Trigger Factors, Allergens and Allergy Testing in Atopic Dermatitis

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disorder affecting between 10-20% of children and 1-3% of adults in the general population. It is associated with high morbidity and has major public health implications. AD is associated with hyper-reactivity of the skin to environmental trigger factors that are harmless in normal individuals. Major contributors to this hyperactivity are the many immune and inflammatory changes taking place in the skin and peripheral blood in AD individuals. AD can be classified into several subgroups, each with different immune and pathological features, suggesting a multifactorial disease and heterogeneity. Historically two types of AD have been identified. They include the “extrinsic or allergic” type of AD, which is characterized by Immunoglobulin E (IgE) mediated sensitization (immediate, type I hypersensitivity) and occurs in 70-80% of individuals. The “non-allergic or intrinsic” type of AD affects 20-30% of individuals and is defined by a more T-cell driven feature (delayed, type IV hypersensitivity), with low IgE levels and absent IgE sensitization. More recently a transition from the intrinsic to the extrinsic type has been reported in young children, and AD individuals can show a combination of above mentioned phenotypes or complete absence of the known features. The clinical diagnosis of AD does not cause major difficulties as there are fairly well defined criteria. Identifying the underlying pathophysiology for the affected individual can be more of a challenge, as there is no gold standard test available for AD and the AD individual might move from one pathophysiological “type” of AD to another. Clinically AD is divided into acute, subacute and chronic forms with correlated histopathological changes. The transition from one clinical form to another is fluent and can be very rapid. AD individuals frequently give a personal and or a family history of asthma and allergic rhinitis, the so called atopic triad. Exacerbation of one of the disorders in this triad can cause concomitant exacerbation of the other two suggesting some underlying common pathways and interdependence (Reitamo et al., 2008). Predisposing factors for AD are multifactorial and involve genetic susceptibility, defects in skin barrier function, immune dysregulation, western life style and exposure to environmental trigger factors. The development of disease is an interplay of gene-gene and gene-environment interactions. The early age of onset and familial predisposition as well as the high concordance rate of AD in monozygotic (77%) and dizygotic (15%) twins suggest a