异氰酸酯诱发职业性哮喘的预后分析。

P L Paggiaro, E Bacci, F L Dente, D Talini, C Giuntini
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引用次数: 0

摘要

几项关于异氰酸酯诱发哮喘预后的研究表明,相当大比例的患者在停止工作后仍会出现哮喘症状和非特异性支气管高反应性,而致敏受试者进一步暴露于异氰酸酯几乎总是会导致呼吸道症状和支气管高反应性持续存在,并导致气道功能恶化。停止工作后,对异氰酸酯的特定支气管反应性可能发生变化;然而,一些受试者在停止工作几个月后仍对TDI敏感。哮喘不良预后的决定因素似乎与其他类型的低分子量化合物职业性哮喘(即红杉哮喘)的决定因素相同:哮喘发病前暴露时间长,诊断前症状持续时间长,气道阻塞,特定激发试验后气道双反应。此外,在工作场所单次急性暴露于高水平的TDI(泄漏)可导致持续的非特异性支气管高反应性。症状持续和非特异性支气管高反应性的潜在机制可能是慢性炎症、支气管平滑肌改变、自主神经系统失调。
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Prognosis of occupational asthma induced by isocyanates.

Several studies on the prognosis of isocyanate-induced asthma show that a significant proportion of patients continue to experience asthmatic symptoms and nonspecific bronchial hyperresponsiveness after cessation of work, and that further exposure to isocyanates in sensitized subjects leads almost invariably to persistence of respiratory symptoms and of bronchial hyperresponsiveness and the deterioration of airway function. Specific bronchial reactivity to isocyanates may change after cessation of work; however, some subjects continue to be sensitive to TDI several months after cessation of work. The determinants of an unfavourable prognosis for asthma seem to be the same as those for other types of occupational asthma due to low molecular weight compounds (i.e. red cedar asthma): long duration of exposure before the onset of asthma, long duration of symptoms before diagnosis, airway obstruction, and dual airway response after specific challenge tests. Also, single acute exposure to high levels of TDI in the workplace (spills) can result in persistent nonspecific bronchial hyperresponsiveness. Potential mechanisms of persistence of symptoms and of nonspecific bronchial hyperresponsiveness may be chronic inflammation, bronchial smooth muscle alteration, autonomic nervous system disregulation.

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Status Asthmaticus The development of an animal model for TDI asthma. The role of neuropeptides as neurotransmitters of non-adrenergic, non-cholinergic nerves in bronchial asthma. Epidemiological measurement of bronchial responsiveness in polyurethane workers. Late asthmatic reactions and changes in histamine responsiveness provoked by occupational agents.
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