Atopic dermatitis (dermatitis atopica)- a hereditary allergic skin disease with a chronic relapsing course and a certain evolutionary dynamics. The concept of atopy refers to a hereditary predisposition to allergic reactions in response to sensitization to certain allergens. Atopic dermatitis is one of the manifestations of atopic disease, which also includes atonic bronchial asthma, allergic rhinoconjunctivitis (pollinosis, "hay fever").

Atopic dermatitis is an urgent problem in pediatric dermatology, as it begins in early childhood, is the most common allergic dermatosis in children with a tendency to a constant increase in incidence, and is also combined with lesions of the respiratory tract. It occurs in 10% of infants and young children; by puberty, most children experience regression of the disease. Only in 3-5% of cases the disease "passes" into adulthood, which is accompanied by a severe course, severe xerosis of the skin, a combination with other atonic conditions.

Atopic dermatitis is a multifactorial disease. Its development is due to the impact on the body of trigger (starting, provoking) factors against the background of hereditary predisposition. Genetic predisposition is characterized by a polygenic type of inheritance. It is not a specific atopic disease that is inherited, but a predisposition to an atopic reaction of certain systems. Approximately 50% of patients have a positive family history of atopy.

Trigger (starting, provoking) factors can be conditionally divided into two groups: specific and nonspecific.

• Specific Factors cause individual reactions and are not irritants for all patients.
  • Food products (milk, eggs, fish, soy, citrus fruits, chocolate, etc.). The role of food irritants is most important in the development of dermatitis in infancy and early childhood. A seasonal change in sensitivity to nutritional factors is characteristic - in the summer it decreases, and often patients better tolerate products for which an exacerbation of the skin process was noted in winter.
  • Aeroallergens (pollen, house dust, dander and animal hair, perfumes, volatile chemicals, etc.) play a significant role in the development of exacerbation of atopic dermatitis when combined with bronchial asthma and rhinitis.
  • medicinal substances.
• Non-specific factors, to which the skin process is aggravated in almost all patients and directly depends on the duration and strength of exposure to the irritating factor.
  • Weather conditions: cold, wind, heat, dry air.
  • Clothing made from fabrics that irritate the skin (wool, synthetic fabric, fabric with a rigid structure), as well as tight-fitting clothing.
  • Detergents (soap, shampoos, household chemicals) and hard water destroy the lipid film on the skin, increasing dryness and
  • Microbial colonization of the skin: coccal flora, herpes simplex virus (HSV), petyrosporal flora, fungi.
  • Emotional influences and stress.

In the development of atopic dermatitis, great importance is given to perinatal risk factors for the development of atopic dermatitis. These include poor diet, occupational hazards, chronic intoxication, and maternal smoking during pregnancy.

Atopic dermatitis

Atopic dermatitis is a chronic allergic disease that develops in individuals with a genetic predisposition to atopy, has a relapsing course with age-related characteristics of clinical manifestations and is characterized by exudative and/or lichenoid rashes, increased levels of serum IgE and hypersensitivity to specific (allergens) and nonspecific irritants.

Prevalence

Atonic dermatitis is one of the most common allergic diseases in children. In economically developed countries, it is diagnosed in 10-28% of children. The frequency of the disease depends on the age of the children. According to the results of epidemiological studies under the ISAAC program, atonic dermatitis occurs on average in 3.4% of children aged 13-14 years in the world. The prevalence of the disease is significantly higher among young children.

Etiology and pathogenesis

The pathomorphological substrate of atopic dermatitis is chronic allergic inflammation of the skin. The disease is characterized by an abnormal immune response to environmental allergens. The immunological concept of the pathogenesis of atopic dermatitis is based on the concept of atopy as a genetically predetermined allergy caused by the overproduction of reagin antibodies in response to contact with environmental allergens. Atopy is the most important identifiable risk factor for the development of atopic dermatitis. Currently, genes that control the production of IgE and cytokines involved in the formation of allergic inflammation have been mapped.

The main route of entry of the allergen into the body during atonic dermatitis is enteral, a rarer one is aerogenic. In the etiology of atopic dermatitis, the leading role belongs to food allergies. Sensitization to food allergens is detected in 80-90% of young children with clinical signs of atopic dermatitis. The most significant antigens are cow's milk, eggs, fish, cereals (especially wheat), legumes (peanuts, soybeans), crustaceans (crabs, shrimp), tomatoes, meat (beef, chicken, duck), cocoa, citrus fruits, strawberries, carrots, grapes . With age, the spectrum of sensitization expands. On top of food allergies is sensitization to indoor aeroallergens, especially to antigens of micromites of the genus Dermatophagoides. Close contact with micromites living in bedding contributes to the activation of allergic skin inflammation at night and increased itching. Some children also develop sensitization to epidermal allergens (especially cats and dogs). Fungal allergens play an important etiological role in the development of atopic dermatitis. The spores of the fungi Cladosporium, Alternaria tenuis, Aspergillus, and Penicillum have the greatest allergenic activity. Drug allergens are one of the common causes of exacerbation of atopic dermatitis. They rarely act as a primary etiological factor. Exacerbation of the skin process is provoked by penicillin antibiotics, non-steroidal anti-inflammatory drugs (analgin, amidopyrine), tetracycline antibiotics, sulfonamides, B vitamins, gamma globulin, plasma, local and general anesthetics. In some patients, sensitization to pollen allergens has etiological significance. Exacerbations of the skin process are observed in them in the spring-summer period of the year and are associated with the timing of pollination of the causally significant plant. Sensitization to bacterial allergens also plays a certain role. Most often, in patients with atonic dermatitis, reagins to antigens of Escherichia coli, pyogenic and Staphylococcus aureus are detected.

The vast majority of patients with atopic dermatitis (80.8%) have a polyvalent allergy. Most often, food allergies are combined with drug allergies and allergies to house dust mites.

Chronic allergic inflammation underlies the formation of skin hyperreactivity. In addition to the specific immune mechanism, nonspecific (“pseudoallergic”) factors play a role in the pathogenesis of atopic dermatitis: an imbalance of the sympathetic and parasympathetic parts of the autonomic nervous system, hyperreactivity of the skin caused by instability of the cytomembranes of mast cells and basophils, etc. Exacerbation of atopic dermatitis can be caused by nonspecific triggers (irritants) . They provoke nonspecific histamine liberation and trigger a cascade of allergic reactions. Nonspecific irritants - synthetic and woolen clothing, chemicals present in topical medications and cosmetics, preservatives and dyes contained in food products, detergent residues remaining on linen after washing, pollutants, low and high temperatures. Some medications can act as nonspecific triggers. In exacerbation of the skin process, the participation of psychogenic mechanisms through the liberation of a number of neuropeptides is possible.

Atopic dermatitis is a genetically determined chronic recurrent skin disease, clinically manifested by primary, often painful itching, age-related evolution of the clinical picture, hypersensitivity to many immune and non-immune stimuli.

Etiopathogenesis. In the etiology of atopic dermatitis, the contribution of genetic factors is an established fact. An autosomal dominant mode of inheritance is assumed. If both parents have dermatosis, then the risk of developing atopic dermatitis in a child is 70-80%; if only the mother or father is sick, the risk of developing the disease is reduced to 30-60%.
In the pathogenesis of atopic dermatitis, leading importance is attached to immune mechanisms.
Among the exogenous factors that have a provoking effect in atopic dermatitis are inhalant food substances, external irritants of a physical nature, animal and plant origin, and negative emotions.
External irritants include wool, fur, latex, synthetic fibers, detergents, nickel, cobalt, lanolin, antibiotics and even topical corticosteroids. In case of drug intolerance in patients, the cause-significant allergens are antibiotics - penicillin and its semisynthetic derivatives, sulfonamides, local anesthetics, non-steroidal anti-inflammatory drugs, B vitamins. The importance of psycho-emotional stress in worsening the condition of patients is known.

Epidemiology. In Ukraine, the incidence ranges from 3-10 per 1000 children. Females are more often affected - 65%, males - 35% less often.
The risk of further respiratory symptoms of allergy in patients with atopic dermatitis is 40-60% (hay fever - 40%, seasonal rhinitis - 25%, atopic asthma - 25%). The chronic course of AD is characterized by seasonal (summer months) and off-season remissions. An exacerbation of the disease usually occurs at the ages of 7-8 and 12-14 years.

Clinical manifestations. The first signs of atopic dermatitis usually appear between the ages of 2-3 months. up to 1.5-2 years. Initial changes appear on the cheeks in the form of "physiological hyperemia" or erythema, peeling on the skin of the scalp, further spreading to the forehead, behind the ear folds, chin, neck, torso.
For the infantile period, erythematous-squamous edematous foci with acute inflammatory small rounded red papules, microvesicles with serous contents, quickly opening, with the formation of "serous wells" are typical. Exudate from dried vesicles forms yellowish-brown crusts. After 6 months of age and in the 2nd year of life, exudative phenomena decrease, and lichenoid and pruriginous components of the lesion begin to appear. The lesions become dry, infiltrative, scaly, small, superficial, barely noticeable polygonal papules appear on the forehead and upper chest. Inflammatory follicular papules develop on the trunk and limbs, sometimes pruriginous and occasionally urticarial rashes. By the end of the 2nd year of life, lesions usually become limited, occupying the extensor and flexion surfaces of the extremities, but a tendency to limit the lesions to the ankle, elbow, and cervical folds begins to appear; the damage to the face is less pronounced.
The second period of development of atopic dermatitis is characterized by the localization of the rash in the folds, the chronic inflammatory nature of the lesions with a more pronounced lichenoid syndrome, the development of secondary skin changes (dyschromia), the undulation of the course, reactions to many provoking influences with a decrease in nutritional hypersensitivity. The main localization of skin lesions is the ulnar and popliteal folds, the flexion surfaces of the upper and lower extremities, the neck, behind the ear folds and the perioral region, the back surface of the hands and fingers, with a more common process - the upper back, the lateral surfaces of the trunk. The face of most patients is free of rashes.
Of the efflorescences, the most common are inflammatory follicular and lichenoid papules, erythematous-infiltrative-squamous and lichenified foci. Skin lesions, which are common at the beginning of the period, later acquire a localized character.
Lesions in the folds are replaced by diffuse changes in the skin of the face, neck, upper body, upper limbs. On the cheeks, they are less pronounced, they are involved in the process of the nasolabial triangle, the skin of the forehead. Only a small part of patients retain pronounced changes in the elbow and popliteal folds, local perioral rashes, and lesions on the hands. The most characteristic rashes are polygonal lichenoid papules, lichenified foci, excoriations.
The main symptom of atopic dermatitis is itching, which persists for a long time even with the disappearance of skin lesions. The intensity of itching is high, especially in lichenoid and pruriginous forms, it can take on the character of biopsy itching. In the period of acute inflammatory rashes, burning, soreness, dryness and tightening of the skin often appear.

In patients with atopic dermatitis, functional disorders of the nervous system and vegetovascular dystonia are naturally found. Manifestations of respiratory atopy in the form of asthmatic bronchitis, atopic rhinitis, bronchial asthma are noted in almost 25% of patients. Eye lesions (conjunctivitis, bilateral “atopic cataracts”) are among the manifestations associated with atopic dermatitis. Characteristic lesions of the gastrointestinal tract are in the form of hypo- or hyperacid states of gastric secretion, gastritis, duodenitis, inflammatory diseases of the biliary tract, pancreatitis, and intestinal dysbiosis.

Diagnostics. The diagnosis, in the vast majority of cases, is made on the basis of the clinical picture of the disease. To identify a specific trigger in atopic dermatitis, skin prick tests with various allergens are used. In patients with extensive skin lesions and severe white dermographism, in vitro tests (RAST or ELISA - determination of specific IgE antibodies) are performed instead of skin tests. To assess the severity of atopic dermatitis and to assess disability, a system for assessing clinical symptoms in SCORAD (scoring of atopic dermatitis) scores has been developed. In the hemogram of patients, eosinophilia is most common (6-10%). A biochemical blood test reveals hypoalbuminemia, changes in globulin fractions, an increase in sialic acid, seromucoid, and sometimes the appearance of C-reactive protein. In the immunogram of patients, the content of T-lymphocytes is reduced due to T-suppressors and T-killers, dysimmunoglobulinemia (increase in the content of IgE and IgG, inhibition of IgA synthesis), as well as an increase in the level of the CEC.

Treatment of atopic dermatitis. Treatment of patients with atopic dermatitis pursues the main goal - reducing the readiness for allergic reactions and eliminating the clinical symptoms of skin lesions. The whole complex of medical and recreational activities, including the organization of the correct regimen and rational nutrition of the child, the use of various pharmacological preparations, physiotherapy procedures; phyto- and reflexotherapy, sanatorium-resort treatment, can be described in a broad sense as non-specific hyposensitization.
Patients should take baths with starch, bran, special products (Triksera - softening baths, Exomega - shower oil). Soap and gel must have a neutral pH. It is necessary to control the temperature and humidity of the air in the apartment, to regularly clean the housing. Sanitation of foci of chronic bacterial, viral and helminthic-protozoal infection with specific preparations is necessary. Normalization of the intestinal microflora is achieved by prescribing preparations containing opportunistic flora antagonist microbes (bactisubtil, biosporin, acilact, biobacton, bifidumbacterin, lactobacterin, bificol, linex, primadolux, lactofiltrum, hilak-forte, normase), agents with antibacterial activity ( metronidazole, hporhinoldol), nitrofuran preparations, herbal medicine (St. John's wort, yarrow, pomegranate, calendula).
Correction of the processes of digestion and absorption is carried out using diet therapy, gastrointestinal enzymes (acidin-pepsin, abomin, pepsidyl, pancreatin, cholenzym, pankurmen, mezim-forte), herbal medicine (wormwood, helichrysum, green tea), restoration of liver functions and the colloidal state of bile - the correct diet, the appointment of hepatoprotectors (legalon, hepabene, essentiale), dietary fiber (wheat bran, oatmeal), sorbents (enterosgel), mineral water. Correction of the pathophysiological and pathochemical effects of allergic (immunopathological) reactions is achieved by antimediator therapy (mast cell membrane stabilizers, Ngistamine receptor blockers), the use of antioxidants and antihypoxants (vitamin E, etimizol, dimephosphone, xydifon).

Intap (1 capsule 4 times a day for 3-4 weeks or in microclysters), H1-histamine lytic - ketotifen (zaditen) have the properties to prevent the destruction of mast cells and the release of allergy mediators with prolonged use. It is prescribed from the age of 6 months. up to 3 years, 0.5 mg 2 times a day; at the age of more than 3 years - 1 mg 2 times a day with meals, with a maximum duration of at least 2 months.
Antihistamines are used to control itching and allergic inflammation of the skin, and their effectiveness is due to the critical role of histamine in the mechanisms of development of most of the clinical symptoms of atopy.
Therapeutic measures for severe and torpid forms may include systemic corticosteroids. Metypred or triamcinolone are preferable at a daily dose of 1-5 mg/kg (30-40 mg per day) with gradual withdrawal. There is also an alternative method of treatment - a double daily dose is prescribed every other day.
In cases of extreme torpidity, the selective immunosuppressant cyclosporine is used in the form of capsules or solution at a dose of 5 mg/kg. A course of extracorporeal detoxification, in particular in the form of plasmapheresis, may be useful for severe blood pressure.
In cases of repeated detection of changes in laboratory parameters (immunograms), immunomodulatory therapy is indicated for patients. Preference should be given to drugs with a pluripotent mechanism of action: sodium nucleinate, ribomunil, bronchovax, some interferon drugs (leukinferon), replacement immunotherapy agents such as titrated donor immunoglobulin (anti-influenza, anti-staphylococcal), native plasma. In all other situations, to restore the functional activity of immunocompetent cells, a regime of antigenic sparing, elimination of the syndrome of endogenous intoxication, stimulation of nonspecific resistance using adaptogens (dibazol, methyluracil, eleutherococcus, Chinese schisandra), some methods of physiotherapy (general ultraviolet radiation, UHF on the sternum or solar plexus) is sufficient ).
Topical therapy for atopic dermatitis includes: suppression or elimination of itching, elimination of biologically active substances and destructive substances, elimination of bacterial and mycotic infections, improvement of microcirculation and metabolism in the affected areas, elimination of lichenification, reduction or elimination of dryness.
When treating the acute stage of the disease, lotions and wet-dry dressings, creams and gels with vitamins A, E, topical corticosteroids with weak or moderate activity are used, it should be remembered that the maximum possible surface for treatment with steroids is no more than 20% of the body surface and duration of use in children - 14 days with return to indifferent therapy; dilute corticosteroids and do not use them under occlusive dressings; Do not use in the area of ​​lips, scrotum, diaper rash.
For children with allergic dermatoses, the safest steroids for a short period are those containing mometasone furoate, methylprednisolone aceponate, hydrocortisone butyrate (Elocom, Advantan, Lokoid) and non-steroidal cream Elidel. If complicated by a bacterial or fungal infection - solutions of aniline dyes, creams or ointments pimafucort, triderm, triacutan, bactroban, baneocin, fusidine, etc. At the stage of the chronic process, preparations of naphthalan, tar, fenistil-gel, psilo-balm, actovegin, solcoseryl, ozokerite, paraffin applications, local baths for hands, feet, sapropels, DARDIA cream (Lipo Balm), soft shampoos of the Freederm series, products for Trixer baths, exomega. After a bath, shower, sauna, emollient creams containing polyunsaturated fatty acids, vitamin E (exomega cream and milk), Trixer creams, and bepanthen are recommended.

Spa treatment: SPA resorts.

Prevention atopic dermatitis. Primary prevention, aimed at preventing the development of the first manifestations of atopic dermatitis in young children, should be carried out in pregnant women at risk (those with a family predisposition to atopy or patients with atopic dermatitis). Secondary prevention involves timely diagnosis of disorders of the immune and nervous systems, diseases of the digestive system, and their adequate therapy.

Atopic dermatitis (or diffuse neurodermatitis, endogenous eczema, constitutional eczema, diathetic prurigo) is a hereditarily determined chronic disease of the entire body with a predominant lesion of the skin, which is characterized by polyvalent hypersensitivity and eosinophilia in the peripheral blood.

Etiology and pathogenesis. Atopic dermatitis is a multifactorial disease. The model of multifactorial inheritance in the form of a polygenic system with a threshold defect is currently considered the most accurate. Thus, hereditary predisposition to atopic diseases is realized under the influence of provoking environmental factors.

An inadequate immune response contributes to increased susceptibility to various skin infections (viral, bacterial and mycotic). Superantigens of bacterial origin are of great importance.

An important role in the pathogenesis of atopic dermatitis is played by the inferiority of the skin barrier associated with impaired ceramide synthesis: the skin of patients loses water, becoming dry and more permeable to various allergens or irritants that enter it.

The characteristics of the psycho-emotional status of patients are essential. Characteristic features of introversion, depression, tension and anxiety. The reactivity of the autonomic nervous system changes. There is a pronounced change in the reactivity of blood vessels and the pilomotor apparatus, which is dynamic in nature in accordance with the severity of the disease.

Children who had manifestations of atopic dermatitis at an early age represent a risk group for developing atopic bronchial asthma and allergic rhinitis.

Diagnostics. To make the correct diagnosis, basic and additional diagnostic criteria are used. The criteria proposed at the First International Symposium on Atopic Dermatitis are used as a basis.

Basic criteria.

1. Itching. The severity and perception of itching may vary. As a rule, itching is more disturbing in the evening and at night. This is due to the natural biological rhythm.

2. Typical morphology and localization of rashes:

1) in childhood: damage to the face, extensor surface of the limbs, torso;

2) in adults: rough skin with an accentuated pattern (lichenification) on the flexor surfaces of the limbs.

3. Family or individual history of atopy: bronchial asthma, allergic rhinoconjunctivitis, urticaria, atopic dermatitis, eczema, allergic dermatitis.

4. The onset of the disease in childhood. In most cases, the first manifestation of atopic dermatitis occurs in infancy. This is often due to the introduction of complementary foods, the prescription of antibiotics for some reason, or climate change.

5. Chronic relapsing course with exacerbations in the spring and autumn-winter seasons. This characteristic feature of the disease usually appears no earlier than 3 to 4 years of age. A continuous off-season course of the disease is possible.

Additional criteria.

1. Xeroderma.

2. Ichthyosis.

3. Palmar hyperlinearity.

4. Follicular keratosis.

5. Increased level of immunoglobulin E in blood serum.

6. Tendency to staphyloderma.

7. Tendency to nonspecific dermatitis of the hands and feet.

8. Dermatitis of the breast nipples.

9. Cheilitis.

10. Keratoconus.

11. Anterior subcapsular cataract.

12. Recurrent conjunctivitis.

13. Darkening of the skin of the periorbital area.

14. Infraorbital Denny–Morgan fold.

15. Facial pallor or erythema.

16. White pityriasis.

17. Itching when sweating.

18. Perifollicular seals.

19. Food hypersensitivity.

20. White dermographism.

Clinic. Age periodization. Atopic dermatitis usually manifests itself quite early - in the first year of life, although its manifestation is possible at a later date. The duration of the course and the timing of remissions vary significantly. The disease can continue into old age, but more often its activity subsides significantly with age. There are three types of atopic dermatitis:

1) recovery up to 2 years (most common);

2) pronounced manifestation up to 2 years with subsequent remissions;

3) continuous flow.

Currently, there is an increase in the third type of flow. At an early age, due to the imperfection of the child’s various regulatory systems and various age-related dysfunctions, the effect of external provoking factors is much more pronounced. This may explain the decrease in the number of patients in older age groups.

In conditions of deteriorating environmental conditions, the role of external factors is increasingly increasing. These include exposure to atmospheric pollution and occupational aggressive factors, increased contact with allergens. Psychological stress is also significant.

Atopic dermatitis occurs with chronic recurrence. Clinical manifestations of the disease change with the age of patients. Long-term remissions are possible during the course of the disease.

The clinical picture of atopic dermatitis in children aged 2 months to 2 years has its own characteristics. Therefore, the infant stage of the disease is distinguished, which is characterized by the acute and subacute inflammatory nature of the lesions with a tendency to exudative changes and a certain localization - on the face, and with widespread lesions - on the extensor surfaces of the limbs, less often on the skin of the body.

In the vast majority of cases, there is a clear connection with nutritional stimuli. Initial changes usually appear on the cheeks, less often on the outer surfaces of the legs and other areas. Disseminated skin lesions are possible. The lesions are located primarily on the cheeks, in addition to the nasolabial triangle, the unaffected skin of which is sharply demarcated from the lesions on the cheeks. The presence of rashes on the skin of the nasolabial triangle in a patient with atopic dermatitis at this age indicates a very severe course of the disease.

The primary ones are erythematoedematous and erythematosquamous lesions. In more acute cases, papulovesicles, cracks, weeping, and crusts develop. Characterized by severe skin itching (uncontrollable scratching movements during the day and during sleep, multiple excoriations). An early sign of atopic dermatitis may be milky crusts (the appearance on the scalp of fatty brownish crusts, relatively tightly fused to the underlying reddened skin).

By the end of the first – beginning of the second year of life, exudative phenomena usually decrease. Infiltration and peeling of lesions increase. Lichenoid papules and mild lichenification appear. Follicular or pruriginous papules may appear, and rarely, urticarial elements. In the future, complete involution of the rash or a gradual change in morphology and localization is possible with the development of the clinical picture characteristic of the second age period.

The second age period (childhood stage) covers the age from 3 years to puberty. It is characterized by a chronically relapsing course, often depending on the season of the year (exacerbation of the disease in spring and autumn). Periods of severe relapses may be followed by long remissions, during which children feel practically healthy. Exudative phenomena decrease, pruriginous papules, excoriations predominate, and a tendency to lichenification, which increases with age. Eczema-like manifestations tend to cluster, most often appearing on the forearms and lower legs, resembling plaque eczema or eczematitis. Erythematosquamous rashes around the eyes and mouth, which are difficult to treat, often appear. At this stage, typical lichenified plaques may be present in the elbow bends, popliteal fossae and on the back of the neck. Characteristic manifestations of this period also include dyschromia, which is especially noticeable in the upper back.

With the development of vegetative-vascular dystonia, grayish pallor of the skin appears.

By the end of the second period, the formation of changes typical for atopic dermatitis on the face is possible: pigmentation on the eyelids (especially the lower ones), a deep fold on the lower eyelid (Denny-Morgan symptom, especially characteristic of the exacerbation phase), in some patients - thinning of the outer third of the eyebrows. In most cases, atopic cheilitis is formed, which is characterized by damage to the red border of the lips and skin. The process is most intense in the area of ​​the corners of the mouth. The part of the red border adjacent to the oral mucosa remains unaffected. The process never spreads to the oral mucosa. Erythema with fairly clear boundaries is typical; slight swelling of the skin and red border of the lips is possible.

After the acute inflammatory phenomena subside, lichenification of the lips is formed. The red border is infiltrated, peels off, and has multiple thin radial grooves on its surface. After the exacerbation of the disease subsides, infiltration and small cracks in the corners of the mouth may persist for a long time.

The third age period (adult stage) is characterized by a lesser tendency to acute inflammatory reactions and a less noticeable reaction to allergic irritants. Patients mainly complain of itchy skin. Clinically, the most characteristic lesions are lichenified lesions, excoriations and lichenoid papules.

Eczema-like reactions are observed mainly during periods of exacerbation of the disease. Characterized by severe dry skin, persistent white dermographism, and a sharply enhanced pilomotor reflex.

Age-related periodization of the disease is not observed in all patients. Atopic dermatitis is characterized by a polymorphic clinical picture, including eczematous, lichenoid and pruriginous manifestations. Based on the predominance of certain rashes, a number of clinical forms of the disease in adults can be distinguished, such as:

1) lichenoid (diffuse) form: dryness and dyschromia of the skin, biopsy itching, severe lichenification, a large number of lichenoid papules (hypertrophied triangular and rhombic skin fields);

2) eczema-like (exudative) form: most typical for the initial manifestations of the disease, but in adults, skin changes such as plaque eczema, eczematid and eczema of the hands may predominate in the clinical picture of the disease;

3) pruriginous form: characterized by a large number of pruriginous papules, hemorrhagic crusts, excoriations.

Among the dermatological complications of atopic dermatitis, the first place is occupied by the addition of a secondary bacterial infection. In cases where staphylococcal infection predominates, they speak of pustulization. If the complication of the disease is caused primarily by streptococci, impetiginization develops. Sensitization to streptococci and eczematization of streptoderma foci often develop.

With prolonged existence of inflammatory changes in the skin, dermatogenous lymphadenopathy develops. Lymph nodes can be significantly enlarged and have a dense consistency, which leads to diagnostic errors.

Treatment. Therapeutic measures for atopic dermatitis include active treatment in the acute phase, as well as constant strict adherence to the regimen and diet, general and external treatment, and climatic therapy.

Before starting therapy, it is necessary to conduct a clinical and laboratory examination to identify factors that provoke exacerbation of the disease.

For successful treatment of atopic dermatitis, detection and control of risk factors that cause exacerbation of the disease (triggers - nutritional, psychogenic, meteorological, infectious and other factors) are very important. The elimination of such factors significantly facilitates the course of the disease (sometimes to complete remission), prevents the need for hospitalization and reduces the need for drug therapy.

In the infant phase, nutritional factors usually come to the fore. Identification of such factors is possible with sufficient activity of the child’s parents (careful keeping of a food diary). In the future, the role of food allergens decreases somewhat.

Patients with atopic dermatitis should avoid foods rich in histamine (fermented cheeses, dry sausages, sauerkraut, tomatoes).

Among non-food allergens and irritants, dermatophagoid mites, animal hair, and pollen occupy a significant place.

Colds and respiratory viral infections can cause atopic dermatitis to worsen. At the first symptoms of a cold, it is necessary to start taking antisensitizing medications.

In young children, nutritional factors such as enzymatic deficiency and functional disorders are of great importance. It is advisable for such patients to prescribe enzymatic preparations and recommend treatment at gastrointestinal resorts. In case of dysbacteriosis and intestinal infections, targeted correction is also carried out.

For mild exacerbations of the disease, you can limit yourself to prescribing antihistamines. The most commonly used are new generation histamine H1 receptor blockers (cetirizine, loratadine), which do not have side sedative effects. Drugs in this group reduce the body’s response to histamine, reducing smooth muscle spasms caused by histamine, reducing capillary permeability, and preventing the development of tissue edema caused by histamine.

Under the influence of these drugs, histamine toxicity decreases. Along with the antihistamine effect, drugs in this group also have other pharmacological properties.

For moderate exacerbations of the disease, in most cases it is advisable to begin therapy with intravenous infusions of solutions of aminophylline (2.4% solution - 10 ml) and magnesium sulfate (25% solution - 10 ml) in 200 - 400 ml of isotonic sodium chloride solution ( daily, 6 – 10 infusions per course). In the lichenoid form of the disease, it is advisable to include atarax or antihistamines with a sedative effect in therapy. For an eczema-like form of the disease, atarax or cinnarizine is added to therapy (2 tablets 3 times a day for 7–10 days, then 1 tablet 3 times a day). It is also possible to prescribe antihistamines that have a sedative effect.

External therapy is carried out according to the usual rules - taking into account the severity and characteristics of inflammation in the skin. The most commonly used creams and pastes contain antipruritic and anti-inflammatory substances. Naftalan oil, ASD, and wood tar are often used. To enhance the antipruritic effect, phenol, trimecaine, and diphenhydramine are added.

In the presence of an acute inflammatory skin reaction with weeping, lotions and wet-dry dressings with astringent antimicrobial agents are used.

When the disease is complicated by the addition of a secondary infection, stronger antimicrobial agents are added to external remedies.

Externally, for mild and moderate exacerbations of atopic dermatitis, short courses of topical steroids and local calcineurin inhibitors are used.

The external use of drugs containing glucorticosteroids for atopic dermatitis is based on their anti-inflammatory, epidermostatic, coreostatic, antiallergenic, and local anesthetic effects.

In case of severe exacerbation of the process, it is advisable to carry out a short course of treatment with glucocorticosteroid hormones. The drug betamethasone is used. The maximum daily dose of the drug is 3–5 mg with gradual withdrawal after achieving a clinical effect. The maximum duration of therapy is 14 days.

For severe exacerbations of atopic dermatitis, it is also possible to use cyclosporine A (daily dose 3–5 mg per 1 kg of patient body weight).

Most patients in the acute phase require psychotropic medications. A long course of itchy dermatosis often provokes the appearance of significant general neurotic symptoms. The first indication for prescribing drugs that inhibit the function of cortico-subcortical centers is persistent night sleep disorders and general irritability of patients. For persistent sleep disturbances, sleeping pills are prescribed. To relieve excitability and tension, small doses of atarax are recommended (25–75 mg per day in separate dosages during the day and at night), a drug that has a pronounced sedative, as well as antihistamine and antipruritic effect.

The use of physical factors in therapy should be strictly individual. It is necessary to take into account the forms of the disease, the severity of the condition, the phase of the disease, the presence of complications and concomitant diseases. In the stabilization and regression phase, as well as as a prophylactic agent, general ultraviolet irradiation is used.

Prevention. Preventive measures should be aimed at preventing relapses and severe complicated course of atopic dermatitis, as well as preventing the occurrence of the disease in risk groups.