Subgroup analysis showed a statistically significant group difference between six molecules in the mean reduction of linear growth velocity during one-year treatment (Chi² = , degrees of freedom (df) = 5, P value < ). The group difference persisted even when analysis was restricted to the trials using doses equivalent to 200 μg/d hydrofluoroalkane (HFA)-beclomethasone. Subgroup analyses did not show a statistically significant impact of daily dose (low vs medium), inhalation device or participant age on the magnitude of ICS-induced suppression of linear growth velocity during a one-year treatment period. However, head-to-head comparisons are needed to assess the effects of different drug molecules, dose, inhalation device or patient age. No statistically significant difference in linear growth velocity was found between participants treated with ICS and controls during the second year of treatment (five trials with 3174 participants; MD - cm/y, 95% CI - to , P value ). Of two trials that reported linear growth velocity in the third year of treatment, one trial involving 667 participants showed similar growth velocity between the budesonide and placebo groups ( cm/y vs cm/y), and another trial involving 1974 participants showed lower growth velocity in the budesonide group compared with the placebo group ( MD - cm/y, 95% CI - to -, P value ). Among four trials reporting data on linear growth after treatment cessation, three did not describe statistically significant catch-up growth in the ICS group two to four months after treatment cessation. One trial showed accelerated linear growth velocity in the fluticasone group at 12 months after treatment cessation, but there remained a statistically significant difference of cm in height between the fluticasone and placebo groups at the end of the three-year trial .
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.
You'll also have a quick-relief inhaler to treat asthma symptoms as they happen. You'll need to use your quick-relief inhaler to treat symptoms when you get them. And you'll use your steroid inhaler regularly to prevent asthma symptoms. You normally breathe these drugs into your lungs with an inhaler. The drug is stored in a small aerosol can attached to a mouthpiece. When you breathe in, some of the drug is released. Taking the drug this way means it gets straight to your lungs. If you find it difficult to use your inhaler, you may like to try another type of inhaler. For instance, some inhalers use a spray, others use a powder. Your doctor will be able to explain the different kinds.