Atopic Dermatitis Knowledge Centre
Acute and long-term treatment options
Topical corticosteroids
Topical corticosteroids, first introduced in the 1950s, have been the mainstay of atopic dermatitis therapy for many years. Their mechanism of action is illustrated in Figure 3.
Figure 3. The mode of action of topical corticosteroids
Following topical application, the corticosteroid molecule crosses skin cell membranes and binds to, thus activating, specific glucocorticoid receptors in the cytoplasm. The steroid-receptor complex is then directed to the cell nucleus where it mediates its anti-inflammatory effects by two main actions. The expression of genes encoding anti-inflammatory proteins, such as lipocortin-1, is increased (transactivation) and, simultaneously, the expression of genes encoding pro-inflammatory mediators such as the cyclo-oxygenase and cytokines (interleukin [IL]-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-11, IL-13, tumour necrosis factor [TNF]-α, and granulocyte macrophage colony-stimulating factor [GM-CSF]), is decreased (transrepression). This has been shown to be effective for the short-term treatment of flares in atopic dermatitis patients.
Different drugs of this class have different potencies, depending on the compound used and the concentration of the active ingredient. In general, topical corticosteroids of mild or moderate potency are prescribed initially and the more potent formulations are reserved for severe flare management or for areas of skin which do not respond to the less potent drugs. Table 1 details the names and potencies of currently available topical corticosteroid drugs.
| Potency | Drugs | Strength formulations |
|---|---|---|
| Low |
Hydrocortisone Fluocinolone acetonide |
0.1%, cream, 0.5% cream & ointment, 1% lipocream 0.0025% cream |
| Medium |
Alclometasone dipropionate Betamethasone valerate Clobetasone butyrate Fludroxycortide Fluocinolone acetonide |
0.05% cream & ointment 0.025% cream & ointment 0.05% cream & ointment 0.0125% cream & ointment 0.00625% cream & ointment |
| High |
Hydrocortisone butyrate Betamethasone valerate Betamethasone dipropionate Diflucortolone valerate Fluocinolone acetonide Fluocinonide Fluticasone propionate Mometasone furoate Triamcinolone acetonide |
0.1% cream & lotion 0.1% cream & ointment 0.05% cream, ointment & lotion 0.1% cream & ointment 0.025% cream, gel & ointment 0.05% cream & ointment 0.05% cream & ointment 0.1% cream & ointment 0.1% ointment |
| Very high |
Clobetasol propionate Diflucortolone valerate |
0.05% cream, ointment, foam & shampoo 0.3% ointment |
*This list is not exhaustive but represents some selected examples.
Despite their effectiveness and tolerability in many patients, the use of topical corticosteroids carries several limitations. The primary concerns centre on adverse effects; the chances and severity of which generally increase in line with the potency of the drug used and the duration of therapy. Accordingly, it is recommended that topical corticosteroid use should be limited to short periods for acute atopic dermatitis, and up to 4–6 weeks to gain initial remission from chronic manifestations.10 In addition, repeated application of these drugs to sensitive areas of the skin, such as the skin around the eyes, is not recommended. In summary, the misuse of topical corticosteroids can cause serious adverse effects, and therefore less potent topical corticosteroid formulations are generally preferred for sensitive areas.
Although topical corticosteroids are clinically beneficial for short-term treatment, their long-term use is associated with a number of local and systemic side-effects. Local adverse effects include skin atrophy, acne, contact dermatitis and exacerbations of skin infections. Tachyphylaxis, where more drug is needed to elicit the same response, is also a potential concern with long-term corticosteroid use. Systemic effects associated with corticosteroid use may be very severe, and include disruption of the pituitary–adrenal axis and Cushing's syndrome.
© February 2010 Astellas Pharma Europe LTD.
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