Simple contact dermatitis

Simple contact dermatitis (synonyms: contact dermatitis, official dermatitis) is characterized by the onset of the lesion solely at the site of the irritant effect, by the absence of sensitization and by the tendency to disseminate and spread along the periphery of the focus.

[1], [2], [3]

Causes of the contact dermatitis

Simple dermatitis arises from the action of chemical (concentrated acids, alkalis), physical (high or low temperature, radiation exposure), mechanical (pressure, friction) and biological factors. It is known that the skin as an organ occupies an exceptional place in the manifestations of hypersensitivity reactions of immediate and delayed types. In addition, according to several authors, the skin is an immune organ, which is confirmed by the presence in it of lymphoid centers, which are involved in hypersensitivity reactions and take part in the formation of foci of inflammation of the immune nature in it. At the heart of contact allergic dermatitis is a kind of delayed-type hypersensitivity, called contact hypersensitivity. Contact allergic dermatitis can have acute, subacute and chronic course.

[4], [5], [6], [7], [8], [9], [10], [11]

Pathogenesis

A number of works describe the morphology of allergic contact dermatitis at different stages of its development, caused in guinea pigs by applying to the skin an obligate allergen - 2,4-dinitrochlorobenzene (DNHB). It is shown that during the primary contact reaction, which develops 24 hours after the application of DHCP, destructive changes in the epidermis are observed, sometimes necrosis and detachment of it. In the dermis - an inflammatory reaction with lesion of vessels of destructive nature and perivascular infiltrates, in which, in addition to mononuclear cells, neutrophilic granulocytes and tissue basophils with degranulation phenomena are found.

With allergic contact dermatitis (on the 15th day after repeated application of the allergen), the morphological changes had a different character. Acanthosis is defined in the epidermis, expressed to a greater or lesser degree depending on the severity of the process, the phenomenon of inter- and intracellular edema, exocytosis. In the dermis - hypertrophy of the endothelium of the vessels of the microcirculatory bed, narrowing of their lumens, perivascular infiltrates, consisting of lymphoid cells, macrophages, active fibroblasts, among which, as a rule, tissue and hematogenic basophils were found.

To diagnose various types of contact dermatitis, a skin test is used in a person. Application of an allergen in allergic contact dermatitis in humans after 3 hours after the application causes alterative changes in the epidermis, vasodilation and extravasation of mononuclear elements from them into the dermis. 8 hours after application, basal spongiosis is formed, and after 12 hours and later spongiosis reaches the upper layers of the epidermis with the formation of blisters.

Histological diagnosis of contact allergic dermatitis in humans is very difficult. This is due to the fact that a biopsy is usually performed a few days after the detection of dermatitis, at the height of its development, when a nonspecific inflammatory reaction is seen. It is also difficult to distinguish between phototoxic and photoallergic dermatitis.

Histogenesis of contact dermatitis

In the development of sensitization in animals, according to the clinical and morphological picture of the skin, three phases are distinguished:

1. primary-contact reaction;
2. a spontaneous inflammatory response, or an inflammation reaction;
3. inflammatory reaction to the permissive application of the allergen (skin test), which simulates allergic contact dermatitis.

Primary-contact reaction is morphologically expressed in the form of nonspecific inflammation. However, the appearance of activated lymphocytes, the detection of contacts between macrophages and lymphocytes on electron diffraction patterns may indicate initial signs of development of sensitization. Necrosis in the epidermis and changes in capillaries during this period can be regarded as a result of the toxic effect of DHCB.

A spontaneous inflammatory reaction has the features of immune inflammation, as evidenced by the appearance in the infiltrate of activated lymphocytes, cells such as immunoblasts, plasmablasts and plasma cells, as well as a large basophil content, accompanied by basophilia in the blood.

In the inflammatory response to the application of the resolving dose of DNCP, the basis of the infiltrate was lymphocytes, macrophages, active protein-synthesizing cells and basophils with signs of degranulation. A similar morphology of the cell infiltrate in the skin test is characteristic for contact allergy and for other forms of delayed type hypersensitivity. However, the presence of basophils in the infiltrate, involved in IgE-dependent reactions, indicates the role of immediate type hypersensitivity in the development of allergic contact dermatitis.

[12], [13], [14], [15], [16], [17]

Symptoms of the contact dermatitis

In the course of the skin-pathological process, acute and chronic simple dermatitis is distinguished. With acute dermatitis, bright redness and puffiness of the skin are noted, small nodules and vesicles are often observed, sometimes wetting, scales and crusts. In some cases, there are larger bubbles and even bubbles, and sometimes necrotic changes. Patients usually experience a feeling of heat, burning, itching, sometimes pain.

Chronic dermatitis occurs with chronic pressure and friction, the strength of which is relatively small. At the same time the skin becomes denser, there is lichenization and infiltration due to thickening of the epidermis and hyperkeratosis. For example, various types of ionizing radiation (sun rays, X-rays, alpha, beta, y-rays, neutron radiation) contribute to the development of acute or chronic radiation dermatitis. Depending on the dose, the penetrating ability of radiation and individual sensitivity, radiation dermatitis can be manifested by erythema (with a peculiar violet or bluish tinge), temporary hair loss, bullous reaction against a background of intense hyperemia and edema. In these cases, the process ends with skin atrophy, persistent alopecia, the formation of telangiectasias, a violation of pigmentation - "motley, x-ray skin," may develop a necrotic reaction with the formation of hard-to-break erosions and ulcers.

Multiple skin irradiation with "soft" X-rays in relatively low doses and exposure to radioactive substances lead to the development of chronic radiation dermatitis. In the lesion focus, dryness, thinning of the skin, loss of elasticity, the presence of telangiectasias, depigmented and hyperpigmented sites, onychodystrophy, pruritus, ie, the clinic of poikilodermia are noted. Chronic radiation damage to the skin contributes to the formation of damaged areas of papillomas, hyperkeratosis, warty growths, ulcers with a tendency to malignant degeneration.

Chemical simple contact dermatitis arise from the action of strong acids and alkalis, salts of alkali metals and mineral acids, etc. Such dermatitis arises sharply, proceeds against the background of necrosis with the formation of a scab, after which the ulcer is found ulcer.

[18], [19], [20]

Treatment of the contact dermatitis

The treatment depends on the severity of the inflammatory phenomena. With an easy flow, the appointment of powders, corticosteroid ointments or antipruritic agents (fenistil-gel, 2% menthol ointment, etc.) is sufficient. In the presence of blisters, clean the surrounding skin with 1% boric alcohol, and then pierce the blisters. Affected areas are smeared with aniline dyes. In severe cases of simple contact dermatitis (tissue necrosis), patients are hospitalized in specialized hospitals.