Toyoshima M, Sato A, Taniguchi M, Imokawa S, Nakazawa K, Hayakawa H, Chida K
Second Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1995 Jul;33(7):691-4.
Urinary excretion of leukotrienes is greater in patients with aspirin-induced asthma (AIA) than in other patients with asthma in remission, and is greater still during an aspirin-induced attack. We therefore hypothesized that increased phospholipase A2 (PLA2) activity leads to increased leukotriene synthesis when non-steroidal antiinflammatory drugs inhibit cyclooxygenase in patients with AIA, and that PLA2 activity increases further during an aspirin induced attack. To test this hypothesis, we measured the serum PLA2 activity in adult asthmatic patients, and compared the activity in those with AIA to the activity in those without AIA. The subjects were 43 patients with asthma in remission, 17 with AIA and 26 without AIA. Serum PLA2 activity was also measured before and after intravenous administration of lysine-aspirin in three patients with AIA and in one without AIA. Serum PLA2 activity was measured by radioimmunoassay. Serum PLA2 activity in patients with AIA, in those without AIA, and in healthy controls was 300.9 +/- 52.9, 294.4 +/- 65.3 and 171.7 +/- 41.8 pmol/ml/min, respectively. Serum PLA2 activity in asthmatic patients was significantly higher than in healthy controls (p < 0.01), but there was no difference between patients with and without AIA. Intravenous lysine-aspirin provoked asthmatic attacks in three patients with AIA. However, intravenous lysine-aspirin did not significantly change serum PLA2 activity in the three patients with AIA or in the patient without AIA. These results indicate that although PLA2 may be involved in the pathogenesis of bronchial asthma, it is not specific to AIA. Thus, the pathophysiology of AIA remains unclear and further investigation is needed.
阿司匹林诱发哮喘（AIA）患者的白三烯尿排泄量高于处于缓解期的其他哮喘患者，在阿司匹林诱发的发作期间排泄量更高。因此，我们推测当非甾体抗炎药抑制AIA患者的环氧化酶时，磷脂酶A2（PLA2）活性增加会导致白三烯合成增加，并且在阿司匹林诱发的发作期间PLA2活性会进一步增加。为了验证这一假设，我们测量了成年哮喘患者的血清PLA2活性，并将AIA患者的活性与非AIA患者的活性进行比较。研究对象为43例处于缓解期的哮喘患者，其中17例患有AIA，26例未患AIA。还对3例AIA患者和1例非AIA患者静脉注射赖氨酸阿司匹林前后的血清PLA2活性进行了测量。采用放射免疫分析法测定血清PLA2活性。AIA患者、非AIA患者和健康对照者的血清PLA2活性分别为300.9±52.9、294.4±65.3和171.7±41.8 pmol/ml/min。哮喘患者的血清PLA2活性显著高于健康对照者（p<0.01），但AIA患者和非AIA患者之间没有差异。静脉注射赖氨酸阿司匹林诱发了3例AIA患者的哮喘发作。然而，静脉注射赖氨酸阿司匹林并未使3例AIA患者或1例非AIA患者的血清PLA2活性发生显著变化。这些结果表明，虽然PLA2可能参与支气管哮喘的发病机制，但它并非AIA所特有。因此，AIA的病理生理学仍不清楚，需要进一步研究。
