This site is intended for health professionals only

At the heart of general practice since 1960

Need to know: Childhood eczema

Dr Malcolm Rustin answers questions from GP Dr Peter Stott

Dr Malcolm Rustin answers questions from GP Dr Peter Stott

The types of eczema for which causes are known are atopic eczema and allergic contact eczema. Identifying the offending allergen by patch testing and the subsequent removal of this allergen from the child's environment will cure the allergic contact eczema. The cause of atopic eczema is more complex and is undoubtedly multifactorial:

  • genetic ­ this provides the tendency for the child to develop the disease
  • immunological activation ­ increased IgE levels in 80 per cent of children and a shift to a Th2 pattern of lymphocyte inflammatory response
  • abnormal epidermal barrier function ­ increased water loss from the skin· allergy to dietary and airborne allergens ­ up to 40 per cent of children may have their atopic eczema triggered by a food
  • infection ­ frequent infection of lesional skin with Staphylococcus aureus contributes to the persisting inflammation of the skin
  • environment ­ the hygiene hypothesis suggests that reduced bacterial and viral infections in infancy prevent the normal development of a dominant Th1 lymphocyte phenotype and contribute to the development of atopy.

The prevalence of atopic eczema peaks at the age of two, whereas hay fever and asthma peak between 15 and 20. Preliminary evidence suggests that early aggressive treatment of atopic eczema may prevent development of the other two diseases.

Many different types of eczema can present in childhood. The common pathology consists of accumulation of fluid between keratinocytes (spongiosis and spongiotic vesicles in the epidermis), oedema of the papillary dermis and a perivascular predominantly lymphocytic infiltrate in the dermis. Children with an atopic diathesis (personal or family history of eczema, asthma or hay fever) have a greater tendency to develop:

  • pityriasis alba ­ hypopigmented scaly patches predominantly on sun-exposed areas of the body, cheeks, around the mouth, arms, trunk and less commonly on the legs
  • infantile seborrheoic eczema ­ this first appears as cradle cap with greasy scaling on the scalp and can extend to involve the skin behind the ears, on the neck and on the face. It can involve other flexural sites, axillae, umbilicus and groin. Usually this eruption clears in a few weeks but in an uncertain number of patients it may be the presenting feature and evolve into atopic eczema.
  • juvenile plantar dermatosis ­ presents as symmetrical erythematous (shiny, scaly, thickened and cracked skin on the forefoot), but may also involve the plantar surface of the toes and all the sole
  • pompholyx ­ characterised by the sudden appearance of vesicles on the palms or fingers (cheiropompholyx) and/or on the soles (podopompholyx). There are usually attacks of vesiculation followed by scaling and cracking of the affected areas
  • irritant eczema ­ this commonly presents as chapping on the cheeks or as a perioral dermatitis secondary to dribbling or thumb-sucking.

Allergic contact dermatitis can occur in any child and such a possibility should always be kept in mind with any child who has persistent eczema.

There is a strong suggestion that priming of the immune system and the tendency to develop atopic eczema occurs in utero. At birth, antigen-specific primed lymphocytes can be found in cord blood. Intervention studies in those families having a high risk of atopy in which probiotics are given to mothers during pregnancy and to the babies for the first six months of life have shown a reduced prevalence of atopic eczema. A diet free of cow's milk and eggs during pregnancy and after birth also seems to reduce the prevalence of atopic eczema.

There is no doubt that a number of children experience a flare-up of their eczema after exposure to food and so it is appropriate to exclude that food. The problem is how to identify such children and whether exclusions are instigated inappropriately, as without a dietitian's input there is a serious risk of nutritional deficiency. Personally I try to gain a history of worsening disease with exposure to foods but often this cannot be obtained. If children have widespread atopic eczema that is urticated and not responding to standard first-line therapy, then dietary exclusions could be implemented.

Unfortunately skin-prick tests and radioallergosorbent tests (RAST), which detect allergen-specific IgE antibodies, are unreliable, with false positive and negative results. Patch tests for foods may provide more useful information.

Patch testing is the only objective method of identifying allergens causing allergic contact eczema. Allergens in skin-care products (perfumes, cetearyl alcohol, quaternium-15, imidazolidinyl urea, propylene glycol, methylchloroisothiazolinone, ethylenediamine), in the leather of shoes (chromate), metal in studs and watches (nickel), topical antibiotics (neomycin), rubber (thiurams, carbamates) and topical steroids themselves are the commonest.

The patch test chemicals are expensive and have a limited shelf life. The reading of patch tests requires training and a detailed knowledge of chemicals that are currently in use and act as allergens. For these reasons I believe patch testing should be undertaken by dermatologists rather than by GPs.

There is no doubt that the type 1 immediate hypersensitivity reaction to peanuts (not a true nut) and to tree nuts (hazelnuts, almonds and brazil nuts) is becoming more common, with a prevalence of 0.8-1.5 per cent, and unfortunately it is usually lifelong. Development of peanut allergy has been noted to be more common in those children with an intake of soya milk and soya formula and having atopic eczema. It has been suggested therefore that children with atopic eczema should not be exposed to peanuts and arachis oil until the age of two. A positive skin-prick test or a high specific IgE is predictive for clinical allergy to peanuts.

Tacrolimus ointment 0.1 per cent and 0.03 per cent are indicated respectively for adults and children between the ages of two and 15 years as second-line treatment of moderate to severe atopic eczema that has not been controlled by topical steroids, where there is a serious risk of important adverse events, particularly irreversible skin atrophy. Pimecrolimus cream is recommended as second-line treatment of moderate atopic eczema on the face and neck only of children aged two to 16 that has not been controlled by topical steroids.

Both are particularly useful in areas such as the flexures and the face, where disease is often severe yet concerns over glaucoma, skin thinning and striae preclude the use of potent topical steroids. It is important parents understand the appropriate quantities of these topical immunomodulators to be applied: 1g should be applied to affected skin the size of an adult palm twice daily. Therapeutic failure with these treatments is invariably due to inadequate quantities being applied.

There is good evidence that treatment of excoriated atopic eczema with topical steroids results in healing of the affected skin even though swabs would invariably grow Staphylococcus aureus. If the eczema is impetiginised (yellow crusts on the surface) or is not settling with appropriate topical steroids then it would be appropriate to swab the sites and prescribe antibiotics such as flucloxacillin. (given for 7-10 days)

If the eczema is recurrently infected it would then be appropriate to undertake nasal swabs and if positive, institute appropriate eradication procedures. The problem with prolonged use of fucidin cream is not one of sensitisation but the organisms, particularly Staph Aureus, can become resistant to it.

Bath additives containing triclosan or benzalkonium chloride certainly reduce the bacterial load on the skin and are helpful if the eczema is recurrently infected however the skin infection must be thought of as a complication of untreated eczema and not the main cause of the eczema. Nevertheless there is increasing evidence that skin infections can be a contributory factor to the eczema. Short pulses of systemic steroids may be required in severe cases but in most cases they should be avoided.

Atopic eczema now affects up to 25 per cent of British schoolchildren and 2 to 10 per cent of adults. Many adults have relapses at some stage in their lives. Factors that may indicate a worse prognosis include severe childhood disease, early onset and a concomitant or family history of asthma or hay fever.

What I will do now

Dr Peter Stott responds to the answers to his questions

  • The answers to my questions support my belief that the earlier we gain control of a child's atopic problems, the better we can achieve long-term control.
  • It is interesting to learn of the evidence that even explosure to antigenic stimuli 'in utero' can play a part.
  • Eczema obviously has multifactorial origins. Avoiding factors elucidated by thehistory plus the judicious use of several different therapeutic approaches is obviously important.

Take-home points

  • The prevalence of atopic eczema peaks at the age of two and up to 40 per cent of children may have food as a trigger
  • Skin-prick tests and RAST are unreliable, with false positives and negatives. Patch tests for foods may be more helpful
  • Children with atopic eczema should not be exposed to peanuts or arachis oil until age two

Rate this article 

Click to rate

  • 1 star out of 5
  • 2 stars out of 5
  • 3 stars out of 5
  • 4 stars out of 5
  • 5 stars out of 5

0 out of 5 stars

Have your say