AH BODY CARE Hand Cream pack 2x50ml

Eczema is a group of skin diseases that present with dermatitis (= skin inflammation) symptoms, either with sudden onset or with a prolonged, slow course (= chronic).

As a synonym for eczema, we generally use the term dermatitis, e.g. atopic dermatitis = atopic eczema, contact dermatitis = contact eczema, irritative dermatitis = irritative eczema (however, not every “dermatitis” can be classified as eczema, e.g. dermatitis herpetiformis).

So-called exogenous eczemas are conditions with varied mechanisms caused by environmental effects. In the development of endogenous eczemas, individual predisposition is the main determining factor.

In dry, flaking, itchy skin, transepidermal water loss (TEWL) increases, which leads to further worsening of dehydration, dryness and flaking, and to the development of inflammation. This creates a so-called vicious cycle, because trauma caused by scratching flaky, itchy skin increases damage to the epidermal layer and induces further inflammatory processes. The skin’s resistance to mechanical stress is weakened; prolonged, recurring inflammatory skin reactions develop, resulting in further damage to the skin barrier. Damaged barrier function is also accompanied by reduced immune defence of the skin. Further consequences of chronic barrier defects include sensitisation (becoming sensitive), i.e. the appearance of various allergic reactions to environmental substances. Early types include atopic dermatitis and contact urticaria; later types include contact dermatitis. Since the skin’s immune system does not function properly due to barrier damage, viral infections are also common, e.g. skin symptoms caused by verruca virus (“wart-like lesions”), as well as pyoderma, i.e. purulent skin inflammation.

Irritative, non-allergic contact eczema reflects a condition in which the skin barrier has been weakened by possible chemical, physical and/or biological effects.

Environmental irritants lead to barrier damage of the stratum corneum of the epidermis. Depending on the dose of the provoking substances, the horn cells (= keratinocytes) are damaged and/or activated, and release pro-inflammatory cytokines.

Chronic irritative eczema develops as a result of prolonged or repeated exposure to weak irritants (e.g. disinfectants). It is characterised by dry skin, flaking, fissures, and sometimes small blisters. It most commonly first appears on the back of the hand and on the skin areas above the finger joints.

Treatment is prevention, i.e. continuous replacement of the lipid and water layer by using protective creams.

Allergic contact eczema is triggered by a provoking substance (= allergen) present in the affected person’s environment. With persistent contact with the allergen, the patient’s skin becomes sensitised. Thereafter, when the allergen enters the skin, it triggers an allergic reaction, a so-called cell-mediated immune response, in the form of skin inflammation. Contact between the provoking substance and the skin lasts approx. 12–24 hours, as a result of which sensitisation begins. This takes a further approx. 6–12 days. In an already sensitised individual, the skin signals dermatitis after the next harmful external effect in about 12 hours, which reaches its peak (= culminates) in approx. 2–7 days. The development of contact sensitisation is influenced by inherited predisposition, the characteristics of the provoking substance, epidermal barrier defects, skin injury, and changes in skin pH.

The immunologically active components of sensitising substances (= haptens) must somehow enter the epidermal layer of the skin in order to trigger an immune reaction. Damage to the epidermal layer may be caused, for example, by dehydration resulting from water-withdrawing substances such as alcohol-based disinfectants, or by epidermal injury caused by scratching. Treatment primarily focuses on prevention, i.e. avoiding provoking substances, using hypoallergenic, acidic pH (pH 5–6), fragrance-free cleansers, and restoring barrier function with protective creams.