In the early 1950s, Hench and colleagues earned a Nobel Prize in medicine and physiology for discovering the dramatic beneficial effect of cortisone on a patient incapacitated by rheumatoid arthritis (RA). Since that time, the exact role of glucocorticoids in the treatment of RA has generated considerable debate.
Glucocorticoids exert both antiinflammatory and immunosuppressive effects via several mechanisms  (see "Glucocorticoid effects on the immune system"). Among those pertinent to patients with RA are the following:
- Inhibition of prostaglandin and leukotriene synthesis
- Reductions in macrophage phagocytosis, in interleukin (IL)-1 secretion, and in the number of circulating monocytes
- Inhibition of the release of collagenase and lysosomal enzymes
These effects are mediated by intracellular glucocorticoid receptors that interact with transcription factors and thus affect gene transcription. Glucocorticoids effects may also be mediated by posttranscriptional and posttranslational mechanisms, by physicochemical interactions with biologic membranes, and by binding to membrane-bound glucocorticoid receptors.
Among patients with RA, glucocorticoids may be administered via several different modalities. These include oral (short-term, chronic, and pulse), intramuscular, intravenous, and intraarticular routes. (See "Pharmacologic use of glucocorticoids".)