**3. Conclusion**

226 Atopic Dermatitis – Disease Etiology and Clinical Management

predisposing risk factors to contact allergen sensitization. Another study evaluating contact sensitization in a series of atopic pediatric patients, that were patch tested, identified 43% positive reactions without commenting on clinical relevance of these reactions (Fonacier & Aquino, 2010 & Jacob S et al., 2008). AD individuals can develop sensitivity to a variety of contact allergens such as topical medicaments including emollients and corticosteroids as well as fragrances, particularly in the presence of recalcitrant periorbital dermatitis. A positive past medical history of AD (44% in patients with periorbital dermatitis) has been found to be a predisposing factor for periorbital dermatitis when compared with all patchtested individuals (29% with peri-orbital dermatitis). Statistically significantly more patients with AD were found in the group of patients with than without periorbital dermatoses. The periorbital region is a prime location for AD and in consequence a defective skin barrier

Hand eczema and compositae allergy may be more common in AD, whereas allergies to topical corticosteroids and antiseptic solutions are only positive in a small subset of AD

Oat sensitization and its clinical manifestations in the form of digestive, respiratory and cutaneous symptoms (including CAD) has been identified in 15-20% of AD children, compared to none in the normal population. It is likely to be due to repeated applications of oat proteins through topical emollients and hygiene products on a predisposed impaired epidermal skin barrier of AD individuals. Oat can also be added to the list of food products (e.g. peanut, ovalbumin, almond) responsible for FA triggered by a possible percutaneous sensitization. Avoiding application of topical containing oat protein products in AD infants

A lower frequency of positive quinoline allergy has been documented in AD individuals, whereas contact allergy to neomycin among atopic subjects is usually found to be equivalent or slightly raised in comparison to non-AD individuals. AD subjects appear to have increased efficiency in orally tolerising haptens but are inefficient in orally tolerising proteins. The reduced contact allergy to quinoline in AD patients might be explained by a higher exposure of haptens in the gut and skin at a young age producing "hapten"-tolerance

History for CAD should always include the patient's personal hygiene environment, medical and medicament history as well as home and care giver environment. PT should be performed in all AD patients where CAD is considered and particularly in children with AD. However because of irritancy interpretation of PT may be difficult in AD individuals and the severity of AD might have an impact on the results obtained through PT. PT should

In summary more and more studies suggest, that CAD might occur as common in AD individuals and particularly in children with AD as in the general population.

alleviates sensitization to contact allergens as well as aeroallergens.

is paramount in reducing sensitization to oat (Boussault P et al., 2007).

• Progression or deterioration of existing dermatitis (AD/Psoriasis)

• Recalcitrant dermatitis by standard therapies

Table 11. Factors that make a diagnosis of CAD likely

• Clinical presentation of dyshidrosis

patients (15%) (Fonacier & Aquino, 2010).

• New-onset dermatitis

(McFadden & White, 2008).

always include the emollients used.

AD is a common chronic skin condition associated with high morbidity and major public health implications. As prevention of disease is not yet a real option, reducing morbidity is main aim of treatment. Identifying the underlying pathomechanism of the individual's AD is very crucial. High levels of specific IgE antibodies and or total IgE levels in serum are significantly associated with severity of dermatitis in individuals with the extrinsic type of AD. Raised specific IgE antibodies can be detected in the peripheral blood for most trigger factors and allergens. Food and aeroallergens, microbes including *S. aureus* and *Malassezia* yeasts, contact allergens and autoallergens have been identified to trigger AD and perpetuate so the underlying immune and inflammatory cascade of AD.

To date no standard test is available to diagnose AD. Sensitization to various allergens is a major part of triggering and perpetuating the inflammatory skin response in AD. Various tests have been developed to investigate the underlying type(s) of hypersensitivity reaction involved in AD patients. None of the available tests so far have proven sensitive and specific enough to identify reliably relevance between clinical reaction and test result. Allergy tests commonly used in practice include measurement of total levels of IgE and allergen specific IgE levels in serum (RAST), SPT, APT, PT and DBPCFC.

Precise understanding of these tests including their limitations together with accurate correlation of patient history, symptoms and signs are required in order to differentiate between allergy, intolerances and hypersensitivities, and achieve an appropriate clinical diagnosis. Results must always be interpreted in the context of clinical history.

In a recent meta-analysis filaggrin gene defects have shown to increase the risk of developing allergic sensitization, AD, and allergic rhinitis. The presence of filaggrin gene mutations correlated strongly with disease severity and treatment failure, and also increased the risk of asthma in AD patients. Gene testing for filaggrin gene mutations might be an additional way to identify atopic individuals in future. Restoring skin barrier function in filaggrin deficient individuals early in life may help prevent the development of sensitization and halt the development and progression of allergic disease.
