E. Inhaled Corticosteroids

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Inhaled corticosteroids are now standard therapy in the management of asthma. Their proven efficacy and safety has led them to be regarded as the mainstay of therapy in the prophylaxis of asthma. The two drugs commonly available are beclomethasone dipropionate (Becotide®, Becloforte®) and budesonide (Pulmicort®). Bextasol is now no longer available.


Both beclomethasone dipropionate (BDP) and budesonide (BUD) are both topically active glucocorticoids that have both anti-inflammatory and immunosuppressive activity. Both have glucocorticoid effects when given systemically in that they bind to the glucocorticoid receptor and have the usual effects on protein and carbohydrate metabolism as hydrocortisone and prednisolone. When inhaled, both drugs inhibit phospholipase A2 locally, thereby reducing the formation of prostaglandins and leucotrienes, and also inhibit neutrophil and macrophage adherence in the capillaries of inflamed tissues, reducing the inflammatory response. Both drugs reduce bronchial hyperresponsiveness in asthmatics and a single dose can modify the late phase response to inhaled allergens. When taken over a period of several days, both drugs may also prevent the early phase response to inhaled allergens and exercise. Clinically, both drugs when taken regularly reduce the frequency of asthma symptoms and "rescue" bronchodilator requirements, and for patients on long term oral corticosteroid therapy, may allow a reduction in dose or complete withdrawal of oral steroids.


Both drugs can be inhaled either as an aerosol from a metered dose inhaler or nebuliser, or as a powder. Although both drugs rely on their topical activity, there may be significant systemic absorption from the lungs. Also, because a large proportion of the inhaled dose impacts in the oropharynx, they are absorbed from the gastrointestinal tract, but undergo significant first pass hepatic metabolism. The plasma half life of BUD is 90-120 minutes in adults and is metabolised in the liver to inactive metabolites. BDP, however, as well as hepatic metabolism in inactive metabolites, also undergoes metabolism in the lung to beclomethasone monopropionate which is pharmacologically active (although less potent than BDP) and cleared four times slower than BUD.

Therapeutic Use

Both drugs are used in the control of asthma (and also rhinitis). It is now recommended that any asthmatic patient that needs to use a bronchodilator more than once or twice a day on a regular basis should be treated with a prophylactic anti-inflammatory agent such as an inhaled corticosteroid. It should be stressed to patients that an inhaled corticosteroid will have no effect when taken for acute symptoms as this misunderstanding can lead to poor compliance with these agents. Also, if a patient is just starting on inhaled corticosteroids, they should also be warned that it may take a week or two before they see an improvement in their symptoms. Inhaled corticosteroids are now preferred to oral steroids because of the reduced incidence of glucocorticoid side effects for the equivalent clinical effect. The usual dose for maintenance treatment is in the range 200-800 µg/day for both BDP and BUD, usually in 2-4 divided doses. BUD is clinically slightly more potent than BDP. For patients who are still poorly controlled, dosages can be increased up to 2000µg /day for BDP and 1600 µg/day for BUD, but it is thought that dosages above this level convey no further advantages, and oral steroid therapy should be added if control is still poor. Also, in patients poorly controlled on high doses of inhaled corticosteroids, 4 times a day dosing is thought to be more effective than twice daily. For BDP, the dose using a powder delivery system for the same clinical effect is usually double that of aerosol, but for BUD, the dose of the powder is equivalent to that of the aerosol. It is now recommended that patients increase the dosage of their inhaled corticosteroids whenever they detect a deterioration in their asthma control (by home peak flow monitoring). They can be given a set of written instructions as to how much to increase the dosage by according to their peak flow, and at what stage to seek further medical advice. By this means, early intervention may avoid further deterioration requiring a course of oral steroids.

Side effects and Overdosage

The side effects of the two drugs can be divided into those caused by local deposition in the oropharynx, and those caused by systemic absorption. Patients may complain of a sore or dry throat, and occasionally, oropharyngeal candidiasis may occur. This can be prevented to some extent by gargling and rinsing of the mouth after inhaling the drug and the use of a large volume spacer device (Volumatic®, Nebuhaler®) to reduce oropharyngeal deposition. Severe cases may need treatment with antifungal lozenges. Hoarseness and dysphonia may occur, and this may be due to atrophy of vocal cord tissues or a localised myopathy of the vocal cord musculature. This is reversible on reducing the dose, using a spacer device or withdrawal of treatment. Systemic side effects are seen in high dosage. Both drugs can cause suppression of the hypothalamic-pituitary-adrenal (HPA) axis (usually at dosages >1500µg/day for BDP and >1600µ g/day for BUD in adults). Suppression of the HPA axis has been seen in children taking 800 µg/day of BDP but there has been no convincing evidence of growth suppression. Although HPA axis is known to occur, no serious effects due to acute glucocorticoid deficiency has been reported in patients taking these drugs. Because most of the systemic activity is due to absorption via the lungs, the use of spacer devices may not prevent this, and may actually increase delivery to the lungs. Recently, there have been reports of increased bone turnover in normal subjects taking BDP but not BUD, which may lead to osteoporosis in long term use. Other systemic effects that have reported include increased easy bruising and dermal thinning and possibly cataract formation. It should be noted that systemic effects may be common with BDP rather than BUD because of the faster systemic clearance of BUD with the formation of inactive metabolites.

Further Reading

Ali NJ, Capewell S, Ward MJ. Bone Turnover during high dose inhaled corticosteroid treatment. Thorax. 1991;46:160-4.

Bisgaard H, Nielson M, Andersson B, Andersson P, Foged N, Fuglsarg G, et al. Adrenal function in children with bronchial asthma treated with beclomethasone dipropionate or budesonide. Journal of Allergy and Clinical Immunology. 1988;81:1088-95.

Boe J, Rosenhall L, Alton M, Carlsson LG, Carlsson U, Hermansson BA, et al. Comparison of dose-response effects of inhaled beclomethasone dipropionate and budesonide in the management of asthma. Allergy. 1989;44:349-55.

Brown PH, Blundell G, Greening AP, Crompton GK. Hypothalamo-pituitary-adrenal axis suppression in asthmatics inhaling high dose corticosteroids. Respiratory Medicine. 1991;85:501-10

Capewell S, Reynolds S, Shuttleworth D, Edwards C, Finlay AY. Purpura and dermal thinning associated with high dose inhaled corticosteroids. British Medical Journal. 1990;300:1548-51.

Ebden P, Jenkins A, Houston G, Davies BH. Comparison of two high-dose corticosteroid aerosol treatments, beclomethasone dipropionate (1500mcg/day) and budesonide (1600mcg/day), for chronic asthma. Thorax. 1986;41:869-74.

European Journal of Respiratory Disease. 1982;63 (Suppl 122).

Gordon ACH, McDonald CF, Thomson SA, Frame MH, Pottage A, Crompton GK. Dose of inhaled budesonide required to produce clinical suppression of plasma cortisol. European Journal of Respiratory Disease. 1987;71:10-4.

Reed CH. Aerosol Glucocorticoid Treatment of Asthma. American Review of Respiratory Disease. 1990; 141:S82-S88.

Smith M.J., Hodson M.E. High-dose beclomethasone inhaler in the treatment of asthma. Lancet 1983i:265-9.

Stead RJ, Cooke NJ. Adverse effects of inhaled corticosteroids. British Medical Journal. 1989;298:403-4.

Toogood JH. Complications of topical steroid therapy for asthma. American Review of Respiratory Disease. 1990; 141:S89-S96.


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