ABSTRACT
It has long been known that anti-inflammatory steroids exert more profound effects than nonsteroidal anti-inflammatory drugs of the aspirin-type. 62 We now have a rational basis for this observation: anti-inflammatory corticosteroids can suppress production of all pro-inflammatory and injurious metabolites of arachidonic acid including both cyclooxygenase and lipoxygenase-derived products. Since the mid 1970s, it has been known that this action of the corticosteroids is exerted through inhibition of arachidonic acid liberation from cell-membrane phospholipids by phosphollpase A2 (see References 21 to 25, 31 and Tables 1 to 4). Indeed, since phospholipase A2 is also involved in production of "platelet-activating factor" (PAF) and its lyso derivative, corticosteroids also inhibit production of this potent inflammatory mediator. 63 Together these mediators may be involved in most, if not all, of the mechanisms of acute and chronic inflammatory disease.
