ATOPIC DERMATITIS
(ATOPIC ECZEMA)

DERMATOLOGY LECTURE NOTES

Debabrata Bandyopadhyay,  Professor & Head,  Dept. of Dermatology,
 R G Kar Medical College, Calcutta, INDIA

Atopic dermatitis (AD) is an itchy, relapsing and recurring skin disease which predominantly affects infants and children. The clinical picture evolves in stages and the condition is frequently associated with a number of cutaneous, ocular, and other features, notably a raised immunoglobulin E (IgE) level and other atopic disorders like allergic rhinitis and asthma. There is a strong familial tendency in atopic disorders. There is no specific laboratory or clinical feature of atopic dermatitis, the condition is diagnosed by the presence of a constellation of symptoms and signs.
 

ETIOLOGY AND PATHOGENESIS

The precise cause of atopic dermatitis is not known. A complex interaction of genetic and environmental factors are believed to induce immunological and biochemical changes that produce the pruritic, inflammatory dermatosis.  

Genetic Factors:
Atopic dermatitis runs in families. The prevalence of AD in children is about 50% when on parent has AD, while it may be as high as about 80% when both parents have the disease  The precise mode of inheritance in not known, it is probably polygenic. Genetic factors may produce disease through abnormality in IgE synthesis, expression of IgE receptors on cells, or through cytokine production by leukocytes.  

Immunologic abnormalities:

	Functionally, there are two subsets of helper T lymphocytes: (a) TH1 cells which mainly produce interferon gamma, interleukin-2 and mediate cell-mediated immune response and (b) TH2 cells, that produce IL-4, IL-5, IL-6, and Il-10 and promotes antibody-mediated immune response. IL-4 induces IgE production and inhibits gamma interferon production and prevents differentiation of TH1 cells. In atopic dermatitis, there is a TH2 cell predominance which leads to increased IgE production by B lymphocytes and by its suppressive action of TH1 cells, diminishes cellular immune response.
	In response to various allergens, AD patients are genetically prone to produce high levels of IgE. IgE-mediated allergic reaction causes mediator release from mast cells, this reaction is biphasic, the immediate reaction producing redness and itching  and the delayed reaction may cause chronic inflammation.
	Langerhans cells of AD patients express high levels of IgE receptors, they capture specific allergens more avidly and present them to TH2 cells more efficiently.
	Tissue specificity of the TH2 cell response is explained by high CLA (cutaneous lymphocyte antigen) expression on circulating T cells that specifically home to the skin.
	Increased prostaglandin E2 (PGE2) secretion by monocytes of atopic dermatitis patients inhibits interferon gamma production, this inhibits TH1 cells.
	Monocytes of AD patients have increased Cyclic AMP-phosphodiesterase enzyme activity – this leads to increased IgE synthesis by B lymphocytes and release of histamine from basophils.
	Keratinocytes, injured by scratching may also secrete cytokines that helps migration of TH2 cells to the skin, thus modulation the immunological phenomenon.

Allergens:  

	Food: a subset of patients, particularly infants and children, may have hypersensitivity to foods, particularly to milk, peanuts, fruits , fish and soybeans.
	Aeroallergens: house dust mites, pollens, and animal danders may exacerbate or perpetuate disease in a number of patients.
	Microbial products: staphylococcal toxins may act as superantigens and stimulates the allergic reaction. Other infections like dermatophytes of pityrosporum may also act as allergens.

Dryness of skin:
Dry skin is a prominent feature in many atopic dermatitis patients. Abnormalities in lipid metabolism with reduced synthesis of ceramide may lead to decreased water-binding capacity of skin. Dryness causes microfissures on the skin surface that promotes entry of irritants, allergens and microbes.  

Climatic factors:
A dry and cool environment increases xerosis of skin. Sweating in hot , humid climates may cause irritation, while sunlight tend to improve the symptoms.

Psychological factors:
The psychological impact of the disease on the patients leading to depression, anxiety, and frustration may cause reduced itch threshold and increase the inherent irritability of the skin, thus contributing to the pathogenesis of the disease.
 

CLINICAL FEATURES

Atopic dermatitis principally affects infants and children, about eighty per cent of the cases are said to occur in children below the age of five.

AD is more prevalent in temperate climate, and the incidence is increasing in recent years.

The dominant symptom of AD is itching. The pruritus of AD persists throughout the day but increases during evening and night. The itching of AD is characteristically paroxysmal and often uncontrollable. It causes varyng degrees of sleep disturbance in affected individuals. There is a reduced threshold for itching to irritants and the itch exacerbates with sweating, and low humidity.

Chronic itching leads to scratching, often violent, and scratching leads to secondary changes in the skin like excoriation, infections and thickening, that leads to more itching. Thus, a vicious cycle (itch-scratch-itch cycle) is established which perpetuates the condition.

The lesions of atopic dermatitis take the form of erythematous papules, vesicles, and oozing with crusting in the acute stage. In the subacute stage the lesions are reddish scaly papules. Chronicity leads to thickened plaques with accentuated skin markings (lichenification). Excoriations due to scratching are the commonest secondary lesions. In all phases of AD, dryness of the skin, exaggerated during conditions of low temperature and humidity, may be a prominent findings.

The morphology and distribution of the lesions evolve in the following phases,

Infantile AD (from two months to two years):

Atopic dermatitis usually starts in the first year of life. During this phase, the there is facial erythema, vesicles, oozing and crusting located mainly on the face, scalp, forehead and extensor surface of the  extremities. Buttocks and diaper area are frequently spared.

Childhood AD:

The lesions tend to be drier and scaly. Flexor surfaces and skin creases are predominantly involved. Facial lesions with eyelid involvement and lesions around the neck also occur. Lichenification from chronic itching and scratching occur over flexor surfaces. Psychological effects often are very prominent.

Adolescent and adult AD:

Flexural predilection of lesions persists. Localized, eczematous or lichenified plaques often predominates the clinical picture. Prurigo papules and nodules tend to occur. Resolved cases show dryness and  irritability of the skin with a tendency to itch with sweating and other triggers. Recurrent and persistent hand dermatitis is a frequent feature.

ASSOCIATED FEATURES AND COMPLICATIONS:

CUTANEOUS:

	Erythroderma (exfoliative dermatitis)
	Pityriasis alba
	Hyperlinear palms
	Ichthyosis vulgaris
	Keratosis pilaris
	Chelitis
	Nipple eczema
	Urticaria including contact urticaria
	Alopecia areata
	Increased incidence of anaphylactic drug reactions
	Increased tendency to irritant dermatitis
	Thinning of lateral eyebrows (Hertoghe sign)
	Vascular phenomena: Perinasal and periorbital pallor Delayed blanching with acetylcholine injection White dermographism

OCULAR:

	Eyelid dermatitis
	Chronic blepharitis
	Recurrent conjunctivitis
	Dennie-Morgan infraorbital fold
	Keratoconus
	Anterior subcapsular cataract
	Retinal detachment

INFECTIONS:

	Staphylococcal infections
	Herpes simplex infection, may lead to severe generalized lesions (Kaposi’s varicelliform eruption, or eczema herpeticum) with characteristic punched-out erosions.
	Small pox vaccination may lead to similar eruptions (eczema vaccinatum)
	Molluscum contagiosum and verruca vulgaris
	Dermatophytosis and tinea versicolor

Associated atopic disorders:

Allergic rhinitis and bronchial asthma

Growth retardation

Psychological effects in the form of anxiety, depression, and frustration. Impaired social and family relations.

Complications of therapy, particularly consequences of steroid therapy.
 

DIAGNOSIS

Diagnosis of atopic dermatitis is done clinically. Since there is no single  diagnostic clinical finding or laboratory abnormality in AD, diagnosis of the disease is based on a combination of clinical features.

The following diagnostic guideline (the UK working group criteria) is simple and useful:

Patients must have an itchy skin condition (or parental report of scratching or rubbing in children).

Provide psychological support.

Avoidance of factors that promotes dryness, itching or inflammation.

Avoidance of contact with local irritants like woolen garments, use soft cotton garments.

Clothing and linens should be washed in mild detergents and rinsed well.

Fingernails should be kept short.

Avoidance of contact with animals, dust, sprays and perfumes.

Avoidance of excessive bathing.

Soaps should be bland and non-irritant

Foods that are suspected to aggravate symptoms in individual patients should be avoided.

Avoidance of extremes of temperature and humidity.

In severe cases, hospitalization for a short period may promote rapid reduction of symptoms mainly by providing a changed environment.

These are the cornerstones of therapy of atopic dermatitis. The following principles should be adhered to while instituting topical steroid therapy:

High potency steroids are used for a short period to rapidly reduce inflammation.

Maintenance therapy, if needed is best done with mild steroids like hydrocortisone.

On face and intertriginous areas, mild steroids should be used, mid-potency formulations are used for trunk and limbs.

Topical steroids are applied initially twice or thrice a day After the symptoms are lessened, frequency of application should be reduced. Intermittent use if topical steroid may be alternated with application of emollients.

Ointments are superior to creams or lotions.

The potential side-effects of topical steroids should always be kept in mind.  

  
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