Inhaled corticosteroids are glucocorticoids with high topical and treatment of asthma. Inhaled corticosteroids are commonly used as Fluticasone, Budesonide, Propionate and also Ciclesonide.
In same note, Inhaled corticosteroids (ICS) should be the first step for all asthma patients, because airway inflammation is present in early mild disease as well, and bronchial remodeling starts developing from the beginning. ICS suppress bronchial inflammation increase peak expiratory flow rate, reduce need for rescue and prevents incident of acute asthma.
Common examples of inhaled corticosteroid
What is the best inhaled corticosteroid?
Fluticasone propionate is known as the best Inhaled corticosteroid because of it high potency, longer duration and negligible oral bioavailability. The dose when given is swallowed after inhalation has little propensity to produce systemic effects. In one direct comparison, fluticasone was equally as effective as twice the dose of beclomethasone, suggesting a potency twice as great. At high doses, systemic effects may be due to absorption from the lungs.
Others include Budesonide which is a nonhalogenated glucocorticoid with high topical systemic activity ratio. Small fraction that is absorbed is rapidly metabolized, less systemic effects are noted too. It is preferred in more severe cases.
Your symptoms that shows up are, Hoarseness of voice, dysphonia, sore throat, asymptomatic or symptomatic oropharyngeal candidiasis are most common side effects. It can be minimized by the use of a spacer, and by gargling after every dose. Oral candidiasis can be prevented as well as treated by tropical clotrimazole. Systemic effects of long term ICS are clinically relevant only at doses.
Use in COPD
The airway inflammation in COPD is not very responsive to corticosteroids. As such, only high dose ICS are beneficial in advanced COPD with frequent exacerbations. It should not be used in early cases. These results are likely to reflect the resistance of pulmonary inflammation to corticosteroids in COPD patients as a result of the reduction in HDAC2 , and no proof for retard progression of COPD.