Atopic dermatitis (AD) is a common condition that affects more than one in ten children, and the incidence is increasing. There are probably several reasons for this, including higher exposure to air pollution, smaller families with less exposure to infections, more pets, higher maternal age, a wider range of foods, and the practice of evidence-based medicine. There is clearly also an important hereditary component to atopic eczema. This is complex because not all affected children are atopic, though the genes implicated in atopy are likely to be involved, together with others as yet unknown. AD usually presents during the first year of life, and when it is severe it is extremely disabling. It may also cause major psychological problems. (1) Most affected children are also allergic to house dust mite, and this is probably a major cause of exacerbation of the condition. Probably less than 10% overall have IgE mediated food allergy, but some have late phase reactions with positive results on patch tests to foods.

Several observations suggest that AD is the cutaneous manifestation of a systemic disorder that also gives rise to asthma, food allergy, and allergic rhinitis. These conditions are all characterized by elevated serum IgE levels and peripheral eosinophilia. AD is often the initial step in the so-called "atopic march," which leads to asthma and allergic rhinitis in the majority of afflicted patients. (2.4) In experimental models of AD, the induction of allergic skin inflammation by epicutaneous application of allergens has been found to augment the systemic allergic response and airway hyperreactivity characteristic of asthma. At least two forms of AD have been delineated: an "extrinsic" form associated with IgE-mediated sensitization involving 70-80% of the patients, and an "intrinsic" form without IgE-mediated sensitization involving 20-30% of the patients. Both forms of AD have associated eosinophilia. In extrinsic AD, memory T cells expressing the skin homing receptor, cutaneous lymphocyte-associated antigen (CLA), produce increased levels of Th2 cytokines. These include IL-4 and IL-13, which are known to induce isotype switching to IgE synthesis, as well as IL-5, which plays an important role in eosinophil development and survival. These CLA+ T cells also produce abnormally low levels of IFN- , a Th1 cytokine known to inhibit Th2 cell function. Intrinsic AD is associated with less IL-4 and IL-13 production than extrinsic AD. (5)

AD is usually the first manifestation of atopy and may coincide with food allergy; asthma often follows, then allergic rhinitis. There is a wide spectrum of presentations of atopic eczema, from minimal flexural eczema to erythroderma. The skin of a child with eczema is generally dry. Dryness of skin or xerosis is the hallmark of atopic dermatitis in children. The eczema can occur anywhere, but there are particular patterns that are more common at certain ages. The face is usually the first to be affected. In crawling infants the forearms, extensor aspects of the knees, and the ankle flexures are often the most affected. In older children the flexor aspects of the elbows and the knees are mostly affected. The eczema may be moist and weeping or may be thickened (lichenified) and dry. In Indian children with darker skin, the rash may have a papular nature. Scratch marks are always seen. The course of the condition fluctuates: causes of exacerbations may be evident but usually are not (particularly with reference to severe cutaneous reaction to mosquito bites). Infective complications are common. Staphylococcal infection may manifest as typical bullous impetigo or simply as a worsening of the eczema with increased redness and oozing. Staphylococcal folliculitis may occur as a result of occlusion from greasy emollients or wet dressings. Streptococcal infection may manifest as increased redness and erosion of the skin or as pustular lesions. Atopic children are particularly prone to severe widespread herpes simplex infections; the spread of the condition is mainly systemic but the areas most affected are the areas of active eczema. The child's life is limited by the constraints of care of the skin, which can separate the child from his or her peers. This can include sport, swimming, and dietary restrictions. The child feels unattractive and different and may have problems with self image and self confidence. Most children with eczema are atopic and are therefore allergic to inhalants such as house dust mite, grass pollens, and animal dander. Some children develop eczema on the face during the pollen season, and many parents report that their child's eczema is worse after close contact with pets. The highest proportion of IgE is produced against house dust mite and mosquitoes, and this must be the most important allergen in the exacerbation of eczema.(6) House dust mite is present in large numbers in children's beds and as well as causing asthma causes exacerbations of eczema. Several studies have shown that actions to reduce dust mite numbers are associated with amelioration of eczema. This is not surprising as in children highly allergic to the mites, skin contact is bound to have a deleterious effect on the eczema. The role of delayed hypersensitivity to house dust mite is also likely to be important. People with AD have positive results to patch tests and positive lymphoproliferative responses to the mite. Unfortunately, in everyday life minimization of house dust mite in bedding is difficult to achieve. In general, food allergy is caused by immunological mechanisms, food intolerance is not. Food intolerance is relatively common: certain chemicals in foods may cause worsening of the eczema for example, tartrazine or other colourings in food by mechanisms that are unclear. Food allergy is age dependent. It may be severe in the infant and become less so with age. Allergy to some foods (such as egg and cows' milk) is relatively transient, whereas allergy to peanuts or shellfish may continue throughout life.

The association between atopic eczema and food allergy is complex, though it is usually children with severe atopic eczema who have food allergy. Probably less than 10% of all children with atopic eczema have IgE mediated food allergy with Angioedema and urticaria, when the diagnosis is obvious from the immediacy of the symptoms and can be confirmed by a wheal more than 5 mm in diameter after a skin prick test. Some of these children have multiple food allergies. There is no doubt that IgE mediated food allergy can act as a trigger for exacerbations of eczema, but most parents recognize the allergy and the food is avoided. What is not clear is the role of late phase food reactions, which cause exacerbations of the eczema without urticaria or angioedema. These can be confirmed by atopy patch tests and food provocation tests. (7-9) This is receiving increasing attention. Woolen material in direct contact with the skin is a major irritant. Shiny nylon materials and some acrylics may irritate, but cotton-polyester mixtures are usually well tolerated. Soap in excess and bubble baths excessively dry the skin, and many perfumed and "medicated" products applied to the skin will cause irritation. Some of the plant extracts preparations favoured by alternative practitioners act as irritants or allergens and a query about the use of these should always be part of the history-taking.

Explanation and counseling are a vital part of the successful management of childhood eczema. Parents will have received a barrage of advice from a range of medical, paramedical, and non-medical "experts" and require a clear understanding of the nature of the condition, a long term management plan, and a realistic expectation of the results of treatment. Terminology is often confusing; the terms atopic eczema and atopic dermatitis are often used synonymously. It is essential to talk in terms of control rather than cure, otherwise parents will search for an end point after which care will no longer be required, and this is an unrealistic expectation. The condition should be explained as a multifactorial disorder, and it must be appreciated that just as there is no "cure" there is no single "cause." Often no explanation can be found for a particular flare up of the condition, and many factors are probably working in combination at all times.

Dealing with xerosis
Bath oils and products containing oatmeal are useful and prevent the drying of the skin that bathing can induce. Bath oils that contain antiseptic may have added benefit in certain cases but have a tendency to over-dry and sometimes actually irritate the skin. The child should have either a bath with additive or a short shower. It is essential to find a suitable moisturizer that can be applied all over twice a day whether or not there is active eczema. Creams containing moisturizing agents, emulsifying ointment, and creams or ointments with lanolin can be used. If a product stings the skin it must be abandoned. The most likely irritant in emollient creams is the stabilizer propylene glycol. Products that contain urea almost always sting broken skin and are unsuitable in these children.

Use of wet dressings
Wet dressings are useful in children with severe widespread eczema. This is essentially an inpatient procedure but can be used for short periods at home.(10) A water based emollient is applied all over; a corticosteroid cream (rather than ointment in this case because cream is more water miscible) is applied to the areas of active eczema. The creams are covered with a double layer of wrapping, the innermost of which is wetted with tepid water. The material may be cotton sheeting covered with a crepe bandage, though an easier alternative is the use of a double layer of tubular elasticized bandage. The procedure is repeated three times a day. This treatment is usually effective in clearing the eczema in three or four days.

Avoidance of allergens
House dust mite is the most important allergen. Avoidance measures have to be carried out assiduously and must include encasing the mattress and pillows as well as dealing with the top covers, either by encasement or by hot (>60°C) washing. If food allergy is suspected, the child should be referred to a pediatric dietician. In general, it is children with severe atopic eczema who have food allergy or food intolerance. Children with flexural eczema are unlikely to have food allergy, unless the history suggests otherwise.

Topical corticosteroids
It is often necessary to spend some time counseling the parents that topical steroid preparations used appropriately are safe. The strength chosen depends on the severity of the eczema and the site affected. The frequency of application depends on the individual product. The caution, however, is to be aware of steroid dependency which can be currently avoided/prevented by the use of topical calcineurin inhibitors (TCI).

Topical antibacterials
Staphylococcus aureus is commonly cultured from eczematous skin, and there may be obvious signs of infection. For localized infections, mupirocin, sisomycin, and fusidic acid ointment may be effective. To prevent infections it is useful to bathe the child in preparations containing triclosan or benzalkonium chloride. (11)

Topical immunosuppressants/ Topical calcineurin inhibitors
Tacrolimus is a potent immunosuppressive drug used in organ transplantation. A topical formulation has been shown to be effective in trials in patients with moderate to severe atopic dermatitis. Studies specifically related to childhood eczema have confirmed its efficacy. The main side effect is a sensation of burning. A concern has been raised as to whether application to skin exposed to sun could increase the long term risk of skin cancer. Pimecrolimus (an ascomycin derivative) is a newer immunosuppressive agent, similar to tacrolimus. Studies in children are very encouraging. The approval of topical calcineurin inhibitors for the treatment of AD represents a significant advance in our management options for this disease. (12-14) The distinction between pimecrolimus and tacrolimus is that the former is a cream while the latter is an ointment. Tacrolimus is currently marketed as an ointment that is more potent but also more irritating. Importantly, there are situations in which these topical calcineurin inhibitors (TCI) may be advantageous over topical corticosteroids and may be useful as first-line therapy. These would include treatment of patients who are poorly responsive to topical steroids or have steroid phobia, and treatment of face and neck dermatitis where ineffective, low-potency topical corticosteroids are usually used due to fears of steroid-induced skin atrophy. The potential use of topical calcineurin inhibitors as maintenance therapy is also intriguing for prevention of AD flares and progression of the atopic march. However, although systemic absorption of these compounds is low, there is a need for careful surveillance to rule out the possibility that skin cancers and increased viral skin infections will appear when such agents are used long term. One has to remember that TCIs are not a substitute for topical steroids. But when used in combination and as the solo therapy, TCIs are by far the best to give the early care and prevent flare.

Oral medications
Immunosuppressive drugs -
Severe atopic eczema is a serious condition, with huge loss of quality of life for the child on a par with juvenile rheumatoid arthritis. It is therefore essential that such children are treated adequately. The use of oral steroids should be avoided because of severe rebound of the eczema on withdrawal, the eczema becoming unstable after several courses, and the long term side effects. There are generally two alternatives for severe eczema, cyclosporin and azathioprine. Cyclosporin - Recent studies have confirmed the efficacy of cyclosporin (2 to 4 mg/Kg) in childhood atopic eczema. Regrettably the improvement is often not maintained after withdrawal of the drug. Continuous treatment is rarely justified in view of the long term risks (such as hypertension and renal dysfunction).(15,16) However, it has a place as an effective, safe, and well tolerated short term option for the management of severe refractory disease in children.

Azathioprine -
(1mg/Kg) is a safer drug for long term use, though it does have several side effects, including nausea, fatigue, myalgia, and liver dysfunction. It is essential to assay for thiopurine methyl transferase before treatment starts as children deficient in this enzyme will experience marked bone marrow suppression. In most children, it is effective at low dosage. The main long term side effect that could theoretically occur (as with cyclosporine) is the development of lymphoma. (17) The advantage of this drug is that it can be used continuously.

Other possibilities include the leukotriene inhibitors zafirlukast and montelukast, given orally (18,19) Chinese herbal medicines have also been used successfully but are not without danger. (20)

Antihistamines -
Sedating antihistamines such as promethazine given at bedtime are useful. The sedation is an important feature of their anti-pruritic action. It is still debatable whether non-sedating antihistamines such as cetirizine and loratadine are useful because generally the role of histamine in eczema is somewhat limited. However, a large study of the use of cetirizine in adults with atopic eczema showed a significant reduction of clinical manifestations in those treated. (21)

• Atopic dermatitis in children is a complex condition


• Four in five children with atopic eczema have IgE-mediated allergy to inhalants or foods


• House dust mite and mosquitoes exacerbates atopic dermatitis


• Food allergy exacerbates eczema in less than one in ten children


• To reduce the need for admission to hospital children with severe eczema can be treated with topical or oral immuno-suppression

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Last updated and Advance Access on 15-12-2007

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