[Blood platelets and asthma caused by aspirin].
Platelets isolated from patients with aspirin-induced asthma (ASA patients) react abnormally in vitro to aspirin and to non-steroid anti-inflammatory drugs (NSAID), by generating cytocidal molecules, that can kill parasitic larvae and to oxygen-dependent free radicles, which may be detected by chemiluminescence, although these drugs do not have a similar effect on platelets from normal donors or allergic asthmatics. The abnormality appears to be associated with the inhibiting properties of NSAID and aspirin on the cyclo-oxygenase pathway, that leads to a defect of the binding of prostaglandin endoperoxide PGH2 to its receptors on the platelet membrane. In addition, another metabolite from the lipoxygenase pathway which is at present poorly defined seems to participate in the anomaly. Sodium salicylate, a naturally produced catabolite of aspirin, that is well-tolerated by ASA patients, inhibits the abnormal response of the platelets and this opens new perspectives in the management of aspirin-sensitive intolerance.
D001241:Aspirin / Q000009:adverse effects* / Q000276:immunology; D001249:Asthma / Q000097:blood / Q000139:chemically induced*; D001792:Blood Platelets / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology; D016861:Cyclooxygenase Inhibitors; D003888:Desensitization, Immunologic; D004342:Drug Hypersensitivity / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D016859:Lipoxygenase Inhibitors
D016861:Cyclooxygenase Inhibitors; D016859:Lipoxygenase Inhibitors; D007073:Immunoglobulin E; D001241:Aspirin
Plaquettes sanguines et asthme à l'aspirine.