Corticosteroids will inhibit phospholipase A2 thereby preventing the generation of substances which mediate inflammation, for example, prostaglandins. Corticosteroids also produce a marked, though transient, lymphocytopaenia. This depletion is due to redistribution of the cells, the T lymphocytes being affected to a greater degree than the B lymphocytes. Lymphokine production is reduced, as is the sensitivity of macrophages to activation by lymphokines. Corticosteroids also retard epithelial regeneration, diminish post-inflammatory neo- vascularisation and reduce towards normal levels the excessive permeability of inflamed capillaries.
Contact lens wear can be an inflammatory influence under normal circumstances, but an alreadysensitized cornea can show rebound inflammation if proper steps aren’t taken. It is imperative to use the immunosuppressive benefits of steroids with a slow taper as contact lens wear is resumed, or the patient will suffer setbacks and require multiple office visits. We typically restart limited contact lens wear when the rehabilitating cornea can tolerate a limited steroid dosage of once to twice daily.