Generally speaking, corticosteroids exert their effects on cells through genomic and non genomic mechanisms. They both suppress and enhance numerous biological phenomena. In asthma, corticosteroids act at different levels. They: inhibit chemical mediators, whether these are performed, like histamine, or newly formed, like arachidonic acid metabolites (prostaglandins and leukotrienes) or the platelet-activating factor (PAF); restore the sensitivity of beta-adrenergic receptors to sympathomimetic drugs; exert a powerful anti-inflammatory effect, notably reducing bronchial mucus secretion; reduce bronchial hyperreactivity and modify the bronchial response to bronchoconstrictors; act on respiratory function and gas exchanges. Many effects of corticosteroids in asthma involve the synthesis of proteins, such as lipomodulin (or macrocortin) which inhibits phospholipase A2, a key-enzyme in the synthesis of numerous chemical mediators derived from membrane phospholipids. The multiple effects of corticosteroids account for their broad spectrum of activity and their effectiveness against both acute and chronic manifestations of asthma.
Corticosteroids can produce reversible hypothalamic- pituitary adrenal (HPA) axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. Adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for up to 12 months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. If the patient is receiving steroids already, dosage may have to be increased.
Intravenous corticosteroids are sometimes needed in patients who need aggressive management of the inflammation, as in a patient with optic nerve involvement, severe VKH, sympathetic ophthalmia, serpiginous choroiditis or in case of panuveitis. The most commonly used drug is methylprednisolone. The usual dosage is 500 mg to 1 gm intravenous infusion with % normal saline or sodium lactate solution over 30 to 60 minutes daily for 3 consecutive days, followed by high dose of oral corticosteroids. Caution should be taken as intravenous methylprednisolone can cause cardiac arrhythmias and cardiovascular collapse. Intravenous methylprednisolone should be followed by high dose oral steroid or immunosuppressive agent