Corticosteroids act in asthma and COPD to reduce the inflammatory response in the airways.
Corticosteroids have an anti-inflammatory effect in many tissues. Virtually all cells contain steroid receptors which then bind to DNA to prevent or induce gene expression.
In the context of inflammation, corticosteroids:
- Decrease neutrophil and macrophage recruitment and action
- Decrease fibroblast formation
- Decrease osteoblast and increase osteoclast activity
- Decrease production of prostanoids
- Decrease production of cytokines
- Decrease histamine release
- Decrease IgG production
This reduces oedema and mucus production in the airways as well as inhibiting allergic reactions.
Beclometasone and budesonide have poor membrane penetration properies, making them useful for topical / local therapy with minimal systemic absoption.
There are a wide range of adverse effects, which are associated with systemic absorption. These include:
- Osteoporosis
- Ischaemic necrosis of femoral head
- Cataract
- Acute Glaucoma
- Cushingoid features including weight gain
- Increased susceptibility to infection, particularly TB, varicella and candida
- Hyperglycaemia potentially leading to type 2 diabetes mellitus.
- Hypertension
- Fluid retention and worsening of heart failure
- Hypokalaemia
- Mask inflammatory response
- Mental disturbance including psychosis
- Addisonian crisis in abrupt withdrawal
Patients admitted to hospital who are treated with long term oral steroids should be treated as if they have Addison's disease.
Pharmacokinetic interactions can occur between liver enzyme inducers and corticosteroids, reducing the effect of the steroids.
Pharmacodynamic interactions can occur where steroid effects increase or antagonise the effect of other drugs. For example:
- Steroids can mask the adverse effects of NSAIDs.
- Hypokalaemia can be made worse if steroids are used in combination with other drugs which lower potassium.
- Antihypertensive and hypoglycaemic agents are antagonised by corticosteroids.
Many asthmatic patents receive dual therapy with corticosteroids and β2 agonists. Ensure the patient understands that short acting β2 agonists only relieve the symptoms of asthma, patients often referred to this as a 'reliever'. In comparison corticosteroids are referred to as a 'preventer'. To achieve maximum efficacy, it is important to stress the different roles these drugs play in the treatment of asthma.
Patients should be informed that it can take several days for inhaled corticosteroids to take effect and so, they should continue taking them even if there is no immediate difference in symptoms within the first few days.
Inhaled corticosteroids need to be taken regularly to gain maximum benefit, therefore patient compliance is very important.
Whilst side effects with inhaled corticosteroids are uncommon, some patients may be at an increased risk of oral thrush. Therefore, it is recommended that patients rinse their mouths with water after taking their inhaled corticosteroids.
Ensure that the patent knows how to use an inhaler device (+/- spacer) correctly. Ask them to demonstrate how to use it.
Patients prescribed long term corticosteroids should be provided with a "steroid card" (pictured) and warned not to stop their medication suddenly. In instances where corticosteroids are used for more than 3 weeks, or in multiple short courses, or at very high doses, patients should be given a reducing regime.
Oral steroids are best taken in the morning to match the body's normal diurnal variation.
All patents with asthma require an annual asthma review, with either a doctor or asthma nurse specialist.

There is no dosage adjustment required in hepatic or renal insufficiency.