VOLUME 21 : NUMBER 1 : January 1998
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Corticosteroids are extremely useful in the treatment of skin disorders. Topical applications are mainly used as the drug is delivered directly to the target organ. The dose can easily be titrated according to response. Intralesional and systemic corticosteroids are warranted in certain circumstances. The newer generation of corticosteroids have improved efficacy, but are not entirely free of adverse reactions. For maximum benefit and minimal adverse effects, various factors have to be taken into account, including the nature of the disease, age of the patient, site affected, and the pharmacology of the corticosteroids and the vehicle.
Key words: skin, vehicle, adverse effects.
Aust Prescr 1998;21:9-11
Dermatology is one of the few disciplines in which we are able to apply therapy directly to the target site. The concentration, the vehicle and the frequency of application can all be altered according to the response, which can easily be monitored.
Corticosteroids have an important role because of their anti- inflammatory and immunosuppressive effects and also their anti-proliferative effects on keratinocytes. They can suppress collagen synthesis by fibroblasts, but this may lead to adverse effects. Conversely, this effect can help in the treatment of keloid scars.
Corticosteroids can also be given orally, parenterally or by injection into the lesion.
Since its introduction in the early 1950s, hydrocortisone has revolutionised dermatology. Modifications to the chemical structure have led to enhanced efficacy, but also more adverse effects.
The vasoconstrictor assay is the primary method of classifying the potency of topical steroids (Table 1). This correlates with clinical efficacy.
The efficacy and possible adverse effects depend on:
- steroid type and the vehicle
- application method - frequency, duration and use under occlusion
- nature and extent of the skin disease
- patient factors - age, site of the disease
All these factors have to be taken into account to obtain the maximum benefit with the minimum adverse effects.
In general, acute inflammatory eruptions respond well to mild/moderate strength topical steroids (Class I and II). Chronic, thickened or hyperkeratotic dermatoses may require potent or very potent steroids (Class III and IV). Table 2 lists the corticosteroid-responsive skin diseases according to likely response. The less responsive the disease, the greater the potency of the corticosteroid that may be required.
For a given strength of the same steroid, ointments are more potent than creams. The occlusive nature of ointment enhances steroid penetration. Ointment is often used for dry, fissured and lichenified skin disease because of its moisturising effect.
Creams (oil in water emulsions) may be drying and thus more suitable for acute and subacute weeping lesions. They are the most suitable vehicle for the moist and intertriginous (flexural) areas. Creams require the addition of emulsifiers and preservatives that have the potential to sensitise and cause allergic reactions.
For the scalp, steroids are often delivered in a lotion or gel. These vehicles lack the moisturising benefit of either creams or ointments. Propylene glycol can act as a penetration enhancer. By using it in a vehicle, the delivery of the topical steroid can be increased.
A classification of the potency of commonly used topical corticosteroid preparations
Class I - mild
|hydrocortisone||0.5 - 1.0%|
|hydrocortisone acetate||0.5 - 1.0%|
|Class II - moderate|
|Class III - potent|
|Class IV - very potent|
|betamethasone dipropionate||0.05% in an optimised vehicle|
A guideline of cutaneous diseases for which corticosteroids are used, and the likely clinical response
|Most responsive||Less responsive||Least responsive|
|Acute inflammatory disease including:||Psoriasis - plaque||Palmoplantar psoriasis|
|- allergic contact dermatitis||Seborrhoeic dermatitis||Discoid lupus erythematosus|
|- atopic eczema||Lichen simplex chronicus||Chronic hypertrophic lichen planus|
|- asteatotic eczema||Lichen planus||Granuloma annulare|
|- discoid eczema||Subacute cutaneous lupus erythematosus||Keloid scars|
|- napkin dermatitis||Papular urticaria (insect bite reactions)|
The efficacy of steroids can be increased by application under occlusion. This increases hydration of the skin and enhances penetration. However, there is an increased risk of adverse effects if the use of steroid under occlusion is prolonged. The occluding materials can include polythene gloves, plastic film (such as 'Gladwrap') and bio-occlusive dressings e.g. hydrocolloid.
Region or sites
The thickness of the stratum corneum, local occlusive factors, warmth and moisture are among the factors that can increase corticosteroid penetration and also the risk of adverse effects. In descending order of ease of penetration are mucous membrane, scrotum, submammary, axillary and perineal flexures, eyelids, face, chest and back, upper arms and legs, lower arms and legs, dorsum of hands and feet, palmar and plantar skin and nails.1
As a rule, Class I steroids are preferred for the face and flexures. If a stronger corticosteroid is required, short-term (1-2 weeks) use is recommended. In contrast, palms and soles tend to require Class III or IV steroids as there is a thick stratum corneum and frequent accidental removal of the steroid may occur. On occasion, two or more different formulations may be required for different regions of the body.
Infants have an increased body surface to weight ratio. Premature babies and the elderly have relatively thin skin so steroid penetration is enhanced. The lower potency steroids are used first in this group. Particular care should be given when steroids are used in the nappy area.
If treatment involves application to a large proportion of the body surface area, low- to medium-strength steroids are preferred because of the risk of extensive absorption.
1. Topical steroids should be stopped when the skin disease has resolved. They are not used for prevention of disease.
2. If possible, intermittent therapy is preferred to continuous application for long-term use. This is to reduce both tachyphylaxis and the risk of adverse effects.
3. Prolonged use should be avoided, where possible, on the face and the flexures.
4. Some people benefit from using a more potent steroid first and then changing to a lower potency as the condition improves.
In general, the greater the potency, the greater the risk of adverse effects (Table 3).
Systemic adverse effects may occur with the use of topical steroids. The risk factors include use in infants and children, prolonged and extensive use, use of high-potency steroids, use over large areas and use under occlusion. The adverse effects include the standard ones of adrenal suppression, growth retardation, Cushing's syndrome and hypertension. Cataracts and glaucoma have been reported with periorbital use.
The steroid is injected directly into the lesion. The common indications include recalcitrant lesions of nodular prurigo, keloid scars, acne cysts, discoid lupus erythematosus, hypertrophic lichen planus, alopecia areata and granuloma annulare.
Triamcinolone acetonide is most often used. It can be diluted with normal saline or lignocaine and is delivered in volumes of 1-2 mL. The concentration used depends on the pathology and skin site. Generally, one commences with a concentration of 5 mg/mL working up to the full concentration of 40 mg/mL, if necessary, when there is no response. If required, the injection can be repeated every 4-6 weeks. The adverse effects include pain, secondary infection, telangiectasia, leucoderma and dermal atrophy. Systemic adverse effects are rare unless large quantities are used. Intralesional steroids are not used for epidermal conditions. Care is required to introduce the steroid deep into the dermis to avoid epidermal atrophy, as well as dermal atrophy in those conditions where there is not a grossly thickened dermis. In the case of keloid, atrophy of the dermis following the use of treatment is unlikely to be a problem.
Adverse effects related to topical corticosteroids
Skin atrophy, stellate scar and striae
Steroids are required systemically for:
- acute and chronic disabling bullous disorders including pemphigus vulgaris, bullous pemphigoid, pemphigoid gestationis
- connective tissue diseases - systemic lupus erythematosus, dermatomyositis, Wegener's granulomatosis, relapsing polychondritis
- acute steroid sensitive disorders, e.g. severe acute allergic contact dermatitis where the allergen is known and can be avoided to prevent relapse on cessation of steroids
- severe, widespread, inflammatory atopic eczema where acute control is required (care is necessary on cessation of the oral steroids to prevent a widespread severe relapse)
- others - severe lichen planus, urticaria, pyoderma gangrenosum, Sweet's disease, Behcet's and severe vasculitis
Oral steroids are perfectly satisfactory in the majority of dermatology patients who are rarely ill enough to require either intramuscular or intravenous administration.
Topical steroids, if the correct potency and base are selected, play an important role in management of skin diseases. They have a beneficial effect, particularly in inflammatory skin diseases. They also have adverse effects, such as dermal atrophy, which may be used with benefit on occasion e.g. in intralesional treatment of keloids.
With experience, a satisfactory therapeutic ratio should be able to be obtained by all practitioners in treating most skin conditions. This will ensure their use for the maximum benefit and the minimal chance of adverse effects.
(See also Dental implications )
Drake LA, Dinehart SM, Farmer ER, Goltz RW, Graham GF, Hordinsky MK, et al. Guidelines of care for the use of topical glucocorticosteroids. American Academy of Dermatology. J Am Acad Dermatol 1996;35:615-9.
Werth VP, Lazarus GS. Systemic glucocorticoids. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, editors. Dermatology in general medicine. New York: McGraw-Hill, 1993:2859-64.
Griffiths WA, Wilkinson JD. Topical therapy. In: Champion RH, Burton JL, Ebling FJ, editors. Textbook of dermatology. 5th ed. Oxford: Blackwell, 1992: 3037-84.
Reynolds JE, editor. Martindale. The extra pharmacopoeia. 31st ed. London: Royal Pharmaceutical Society, 1996.
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