[在有或没有阿司匹林超敏反应的哮喘患者和健康对照者口服阿司匹林期间诱导的痰上清前列腺素E2 -初步研究]。

Przeglad lekarski Pub Date : 2016-01-01
Maria Ignacak, Natalia Celejewska-Wójcik, Krzysztof Wójcik, Kinga Sałapa, Ewa Konduracka, Marek Sanak, Katarzyna Tyrak, Krzysztof Sładek, Jacek Musiał, Lucyna Mastalerz
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引用次数: 0

摘要

本初步研究的目的是评价非甾体抗炎药加重呼吸系统疾病(NERD)、阿司匹林耐受性哮喘(ATA)和健康对照(HC)患者在口服阿司匹林刺激试验前后诱导痰上清中前列腺素E2 (PGE2)浓度的变化。本研究于2014-2015年在克拉科夫大学医院肺内科临床科室进行,共纳入43例患者(NERD - n = 15, ATA - n = 15, HC - n = 13)。所有人都接受了安慰剂控制的口服阿司匹林挑战。在攻毒前24小时和试验后立即诱导痰。对诱导痰进行处理,以获得描绘炎症细胞模式和上清的囊旋玻片,其中测量PGE2。采用质谱联用气相色谱法(气相色谱/质谱联用- GC/MS)测定PGE2浓度。阿司匹林刺激后,阿司匹林过敏组和阿司匹林耐受良好组诱导痰上清中PGE2浓度均下降(p = 0.01)。健康对照组的变化无统计学意义。这些结果支持阿司匹林抑制PGE2的环加氧酶理论。然而,非甾体抗炎药加重呼吸系统疾病患者单独服用阿司匹林后支气管收缩的机制尚不清楚。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Induced sputum supernatant prostaglandin E2 during oral aspirin challenge of asthmatic patients with and without aspirin hypersensitivity and healthy controls--pilot study].

The aim of this pilot study was to evaluate changes in the concentration of prostaglandin E2 (PGE2) in induced sputum supernatant in 3 groups: sub- jects with NSAID-exacerbated respira- tory disease (NERD), aspirin tolerant asthma (ATA) and healthy controls (HC), before and after oral aspirin chal- lenge test. The study was conducted in the years 2014-2015 at the Clinical Department of the Pulmonology Clinic at the University Hospital in Cracow. 43 patients were enrolled in the study (NERD - n = 15, ATA - n = 15 and HC - n = 13). All of them underwent a placebo-controlled oral aspirin challenge. Sputum was induced 24 hours before the challenge and immediately after the test. Induced sputum was processed in order to obtain cystospin slides to depict inflammatory cell patterns and supernatants, in which PGE2 was measured. The concentration of PGE2 was determined using mass spectrometry coupled with gas chromatography (gas chromatography/mass spectrometry - GC/MS). After aspirin challenge, the concentration of PGE2 in induced sputum supernatant decreased in both asthmatics hypersensitive to aspirin (p = 0.01) and those who tolerated aspirin well (p = 0.17). The change in the healthy control group was not statistically significant. These results support the cyclooxygenase theory of PGE2 inhibition by aspirin. However, the mechanism of bronchoconstriction after aspirin administration alone in patients with NSAID-exacerbated respiratory disease remains unclear.

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