For Patients

Skin – Atopic Dermatitis

Written by Dr Cassim Motala

Atopic dermatitis is a form of eczema that is most prevalent during infancy and childhood (paediatric cases: 80% by 1 year of age, 95% by years). The estimated incidence of atopic eczema in the general population varies between 1% and 5%. Over the past few decades there has been a steady increase worldwide in the incidence of this disorder.

Pathogenesis

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The exact pathogenesis of atopic dermatitis is unknown. Currently, it is believed that IgE-mediated reactions and cellular responses contribute to the chronic inflammation of this disorder. Atopic eczema typically runs a chronic course with exacerbations and remissions. A variety of ‘trigger factors’ may exacerbate eczema: irritants (e.g. soap, harsh chemicals), heat and humidity, stress and anxiety, certain foods, inhalant allergens and certain infections.

Eggs, milk, wheat, soya protein and peanut are the most common offending foods. Inhalant allergens such as house dust mite, pets, pollen and cut grass may also cause acute flare-up of eczema.

Patients with atopic eczema are highly susceptible to secondary bacterial (e.g. staphylococcal and streptococcal) and viral infections, (e.g. Warts, Molluscum contagiosum and Herpes simplex) and occasionally to fungal infections (e.g. Pitysporium ovale).

Infection in atopic dermatitis

Staphylococcus aureus (S. aureus) is a frequent cause of secondary infection in atopic dermatitis. S. aureus is not part of the normal resident flora of the skin. Patients with atopic dermatitis are colonised with S. aureus and the organism has been isolated from infected eczema, from chronic lesions and from clinically normal skin in patients with atopic dermatitis. S. aureus may also influence disease activity in the absence of overt clinical infection. S. aureus may exacerbate eczema by several mechanisms: protein A, contained in the S. aureus cell wall causes a biphasic reaction – an initial wheal and flare and a late indurated response when injected intradermally. Circulating antistaphylococcal IgE antibodies have been found in up to 30% of patients with atopic dermatitis and these may cause mast cell degranulation via an IgE-mediated reaction. S. aureus isolated from patients with atopic dermatitis has the ability to produce superantigens. These cause inflammation by activating T-lymphocyte and macrophages, release cytokine, cause mast cell degranulation and enhance IgE-mediated reactions.

Herpes simplex infections may result in eczema herpeticum which may progress to disseminated herpes infection (a potentially life-threatening condition).

Clinical Features

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Atopic eczema may be acute with erythema, scaling and vesicles or chronic with thickening, altered pigmentation and increased markings (lichenification). Severity of eczema is variable, ranging from localised mild scaling to generalised involvement with redness, oozing and secondary infection. Itching and scratching are the predominant symptoms. Scratching not only inflicts gross damage, perpetuating the itch/scratch cycle, but also disturbs other household members.

  

The distribution of the rash typically varies with age. (Plate 1 on page 121). In infancy (3 months to 2 years) the cheeks, wrists and extensor aspects of the arms and legs are usually involved. The entire body may be affected but the nappy area is usually spared. In young children (2 years to 12 years) flexor surfaces, the neck, wrists and ankles are generally involved. In teenagers and young adults flexural surfaces, the face (especially periorbital region), hands and feet are frequently affected.

  

Bacterial infection is usually recognised by crusting of the eczematous lesions. Pustules are generally less common except with infections of the palms and soles. A subgroup of patients with infected eczema who may be clinically distinct are those with diffuse erythema of a characteristic beefy red colour. These features are very suggestive of streptococcal infection. Patients with eczema complicated by streptococcal infection are at risk for developing acute glomerulonephritis.

  

A high index of suspicion is needed for the diagnosis of herpes simplex infection in patients with atopic eczema. Typical herpetic lesions are vesicular, but in patients with eczema the blisters have often ruptured, leaving discreet characteristic punched out ulcers. Herpetic lesions in atopic dermatitis are much more widespread than the typical herpes labialis seen in non-atopic people. Herpetic infection may also affect other sites, including the flexures and genital area. A few have widespread involvement: Kaposis varicelli form eruption. Severity of herpes simplex infection is not necessarily related to severity of the eczema. Patients with mild eczema can have herpetic infection that is severe and recurrent.

Natural History

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Atopic dermatitis usually becomes less severe in the teens, and may be completely “outgrown” around puberty. The majority of these patients will remain asymptomatic apart from possible hand dermatitis due to contact with irritants such as detergents and oils. However, eczema may relapse in some patients around the age of 20; the reason for this is unclear, but it might be associated with infectious mononucleosis infection causing immunomodulation. If atopic dermatitis continues into the third, fourth and fifth decade, it is commonly “outgrown” at the menopause in females. It is rare for atopic dermatitis to continue into old age, but when it does it is often severe and widespread.

Diagnosis

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The diagnosis rests primarily on clinical evaluation. The main features include the extreme pruritic nature of the rash, its typical morphology and distribution, and its tendency towards a chronic or relapsing course. No routine laboratory test is helpful in making the diagnosis of atopic dermatitis. Peripheral blood eosinophilia, elevated total serum IgE concentrations and specific IgE antibodies to foods and inhalants (skin prick testing or RAST tests) are present in about 80% of children with atopic dermatitis. Allergic contact dermatitis and infantile seborrheic dermatitis may be mistaken for atopic dermatitis. Differences between atopic dermatitis and the other two disorders are listed in Table 1.

Table 1

Differences between seborrhoeic dermatitis, atopic eczema and Contact dermatitis

 

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	Infantile seborrhoeic dermatitis	Atopic eczema		Allergic contact dermatitis
Age	<3 months	>2-3 months	Any – NB. Infrequent in children
General Condition	Good	Irritable	Good
Pruritus	Nil	++++	+++
Sleep	Normal	Restless	Usually normal
Distribution ofRash	May involve nappy area	Nappy area usually spared	Localised to certain areas of the body.(indicate particular irritant factors)
F/H Atopy	Usually negative	Often positive	Usually negative
Skin test o RAST	Usually negative	Positive (80%)	Negative NB.Patch Test +ve
Prognosis	Self-limiting Clears in few Weeks	Chronic rash waxes and wanes	Usually clears up when cause removed