamine release test revealed that Danggui extract could release a greater amount of histamine from basophils in the patient than in a healthy control. CONCLUSIONS: Chunkung, Banha, and Sanyak may induce IgE-mediated bronchoconstriction in an exposed worker, and Danggui can cause bronchoconstriction by direct histamine-releasing effect from mast cells in a sensitized patient.
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ranking = 0.7
keywords = asthma
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7/34. Occupational asthma caused by exposure to cyanoacrylate.

    BACKGROUND: Exposure to acrylates may give rise to rhinitis and asthma in both industrial and domestic environments. The mechanisms underlying these respiratory conditions caused by acrylates remain largely unknown. methods: We studied two assembly operators exposed to cyanoacrylate glue who developed rhinitis and asthma symptoms. The causal relationship of these symptoms to cyanoacrylate glue exposure was investigated by serial peak expiratory flow (PEF) monitoring at work and off work. Moreover, inhalation testing was performed by asking the patients to mimic exposure at work with the cyanoacrylate glue in a 7-m3 challenge chamber. RESULTS: Serial PEF monitoring at work and away from work was consistent with occupational asthma in both patients. The methacholine inhalation test was negative in patient 1 (off work) and showed bronchial hyperresponsiveness in patient 2. After 20-min exposure to cyanoacrylate, the patients had late and progressive asthmatic reactions, respectively, and the methacholine test became positive in patient 1. Induced-sputum samples obtained 3 and 24 h after the cyanoacrylate challenge showed a marked increase in sputum eosinophils. CONCLUSION: Exposure to cyanoacrylate in these patients provoked not only variable airflow limitation and bronchial hyperresponsiveness, but also pronounced eosinophilia in sputum.
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ranking = 0.8
keywords = asthma
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8/34. Dentist's occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.

    BACKGROUND: Allergic contact dermatitis (ACD) caused by (meth)acrylates (MA) is common in dental personnel. MAs have also caused asthma and rhinoconjunctivitis, but asthma, rhinoconjunctivitis and ACD caused by MAs in the same patient appears to be very rare. methods: Occupational asthma and rhinoconjunctivitis were diagnosed in a dentist according to patient history, PEF monitoring, and a work-simulated bronchial provocation test. ACD was diagnosed by skin-patch testing with MAs with the occlusive Finn Chamber-technique. RESULTS: The patient's skin-prick test reactions to common environmental allergens and MAs were negative. The total IgE was not elevated. Occupational asthma was diagnosed by a specific inhalation challenge test in which the patient handled liquid dental MAs for 30 min causing a delayed 23% reduction in FEV1. The provocation test also resulted in rhinoconjunctivitis. On patch testing, positive reactions were provoked by several MAs including 2-hydroxyethyl methacrylate (2-HEMA) to which the patient was occupationally exposed. The patient has not been able to continue her work with dental MAs. CONCLUSIONS: A case of occupational asthma, rhinoconjunctivitis and ACD caused by dental acrylate compounds is presented. patients with respiratory hypersensitivity from MAs have to stop working with MAs, whereas patients with ACD from MAs need to avoid direct contact with MAs, but can often continue in their present job if they use no-touch techniques.
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ranking = 0.9
keywords = asthma
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9/34. Reactive airways dysfunction syndrome following metal fume fever.

    Metal fume fever (MFF) is an acute response to the inhalation of heavy metals used in industry. The patient typically experiences symptoms of cough, fever, chills, malaise, and myalgia that are self-limited and of short duration. Wheezing may occur and pulmonary function may be acutely impaired with a decrease in lung volumes and diffusing capacity of carbon monoxide. Nevertheless, respiratory function quickly returns to normal, and persistent pulmonary insufficiency is unusual. Irritant-induced asthma is a non-immunogenic form of airway injury that may be associated with industrial inhalation exposure. In this situation, the direct toxic effect on the airways causes persistent airway inflammation and bronchial hyperreactivity. The two conditions are considered distinct entities, but we report a previously healthy worker who had classic MFF and was left with irritant-induced asthma or reactive airways dysfunction syndrome (RADS).
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ranking = 0.2
keywords = asthma
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10/34. Bronchial hyperresponsiveness in a patient with systemic mastocytosis.

    In order to investigate the possible involvement of airway mast cells in bronchial hyperresponsiveness (BHR), we examined whether a patient with systemic mastocytosis would demonstrate BHR against ultrasonically nebulized distilled water (UNDW) and histamine inhalation challenge. A 56-year-old man with systemic mastocytosis underwent both UNDW and histamine inhalation challenge. We also evaluated the effect of beclomethasone dipropionate inhalation (BDI) treatment on the histamine inhalation challenge. The results showed that UNDW inhalation caused no changes in forced expiratory volume in 1 s (FEV1) for this patient. The provocative dose causing a 20% fall (PC20) in FEV1 in the histamine inhalation challenge was 625 microg/mL. After BDI treatment for 8 weeks, the histamine PC20 was still 625 microg/mL. These data suggest that UNDW-induced bronchoconstriction may be independent of airway mast cells and that the mechanism of histamine-induced bronchoconstriction in systemic mastocytosis may be independent of airway inflammation, which is often present in asthmatics.
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