Experts talks
Atopic dermatitis is a non-contagious inflammatory skin disorder characterised by intense pruritus, excessive skin dryness, and eczematous eruptions with chronic, fluctuating, exacerbations and remissions that usually occur in childhood.
In 80% of patients, it starts before the age of 5, but in 60% of those, especially in those with mild symptoms, the symptoms improve or disappear after puberty. In those with moderate/severe manifestations, AD tends to continue after puberty, and even persist in adult life, affecting quality of life.
Diagnosis of AD is mainly clinical. The main symptom is intense pruritus leading to the “itching-scratching” cycle. It is said that AD is itching that erupts, and not the eruption that causes itching (i.e., itching on the skin).
The causes are complex and multifactorial, involving the interaction between genetic predisposition, environmental factors, certain immunological changes, and skin barrier dysfunction. Although all of these are closely correlated, the key role in atopic dermatitis pathogenesis is the alteration of the skin barrier function.
A skin protein with non-functional mutations is the most important genetic risk factor for atopic dermatitis. Loss of this protein’s functions leads to significant transepidermal water loss, increased skin permeability for food allergens and from the environment, allowing them to penetrate, causing sensitisation and inflammation, which could lead to an “atopic march”. (i.e. the sequence: bronchial asthma, allergic rhinitis).
Sensitisation of IgE mediated to a particular food can be induced by contact with skin that does not effectively fulfil the barrier role, secondary to gene mutation of that protein in the skin. Barrier defects allow skin penetration by various allergens, including by food proteins, promoting sensitisation induction and IgE synthesis, which may contribute to skin inflammation characteristic of atopic dermatitis.
It is estimated that 40% of children with moderate forms, and probably much more of those with severe AD, have associate food allergies. An even greater proportion of children with atopic dermatitis often have elevated levels of specific IgE, sometimes even in the absence of a genuine allergy. This explains why the role of allergies in the pathogenesis and severity of AD is intensely debated.
Skin manifestations of food allergies (IgE-mediated) consist of acute urticaria, angioedema, and contact reactions. If AD is aggravated by exposure to a food product, such reactions are not IgE-mediated hypersensitivity reactions, but rather delayed and usually develop 2 to 6 hours after exposure.
Milk, egg white, wheat flour, soy, fish and peanuts are among the foods most often involved in worsening AD symptoms.
The diagnostic approach includes a detailed history, including information about the child’s or mother’s diet if the baby is breast-fed, prick/patch skin tests, serological tests to identify mediated IgE sensitisation and the clinical significance of positive tests.
AD treatment implies avoiding factors triggering lesions, controlling pruritus, suppressing inflammation, and restoring the skin barrier.
Topical medication consists of:
Food allergies are an indisputable factor in the worsening of atopic dermatitis in children. The history of reactions, diet, skin tests, and establishing the specific IgE help identify foods which are possibly involved in the persistence and worsening of AD, the oral challenge tests being the gold standard for establishing the diagnosis with certainty and implementing a personalised diet.
Although the pathogenesis of AD is complex, recent research supports the role of an abnormal skin barrier.
This new knowledge reinforces the main role of the cutaneous barrier function in the emergence and development of atopic dermatitis and underlines the need for targeted therapies to maintain its integrity, with proper skin hydration playing a crucial role in this process.
