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An overview of atopic dermatitis


Eczema, or  atopic dermatitis, is a common inflammatory disease of the skin. The condition often has its start in childhood and follows a variable and sometimes unremitting course. Historically, this disease has been considered a part of a triad of “atopy” that included asthma and allergic rhinitis, though this association has recently come into question.


Although not a cause of significant mortality, the visible and chronic nature of eczema can be a source of emotional stress.

Good evidence indicates that genetic factors are important in the development of atopic dermatitis, but the pathophysiology is still poorly understood. Two main hypotheses have been proposed regarding the development of the inflammatory lesions. The first suggests an immune dysfunction resulting in IgE sensitisation and a secondary epithelial-barrier disturbance. The second proposes a defect in epithelial cells leading to the defective barrier problem, with the immunological aspects being epiphenomena.

The epidermis is the first line of defense between the body and the environment and, when intact, shields the body from a variety of irritants, allergens, and microbes. This barrier, which is maintained by differentiated keratinocytes and structural proteins, can be compromised by inheritance, trauma, decreased humidity, change in pH, and infection.

Atopic skin additionally has diminished ability to retain water; this dry skin leads to scratching, which further contributes to the release of pro-inflammatory mediators. Eczema is a biphasic T cell mediated disease: TH2 is more prevalent in the acute phase, and TH1 predominates in the chronically affected skin. Patients with atopic dermatitis have elevated serum IgE levels, peripheral eosinophilia, and overall greater numbers of immune mediators and cytokines.

Incessant itch and work loss in adult life is a great financial burden. A number of studies have reported that the financial burden to families and government is similar to that of asthma, arthritis, and diabetes mellitus. In children, the disease causes enormous psychological burden to families and loss of school days. Mortality due to atopic dermatitis is unusual, however.

The prevalence rate of atopic dermatitis is rising, and it affects 15-30 per cent of children and two-10 per cent of adults. This figure estimates the prevalence in developed countries.

Bacterial infection with Staphylococcus aureus or Streptococcus pyogenesis is not infrequent in the setting of atopic dermatitis. The skin of patients with atopic dermatitis is colonised by S.aureus. Colonisation does not imply clinical infection, and physicians should only treat patients with clinical infection. Eczematous and bullous lesions on the palms and soles are often infected with beta-haemolytic group A Streptococcus.

Incessant pruritus is the only symptom of atopic dermatitis, children often scratch themselves uncontrollably.  Although pruritus may be present in the first few weeks of life, parents become more aware of the itch as the itch-scratch cycle matures when the patient is aged approximately three months. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons.

Primary findings of atopic dermatitis include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common. The eczematous changes and its morphology are seen in different locations depending on the age of the patient.


• Atopic dermatitis is usually noticed soon after birth. Xerosis occurs early and often involves the whole body; the diaper area is usually spared.

• The earliest lesions affect the creases (antecubital and popliteal fossae), with erythema and exudation. Over the following few weeks, lesions usually localise to the cheeks, the forehead and scalp, and the extensors of the lower legs; however, they may occur in any location on the body, usually sparing the nappy area. Lesions are ill-defined, erythematous, scaly, and crusted (eczematous) patches and plaques.

• Lichenification is seldom seen in infancy.


• Xerosis is often generalised. The skin is flaky and rough.

• Lichenification is characteristic of childhood atopic dermatitis. It signifies repeated rubbing of the skin and is seen mostly over the folds, bony protuberances, and forehead.

• Lesions are eczematous and exudative. Pallor of the face is common; erythema and scaling occur around the eyes. Dennie-Morgan folds (i.e., increased folds below the eye) are often seen. Flexural creases, particularly the antecubital and popliteal fossae, and buttock-thigh creases are often affected.


• Lesions become more diffuse with an underlying background of erythaema. The face is commonly involved and is dry and scaly.

• Xerosis is prominent.

• Lichenification may be present.

• A brown macular ring around the neck is typical but not always present. It represents localised deposition of amyloid.


Patients with atopic dermatitis do not usually require emergency therapy, but they may visit the emergency department for treatment of acute flares caused by eczema herpeticum and bacterial infections. For further information on treatment, see the NICE guidelines on treating atopic eczema in children.

Moisturisation in atopic dermatitis

Depending on the climate, patients usually benefit from five-minute, lukewarm baths followed by the application of a moisturiser such as white petrolatum. Frequent baths with the addition of emulsifying oils (one capful added to lukewarm bath water) for five-10 minutes hydrate the skin.

The oil keeps the water on the skin and prevents evaporation to the outside environment. In infants, three times a day is not a great burden; in adults, once or twice a day is usually all that can be achieved. Leave the body wet after bathing. Advise patients to apply an emollient all over the body while wet, to seal in moisture and allow water to be absorbed through the stratum corneum. The ointment spreads well on wet skin. The active ingredient should be applied before the emollient.

Topical steroids in atopic dermatitis

• Topical steroids are currently the mainstay of treatment. In association with moisturisation, responses have been excellent.

• Ointment bases are preferred, particularly in dry environments.

• Initial therapy consists of hydrocortisone one per cent powder in an ointment base applied three times daily to lesions on the face and in the folds.

• A mid-strength steroid ointment (triamcinolone or betamethasone valerate) is applied two-three times daily to lesions on the trunk until the eczematous lesions clear.

• Steroids are discontinued when lesions disappear and are resumed when new patches arise.

• Flares may be associated with seasonal changes, stress, activity, Staphylococcal infection, or contact allergy.

• Contact allergy is rare but accounts for increasing numbers of flares. These are seen mostly with hydrocortisone.

• The results of a study from the Netherlands suggest that the use of topical corticosteroids for atopic dermatitis on the eyelids and periorbital region is safe with the respect to induction of glaucoma or cataracts.

References on request


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