par Famaey, Jean Pierre 
Référence Journal Belge de Rhumatologie et de Medicine Physique, 30, 1, page (15-27)
Publication Publié, 1975
Référence Journal Belge de Rhumatologie et de Medicine Physique, 30, 1, page (15-27)
Publication Publié, 1975
Article révisé par les pairs
| Résumé : | After a brief review of recent progress made in the field of the biochemistry of non steroid antiinflammatory drugs (NSAID), the author presents the four most coherent theories currently being put forward to explain the mode of action of these drugs. These hypotheses are namely the shifting of a natural polypeptide X with antiinflammatory properties, of which plasma tryptophan would be the reflection; the uncoupling of the mitochondrial oxidative phosphorylation which would entail a waste of the ATP reserves required for the various syntheses having their seat in the inflammatory focus; the stabilization of the lysosomal membrane which prevents the release into the inflammatory focus of lytic enzymes, which would self maintain the inflammatory phenomena (this effect is in relation to others of the NSAID on the membrane); and the inhibition of the synthesis of the prostaglandins local mediators which at the same time act as agents responsible for the inflammatory phenomena, such as pyrogenous agents and sensitizing agents to the pain awakened by other mediators (histamine, bradykinin). The triple antiinflammatory, antipyretic and antalgic action of NSAID would thus be explained. Some of these biochemical properties, in particular the action on the synthesis of the prostaglandins are discussed with respect to certain side effects of NSAID, such as the ulcerogenic effect, and with respect to the new therapeutic fields which are open to the use of those products (for example antiplatelet aggregation activity). |
