**4. Pathophysiology**

The pathophysiological mechanism of AD is multifactorial involving genetic, structural and immunological elements. The hallmark characteristic of AD is epidermal barrier dysfunction.

Clinical Management of Atopic Dermatitis 253

The clinical appearance of AD varies with disease severity. At all stages, patients have dry skin. Intensely pruritic, erythematous papules associated with exudates are seen in the acute phase of AD in infants. In the infantile stage (0-2 years old), the distribution of the rash is normally located on the face, chin, cheeks, scalp, trunk and extensor surfaces, but not on the nose or the diaper area (Deshazo, 2009). As the disease becomes more chronic, there is associated lichenification and the distribution of the rash is mostly seen on the wrists, ankles and neck in the childhood stage (2 years old-puberty) (Deshazo, 2009; Lipozencic, 2010). Approximately, 40% of childhood AD persists into adulthood (Bettrani, 2007). The distribution of rash in adults is similar to the childhood form mostly noticeable on the upper arms, back, wrists, dorsa of hands, fingers, feet and toes (Deshazo, 2009). The presence of pustules within areas of dermatitis suggests a secondary infection. Lesions with a less

The diagnosis of atopic dermatitis is based on a constellation of clinical signs and symptoms, physical examination and history. Laboratory tests are unnecessary and skin biopsy has been found to be little value, but they can exclude other diagnosis in adults. Although the majority of AD patients have elevated total serum IgE, up to 30% of these patients have normal total serum IgE and show no allergic sensitization to food or aeroallergens (Schmid-Grendelmeier, et al. 2005). However, monitoring of IgE remains a

Normally, diagnosis is confirmed by chronicity of symptoms, pruritis, and age-specific morphology and distribution of symptoms (Ong P, et al. 2008). However, well-defined criteria are important in the diagnosis of AD and diagnostic criteria developed by Hanifin and Rajka are widely accepted (see Table 1). The American Academy of Dermatology has

There are many exacerbating factors that are triggers, which can expedite the progress of inflammation. These triggers are found in food allergens, bacteria, viruses, stress and opportunistic pathogens. One of the major triggers is the microorganism *Staphylococcus Aureus* due to the fact that is organism secretes a toxin which can stimulate action of T cells (Ghazvini, et al. 2010). Among viruses, herpes simplex virus has been identified as one of the possible triggers of AD (Ghazvini, et al. 2010). Diagnostic testing is mainly utilized to



also developed diagnostic criteria for AD (Leung & Hong, 2007). Please see Table 2.

determine specific allergens that may be causing the condition. These tests include:

distinct distribution should prompt a search for an alternative diagnosis.

**5. Clinical presentation** 

**6. Diagnosis** 

nonspecific finding of AD.

food challenges (Ghazvini, et al. 2010).

creams or ointments (Akdis, et al. 2006; Lipozencic, 2010).

In normal individuals there are three factors that contribute to intact epidermal barrier function; structural proteins, lipids and proteases. Alterations in these components contribute to epidermal barrier dysfunction in AD patients. Additionally, genetic dysfunctions can be classified into two distinct groups; mutations occurring in genes encoding for epithelial structures and mutations occurring in genes encoding for elements of the immune system (Bieber, 2008). Lastly, immunological dysfunction appears to play a critical role in the pathogenesis of AD and involves alterations in T-cells, B-cells, eosinophils and IgE production.
