Abstract
The mechanism by which salicylates exert their effects always has been an enigma. Because the therapeutic response to cortisone and corticotropin is similar to that obtained from salicylates, it has been suggested that the mechanism of action of the salicylates might be pituitary-adrenocortical stimulation. In this critical analysis of the evidence for and against this hypothesis, the author observes that current investigations do not indicate that the antirheumatic effects of salicylates are mediated through the pituitary-adrenal system.