Atopic individuals are predisposed to skin infections because of a compromised physical barrier, coupled with diminished immune recognition and impaired antimicrobial peptide production.

AD follows a relapsing course and is associated with elevated serum immunoglobulin( IgE) levels and a personal or family history of type I allergies, allergic rhinitis, and asthma. Most patients improve in summer and are worse in winter.

RISK FACTORS According to the updated American Academy of Dermatology guideline, two risk factors appear to be consistently and strongly associated with the development of atopic dermatitis: A family history of atopy and a loss of function mutations in the filaggrin( FLG) gene.

Approximately 70 % of AD patients have a positive family history of atopic diseases. The odds of developing AD are two- to three-fold higher in children with one atopic parent, and this increases to three- to five-fold if both parents are atopic.

TREATMENT The goals of treatment are to reduce symptoms( pruritus and dermatitis), prevent exacerbations, and minimise therapeutic risks. Standard treatment modalities for the management of these patients are centered around the use of topical anti-inflammatory preparations and moisturisation of the skin, but patients with severe disease may require phototherapy or systemic treatment.

Topical agents include topical

corticosteroids( TCS), calcineurin inhibitors( TCI), antimicrobials and antiseptics and antihistamines.

TOPICAL CORTICOSTEROIDS Topical corticosteroids( TCS) have been used to treat AD for more than 60 years. TCS are used in the management of AD in both adults and children and are the mainstay of antiinflammatory therapy.

TCSs are used for both active inflammatory disease and for prevention of relapses. They are typically introduced into the treatment regimen after failure of lesions to respond to good skin care and regular use of moisturisers alone.

TCS are grouped into seven classes, from very low / lowest potency( VII) to very high potency( I), based on vasoconstriction assays. TCSs are recommended for AD-affected individuals who have failed to respond to good skin care and regular use of emollients alone.

A variety of factors should be considered when choosing a particular topical corticosteroid for the treatment of AD, including patient age, areas of the body to which the medication will be applied, and other patient factors such as degree of xerosis, patient preference, and cost of medication.

Twice-daily application of corticosteroids is generally recommended for the treatment of AD, however, evidence suggests that once-daily application of some corticosteroids may be sufficient.

Proactive, intermittent use of TCS as maintenance therapy( one to two times weekly) on areas that commonly flare is recommended to help prevent

relapses and is more effective than use of emollients alone.

No universal standard exists for quantity of application, although suggested methods include use of the adult fingertip unit( the amount from the distal interphalangeal joint to the fingertip, or approximately 0.5g, being applied over an area equal to two adult palms), following the rule of nines that measures the percent affected area, and use of charts that propose amounts based on patient age and body site.

Children have a proportionately greater body surface area to weight ratio, and as a result, have a higher degree of absorption for the same amount applied. But during significant acute flares, the use of mid- or higherpotency TCS for short courses may be appropriate to gain rapid control of symptoms, even in children.

However, for long-term management, the least-potent corticosteroid that is effective should be used to minimise the risk of adverse effects.

Greater caution regarding TCS potency is also needed when treating thin skin sites( e. g. face, neck, and other skin folds), where there is greater penetration and higher likelihood for systemic absorption. It is important to monitor quantities of TCS used over time, which may impact efficacy and safety.

TOPICAL CALCINEURIN INHIBITORS

Topical calcineurin inhibitors( TCI) are a second class of anti-inflammatory therapy introduced in 2000. They are naturally produced by Streptomyces bacteria and inhibit calcineurindependent

T-cell activation, blocking the production of proinflammatory cytokines and mediators of the AD inflammatory reaction.

They have also been demonstrated to affect mast cell activation, and tacrolimus decreases both the number and costimulatory ability of epidermal dendritic cells.

Two TCIs are available, topical tacrolimus ointment( 0.03 % and 0.1 % strengths) and pimecrolimus cream( 1 % strength). Both agents have been shown to be more effective than vehicle in short-term( three to 12 weeks) and long-term( up to 12 months) studies in adults and children with active disease.

Physician global evaluation scores showed decline, as did the percent body surface area involved and patient evaluation of symptoms and signs of disease. Tacrolimus is approved for moderate to severe disease, whereas pimecrolimus is indicated for mild to moderate AD, and six-week comparative studies support a greater effect for tacrolimus over this time period for all AD severities.

In the US, TCIs are approved as second-line therapy for the short-term and non-continuous chronic treatment of AD in non-immunocompromised individuals who have failed to respond adequately to other topical prescription treatments for AD, or when those treatments are not advisable.

TCIs have the benefit of not carrying risk for cutaneous atrophy, with little negative effect on collagen synthesis and skin thickness. TCI can therefore be used as steroid-sparing agents and long-term studies.

References available on request.