Bronchial aspirin challenge causes specific eicosanoid response in aspirin-sensitive asthmatics.
Bronchial aspirin challenge causes specific eicosanoid response in aspirin-sensitive asthmatics.
复制标题
支气管阿司匹林激发会引起阿司匹林敏感哮喘患者的特异性类二十烷酸反应。
DOI：
10.1164/ajrccm.154.6.8970343
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Oates,J
中科院分区：
文献类型：
--
作者：
Szczeklik,A;Sladek,K;Dworski,R;Nizankowska,E;Soja,J;Sheller,J;Oates,J
我们已经证明，吸入赖氨酸阿司匹林增强了阿司匹林诱导的哮喘（AIA）患者肺中白三烯的产生。为了评估这种反应的特异性，我们比较了两组匹配良好的患者：11例AIA患者和14例阿司匹林耐受性哮喘患者（ATA）。所有受试者均接受了盐水支气管肺泡灌洗（BAL），随后立即向右中叶肺段支气管滴入10 mg赖氨酸阿司匹林，15 min后灌洗。基线时，两组在环氧化酶产物、肽-白三烯、组胺、类胰蛋白酶、白细胞介素-5（IL-5）、嗜酸性粒细胞阳离子蛋白（ECP）或嗜酸性粒细胞数量的BAL液浓度方面无差异。阿司匹林滴注15分钟后，AIA患者的肽-白三烯、IL-5和嗜酸性粒细胞数量出现统计学显著性升高，但ATA患者无此现象。在前者中，但不是在后者组中，平均组胺浓度上升响应阿司匹林，接近统计学意义的水平。类胰蛋白酶和ECP水平没有显着变化。阿司匹林显著降低了两组的PGE 2和血栓素B2（TXB 2），但仅ATA患者的PGD 2、PGF 2 α和9 α，11 β-PGF 2降低。对阿司匹林不耐受的病人，其花生酸类平衡的一种特征性紊乱可能解释哮喘发作的发生。
We have shown that inhalation of lysine aspirin enhances leukotriene production in the lungs of patients with aspirin-induced asthma (AIA). To assess the specificity of this reaction, we compared two well-matched groups of patients: eleven with AIA versus 14 asthmatics tolerant to aspirin (ATA). All subjects underwent bronchoalveolar lavage (BAL) with saline followed immediately by instillation of 10 mg of lysine aspirin, into a right middle lobe segmental bronchus, which was lavaged 15 min later. At baseline the two groups did not differ with respect to BAL fluid concentrations of cyclooxygenase products, peptido-leukotrienes, histamine, tryptase, interleukin-5 (IL-5), eosinophil cationic protein (ECP), or eosinophil number. Fifteen minutes after aspirin instillation, there was a statistically significant rise in peptido-leukotrienes, IL-5, and eosinophil number in AIA, but not in ATA, but not in ATA patients. In the former, but not in the latter group, mean histamine concentrations rose in response to aspirin, approaching the level of statistical significance. Tryptase and ECP levels showed no significant change. Aspirin significantly depressed PGE2 and thromboxane B2 (TXB2) in both groups, however PGD2, PGF2 alpha, and 9 alpha, 11 beta-PGF2 decreased only in ATA patients. A characteristic disturbance in eicosanoid balance, produced by aspirin in patients intolerant to this drug, might explain precipitation of asthma attacks.