DERMATITIS (ECZEMA) PRINCIPLES OF TREATMENT Avoid precipitating factors Emollients Dry, fissuring Weeping, exudating Aqueous cream Emulsifying ointment Ichthammol and zinc cream (chronic lichenified eczema) Yes No Inflamed? The most common forms of dermatitis that present to physicians are atopic dermatitis, synonymous with atopic eczema, seborrhoeic dermatitis and contact dermatitis. An algorithm for treatment of dermatitis is shown in Figure 51.2. Management of atopic eczema should include avoidance of trigger factors and the use of emollients. Dry skin is a major factor and emollients should be used when bathing and applied as often as necessary. A simple emollient (an aqueous cream, e.g. E45 or Alpha Keri) is usually all that is necessary for dry, fissured scaly lesions. Inflammation should be treated with short courses of mild to moderate topical glucocorticosteroids. A more potent glucocorticosteroid may be required for particularly severely affected areas or for a more general flare up. Oral antihistamines are often effective in reducing pruritus. Ichthammol and zinc cream may be used in chronic lichenified forms of eczema. Potassium permanganate solution can be used in exudating eczema for its antiseptic and astringent effect; treatment should be stopped when weeping stops. Potassium permanganate solution Antibiotics (if secondary infection) Topical glucocorticosteroid (systemic if exfoliative) Continue till improved Healing? No Yes Consider UVB, PUVA, azathioprine, ciclosporin, mycophenolate mofetil SPECIALISTS ONLY DERMATITIS (ECZEMA) 413 Figure 51.2: Pathway for treatment of dermatitis. Weeping eczema may require topical glucocorticosteroids andoften antibiotics to treat secondary infection. Immunosuppressant therapy, such as ciclosporin, is sometimes effective in severe, resistant eczema. Ultraviolet B or psoralen � ultraviolet A (PUVA), or an immunosuppressive agent (e.g. azathioprine, ciclosporin or mycophenolate mofetil, Chapter 50) are also used. Seborrhoeic dermatitis may respond to a mild topical glucocorticosteroid. Scalp seborrhoeic dermatitis is often improved by coal tar, salicylic acid and sulphur preparations. (Fungal infection should be ruled out if there is no response.) Contact dermatitis is caused by external agents (e.g. nickel), but often complicates a pre-existing dermatitis. Avoidance of precipitating factors, emollients and topical glucocorticosteroids are used. GLUCOCORTICOSTEROIDS Topical glucocorticosteroids act as anti-inflammatory vasoconstrictors and reduce keratinocyte proliferation. They include hydrocortisone and its fluorinated semi-synthetic derivatives, which have increased anti-inflammatory potency compared to hydrocortisone (Chapter 40).
414 DRUGS AND THE SKIN Table 51.1: Topical glucocorticosteroids and their anti-inflammatory potency Potency Drug and strength Extremely potent Clobetasol (0.05%) Halcinonide (0.1%) Diflucortolone (0.3%) Potent Beclometasone (0.025%) Budesonide (0.025%) Fluocinolone (0.025%) Fluocinonide (0.05%) Moderately potent Clobetasone (0.05%) Flurandrenolone (0.0125%) Mild Hydrocortisone (0.5–2.5%) Alclometasone (0.05%) Methylprednisolone (0.25%) Uses The use of systemic glucocorticosteroids (e.g. oral prednisolone) is limited to serious disorders such as pemphigus or refractory exfoliative dermatitis (e.g. Stevens Johnson syndrome). Topical glucocorticosteroids are widely used and effective in treating eczema, lichen planus, discoid lupus erythematosus, lichen simplex chronicus and palmar plantar pustulosis, but rarely in psoriasis. The symptoms of eczema are rapidly suppressed, but these drugs do not treat the cause. In the presence of infection, they are combined with an antimicrobial agent. The lowest potency glucocorticosteroid preparation that will control the disease is preferred. Occlusive dressings should be used only in the short term (two to three days) and increase potency considerably. Potent fluorinated glucocorticosteroids should not be used on the face because they cause dermatitis medicamentosa. Many preparations are available, some of which are listed in descending order of anti-inflammatory potency in Table 51.1. Adverse effeccts of cutaneoulsly applied glucocorticosteroids These include the following: • hypothalamic–pituitary–adrenal suppression where very potent drugs are used long term on large areas of skin or when systemic absorption is increased under occlusive dressing; • spread of local infection – bacterial or fungal; • atrophic striae; • depigmentation and vellus hair formation; • perioral dermatitis when applied to the face; • rebound exacerbation of disease (e.g. pustular psoriasis) when treatment is stopped; • exacerbation of glaucoma if applied to the eyelids; • contact dermatitis (rare); • hirsutism and acne if systemic absorption is very high. PSORIASIS Psoriasis occurs in approximately 2% of the population. Its cause is unknown and no treatment is curative. The skin lesions are characterized by epidermal thickening and scaling due to increased epidermal undifferentiated cell proliferation with abnormal keratin. Figure 51.3 shows an algorithm for treatment. Therapy in mild cases consists of reassurance and a simple emollient cream. More resistant cases are treated with a keratolytic, e.g. salicylic acid, coal tar or dithranol applied accurately to the lesions. Topical and systemic steroids are reserved for cases that do not respond to these simple remedies and their use should be monitored by a specialist, as they can worsen the disease in some patients (e.g. pustular psoriasis on stopping treatment). Calcitriol (a vitamin D analogue) is effective topically. In some cases, therapy with PUVA (see below) is effective. Refractory cases are treated with oral retinoids (e.g. acetretin). Occasionally refractory cases justify immunosuppression with methotrexate (Chapters 48 and 50), but chronic use can cause cirrhosis. Potential recipients need to be warned about this and their liver function must be monitored meticulously. Ciclosporin is an alternative (Chapter 50), but causes hypertension and nephrotoxicity. Regular monitoring of blood pressure and plasma ciclosporin concentration is essential. Recently, the use of biological agents (alefacept, etanercept, efalizumab, infliximab) has been found to produce good remissions in otherwise refractory psoriasis (see Table 51.2); these agents are discussed more fully in Chapter 50. Secondline therapies (phototherapy or systemic drugs) should only be used under the supervision of a dermatologist. CALCIPOTRIOL (1-α, 24-DIHYDROXYVITAMIN D3) This analogue of vitamin D3 is used as a cream applied to mild to moderate psoriasis. Vitamin D receptors are present in keratinocytes, T and B lymphocytes and dermal fibroblasts of psoriatics, and the stimulation of vitamin D receptors on keratinocytes inhibits proliferation and differentiation. Adverse effects include local irritation, facial and perioral dermatitis, and possible hypercalcaemia and hypertriglyceridaemia if used too extensively. It should not be used in pregnancy. PSORALEN WITH ULTRAVIOLET A LIGHT Psoralen with ultraviolet A light (PUVA) is a well-established but somewhat inconvenient therapy for chronic plaque psoriasis. Psoralens intercalate DNA bases and, when activated by light, produce highly reactive oxygen species which sensitize the skin to the cytotoxic effects of long-wave UVA (320– 400 nm wavelength) radiation. Psoralen is taken orally two hours before phototherapy, or applied topically immediately before phototherapy; the usual course lasts for four to six weeks. Skin burning and ageing, cataracts and skin cancer are potential complications, especially with the higher total doses of UVA. Sunglasses are worn during UVA exposure in order to reduce the risk of cataract formation, if the psoralen has been administered orally. Technological advances in psoralens and