Ogino S, Irifune M, Harada T, Kikumori H, Matsunaga T
Department of Otolaryngology, Osaka University Medical School, Japan.
Acta Otolaryngol Suppl. 1993;501:85-7. doi: 10.3109/00016489309126222.
Arachidonic acid metabolites (AAMs) are known to be involved in inflammation. It is suggested that AAMs play an important role in the pathogenesis of nasal polyp. We have measured the levels of prostaglandin E2, 6-keto prostaglandin F1 alpha, thromboxane B2, leukotriene B4 and a mixture of leukotriene C4, D4 and E4 in both nasal polyp and maxillary sinus mucosa by radioimmunoassay. Our results showed that arachidonic acid metabolism in nasal polyps from allergic patients was more active than that from non-allergic patients. The arachidonic acid metabolism in nasal polyp was more active than in maxillary sinus mucosa among allergic patients. On the other hand, arachidonic acid metabolism in maxillary sinus mucosa was more active than that in nasal polyps among non-allergic patients. On the basis of these results, we hypothesized the causal mechanisms of nasal polyps as follows: The nasal polyp in allergic patients is caused by primary inflammation of the nasal mucosa, and sinusitis occurs secondarily. In non-allergic patients, the primary side of inflammation is located in the maxillary sinus mucosa, leading to the secondary formation of nasal polyp.
已知花生四烯酸代谢产物(AAMs)参与炎症反应。有人提出,AAMs在鼻息肉的发病机制中起重要作用。我们通过放射免疫分析法测量了鼻息肉和上颌窦黏膜中前列腺素E2、6-酮前列腺素F1α、血栓素B2、白三烯B4以及白三烯C4、D4和E4混合物的水平。我们的结果表明,过敏患者鼻息肉中的花生四烯酸代谢比非过敏患者更活跃。在过敏患者中,鼻息肉中的花生四烯酸代谢比上颌窦黏膜更活跃。另一方面,在非过敏患者中,上颌窦黏膜中的花生四烯酸代谢比鼻息肉更活跃。基于这些结果,我们对鼻息肉的因果机制提出如下假设:过敏患者的鼻息肉是由鼻黏膜的原发性炎症引起的,鼻窦炎是继发的。在非过敏患者中,炎症的原发部位位于上颌窦黏膜,导致鼻息肉的继发形成。