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[血小板中褪黑素的产生及其在阿司匹林哮喘患者中的功能活性]

[Melatonin production in thrombocytes and their functional activity in patients with aspirin asthma].

作者信息

Evsiukova E V, Muraia E V, Zubzhitskaia L B, Kveshnoĭ I M

出版信息

Klin Med (Mosk). 2007;85(10):37-41.

Abstract

The aim of the investigation was to study melatonin production in thrombocytes and their functional activity in correlation with 6-sulfatoximelatonin (6-SOM) urinary excretion in patients with aspirin-induced bronchial asthma (AIBA). Forty-three patients with bronchial asthma (BA) were examined. The main group consisted of 26 AIBA patients; the comparison group consisted of 17 BA patients with no intolerance to aspirin or other non-steroidal anti-inflammatory drugs; 30 practically healthy individuals constituted the control group. The study found no melatonin production in thrombocytes of AIBA patients: only 13.0 +/- 1.3% of platelets expressed melatonin, while in healthy people 97.7 +/- 0.6% of the cells did. Besides, daytime urinary excretion of 6-SOM, the main melatonin metabolite, was lower in AIBA patients. Lower daytime and higher nighttime melatonin production in AIBA patients correlated with the acceleration of the 1st phase and increased intensity of thrombocyte aggregation, which evidences high thrombocyte reactivity to the inducing agent. The presence of a pathologic reaction of thrombocytes to exogenous melatonin, manifesting by changes in the 1st stage of aggregation, suggests the presence of pathology in thrombocyte membrane-receptor complex and the calcium homeostasis of the cell, which determines constant activation and the participation of thrombocytes in the development of asthmatic syndrome.

摘要

本研究旨在探讨阿司匹林诱发的支气管哮喘(AIBA)患者血小板中褪黑素的生成及其功能活性与尿中6-硫酸氧褪黑素(6-SOM)排泄的相关性。对43例支气管哮喘(BA)患者进行了检查。主要组由26例AIBA患者组成;比较组由17例对阿司匹林或其他非甾体抗炎药无不耐受的BA患者组成;30名健康个体构成对照组。研究发现,AIBA患者的血小板中不产生褪黑素:只有13.0±1.3%的血小板表达褪黑素,而健康人中有97.7±0.6%的细胞表达。此外,AIBA患者白天尿中主要褪黑素代谢产物6-SOM的排泄量较低。AIBA患者白天褪黑素生成较低而夜间较高,这与第一阶段加速和血小板聚集强度增加相关,这表明血小板对诱导剂的反应性较高。血小板对外源性褪黑素存在病理反应,表现为聚集第一阶段的变化,这表明血小板膜受体复合物和细胞钙稳态存在病理,这决定了血小板的持续激活以及其在哮喘综合征发展中的参与。

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