M. Schmid et al., Arachidonic acid metabolism in nasal tissue and peripheral blood cells in aspirin intolerant asthmatics, ACT OTO-LAR, 119(2), 1999, pp. 277-280
Aspirin intolerance (AI) is characterized by polypous rhinosinusitis, bronc
hial asthma and adverse reactions to aspirin. The common intolerance to all
cyclo-oxygenase inhibitors allows us to focus study of the pathogenesis of
AI on the metabolism of arachidonic acid (AA). We studied the metabolism o
f AA in nine aspirin intolerant asthmatics (AIA) and eight healthy voluntee
rs (controls) by measuring prostaglandin E-2 (PGE(2)) and peptido-leukotrie
nes (pLT = LTC4/D-4/E-4) in nasal tissue and peripheral blood cells (PBCs)
using a specific immunoassay. In all patients with AI the tests were perfor
med before and after bronchial provocation with lysine-ASA. In the control
group the tests were done before and after 500 mg ASA p.o. The release of p
LT in nasal polyps of AIA was found to be significantly higher than in norm
al mucosa of AIAs and controls. In every tissue a significant increase of p
LT after aspirin challenge was observed. Nasal polyps of AIA show a signifi
cantly lower release of PGE(2) than normal mucosa of AIAs and controls. Per
ipheral blood cells of AIA show a significantly higher release of pLT and a
significantly lower release of PGE(2) than PBCs of controls. Therefore cli
nical manifestations of AI may be based on an alteration of AA metabolism i
n AIA.