Nebulized budesonide reduces the need for oral corticosteroids and also improved lung function in children under the age of three [ 46 ]. ICS given via a large volume spacer improve asthma symptoms and reduce the number of exacerbations in preschool children and in infants.
Surprisingly, the dose-response curve for the clinical efficacy of ICS is relatively flat and, while all studies have demonstrated a clinical benefit of ICS, it has been difficult to demonstrate differences between doses, with most benefit obtained at the lowest doses used [ 47 , 48 ]. This is in contrast to the steeper dose-response for systemic effects, implying that while there is little clinical benefit from increasing doses of ICS the risk of adverse effects is increased.
However, the dose-response effect of ICS may depend on the parameters measured and, while it is difficult to discern a dose-response when traditional lung function parameters are measured, there may be a dose-response effect in prevention of asthma exacerbations.
These findings suggest that pulmonary function tests or symptoms may have a rather low sensitivity in the assessment of the effects of ICS. This is obviously important for the interpretation of clinical comparisons between different ICS or inhalers. It is also important to consider the type of patient included in clinical studies. Patients with relatively mild asthma may have relatively little room for improvement with ICS, so that maximal improvement is obtained with relatively low doses.
Patients with more severe asthma or with unstable asthma may have more room for improvement and may therefore show a greater response to increasing doses, but it is often difficult to include such patients in controlled clinical trials. More studies are needed to assess whether other outcome measures such as AHR or more direct measurements of inflammation, such as sputum eosinophils or exhaled NO, may be more sensitive than traditional outcome measures such as symptoms or lung function tests [ 50 , 51 , 52 , 53 ].
Higher doses of ICS are needed to control AHR than to improve symptoms and lung function, and this may have a better long-term outcome in terms of reduction in structural changes of the airways [ 54 ]. Measurement of sputum eosinophils to adjust the dose of ICS may reduce the overall dose requirement for ICS and exacerbations [ 55 , 56 ].
Monitoring of exhaled NO may also reduce the requirement for corticosteroids but is not yet practical in clinical practice [ 57 ]. Some patients with asthma develop an element of irreversible airflow obstruction, but the pathophysiological basis of these changes is not yet understood. It is likely that they are the result of chronic airway inflammation and that they may be prevented by treatment with ICS.
There is some evidence that the annual decline in lung function may be slowed by the introduction of ICS [ 58 ] and this is supported by a five year study of low dose budesonide in patients with mild asthma [ 59 , 60 ]. Increasing evidence also suggests that delay in starting ICS may result in less overall improvement in lung function in both adults and children [ 61 , 62 , 63 ].
These studies suggest that introduction of ICS at the time of diagnosis is likely to have the greatest impact [ 62 , 63 ]. So far there is no evidence that early use of ICS is curative and even when ICS are introduced at the time of diagnosis, symptoms and lung function revert to pretreatment levels when corticosteroids are withdrawn [ 61 ].
In a retrospective review of the risk of mortality and prescribed anti-asthma medication, there was a significant protection provided by regular ICS therapy [ 64 ]. The increase in use of rescue therapy should result in an increase in the maintenance dose of ICS. Several ICS are currently on the market for use in asthma, although their availability varies between countries.
There have been relatively few studies comparing efficacy of the different ICS, and it is important to take into account the delivery system and the type of patient under investigation when such comparisons are made. Because of the relatively flat dose-response curve for the clinical parameters normally used in comparing doses of ICS, it may be difficult to see differences in efficacy of ICS.
Most comparisons have concentrated on differences in systemic effects at equally efficacious doses, although it has often proved difficult to establish dose-equivalence [ 68 ]. There are few studies comparing different doses of ICS in asthmatic patients. Budesonide has been compared with BDP and in adults and children it appears to have comparable anti-asthma effects at equal doses, whereas fluticasone propionate FP appears to be approximately twice as potent as BDP and budesonide [ 48 ].
Studies have consistently shown that FP and budesonide have less systemic effects than BDP, triamcinolone and flunisolide [ 33 ]. The newer ICS mometasone and ciclesonide are claimed to have less systemic effects [ 69 , 70 ]. ICS are now recommended as first-line therapy for all patients with persistent symptoms. It is conventional to start with a low dose of ICS and to increase the dose until asthma control is achieved. It may take as long as three months to reach a plateau in response and any changes in dose should be made at intervals of three months or more.
ICS are usually given as a twice daily dose in order to increase compliance. When asthma is unstable four times daily dosage may be preferable [ 71 ]. It may be preferable to add a low dose of oral corticosteroid, since higher doses of ICS are expensive and have a high incidence of local side effects. Nebulized budesonide has been advocated in order to give an increased dose of inhaled corticosteroid and to reduce the requirement for oral corticosteroids [ 72 ], but this treatment is expensive and may achieve its effects largely via systemic absorption.
The dose of inhaled corticosteroid should be the minimal dose that controls asthma and once control is achieved the dose should be slowly reduced [ 73 ]. Patients with COPD have a poor response to corticosteroids in comparison to asthma with little improvement in lung function [ 39 ]. However, several large studies have shown that corticosteroids fail to reduce the progression in COPD measured by annual fall in FEV 1 [ 75 ] and they have not been found to reduce mortality in a large study [ 76 ].
These results are likely to reflect the resistance of pulmonary inflammation to corticosteroids in COPD patients as a result of the reduction in HDAC2 [ 22 ]. Previously it was recommended to increase the dose of ICS if asthma was not controlled, on the assumption that there was residual inflammation of the airways.
However the dose response effect of ICS is relatively flat, so that there is little improvement in lung function after increasing the dose of ICS. An alternative strategy is to add some other class of controller drug and this is more effective than increasing the dose of ICS for most patients [ 77 ]. This has been confirmed in several other studies [ 79 ].
Analysis of several studies clearly show that adding a LABA is more effective than increasing the dose of ICS in terms of improving asthma control and reducing exacerbations [ 81 ]. These fixed combination inhalers also ensure that patients do not discontinue their ICS when a long-acting bronchodilator is used.
For patients with mild persistent asthma combination inhalers are no more effective than the ICS alone in controlled trials [ 82 ], but may have an advantage in the real world where adherence to regular ICS is very low. This advantage is particularly striking in terms of reducing the number of severe exacerbations.
The mechanisms by which corticosteroids as required improve asthma control and reduce exacerbations are not completely understood, but exacerbations of asthma evolve over several days when patients take increasing amounts of rescue medication [ 86 ]. During this time there is increasing inflammation of the airways, as may be measure by exhaled nitric oxide and sputum eosinophils [ 44 ].
Taking the inhaled corticosteroid at the same time as the formoterol to relieve symptoms may suppress this evolving inflammation, particularly since corticosteroids appear to have a relatively rapid onset of effect in suppressing airway inflammation [ 87 ]. They are more effective than LABA alone in reducing exacerbations [ 90 ]. This may be explained by molecular interactions between LABA and corticosteroids as discussed above.
Theophylline has not been examined as an add-on therapy in COPD patients but there are theoretical reasons to believe that low dose theophylline may reverse corticosteroid resistance in COPD. There is no role for anti-leukotrienes in COPD patients. The efficacy of ICS is now established in short- and long-term studies in adults and children, but there are still concerns about side effects, particularly in children and when high inhaled doses are used.
Several side effects have been recognized Table 2. Side effects due to the local deposition of the ICS in the oropharynx may occur with steroid, but the frequency of complaints depends on the dose and frequency of administration and on the delivery device used. Dysphonia is not appreciably reduced by using spacers, but may be less with dry powder devices. Dysphonia may be due to myopathy of laryngeal muscles and is reversible when treatment is withdrawn [ ]. For most patients it is not troublesome but may be disabling in singers and lecturers.
Oropharyngeal candidiasis thrush may be a problem in some patients, particularly in the elderly, with concomitant oral corticosteroids and more than twice daily administration [ ]. Large volume spacer devices protect against this local side effect by reducing the dose of ICS that deposits in the oropharynx. There is no evidence that ICS, even in high doses, increase the frequency of infections, including tuberculosis, in the lower respiratory tract in asthmatic patients.
Recently several large controlled studies have shown that high dose ICS increase physician-diagnosed pneumonias, either used alone or in combination with a LABA [ 75 , 90 ] and this has been confirmed in an epidemiological study of hospital admissions for pneumonia amongst COPD patients [ ]. The mechanism of pneumonia in COPD is uncertain, but is apparently seen more often with FP than with budesonide [ ].
The efficacy of ICS in the control of asthma is undisputed, but there are concerns about systemic effects of ICS, particularly as they are likely to be used over long periods and in children of all ages [ 33 , ]. The safety of ICS has been extensively investigated since their introduction 30 years ago [ 32 ]. One of the major problems is to decide whether a measurable systemic effect has any significant clinical consequence and this necessitates careful long-term follow-up studies.
As biochemical markers of systemic corticosteroid effects become more sensitive, then systemic effects may be seen more often, but this does not mean that these effects are clinically relevant. There are several case reports of adverse systemic effects of ICS, and these may be idiosyncratic reactions, which may be due to abnormal pharmacokinetic handing of the inhaled corticosteroid. The systemic effect of an inhaled corticosteroid will depend on several factors, including the dose delivered to the patient, the site of delivery gastrointestinal tract and lung , the delivery system used and individual differences in the patient's response to the corticosteroid.
Recent studies suggest that systemic effects of inhaled corticosteroid are less in patients with more severe asthma, presumably as less drug reaches the lung periphery [ , ]. The systemic effect of an ICS is dependent on the amount of drug absorbed into the systemic circulation. Use of a large volume spacer device markedly reduces the oropharyngeal deposition, and therefore the systemic effects of ICS, although thus is less important when oral bioavailability is minimal, as with FP.
For dry powder inhalers similar reductions in systemic effects may be achieved with mouth-washing and discarding the fluid. As the fraction of ICS deposited in the oropharynx is reduced, the proportion of the inhaled dose entering the lungs is increased.
More efficient delivery to the lungs is therefore accompanied by increased systemic absorption, but this is offset by a reduction in the dose needed for optimal control of airway inflammation. For example, a multiple dry powder delivery system, the Turbuhaler, delivers approximately twice as much corticosteroid to the lungs as other devices, and therefore has increased systemic effects.
However this is compensated for by the fact that only half the dose is required. Adrenal Suppression. Corticosteroids may cause hypothalamic-pituitary-adrenal HPA axis suppression by reducing corticotrophin ACTH production, which reduces cortisol secretion by the adrenal gland. The degree of HPA suppression is dependent on dose, duration, frequency and timing of corticosteroid administration.
Measurement of HPA axis function provides evidence for systemic effects of an inhaled corticosteroid. Basal adrenal cortisol secretion may be measured by a morning plasma cortisol, 24h urinary cortisol or by plasma cortisol profile over 24 h. Other tests measure the HPA response following stimulation with tetracosactrin which measures adrenal reserve or stimulation with metyrapone and insulin which measure the response to stress.
There are many studies of HPA axis function in asthmatic patients with ICS, but the results are inconsistent as they have often been uncontrolled and patients have also been taking courses of oral corticosteroids which may affect the HPA axis for weeks [ 32 ].
The clinical significance of these effects is not certain, however. Bone Metabolism. Corticosteroids lead to a reduction in bone mass by direct effects on bone formation and resorption and indirectly by suppression of the pituitary-gonadal and HPA axes, effects on intestinal calcium absorption, renal tubular calcium reabsorption and secondary hyperparathyroidism [ ]. The effects of oral corticosteroids on osteoporosis and increased risk of vertebral and rib fractures are well known, but there are no reports suggesting that long-term treatment with ICS is associated with an increased risk of fractures.
Bone densitometry has been used to assess the effect of ICS on bone mass. Although there is evidence that bone density is less in patients taking high dose ICS, interpretation is confounded by the fact that these patients are also taking intermittent courses of oral corticosteroids. Changes in bone mass occur very slowly and several biochemical indices have been used to assess the short-term effects of ICS on bone metabolism.
Bone formation has been measured by plasma concentrations of bone-specific alkaline phosphatase, serum osteocalcin or procollagen peptides. Bone resorption may be assessed by urinary hydroxyproline after a 12 hours fast, urinary calcium excretion and pyridinium cross-link excretion. Budesonide consistently has less effect than BDP at equivalent doses and only BDP increases urinary hydroxyproline at high doses.
It is important to monitor changes in markers of bone formation as well as bone degradation, as the net effect on bone turnover is important. There is no evidence that ICS increase the frequency of fractures. Long-term treatment with high dose ICS has not been associated with any consistent change in bone density. Indeed, in elderly patients there may be an increase in bone density due to increased mobility.
Connective Tissue Effects. Oral and topical corticosteroids cause thinning of the skin, telangiectasiae and easy bruising, probably as a result of loss of extracellular ground substance within the dermis, due to an inhibitory effect on dermal fibroblasts. There are reports of increased skin bruising and purpura in patients using high doses of inhaled BDP, but the amount of intermittent oral corticosteroids in these patients is not known. Easy bruising in association with ICS is more frequent in elderly patients [ ] and there are no reports of this problem in children.
Long-term prospective studies with objective measurements of skin thickness are needed with different ICS. Long-term treatment with oral corticosteroids increase the risk of posterior subcapsular cataracts and there are several case reports describing cataracts in individual patients taking ICS [ 32 ]. A slight increase in the risk of glaucoma in patient staking very high does of inhaled corticosteroids has also been identified [ ]. There has been particular concern that ICS may cause stunting of growth and several studies have addressed this issue.
Asthma itself as with other chronic diseases may have an effect on the growth pattern and has been associated with delayed onset of puberty and decceleration of growth velocity that is more pronounced with more severe disease [ ]. However, asthmatic children appear to grow for longer, so that their final height is normal. The effect of asthma on growth make it difficult to assess the effects of ICS on growth in cross-sectional studies, particularly as courses of oral corticosteroids is a confounding factor.
A meta-analysis of 21 studies, including over children, showed no effect of inhaled BDP on statural height, even with higher doses and long duration of therapy [ ] and in a large study of asthmatics treated with ICS during childhood there was no difference in statural height compared to normal children [ ].
Another long-term follow-up study showed no effect of corticosteroids on final height in children treated over several years [ ]. Short-term growth measurements knemometry have demonstrated that even a low dose of an oral corticosteroid prednisolone 2. The relationship between knemometry measurements and final height are uncertain since low doses of oral corticosteroid that have no effect on final height cause profound suppression.
Metabolic Effects. Several metabolic effects have been reported after ICS, but there is no evidence that these are clinically relevant at therapeutic doses. In normal individuals high dose inhaled BDP may slightly increase resistance to insulin. However, in patients with poorly controlled asthma high doses of BDP and budesonide paradoxically decrease insulin resistance and improve glucose tolerance, suggesting that the disease itself may lead to abnormalities in carbohydrate metabolism.
Psychiatric Effects. There are various reports of psychiatric disturbance, including emotional liability, euphoria, depression, aggressiveness and insomnia, after ICS. Only eight such patients have so far been reported, suggesting that this is very infrequent and a causal link with ICS has usually not been established. Based on extensive clinical experience ICS appear to be safe in pregnancy, although no controlled studies have been performed.
There is no evidence for any adverse effects of ICS on the pregnancy, the delivery or on the foetus [ ]. It is important to recognise that poorly controlled asthma may increase the incidence of perinatal mortality and retard intra-uterine growth, so that more effective control of asthma with ICS may reduce these problems. Patients with COPD are elderly and are likely to have increased systemic side effects from ICS as they have several additional risk factors.
There have been fewer studies of systemic side effects in COPD patients. However, a systematic review found no reduction in bone mineral density or increase in fractures in COPD patients treated for up to 3 years with ICS [ 75 ]. An epidemiological study showed an increase in cataracts which are more common in an elderly population [ ].
Many patients with COPD suffer from co-morbidities, including hypertension, metabolic syndrome and diabetes, and may therefore have a worsening of these conditions, but this has not yet been systematically investigated. National Center for Biotechnology Information , U. Journal List Pharmaceuticals Basel v. Pharmaceuticals Basel. Published online Mar 8.
Peter J. Author information Article notes Copyright and License information Disclaimer. Received Jan 29; Accepted Mar 2. This article has been cited by other articles in PMC. Abstract Inhaled corticosteroids ICS are the most effective controllers of asthma. Introduction Inhaled corticosteroids ICS, also known as glucocorticosteroids, glucocorticoids, steroids are by far the most effective controllers used in the treatment of asthma and the only drugs that can effectively suppress the characteristic inflammation in asthmatic airways, even in very low doses.
Mechanisms of Action There have been major advances in understanding the molecular mechanisms whereby ICS suppress inflammation in asthma, based on recent developments in understanding the fundamental mechanisms of gene transcription [ 1 , 2 ]. Table 1 Effect of corticosteroids on gene transcription. Open in a separate window.
Cellular Effects At a cellular level inhaled corticosteroids reduce the numbers of inflammatory cells in asthmatic airways, including eosinophils, T-lymphocytes, mast cells and dendritic cells Figure 1.
Figure 1. Figure 2. Glucocorticoid Receptors Corticosteroids diffuse across the cell membrane and bind to glucocorticoid receptors GR in the cytoplasm 2. Figure 3. Switching off Inflammation The major action of corticosteroids is to switch off multiple activated inflammatory genes that encode for cytokines, chemokines, adhesion molecules inflammatory enzymes and receptors [ 1 ].
Figure 4. Corticosteroid Resistance Patients with severe asthma have a poor response to corticosteroids, which necessitates the need for high doses and a few patients are completely resistant. Figure 5. Figure 6. Pharmacokinetics The pharmacokinetics of ICS is important in relation to systemic effects [ 32 , 33 , 34 ].
Figure 7. Pharmacokinetics of inhaled glucocorticoids. Clinical Use There is no doubt that the early use of ICS has revolutionized the management of asthma, with marked reductions in asthma morbidity and improvement in health status.
Figure 8. Use in Asthma As experience has been gained with ICS they have been introduced in patients with milder asthma, with the recognition that inflammation is present even in patients with mild asthma. Dose-Response Studies Surprisingly, the dose-response curve for the clinical efficacy of ICS is relatively flat and, while all studies have demonstrated a clinical benefit of ICS, it has been difficult to demonstrate differences between doses, with most benefit obtained at the lowest doses used [ 47 , 48 ].
Prevention of Irreversible Airway Changes in Asthma Some patients with asthma develop an element of irreversible airflow obstruction, but the pathophysiological basis of these changes is not yet understood. Reduction in Mortality In a retrospective review of the risk of mortality and prescribed anti-asthma medication, there was a significant protection provided by regular ICS therapy [ 64 ]. Comparison between ICS Several ICS are currently on the market for use in asthma, although their availability varies between countries.
Clinical Application in Asthma Patients ICS are now recommended as first-line therapy for all patients with persistent symptoms. Add-on Therapy Previously it was recommended to increase the dose of ICS if asthma was not controlled, on the assumption that there was residual inflammation of the airways. Side Effects The efficacy of ICS is now established in short- and long-term studies in adults and children, but there are still concerns about side effects, particularly in children and when high inhaled doses are used.
Table 2 Side effects of inhaled corticosteroids. Local Side Effects Side effects due to the local deposition of the ICS in the oropharynx may occur with steroid, but the frequency of complaints depends on the dose and frequency of administration and on the delivery device used. Infections There is no evidence that ICS, even in high doses, increase the frequency of infections, including tuberculosis, in the lower respiratory tract in asthmatic patients.
Systemic Side Effects The efficacy of ICS in the control of asthma is undisputed, but there are concerns about systemic effects of ICS, particularly as they are likely to be used over long periods and in children of all ages [ 33 , ]. References 1. Barnes P. How corticosteroids control inflammation. Rhen T. Antiinflammatory action of glucocorticoids--new mechanisms for old drugs. New Engl.
Glucocorticoid resistance in inflammatory diseases. Gibson P. Acute anti-inflammatory effects of inhaled budesonide in asthma: a randomized controlled trial. Care Med. Ketchell R. Rapid effect of inhaled fluticasone propionate on airway responsiveness to adenosine 5'-monophosphate in mild asthma.
Allergy Clin. Erin E. Rapid anti-inflammatory effect of inhaled ciclesonide in asthma: a randomised, placebo-controlled study. Juniper E. Long-term effects of budesonide on airway responsiveness and clinical asthma severity in inhaled steroid-dependent asthmatics.
Lewis-Tuffin L. The physiology of human glucocorticoid receptor beta hGRbeta and glucocorticoid resistance. NY Acad. Pujols L. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Allergy Asthma Rep. Corticosteroid effects on cell signalling. Clark A. Role of dual specificity phosphatases in biological responses to glucocorticoids.
Dostert A. Negative glucocorticoid receptor response elements and their role in glucocorticoid action. Histone acetylation and deacetylation: importance in inflammatory lung diseases. Hart L. Effects of inhaled corticosteroid therapy on expression and DNA-binding activity of nuclear factor-kB in asthma. Ito K. Glucocorticoid receptor recruitment of histone deacetylase 2 inhibits IL-1b-induced histone H4 acetylation on lysines 8 and Cell Biol.
Bergmann M. Brook M. Posttranslational regulation of tristetraprolin subcellular localization and protein stability by p38 mitogen-activated protein kinase and extracellular signal-regulated kinase pathways. Thomson N. The influence of smoking on the treatment response in patients with asthma.
Adcock I. Molecular mechanisms of corticosteroid resistance. Decreased histone deacetylase activity in chronic obstructive pulmonary disease. Hew M. Relative corticosteroid insensitivity of peripheral blood mononuclear cells in severe asthma. Irusen E. Matthews J. Defective glucocorticoid receptor nuclear translocation and altered histone acetylation patterns in glucocorticoid-resistant patients. Scientific rationale for combination inhalers with a long-acting b2-agonists and corticosteroids. Mak J.
Glucocorticosteroids increase b 2 -adrenergic receptor transcription in human lung. Baraniuk J. Glucocorticoids induce b 2 -adrenergic receptor function in human nasal mucosa. Protective effects of a glucocorticoid on down-regulation of pulmonary b 2 -adrenergic receptors in vivo.
Increased expression of G protein-coupled receptor kinases in cystic fibrosis lung. Roth M. Interaction between glucocorticoids and b2 agonists on bronchial airway smooth muscle cells through synchronised cellular signalling. Usmani O. Glucocorticoid receptor nuclear translocation in airway cells following inhaled combination therapy.
Crit Care Med. Published online May 7. David M. Halpin , 1, 2 Dave Singh , 2, 3 and Ruth M. Hadfield 2, 4. Ruth M. Author information Article notes Copyright and License information Disclaimer. E-mail: ten. Received Apr 3; Accepted Apr This article has been cited by other articles in PMC.
Open in a separate window. Footnotes Conflict of interest: D. References 1. JAMA ; in press [ Clinical features of patients infected with novel coronavirus in Wuhan, China. Lancet ; : — Viral infections and asthma: an inflammatory interface?
Eur Respir J ; 44 : — Nasal cytokine responses to natural colds in asthmatic children. Clin Exp Allergy ; 42 : — Diversity in the bronchial epithelial cell response to infection with different rhinovirus strains. Respirology ; 14 : — Lancet Respir Med ; in press [ China CDC Weekly ; 2 : — Global Initiative for Asthma. Global strategy for asthma management and prevention Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease Inhaled corticosteroids and risk of upper respiratory tract infection in patients with asthma: a meta-analysis.
Infection ; 47 : — Long-term use of inhaled corticosteroids and risk of upper respiratory tract infection in chronic obstructive pulmonary disease: a meta-analysis. Inhal Toxicol ; 29 : — Inhaled corticosteroids for stable chronic obstructive pulmonary disease.
Long-term effects of inhaled corticosteroids on sputum bacterial and viral loads in COPD. Eur Respir J ; 50 : Inhaled corticosteroids and the risk of pneumonia in people with asthma: a case—control study. Chest ; : — Budesonide and formoterol reduce early innate anti-viral immune responses in vitro. PLoS One ; 6 : e Reduced antiviral interferon production in poorly controlled asthma is associated with neutrophilic inflammation and high-dose inhaled corticosteroids.
Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations. Nat Commun ; 9 : Increased type 2 inflammation post rhinovirus infection in patients with moderate asthma. Cytokine ; : Inhibitory effects of glycopyrronium, formoterol, and budesonide on coronavirus HCoVE replication and cytokine production by primary cultures of human nasal and tracheal epithelial cells.
Respir Investig ; in press [ Johnston SL. Overview of virus-induced airway disease. Proc Am Thorac Soc ; 2 : — Budesonide and formoterol effects on rhinovirus replication and epithelial cell cytokine responses. Respir Res ; 14 : SARS: systematic review of treatment effects. PLoS Med ; 3 : e World Health Organization. Interim guidance www.
They must be used every day. Symptoms should get better in 2 to 3 weeks. Your child breathes these medicines into his lungs to treat asthma. They help reduce swelling in the airways on a daily basis and help prevent flare-ups. They may not help your child during an asthma flare-up, but your child should still use the medicine during episodes that have increased symptoms. If you forget to give a dose of this medicine, give it as soon as possible.
If it is almost time for the next dose, do not give the missed dose at all. Do not double the next dose. If you have any questions about this, check with your child's doctor or pharmacist. If a skin rash occurs, call your child's doctor. He should brush his teeth or drink water after each dose.
This will prevent thrush and a sore throat. Skip to Content. Urgent Care. In This Section. How to give this medicine Read the label carefully and make sure you are giving your child the right dose. It is easy to confuse the many different dosage forms and strengths. Stay with your child until he has used the right dose of medicine. Shake this medicine before giving it if it is a metered dose inhaler or liquid for use in a nebulizer. Do not shake this medicine if it is a dry powder inhaler. It is very important to give the medicine every day as ordered, even if your child is feeling fine.
After each dose, your child should rinse his mouth with water or brush his teeth to wash the steroid medicine out of his mouth. Keep track of the remaining doses. It is important to keep a record of when the medicine is given. This is very important. If you forget to give a dose If you forget to give a dose of this medicine, give it as soon as possible.
Medicine storage Store all medicine out of the reach of children. Keep the bottle tightly closed and store it in a dark, dry place not in the bathroom or above the kitchen sink. This medicine does not work as well when kept in a light or humid place. Do not keep this medicine in the refrigerator.
Store it at room temperature. Keep this medicine away from heat or direct sunlight. Do not use this medicine after the expiration date printed on the container. Each medicine container has directions to throw it away after being open for 30 to 60 days, even if the medicine is not gone. Drug interactions This medicine should not be taken with these foods, products or medicines: Tobacco products — your child should not smoke. Smoking irritates the lungs and makes the asthma worse.
Inhaled corticosteroids help to prevent asthma attacks and improve lung function. They may also be used in the treatment of certain other lung conditions, such as chronic obstructive pulmonary disease COPD. Because inhaled corticosteroids deliver the medicine directly into the lungs, much smaller doses of corticosteroid are needed to effectively control asthma symptoms compared to what would be needed if the same medication was taken orally.