ABSTRACT
I. INTRODUCTION Despite the broad use of glucocorticoids in inflammatory diseases (Table 1), a major question remains unanswered: why some patients with inflammatory diseases respond well to glucocorticoids while others are refractory or need chronic glucocorticoid therapy to maintain their disease in remission. Indeed, some patients are steroid-sensitive (50-75%), while others are steroid-dependent (30-35%) or resistant (10-15%). Most steroid-dependent or steroid-resistant patients develop a cushingoid appearance or metabolic dysfunction, which suggests that their poor glucocorticoid sensitivity is limited to the immune system rather than involving nonimmune tissues. Recent studies have revealed that both the process of inflammation or the disease itself and the genetic and constitutional background of the patient may influence his or her variable response to glucocorticoids [1-4].
