Skin Care World

The views expressed below are those of the author, and are not necessarily those of Mölnlycke Health Care.

Dr Ruwani Katugampola BM, MRCP, Specialist Registrar in Dermatology, Welsh Institute of Dermatology, University Hospital of Wales, Cardiff.

Dr Katugumpola graduated from the University of Southampton in 1998 and completed training at Southampton General Hospital before joining the South East Wales Medical Senior House Officer rotations to gain wider experience of dermatology. Dr Katugampola joined the Welsh Institute of Dermatology in March 2003 as a Specialist Registrar.

Atopic eczema (atopic dermatitis, AD) is a common inflammatory skin disease. It is characterised by dry itchy skin. AD mainly affects infants, children and young adults. The prevalence of AD has increased over the last few decades, affecting 5-15% of schoolchildren (1-2) More than two thirds of patients demonstrate the onset of the disease within the first year of life (3). Although usually not life threatening, AD has a significant effect on the quality of life of the affected child and their family.

At present there is no cure for AD. Therefore, the aim of treatment is disease control, patient and parent education, and improving the quality of life of patients and their families.

DIAGNOSIS OF ATOPIC ECZEMA

AD is a clinical diagnosis. The distribution of AD may vary in different age groups of patients. AD commonly affects the face, scalp and trunk in infants, and skin creases in older children.

Diagnostic criteria for atopic eczema (2)

Must have:
Itchy skin condition (scratching or rubbing in a child)

Plus three or more of the following:

• Itching in skin creases (or cheeks in children < 4 years)
• History of asthma or hay fever (or history of atopy in first degree relatives in children < 4 years)
• General dry skin in the past year
• Visible flexural eczema (or eczema affecting the cheeks or forehead and outer limbs in children < 4 years)
• Onset in the first two years of life (not always diagnostic in children < 4years)

AETIOLOGY OF ATOPIC ECZEMA

AD is thought to occur due to preferential activation of Th2 CD4 lymphocytes, epidermal defects and environmental influences in genetically predisposed individuals. (4-5)

In AD, there is damage to the barrier function of the skin, providing an opportunity for exogenous agents to penetrate the skin, and stimulate an inflammatory process. (6-7) Soap and detergents can exacerbate AD by removing the lipid layer of the epidermis and drying the skin. Dry skin causes itching, which leads to a vicious itch-scratch cycle with release of further inflammatory mediators.

The skin of patients with AD is often colonized by Staphylococcus aureus. The exotoxins released by these bacteria activate perpetuate the inflammatory process in AD. (8)

MANAGEMENT OF ATOPIC ECZEMA

Aims of atopic eczema management

• Patient and parent eductation
• Participation of patient and parents with treatment
• Maintaining long-term control of skin inflammation
• Restore epiderman lipid barrier
• Control acute flare
• Eliminate exacerbating factors<
• Discuss and alleviate anxieties regarding the disease or its treatment

In general, when treating AD, ointments are preferred for use on dry skin, and creams on acutely inflamed weepy skin. However, the individual child’s preference should be taken into account when prescribing these treatments. It is important to supply adequate quantities of topical preparations, and written instructions of the treatment regime to improve treatment compliance.

Emollients

Emollients are the mainstay of treatment in AD. It helps maintain the water content, reduce dryness and restore the barrier function of the skin. Emollients relieve the itch in AD, and help break the itch-scratch cycle. Emollients could also be used as soap substitutes and prevent the drying effect of conventional soap. It also has a steroid-sparing effect. (6) It is recommended that emollients be continued, at least twice daily, during and after a flare-up of eczema when topical corticosteroid treatment has been discontinued. (6-7)

Topical corticosteroids

Topical corticosteroids are used for short periods during acute flare-up of AD. The fingertip unit measurement is helpful when advising patients and parents the amount of topical steroids to use to a given surface area. (9) One fingertip unit is the amount of topical agent squeezed from a 5mm nozzle from the distal finger crease to the tip. This is equivalent to approximately half a gram, and adequate to cover both sides of one adult hand. However, infants and children under 10 years require much less topical corticosteroid per unit area.

The potency of topical corticosteroid used depends on the severity of the disease, the part of the body affected and the age of the patient. Most infants can be managed with mildly potent corticosteroids such as hydrocortisone 1%. Young children can be given moderately potent agents such as betamethasone valerate 0.025% or clobestasone butyrate during acute flare up of their AD. In older children short courses of more potent agents such as betamethasone valerate 0.1% can be used during severe disease. No more than mild (infants) and moderate (older children) potent corticosteroids should be used on body surfaces with thin skin such as the face.

Topical immunosuppressant agents

Tacrolimus (10) (0.1%, 0.03% ointment) and pimecrolimus (11) (1% cream) are topical immunosuppresasants that have recently been introduced as steroid-sparing agents for the treatment of AD. Both agents are licensed for use only in children 2 years and older under specialist supervision.

Only tacrolimus 0.03% is licensed for use in children between 2-16 years. It is licensed for use in moderate to severe AD involving 15-50% of body surface area, inadequately responsive to conventional therapy. Pimecrolimus is licensed for use in mild to moderate AD. In clinical studies, pimecrolimus has been shown to prevent disease progression and reduce the incidence of flares, suggesting that this maybe used for maintenance therapy of AD. The conflicting results from studies regarding the efficacy of these agentscompared to mild and potent topical corticosteroids warrants further investigation.

The advantages of these agents over topical corticosteroids are that they can be used on all body surfaces including the face, and lack the potential side effects of long-term topical corticosteroid use. The main side effect of these preparations is local discomfort after application. The risk of carcinogenicity in humans from topical immunosuppressants is still undetermined. Therefore, protection from exposure to excessive sunlight and ultraviolet light should be advised when these treatments are used. Occlusive bandaging should not be applied when using these topical agents.

Antibiotics

Combination of topical steroid (anti-inflammatory) and topical antibiotic (anti-Staph aureus, such as fusidic acid or mupirocin) has been proposed to prevent exacerbation of AD. (12) Systemic antibiotics (flucloxacillin, or erythromycin in penicillin allergy) maybe required in short courses during acute exacerbation of AD secondary to Staph aureus infection. If recurrent Staph aureus infection occurs, nasal and perineal swabs should be obtained from the patient and parents/carers. Carriers should be treated with topical mupirocin for about 10 days. (12)

Occlusive bandaging

Topical corticosteroids and/or emollients can be used under occlusive bandaging, to enhance its absorption. Therefore, it is important to use a less potent corticosteroid in these circumstances. Occlusive bandaging also helps break the itch-scratch cycle and is especially useful in children at bedtime. The bandages used maybe dry, or impregnated in zinc. More recently, bandages have been introduced as garments that are more acceptable to children.

Anti-histamines

In AD, anti-histamines are used for their sedative effect rather than for anti-pruritic effect. (13)

Treatment not routinely recommended for childhood atopic eczema

Systemic immunosuppressants, phototherapy and photochemotherapy are also not generally used in childhood AD.

Although exclusion diets have been shown to improve AD in some individuals (14), it is not recommended as part of routine management.

Oral Chinese herbal medicines have been shown to benefit children with extensive AD. (15) However, these medicines are hepatotoxic, and are not used in routine clinical practice.

The product license for evening Primrose oil in AD has recently been withdrawn as there is no convincing evidence that it improves AD.

FAILURE TO RESPOND TO TREATMENT

Failure to respond to treatment and/or deterioration of the condition may be due to poor treatment compliance or superimposed infection. The development of hypersensitivity to topical treatment is also possible, for example to the preservatives or to hydrocortisone itself. This can be confirmed with patch testing for these agents.

CONCLUSION

AD is a common chronic inflammatory skin disease seen in children. Emollients are the mainstay of treatment, with the use of short courses of topical corticosteroids to control acute flares. The absorption of these two agents can be enhanced by the use of occlusive bandaging. The topical immunosuppressant agents are an exciting new alternative to topical corticosteroids. The potential long-term side effects of all topical agents used in children with a chronic skin disease should be considered at all times.