Side effects are minimized by taking the lowest doses possible (that still yields positive results) and following doctor's orders. It is important to avoid self-regulation of the dosage, either by adding more or stopping the drug without a schedule. After prolonged use, steroids must be gradually reduced to permit the adrenal glands to resume natural cortisol production. Eliminating doses too quickly can result in glucocorticoid withdrawal symptoms, worsening of underlying inflammatory disease (rebound effect), or rarely, adrenal crisis (a life-threatening state caused by insufficient levels of adrenal steroids).
Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.