<h3>Introduction</h3> Similarities between the anti-inflammatory effects obtained from salicylate and glucocorticoid therapy in rheumatic diseases have led to speculation as to a common mode of action of these two substances. Metabolic studies using current laboratory procedures have, however, often produced conflicting results. Data have been reported supporting the concept that salicylates stimulate the pituitary-adrenal axis in man. In other studies these data have not been confirmed and, indeed, appear to have been contradicted. Some investigators have reported an<i>increase</i>in the urinary reducing steroids and no change in neutral 17-ketosteroids after salicylate therapy.^1-3Others have reported a significant<i>decrease</i>in the urinary 17-hydroxycorticosteroid excretion with a slight decrease in 17-ketosteroid excretion in individuals who have been given large doses of salicylates.⁴Other reports have shown no significant alteration in either urinary 17-ketosteroids^5-7or 17-hydroxycorticosteroids^6,7following salicylate administration. In many of the earlier studies in man, massive