Dermatitis contacta allergica

 'Allergic contact dermatitis'  is a manifestation of immunopathological reaction type IV. to substances coming into direct contact with the skin (usually haptens ).

Etiology and pathogenesis
The development of contact allergic eczema takes place in two phases: sensitizing and equipment. Due to their size, haptens acquire antigenic properties only after binding to epidermal protein carriers. Antigen is recognized and processed by Langerhans cells, which present it to T-lymphocytes. Langerhans cells then migrate to the regional lymph nodes, changing their phenotype. They elute "IL-1", "IL-6" and "TNF-α", leading to the proliferation of T cell clones that have receptors for the respective antigen. T-lymphocytes then migrate to various organs, including the skin (10-20%). The sensitization process spreads throughout the body, requiring at least 5-7 days to fully sensitize. The onset of sensitization is influenced by a number of factors such as the time and intensity of action of allergen, its allergenic properties, the state of immunity and the disposition of the individual. The resulting hypersensitivity is usually permanent.


 * Common sensitisers:
 * metals (Ni, Co – jewelry, watches);
 * cosmetics ingredients;
 * chemicals from the work environment;
 * local anesthetics;
 * dyes, etc.

After leaving the vessels, the T-lymphocytes can be activated by contact with the appropriate antigen and macrophages, mast cells and possibly keratinocytes are used as the accessory phase. Each new contact between the allergen and the sensitized T-lymphocytes triggers the immediate release of cytokines, that direct the immune response to remove the allergen from the body as quickly as possible.

If contact eczema is caused by a single substance, it is a so-called monovalent hypersensitivity, more than 1 and less than 5 substances produce oligovalent hypersensitivity , and more causative agents are polyvalent hypersensitivity. Group hypersensitivity refers to a specific part of the primary antigen molecule, resulting in hypersensitivity to a number of chemicals that contain this structure in their molecule. Combined hypersensitivity is caused by the simultaneous or sequential action of two allergens in one substance.

Klinický obraz
Manifestations 24-48 h. after contact with the allergen and are limited to the point of contact. In the acute phase, a strongly reddish edematous deposit with rapidly eroding papulovesicles and wetting on the surface is formed, rarely with the formation of bul. Microscopically,spongiosis and intracellular edema are visible, intraepidermal blisters form. Later, crusts form. In the chronic phase, the surface becomes hyperkeratotic and ragads form on it, or lichenification predominates.

The hematogenous form caused by a substance to which the patient is sensitized by blood to the skin, where it causes urticaria. Chematically or lymphogenically, chronic contact eczema may also spread beyond the primary site of contact.

Diagnostics
Kromě pečlivé anamnézy je základním vyšetřením epikutánní test. Principem je nanesení vyšetřované látky za standardních podmínek a ve správné koncentraci na zdravou kůži v časovém odstupu 2−3 týdnů od zhojení kožních projevů. Následuje hodnocení a interpretace.

Diferenciální diagnóza
Je třeba odlišit: U chronických projevů odlišujeme
 * toxickou dermatitidu,
 * atopický ekzém,
 * povrchové dermatofytózy,
 * erysipel.
 * psoriázu,
 * lichen planus,
 * m. Paget,
 * m. Bowen.

Terapie
Základním předpokladem je odstranění antigenu a zamezení jeho dalšího působení. V akutní fázi aplikujeme vysychavé obklady, později roztoky organických barviv, krémy, masti. Účinné jsou lokální kortikosteroidy, u chronických forem ekzému se kombinují s ichtamolem nebo dehtovými přípravky. U odolných forem je někdy účinné rentgenové ozáření Buckyho lampou.

Související články

 * Alergeny
 * Léčba alergie
 * Urticaria
 * Erytrodermie