It is the leading non-fatal health burden attributable to skin diseases and inflicts a substantial psychosocial burden on patients.

Atopic dermatitis is one of the most common chronic diseases and affects 10% to 30% of children and 2% to 10% of adults in developed countries.⁽²⁾ It occurs in phenotypes differently at different ages; then it is useful to divide the disease into three phases:

• > Infant or toddler phase, or pre-infancy, from 4 months to two years old;
• > Child phase, after 2 years old till 8-10 years old;
• > Adolescent and adult phase, after 10 years old till adulthood.⁽³⁾

In the first months, the AD may start with the so-called cradle crap on the head, then the disease may spread on the face and on the extendible surfaces of the infant's limbs. Later, the typical topography develops involving the folds.⁽⁴⁾

In adults it is very common for the face and upper part of the trunk to be affected. The AD may also appear as nummular eczema.⁽⁴⁾

Depending on the type of lesion, two clinical phases of AD can be differentiated:

• > acute or exudative phase, characterised by inflammation of the skin, with exudation, which frequently tends to microbial over-infection;
• > chronic phase, characterised essentially by a patchy, dry dermatitis with a desquamating surface and in which frequent scrapping lesions are found, predominantly located in the flexural folds of the limbs. At this stage the skin becomes thickened, infiltrated, greyish-brown and finely desquamated.⁽²⁾

In acute phase, skin lesions are typically eczematous, erythematous-vesicular, while erythematous-squamous and lichenified in chronic phase. The lesions can hit any part of the body, typically they have morphology and distribution correlated with age.⁽⁴⁾The disease is characterised in both phases by intense itching, with night exacerbation (the small patient scratches even at night, sometimes even during sleep).⁽³⁾

Although the clinical picture, characterized by acute flare-ups of eczematous, pruritic lesions on dry skin at typical predilection such as the flexural folds, is quite homogenous, the trigger factors of the disease are diverse and the pathophysiologic network involved is complex.

Therefore, first attempts have been made to classify subtypes of AD based on the most relevant causal factors in the individual patient.⁽⁵⁾

Recently Atopic Dermatitis pathogenesis has evolved from the trinity pathogenesis concept – the interplay between 3 key factors:

1. Skin barrier
2. Allergy/Inflammatory
3. Pruritus⁽⁶⁾

When the skin barrier is disrupted by, for example, the filaggrin gene mutation and/or environmental factors, the skin is predisposed to being penetrated by external stimuli.

Foreign antigens can be subdivided into two subsets by size: haptens (including metals) and protein antigens.⁽⁶⁾

Furthermore, it is becoming increasingly evident that oxidative stress is involved in numerous skin diseases and that antioxidative strategies can serve as effective and easy methods for improving these conditions.⁽⁷⁾

We should consider the antioxidant strategy for better disease control and improve quality of life for AD patients.⁽¹¹⁾

The pathology treatment is based on the severity of the disease, structured as a pyramid where the baseline is used for every type and severity of dermatitis.

The pathology can vary from mild to severe, for every phase, additional therapeutic options are given. ⁽¹³⁾ 

Given the importance of appropriate diagnosis and appropriate assessment of cutaneous symptoms in treatment of atopic dermatitis, the basics of therapy in adult and children include emollients, bath oils and avoidance of clinically relevant allergens (encasings, if diagnosed by allergy tests). 

Moreover, educational programs involving dermatologists, paediatricians, psychologists / psychosomatic counsellors, and dietary counselling have been demonstrated to support the improvement of subjective and objective symptoms, and optimize medication use in patients, and result in a significant gain in quality of life.⁽¹³⁾ 

More details on the specifics of the basic therapy for atopic dermatitis and skin care are outlined below.

BASIC THERAPY FOR ATOPIC DERMATITIS AND SKIN CARE.

Atopic dermatitis is a chronic condition.

Therefore,

treatment has to be planned with a long-term perspective

special attention must be given to long-term safety aspects.

The four major components of treatment include trigger avoidance, daily skin care, anti-inflammatory therapy, and other complementary modalities.

Atopic dermatitis is not curable, and many patients will experience a chronic course of the disease. Accordingly, the treatment of atopic dermatitis aims to:

• > minimise the number of exacerbations of the disease, so-called flares,
• > reduce the duration and degree of the flare, if flare occurs.

The first aim relates primarily to prevention; the second aim relates to treatment.

Prevention is best attained by trying to reduce the dryness of the skin, primarily via daily use of skin moisturising creams or emollients along with avoidance of specific and unspecific irritants such as allergens and noncotton clothing.

When dryness is reduced, the desire to scratch will lessen and the risk of skin infection will decrease. 

Avoiding long, hot baths further prevents skin dryness, but when a bath is taken, an emollient should be applied directly after it to secure a moist epidermis and augment the skin barrier function. Reducing the flare is warranted when actual eczema occurs or when mild intermittent eczema worsens. Management of AD exacerbation requires medical treatment often in the form of corticosteroid creams. In addition to topical treatment, severe acute or chronic AD often requires systemic immunosuppressant drugs or phototherapy (ultraviolet, UV light).⁽¹⁾

CLEANSING.

The skin must be cleansed throughly with a gentle and hydrating cleanse in non-irritant and low allergenic formulas may be used and the pH should be in a physiological cutaneous range around 5-6.⁽¹²⁾

EMOLLIENT THERAPY.

The use of emollients in the management of atopic dermatitis is pivotal: atopic dermatitis is associated with skin barrier anomalies that facilitate an easier allergen penetration into the skin with an increased proneness to irritation and subsequent cutaneous inflammation.
Hydration of the skin is usually maintained by daily application of emollients.

Bath oils may also help to reduce the flares.

Use of emollients improves dryness and subsequently pruritus during the eczema treatment and especially improves the barrier function.⁽¹³⁾

^{(1) Spałek M. Chronic radiation-induced dermatitis: challenges and solutions. Clinical, Cosmetic and Investigational Dermatology 2016; 9: 473–82.}

^{(2) Atopic Dermatitis Logan Kolb; Sarah J. Ferrer-Bruker.}

^{(3) Gelmetti C. Eczemi o dermatiti. From “Manuale di dermatologia medica” of Paolo Fabbri, Carlo Gelmetti, Giorgio Leigheb. Elsevier srl, 2010.}

^{(4) Società Italiana di Dermatologia Medica, Chirurgica, Estetica e delle Malattie Sessualmente Trasmesse. Dermatite Atopica – Linee guida SIDeMaST 2016-2017. Pacini Editore Medicina. Available on: http://www.pacinimedicina.it/dermatite-atopica-linee-guida-sidemast-2016-2017/ [accessed February 2017].}

^{(5) Pathogenesis of atopic dermatitis. Peng W1, Novak N.}

^{(6) Kenji Kabashima (2013) New concept of the pathogenesis of atopic dermatitis: interplay among the barrier, allergy, and pruritus as a trinity}

^{(7) Jinok Baek & Min-Geol Lee (2016) Oxidative stress and antioxidant strategies in dermatology, Redox Report, 21:4, 164-169, DOI: 10.1179/1351000215Y.0000000015}

^{(8) Academic and occupational impact (Drucker, 2017)
(9) QoL in families of AD patients (Drucker, 2017)}

^{(10) Sleep Disturbance in AD (Caleb, 2017)}

^{(11) Ji Hongxiu (2016) Oxidative Stress in Atopic Dermatitis}

^{(12) Management of Patients with Atopic Dermatitis: The Role of Emollient Therapy M. Catherine Mack Correa* and Judith Nebus}

^{(13) ETFAD/EADV Eczema task force 2015 position paper on diagnosis and treatment of atopic dermatitis in adult and paediatric patients A. Wollenberg,,* A. Oranje, M. Deleuran, D. Simon, Z. Szalai, B. Kunz, A. Svensson, S. Barbarot, L. von Kobyletzki, A. Taieb, M. de Bruin-Weller, T. Werfel,11 M. Trzeciak, C. Vestergard, J. Ring, U. Darsowfor the European Task Force on Atopic Dermatitis/EADV Eczema Task Force†}