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.
Allergic sensitivity to a topical corticosteroid is usually only picked up when an eczematous dermatitis being treated by a topical corticosteroid fails to respond to treatment or worsens. In cases of persistent or exacerbating dermatitis treated with corticosteroid preparations, corticosteroid sensitivity should be considered. However, it may also be due to irritation from or allergy to other components of the preparation such as preservatives . Lanolin , ethylenediamine , quaternium-15 and the antibacterial agent neomycin , are all known to be potent sensitisers.