Corticosteroid mechanism in asthma

It would be difficult for physicians or allergists to imagine doing without corticosteroids in managing difficult cases of bronchial asthma. It is beyond any doubt that CS act on many sites to help reverse the pathologic process of bronchial asthma. Corticosteroids enhance the beta-adrenergic response to relieve the muscle spasm. They also act by reversing the mucosal edema, decreasing vascular permeability by vasoconstriction, and inhibiting the release of LTC4 and LTD4. Corticosteroids reduce the mucus secretion by inhibiting the release of secretagogue from macrophages. Corticosteroids inhibit the late phase reaction by inhibiting the inflammatory response and interfering with chemotaxis. This action may be due to the inhibition of LTB4 release. The eosinopenic effect of corticosteroids may help to prevent the cytotoxic effect of the major basic protein and other inflammatory mediators released from eosinophils. Corticosteroids have no effect on the immediate hypersensitivity reaction and have no direct role in bronchial reactivity. By blocking the late reaction, they prevent the increased airway reactivity observed with late bronchial reactions. The limitation of using corticosteroids are their side effects. They vary from tolerable to life threatening side effects. Each tissue in the body is a target for corticosteroids. The mechanism of adverse effects have been studied in extensive detail but many questions are yet to be answered. Alternate-day therapy and inhalation therapy are meant to minimize these side effects. The expansion of using inhaled steroid therapy and finding some inhaled preparations that have even less systemic side effects seems a reasonable approach to deal with severe asthma.

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

Decreases in bone mineral density (BMD) have been observed with long-term administration of products containing inhaled corticosteroids, including flunisolide. The clinical significance of small changes in BMD with regard to long-term outcomes is unknown. Monitor patients with major risk factors for decreased bone mineral content, such as prolonged immobilization, family history of osteoporosis , postmenopausal status, tobacco use, advanced age, poor nutrition, or chronic use of drugs that can reduce bone mass (., anticonvulsants and corticosteroids) and treat with established standards of care.

Corticosteroid mechanism in asthma

corticosteroid mechanism in asthma


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