Cases reported "Bronchial Hyperreactivity"

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1/18. 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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2/18. Persistent anaphylactic reaction after induction with thiopentone and cisatracurium.

    A 6-year-old boy presented for surgery for phimosis. The anaesthetic technique included intravenous induction with thiopentone and neuromuscular blockade with cisatracurium. Severe persistent bronchospasm and central cyanosis followed the administration of these drugs. A continuous i.v. infusion of epinephrine at 0.2 microg. kg(-1) x min(-1) was necessary to break the severe refractory bronchial hyperresponsiveness. There was no previous exposure to anaesthetic drugs and no definite family history of allergy. Through increased serum eosinophil cationic protein, tryptase and histamine levels and IgE levels specific to cisatracurium, we demonstrated an IgE-mediated anaphylactic reaction to cisatracurium in the child's first exposure to this new neuromuscular blocking agent. Anaphylactic reactions to new anaesthetic drugs may be challenging to recognize and treat during general anaesthesia in children. The pathogenesis, diagnosis and management of life threatening persistent allergic reactions to intravenous anaesthetics are discussed.
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3/18. 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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4/18. 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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5/18. 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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6/18. Influence of natural exposure to pollens and domestic animals on airway responsiveness and inflammation in sensitized non-asthmatic subjects.

    BACKGROUND: Atopy may be a risk factor in the development of asthma. Indoor allergens are considered to be more potent asthma inducers than outdoor ones such as pollens. Lower airway inflammation may be present in non-asthmatic subjects during natural exposure to relevant allergens and may eventually lead to the development of asthma. AIMS: To document seasonal variation in lower airway responsiveness and inflammation in sensitized non-asthmatic subjects, during natural exposure to allergens, and to determine whether it is more marked in those exposed to animals to which they are sensitized. methods: Twenty-two atopic subjects were seen during and out of the pollen season. All (but the controls) were sensitized to domestic animals, and to trees, grasses or ragweed. Eleven were not exposed to animals at home and 8 were exposed. They were compared with 3 normal controls. A respiratory questionnaire was administered, allergy skin prick tests, spirometry, methacholine challenge, blood and induced sputum with differential cell counts were obtained during the pollen season for all subjects. These tests were repeated out of the pollen season. RESULTS: Throughout the study, none of the subjects had asthma symptoms. Mean PC(20) was significantly lower in subjects exposed to animals compared with unexposed subjects or controls, both during and out of the pollen season. In season, subjects exposed to animals had significantly higher sputum eosinophil numbers than unexposed or normal control subjects. CONCLUSIONS: Non-asthmatic atopic subjects show variable degrees of airway responsiveness and inflammation. However, subjects exposed to animals show higher airway eosinophilia, which may suggest they are at increased risk of developing airway hyperresponsiveness and asthma.
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ranking = 6
keywords = exposure
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7/18. Bronchial asthma due to sensitization to chloramine T.

    Chloramine T, an organic, highly reactive derivative of chlorine with potent bactericidal properties, is used as a disinfectant in the food industry. Described as an occupational sensitizer in 1945 for the first time, it produces late or dual asthma, occasionally accompanied by fever and leukocytosis, which is mediated by IgE. We present the case of a male dairy worker who, after 4 years of exposure to the product, developed rhinitis and asthma. skin tests with chloramine T were positive at a concentration of 10 mg/ml, while all other allergens tested negative. RAST detected specific IgE at 12 PRU and bronchial provocation induced immediate and late bronchoconstriction.
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8/18. Reactive airways dysfunction syndrome caused by bromochlorodifluoromethane from fire extinguishers.

    Although the neurological and cardiovascular effects of Freons have been extensively described, the respiratory effects have been less well documented. We report four cases of occupational asthma following accidental exposure to bromochlorodifluoromethane (Halon 1211) due to release of the contents of a fire extinguisher. All subjects developed an irritative reaction of the upper airways and lower respiratory symptoms immediately after exposure. Non-specific bronchial hyperreactivity was present for at least two months in all subjects and was still present more than two years after exposure in one case. The diagnosis of reactive airways dysfunction syndrome can be adopted in at least three of these four cases.
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ranking = 3
keywords = exposure
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9/18. Pulmonary toxicity following exposure to methylene chloride and its combustion product, phosgene.

    Chemical paint removers containing methylene chloride are widely used in domestic and industrial settings where exposure to a heat source with conversion to phosgene is possible. We describe a case of noncardiogenic pulmonary edema and subsequent hyperreactive airways following such an exposure. In addition, the various problems that have been associated with exposure to methylene chloride and phosgene are reviewed.
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ranking = 7
keywords = exposure
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10/18. Occupational asthma due to piperazine citrate.

    BACKGROUND: Piperazine is a secondary heterocyclic amine that may give rise to occupational asthma of uncertain mechanism. methods: We report on a 42-year-old woman, a process operator in a chemical factory, who developed work-related symptoms of rhinitis and asthma upon exposure to piperazine citrate. She remained symptom free during holidays and days off work. RESULTS: Skin prick test with piperazine citrate was positive. Specific inhalation challenge with piperazine citrate at a concentration of 5 mg/m3 for 30 minutes elicited an isolated late asthmatic response. Airway hyperresponsiveness to methacholine significantly increased 3 hours after the piperazine challenge, preceding the late asthmatic response. CONCLUSION: This patient had developed occupational asthma caused by piperazine, as confirmed by the specific inhalation challenge test, possibly due to an immunological mechanism.
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