Aspirin intolerance: unaltered susceptibility of platelet cyclo-oxygenase to inhibition by aspirin in vitro.
Inhibition of prostaglandin (PG) biosynthesis has been proposed as a mechanism of aspirin-induced asthma. In order to verify the existence of a generalized abnormal sensitivity of the PG cyclo-oxygenase in intolerant patients, we have compared the inhibitory effects of aspirin on platelet PGE2 and PGF2alpha spontaneous formation in vitro, in 10 healthy subjects, 10 aspirin-sensitive asthmatics, and 10 nonasthmatic aspirin-sensitive patients. No statistically significant differences were found in the pattern nor in the absolute concentrations of both PGs in the control platelet superfusates. Moreover, the synthesis and release of both PGs were inhibited by aspirin with the same potency in the three groups studied.
D000328:Adult; D000368:Aged; D001241:Aspirin / Q000494:pharmacology*; D001249:Asthma / Q000139:chemically induced / Q000276:immunology; D001792:Blood Platelets / Q000201:enzymology*; D016861:Cyclooxygenase Inhibitors; D004342:Drug Hypersensitivity; D004361:Drug Tolerance; D006801:Humans; D008875:Middle Aged; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
D016861:Cyclooxygenase Inhibitors; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin