The problem of atopic dermatitis (AD) is becoming increasingly important in modern medicine. The increase in the incidence in the last decade, the chronic course with frequent relapses, the insufficient effectiveness of existing methods of treatment and prevention today put this disease among the most urgent problems of medicine. |
The term "atopy" (from the Greek atopos - unusual, alien) was first introduced by A.F. Sosa in 1922 to determine the hereditary forms of increased sensitivity of the body to various environmental influences. According to modern concepts, the term "atopy" is understood as a hereditary form of allergy, which is characterized by the presence of reagin antibodies. The causes of Bactrim dermatitis are unknown and this is reflected in the lack of commonly accepted terminology. "Atopic dermatitis" is the most common term in the world literature. Its synonyms are also used - constitutional eczema, prurigo Besnier and constitutional neurodermatitis.
The etiology and pathogenesis of atopic dermatitis remain largely unclear. There is a widespread theory of the allergic genesis of atopic dermatitis, which links the appearance of the disease with congenital sensitization and the ability to form reaginic (IgE) antibodies.
In patients with atopic dermatitis, the content of Bactrim antibiotic immunoglobulin E, which includes both antigen-specific IgE antibodies to various allergens, and IgE molecules, is sharply increased. The role of the trigger mechanism is played by ubiquitous allergens penetrating the mucous membrane.
This is due to congenital and acquired disorders of the digestive tract, improper feeding, early introduction of highly allergenic foods into the diet, intestinal dysbiosis, disruption of the cytoprotective barrier, etc., which contributes to the penetration of antigens from food pulp through the mucous membrane into the internal environment of the body and the formation food sensitization..
Sensitization to pollen, household, epidermal and bacterial allergens is more typical at an older age. However, the reaginic type of allergic reaction is not the only one in the pathogenesis of atopic dermatitis. In recent years, disturbances in the cell-mediated link of immunity have attracted the greatest interest. It has been shown that AD patients have an imbalance of Th1/Th2-lymphocytes, impaired phagocytosis, other nonspecific immunity factors, and barrier properties of the skin. This explains the susceptibility of AD patients to various infections of Bactrim, bacterial and fungal origin.
The immunogenesis of AD is determined by the features of a genetically programmed immune response to an antigen under the influence of various provoking factors. Long-term antigen exposure, stimulation of Th2 cells, production of allergen-specific IgE antibodies, mast cell degranulation, eosinophilic infiltration, and inflammation exacerbated by scratching keratinocyte damage all lead to chronic inflammation in the skin in AD, which plays a critical role in the pathogenesis of skin hyperreactivity.
Also of interest is the hypothesis of intradermal absorption of staphylococcal antigens, which cause a slow, sustained release of histamine from mast cells, either directly or through immune mechanisms. Disturbances in the autonomic nervous system can play an important role in pathogenesis.
Behind these changes in the skin lies, obviously, the main biochemical defect, the essence of which is still largely unclear. In patients with atopic dermatitis, the altered reactivity is also explained by unstable adrenergic influences. This instability is considered as the result of a congenital partial blockade of beta-adrenergic receptors in tissues and cells in patients with atopy. As a result, a significant violation in the synthesis of the cycle was noted.ic adenosine monophosphate (cAMP).
An important place in the pathogenesis of atopic dermatitis is given to endocrinopathies, various types of metabolic disorders. The role of the central nervous system is great, which has been recognized and is recognized at the present time and is reflected in the neuro-allergic theory of the origin of atopic dermatitis.
The clinical manifestations of atopic dermatitis are extremely diverse and depend mainly on the age at which the disease manifests itself. Starting in infancy, atopic dermatitis, often with remissions of varying duration, may continue until puberty, and sometimes does not go away until the end of life.
Skin status of the asymptomatic atopic patient The skin of those suffering from atopic dermatitis, especially during the period of remission or "dormant course", is characterized by dryness and ichthyosiform peeling. The frequency of ichthyosis vulgaris in atopic dermatitis varies from 1.6 to 6%, according to different phases of the disease. Hyperlinearity of the palms (folded palms) is observed when combined with ichthyosis vulgaris.
The skin of the trunk and extensor surfaces of the limbs is covered with shiny, flesh-colored follicular papules. On the lateral surfaces of the shoulders, elbows, sometimes in the region of the shoulder joints, horny papules are determined, usually regarded as Keratosis pilaris. At an older age, the skin is characterized by dyschromic variegation with the presence of pigmentation and secondary leucoderma. Quite often at patients in the field of cheeks whitish spots of Pityriasis alba are defined.
The infant phase begins after 18 months of age and continues until puberty. Eruptions of atopic dermatitis in the early stages of this phase are represented by erythematous, edematous papules, prone to the formation of continuous lesions. In the future, lichenoid papules and foci of lichenification begin to predominate in the clinical picture.
As a result of scratching, the lesions are covered with excoriations and hemorrhagic crusts. Eruptions are localized mainly in the elbow and popliteal folds, on the lateral surfaces of the neck, upper chest and hands. Over time, in most children, the skin is cleared of rashes, and only the popliteal and elbow folds remain affected.