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Prostaglandins, leukotrienes, and other arachidonic acid metabolites in nasal polyps and nasal mucosa
Author(s) -
Jung Timothy T. K.,
Stewart Robert,
Juhn S. K.,
Hwang Daniel
Publication year - 1987
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1288/00005537-198702000-00009
Subject(s) - arachidonic acid , nasal polyps , mucous membrane of nose , aspirin , metabolite , leukotriene , hydroxyeicosatetraenoic acid , medicine , leukotriene b4 , thromboxane b2 , pathogenesis , chemistry , pathology , platelet , biochemistry , asthma , inflammation , enzyme
Prostaglandins (PGs) and leukotrienes (LTs) are known to play an important role in allergic inflammatory reactions. The triad of aspirin sensitivity, nasal polyposis, and asthma led us to suspect that PGs, LTs and other arachidonic acid metabolites may be involved in the pathogenesis of nasal polyps. The purpose of this study was to determine arachidonic acid metabolites and to measure concentrations of PGs and LTs in nasal polyps and nasal mucosa. Samples of nasal polyps and nasal mucosa were obtained at the time of polypectomies and nasal procedures. Metabolites of arachidonic acid in tissue were determined by incubation of tissue‐homogenates with 14 C‐arachidonic acid and analyses with thin‐layer chromatography and high performance liquid chromatography (HPLC). Levels of PGE 2 , 6‐keto‐PGF 1α , throm‐boxane (Tx)B 2 , 15‐hydroxyeicosatetraenoic acid (HETE), LTC 4 , LTB 4 were measured by radioimmunoassay. The predominant arachidonic acid metabolite in both nasal polyps and mucosa was 15‐HETE. The HPLC analysis showed that the predominant metabolite in nasal polyp was 15‐HETE, especially in polyps from aspirin sensitive patients. Levels of 15‐HETE and PGE 2 were higher in polyps from patients with a history of allergy than from nonallergic patients. Levels of LTC 4 and LTB 4 in nasal polyps were determined. The findings of this study will help to explain biochemical basis of the pathogenesis of aspirin‐sensitive nasal polyps and to develop better medical treatment for them.