与阿司匹林敏感性哮喘相关的鼻息肉病因学。

Rhinology. Supplement Pub Date : 1989-01-01
T Yamashita, H Tsuji, N Maeda, K Tomoda, T Kumazawa
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引用次数: 0

摘要

众所周知,在阿司匹林敏感性哮喘(ASA)中,鼻息肉的发生率很高。然而,其病因尚不清楚。因此,我们通过组织病理学观察和花生四烯酸代谢物的测定来研究ASA鼻息肉的发病机制。在鼻息肉相关的ASA病例中发现大量嗜酸性粒细胞和脱颗粒肥大细胞。这些嗜酸性粒细胞的电镜分析显示,高电子密度的物质已经从细胞质颗粒的中心晶体中消失。采用气相质层析法测定环加氧酶途径花生四烯酸代谢产物(PGE2、PGF2、6-酮- pgf1和TXB2)。采用高效液相色谱-放射免疫法测定脂氧合酶途径白三烯(LTC4和LTD4)含量。特别值得注意的是鼻息肉相关性ASA中白三烯的高水平和前列腺素的低水平。假定阿司匹林敏感性哮喘鼻息肉的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Etiology of nasal polyps associated with aspirin-sensitive asthma.

It is well known that nasal polyps occur at high frequency in aspirin-sensitive asthma (ASA). Their etiology, however, remains obscure. Therefore, histopathologic observations and measurements of arachidonic acid metabolites were carried out to investigate the etiopathogenesis of nasal polyps in ASA. Abundant eosinophils and degranulated mast cells were found in the tissue of nasal polyp-associated ASA cases. Electron-microscopic analyses of these eosinophils revealed that high-electron-dense material had disappeared from the cytoplasmic granules' central crystalloids. Arachidonic acid metabolites (PGE2, PGF2, 6-keto-PGF1 and TXB2) from the cyclooxygenase pathway were measured via gas mass-chromatography. Leukotrienes (LTC4 and LTD4) from the lipoxygenase pathway were measured via HPLC-radioimmunoassay. Especially noteworthy are the high level of leukotrienes and low level of prostaglandins in nasal polyp-associated ASA. The etiopathogenesis of nasal polyps in aspirin-sensitive asthma is postulated.

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