ANNOTATION

The information and methodological letter was prepared as part of the implementation of the Moscow Regional Program of State Guarantees for citizens of the Russian Federation of free medical care.

The letter provides information on etiology, pathogenesis, clinical picture, diagnostic criteria, medical and preventive measures, dispensary accounting with atopic dermatitis.

The information letter is intended for the doctors of dermatovenerologists, pediatricians, clinical orders and interns doctors.

Compilers:

Mostbin L.B. - chief doctor of the State University "Moscow Regional Clinical Skin-Venereological Dispensary";

Shuvalova T.M. - Ph.D., head of the organizational and methodological department of the State University "Moscow Regional Clinical Skin-Venereological Dispensary", the main children's dermatovenerologist of the Moscow region;

Maksimova I.V. - Head of the Consultative and Polyclinical Department of the State University "Moscow Regional Clinical Skin-Venereological Dispensary";

Leswin E.M. - D.M., doctor of the State University "Moscow Regional Clinical Skin-Venereological Dispensary";

Klochakova TA - Ph.D., doctor of the State University "Moscow Regional Clinical Skin-Venereological Dispensary";

Kalenichenko N.A. - doctor of the State University "Moskovsky Regional Clinical Skin-Venereological Dispensary";

Ophdovova E.D. - doctor of the State University "Moscow Regional Clinical Skin-Venerologian Dispensary".

Reviewer - D.N., Professor, Suvorova K.N.

Introduction

Atopic dermatitis (hell) - The actual problem of child dermatovenerology, since his debut in most cases falls on early children's age (60-70% of children in the first year of life). AD is 20-30% among all allergic diseases of children's age.

Despite the large number of adhesives, such as "endogenous eczema", "Children's eczema", "Atopic neurodermatitis", "Diffuse Neurodermit of Brock", "Prurigo Bempi", they all at the moment of time are outdated and in their essence reflect the development stages a single pathological process.

AD is a chronic allergic disease, developing in individuals with a genetic predisposition to atopy, having a recurrent flow with age-related evolutionary features of clinical manifestations and hypersensitivity to specific (allergenic) and nonspecific stimuli.

The most characteristic distinctive feature of the blood pressure is the itching and age-related change in topography and clinical morphology of skin lesions that are not characteristic of other multifactorial dermatoses.

Skin diseases, clinically similar to blood pressure, but not having an atopic basis pathogenesis are not blood pressure. The main purpose of the preparation of these methodological recommendations is to reduce diagnostic errors in practicing dermatologists, an increase in the level of medical and prophylactic assistance to patients with blood pressure.

The hard forms of hell sharply reduce the quality of life of the patient and his whole family, contribute to the formation of psychosomatic disorders. 40 - 50% of children suffering from hell, subsequently develops pollinosis and / or allergic rhinitis, bronchial asthma.

The risk group includes:

• Children whose parents in the family history have allergic diseases (extempus, bronchial asthma, allergic rhinitis, etc.), mainly through the mother's line (the detection of burded family anamnesis reaches 80%);
• Children born with a mass of the body of more than 4 kilograms;
• Children born with a body weight of less than 3 kilograms - low-tech children;
• Children who have appeared by cesarean section;
• In addition, the risk group includes children born from mothers, which during pregnancy had chronic foci of infection, including wicked invasions and giardias, endocrinopathies, suffered from vegetative dystonia, severe toxicosis, anemia, transferred acute infectious diseases, were stressful, taken various medicines. There were irrational habits and professional harm to the diseases.

Etiology

The beginning of the disease, as well as its flow and degree of gravity, is due to the interaction of predisposing genes and trigger (launcheling) factors. Trigger factors can be the most diverse: physical and mental overvoltage; Emotional injuries; Inhalation of poisoning gases, chemicals and drugs; pregnancy and childbirth; Moving to permanent place Residence in an ecologically unfavorable area, etc. (See Table 1). Susceptibility to trigger factors depends on the age of patient, its endogenous constitutional features, such as morphofunctional characteristics gastrointestinal intestinal tract, endocrine, nervous, immune systems.

In breast and early childhood Among the trigger factors, food allergens are dominated, irrational feeding and nutrition, infectious agents, preventive vaccinations, and their effect becomes more pronounced if there is immunodeficient states, chronic foci of infection, food allergies, immaturity of enzyme systems, liver diseases, vitamin metabolic disorders. Often, the manifestation of the skin manifestations occurs after unreasonably early translation of infant children on artificial feeding

In the future, the significance of inhalation allergens increases: household, epidermal, pollen. Among the household allergens is the greatest importance of home dust. When allergic to pollen plants during flowering period, it is necessary to seal windows, limit walks into windy and sunny weather, use hygiene products containing vegetable components with caution.

Parents of sick children and patients themselves must be explained that woolen or synthetic clothing, detergents can also provoke exacerbation. In addition, it is necessary to bear in mind nonspecific, non-allergenic aggravation factors, which include stress, extreme values \u200b\u200bof air and humidity temperature, intense physical activity, infectious diseases.

In adult development of exacerbations of the disease, contact allergens are promoted, drugs taken on the concomitant somatic pathology, irrational nutrition.

Table 1

Trigger factors hell

Food allergens	High allergizing activity products: proteins of cow milk, cereals, eggs, fish, soybeans, cocoa, chocolate, caviar and seafood, mushrooms, carrots and tomatoes. Products with medium allergizing activity include: peaches, apricots, cranberries, bananas, green peppers, potatoes, peas, rice, corn, Grech. Weak allergizing activity have green and yellow apples, pears, white currants and sweet cherries, gooseberries, zucchini, patissons, fermented milk products
Inhalation allergens	Home and Library Dust, Pillock Feather, Flowering Plant Pollen, Mold, Dandruff, Pet Epidermis, Tobacco Smoke. The main source of allergens in home dust is DERMATOPHAGOIDES PERONYSSSIMUS tick, and tick feces have the main allergenity
Contact stimuli and allergens	Soaps, Solvents, Wool Clothes, Mechanical Studies, Detergents, Preservatives, Flavoring
Infectious agents	Staphylococcus Aureus, Helicobacter Pylori, Trichophyton Rubrum and Malassezia Furfur (Pityrosporum Ovale or Pityrosporum Orbiculare), Mushrooms of Candida, Herpes Simplex virus, cytomegalovirus, worms and giardia
Reception of drugs	Antibiotics, sulfonamides, vitamins, nonsteroidal anti-inflammatory drugs
Psycho-emotional factors	Fear, overvoltage, overexcitation
Endocrine factors	The aggravation of the disease during pregnancy, in breast children, the aggravation of hell during menstruation at a nursing mother.
Increased exercise	Increased sweating promoting secondary skin infection
Eranny food	Early artificial feeding, later applying to the chest, violation of the power mode, excessive use of products rich in histaginolybers
Preventive vaccinations	Can provoke both the beginning of the disease and the exacerbation of the process (especially DC)
Climatic influences	Frequent exacerbations in spring and autumn periods

Sensitivity to several allergens is often recorded, which is often associated with the development of allergic cross-reactions due to the presence of general antigenic determinants. There are simultaneous intolerance to fresh cow's milk, eggs, meat broths, citrus, chocolate.

Between allergens of the pollen of trees, there is also structural homology, and it is expressed much weaker than also the existing affinity of allergens pollen of herbs. Therefore, patients who have increased sensitivity to the pollen of the birch, at the same time react to the pollen of the hazel and alder. Similar allergenic properties may have antigenic determinants of pollen and other classes of allergens (for example, when eating leaves and fruits of the same plants) (Table 2).

table 2

Possible options for intolerance of related vegetable allergens, food products and phytopreparatics with allergies to pollen plants

Ecological factor (pollen)	Possible cross-reactions
	Pollen, leaves and stalks of plants	Vegetable foods	Medicinal plants (phytopreparations)
Birch	Leschina, alder, apple tree	Apples, Cherry, Nuts (Hazelnuk), Peaches, Plums, Carrots, Celery, Potatoes, Tomatoes, Cucumbers, Onions, Kiwi	Birch leaf (kidneys), Olkhovy bumps
Cereals		Food grasses (Wheat, wheat, barley, and D.R.), sorrel
Sagebrush	Dahlia, chamomile, dandelion, sunflower	Citrus, sunflower seed (oil, halva), chicory, honey	Wormwood, chamomile, calendula, mother and machech, nine, series
Wan Ambrosia	Sunflower, dandelion.	Beets, spinach, melon, bananas, sunflower seed

Pathogenesis of atopic dermatitis

At the heart of the development of blood pressure lies a genetically programmed feature of the organism's immune response to allergens, as a result of which immunopathological reactions arise. The most significant in pathogenesis is the reaction of the hypersensitivity of a slow-type (GZT), in which sensitized lymphocytes and their interaction with allergens play a leading role. The final result of this reaction is the production of mediators GZT and the development of chronic immune inflammation. Morphologically, this is manifested by a lymphic histiocytic reaction around the vessels of the dermis. At the same time, in cases of active products of the IGE class antibodies in the pathogenesis, the adhesiveness of the immediate type (GTT) is often involved, with the reaction of fat cells and basophils. With their subsequent degranulation and emissions into the blood of the GNT mediators, the main of which are histamine, slowly reacting anaphylaxis. Clinically, it is manifested by erythematous-urticular rashes. Treatment should be determined taking into account the prevalence of the type of immunopathological reactions (immediate or slow-type).

The basis of pathogenesis is immunopathological processes. The most characteristic violations of immune status are:

1. Changes in the phagocytic system: more often observed the phase of the absorption phase of the antigenic material by phagocyant cells and completed phagocytosis;
2. Reducing the content of T-lymphocytes, an increase in lymphocytes, imbalance of immunoregular T-lymphocytes: an increase in T-helpers and suppressing T-suppressors;
3. The predominance of TH-2 subpopulation leads to increased cytokine products with a pro-inflammatory and disposable effect (interleukin -3, interleukin - 4, interleukin - 5);
4. Diskimumunoglobulinemia - the content of IGE, IgG is more often increased;
5. Increased the content of circulating immune complexes;
6. Violation of the function of local immunity of the gastrointestinal tract, a decrease in the synthesis of secretory immunoglobulin A, which deprives the intestine of the necessary protective secret and creates a background for the damaging effect on the microbial and antigenic factors;
7. Insolvency of local immune protective functions of the skin and local skin immunity.

Along with violations in the immune status of patients in the formation of pathogenesis, other factors are also involved:

• imbalance of intracellular regulatory mechanisms (the ratio of CAMF / TSGMF);
• disruption of the membrane reception (fat cells of patients with atopic diseases contain 10 times more receptors to IgE than cells of healthy people);
• activation of non-immune mechanisms for the release of allergic inflammation mediators;
• violation of the neareegetative function and peripheral blood circulation (spasm of peripheral vessels);
• psycho-physiological and psychosomatic deviations;
• violations of the equilibrium of sympathetic and parasympathetic systems (blockade of β-adreno-receptors and the predominance of α receptors);
• the genetic violation of the barrier function of the skin leads to the penetration of allergens from the environment in the skin, which causes immunological reactions and inflammation, as well as colonization of piococcal and mushrooms;
• endocrine dysfunctions (hypercorticism, hypoandrogenation, hypoestroaction, hyperthyroidism);
• dysfunction of the gastrointestinal organs (food enzymes, intestinal dysbiosis, gastritis, hepatobiliary dysfunction);
• the presence of chronic foci of infection (more often than Lor organs and the gastrointestinal tract);
• glice and protozoa invasion;
• spinal diseases;
• dysmetabolic nephropathy;
• metabolic disorders of fatty acids in uniform elements, blood plasma, adipose tissue.

Clinical picture

Manifestation of blood pressure occurs in infancy, proceeds with remissions of various duration, can last up to puberty, and sometimes it does not pass until the end of life. Recurrements usually occur seasonally (autumn, winter, sometimes spring), improving or disappearance of manifestations, as a rule, is marked in the summer.

In severe cases, hell flows torpidly, without remission, with the development of atopic erythrodermia.

Hell is characterized by clinical polymorphism of rash. The true polymorphism of the rash is a common feature of all clinical forms of blood pressure, they create a complex clinical syndrome with combining features of the eczematosis and dynamoid lesions, accompanied by itching.

Each age of the period is characterized by their clinical and morphological features, which is manifested in the age evolution of the elements of the rash. In this regard, five clinical and morphological forms are isolated (exudative, erythematous-squamous, erythematous-squamous with liquidification, lihenoid, barginin) and three stages of development of the disease - infant, children's and adolescent-adult (Table 3).

Table 3.

Age stages of development and clinical and morphological forms of atopic dermatitis

By the severity of the flow of blood pressure, they allocate a lung, medigative and heavy forms of the disease. For course, they allocate acute, subacute periods and remission (Table 4).

Table 4.

Working classification of atopic dermatitis

Diagnosis examples:

Atopic dermatitis, exudative form, infant stage, II Art. gravity, period of exacerbation.

Atopic dermatitis, erythematosno-squamous form, Children's stage, I Art. gravity, subacute period.

Atopic dermatitis, Lichnemoid form, Teenage stage, III Art. gravity, period of exacerbation

Appendix 2.

Atoderm Mousse, Soap (BIODERMA) (from the newborn period)

CU-ZN + Gel, Cu-Zn + Dermatological Soap (URIAGE) (from the newborn period)

Cemezoz shiny, soft cleansing cream gel without soap (UriAGE) (from the newborn period)

Trixer + Cleansing Softening Gel (Avene) (from the newborn period)

Trizzer + Cleansing Soften Bath (Avene) (from the newborn period)

Exomega Cleansing Oil for the Soul (A-Derma) (from the newborn period)

Cleansing softening gel (Avene) (from the newborn period)

Shampoo for the removal of dairy crusts in babies (A-Derma)

Friterm RN-Balance Shampoo (MSD)

Dermalibor Antibacterial Cleansing Gel For Irished Skin With Risk of Infection (A-Derma) (from the newborn period)

Lipicar Shinet Gel (La Roche Posay) (from 1 year)

Skin-Cap Shampoo (Cheminova Internacional S.A.) (from 1 year)

Appendix 3.

Nonteroid drugs used for the treatment and care of the skin of patients with blood pressure.

Name of the drug	Age with which is allowed to use	Indications
Atoderm R.O. Zinc Cream (BIODERMA)	From the newborn period	In the sharp period, it is possible to use in the period of mocking
Atoderm RR Antreesidivnaya Balm (Bioderma)	From the newborn period	When poeing acute phenomena, before the onset of remission
ATODERM CREAM (BIODERMA)	From the newborn period	During the remission
Spray with CU-Zn + Refrigerate (Uriage)	From the newborn period	In the sharp period when moknuti
Cu-Zn + Cream (Uriage)	From the newborn period
Crembam Cream-Emoljante, Captoz Cerat (Uriage)	From the newborn period	During the remission
Lockobays Ripea (ASTELLAS)	From the newborn period
Lipokrem Lockoise (ASTELLAS)	From the newborn period	In a sharp period (in the absence of a mock) and during remission
Dermalibe Cream (A-Derma)	From the newborn period	In a sharp period, possibly when weaving
Sitelium Lotion (A-Derma)	From the newborn period	In the period of mocking
TRIKSER + CREAM AND BALM (Avene)	From the newborn period
Dardia Cream, Milk, Balm (Intendis)	From the newborn period cream, from 1 year old balsam and milk.	During remission
Lockobays Ripea (ASTELLAS)	From the newborn period	In the acute period in the absence of a mock, as well as during remission
Lipicar Balsam (La Roche Posay)	From the 1st year	In the acute period in the absence of mocking, as well as during remission.

The content of the article

Dermatitis - inflammatory lesion of the skin, developing at the exposure to Piz. or chemical. factors.
Domestic dermatological school The concept of "dermatitis" identifies with the concept of "contact dermatitis" and considers it to be wrong to call dermatitis of skin lesion due to the uncomfortable path of impact on the body. For example, changes on the skin arising from the oral or parenteral route of administration of medicines, it is necessary to be called toxidermia. At the same time, the term "dermatitis" is still used to designate certain skin diseases with various mechanisms of development: Durring Disease, Dermatitis of pigment progressive, dermatitis of atonic and AR.
The term "dermatitis" is traditionally used in two cases: for the characteristics of any changes resulting from contacting the substance with skin, simple dermatitis (artiffical, toxic) and as a synonym for dermatitis of allergic contacts.
In the occurrence of simple dermatitis, allergic mechanisms do not take part. It is the so-called bondnant stimuli, that is, such that cause an inflammatory response from any person. This is chemical. Substances (acids, alkalis), mechanical (scuff) and physical. Factors (temperatures, x-rays and ultraviolet rays), plants (caustic buttercup, ash, scarce, poisonous Badyan, Mokha, nettles, Pasternak, etc.). The cause of allergic contact dermatitis is optional stimuli, which cause the inflammatory skin reaction to only people with genetic predisposition to the development of this disease and altered immunity. These include metal ions, rubber, synthetic polymers, cosmetics, medicines, some plants. Simple dermatitis may occur after a single contact with a strong stimulus or after repeated contacts with the average. Unlike allergic contact dermatitis, the incubation period is not required for the occurrence of simple dermatitis. Some chemical. substances, eg. Cement, possess the properties of bond irritants and allergens.

Allergic contact dermatitis

Allergic contact dermatitis Dermatitis allergic, dermatitis Eczema, eczema Allergic contact - inflammatory allergic lesion of the skin, developing on the site of direct contact of the substance to which the body was sensitized as a result of the previous exposure.

Etiology and pathogenesis of allergic contact dermatitis

The amounts of substances with the potential properties of contact allergens are very large in the same way as endless capabilities in which they can contact with the skin. However, only certain chemicals. Substances are responsible for the occurrence of allergic contact dermatitis. These substances called haptenses have a low mole. Mass (500-1000 Dalton), easily penetrate the skin and are able to bind covalently with chemical. elements of organism proteins. In some cases, not the substances themselves, but their metabolic products, can act as hapten. The hypersensitivity of the slow-type contact is most easily induced by substances that are dissolved by skin fats or products capable of penetrating the horn layer of the epidermis and having affinity to epidermal cells. The property of this or that agent to cause allergic contrast dermatitis depends on its ability to bind to proteins. The cause of allergic contact dermatitis can be different chemical. Substances, medicines, plants. Unlike simple dermatitis, allergic contact dermatitis occurs only in certain persons in contact with this substance, and only when repeated contact with it. Allergic contact dermatitis may be the result of the systemic use of the medication in persons pre-sensitized by this preparation or chemical. Substance having similar antigenic determinants. Allergy is occurring 7-10 days after first contact with a potential allergen, more often for the development of contact allergies, a re-and long exposition by a sensitizing agent is necessary, even years in case of professional allergyization.
One of the most powerful contact allergens is the juice of plants from the Summy family, which have 100-150 varieties. About 70% of those in contact with the "poison" of the suma suffer from allergic contact dermatitis. The allergic genesis of allergic contact dermatitis is confirmed by the fact that people who have never contacted with this plant (residents of Europe), allergic contact dermatitis does not develop.
For the occurrence of allergic contact dermatitis, Hapten must penetrate the skin, contact protein, form an antigen. Of great importance in this process is attached to the Langerhans cells, which are found in the epidermis, thymus and lymph nodes. Langerhans cells have a specific affinity to substances with low mole. Mass (hapten). In this regard, it is assumed that these cells absorb hapten when it passes through the epidermis, conjugate it with proteins and turn into a complete antigen. Then the antigen is then transferred to regional lymph nodes, in which the number of lymphocytes of T. sensitized lymphocytes of t from lymph nodes is migrated into the skin and blood. This process lasts almost 10 days - the incubation period. If chem. The agent again contacts the patient's skin, allergic contact dermatitis develops after 12-48 hours. This time (reaction time) is shorter than the incubation period, since the lemphocytes T, sensitized to this substance are in the skin. The interaction of lymphocytes T with an antigen leads to the products of lymphokinov, admission to the focus of inflammation of neutrophils, basophils, lymphocytes, eosinophils, damage to skin cells, which manifests the symptoms of allergic contact dermatitis. This contact hypersensitivity is a classic example of a slow-type hypersensitivity, which is confirmed by the following facts: an inflammatory process with an allergic contact dermatitis. associated with the accumulation of mononuclear cells of the lymphoid series; Contact sensitivity can be passively transferred by suspension of lymphoid cells (but not serum) taken from a sensitized animal; Contact sensitivity is accompanied by changes in drainage lymph nodes (proliferation of lymphocyte T), which is typically for cellular allergic reactions; When cultivating lymphocytes with allergic contact dermatitis patients. Gapden conjugates - protein is observed RBTL, which also indicates sensitization of lymphocytes T. Confirming the role of the T-system of immunity in the pathogenesis of the disease serves the functional insufficiency of lymphocytes T in patients with allergic contact dermatitis.
The development of allergic contact dermatitis is associated with hereditary predisposition. Children of parents sensitive to DNHB are easier sensitizing than parents who are not sensitive to DNHB. Such a genetic predisposition was revealed by twins and in animal experiment.
The role of antibodies in the development of allergic contact dermatitis is discussed. Around the vessels, in the dermis and vesicles patients with allergic contact dermatitis, lymphoid cells with immunoglobulin membrane, mainly immunoglobulin E and immunoglobulin D are determined. These cells are in the skin and in the absence of clinical symptoms of allergic contact dermatitis. It is assumed that they are memory cells that carry a predisposition to the disease. In patients experimentally sensitized with DNHB, there are lymphocytes carrying immunoglobulin D, and in patients with allergic contact dermatitis, the number of circulating lymphocytes with surface immunoglobulin D is increasing.

Pathomorphology of allergic contact dermatitis

Histological changes in the skin with allergic contact dermatitis are not specific. Before the occurrence of clinical signs of the disease in the skin of a sensitized person after 3 hours after contact with the allergen, vasodyolates and perivascular infiltration of mononuclears occur, after 6 - the infiltration of the skin by mononuclears, intracellular swelling (spongiosis) in the deep layers of the epidermis. In the next 12-24 hours, spongiosis intensifies and intapidermal vesicles are formed; Mononuclear infiltration captures all epidermis. Thickening (acanthosis) of the epidermal layer becomes visible naked eye. Two days later, spongiosis disappears and vesicular changes are dominated, as well as acanthosis, pararacratosis occurs. Characteristic for acute allergic contact dermatitis spongiosis, visication, acanthosis, pararacratosis, exocytosis. Microscopic changes in the disease tend to vary in different parts of the amazed epidermis (spotting histological picture). Skin biopsy with allergic contact dermatitis can only help in cases if it is necessary to distinguish this condition from dermatological disorders with a characteristic histological picture. Simple dermatitis differs from allergic contact dermatitis with a more pronounced destruction of the epidermis and the presence of polymorphic nuclear cells in infiltrates.

Allergic contact dermatitis clinic

Allergic contact dermatitis is characterized by papuo-vesiculous and urticular elements, erythema, edema, bubbles, cracks, which causes wet dermatitis. In later stages, crusts appear, peeling. When recovering scars does not remain if there is no secondary infection; There is rarely pigmentation (exception - phytofotocontact dermatitis from meadow herbs). Depending on the etiological cause, localization, prevalence, outlines and clinical picture of the disease have features.
For phytoderotitis, linear damage to the dorsal surfaces of the hands, interfallated gaps, ankles, sometimes in the form of leaves of that plant, which caused allergic contact dermatitis was characterized. Such allergic contact dermatitis can be combined with the defeat of other organs (conjunctivitis, allergic, bronchitis rhinitis) and symptoms of general lesion (fatigue, temperature increase, headache).
Professional allergic contact dermatitis is manifested by thickening of the skin, peeling, liquidification, cracks and pigmentation. In some cases, the process is involved in the process itself and to a lesser extent - the epidermis, which is clinically expressed by Erythema and Edema, for example. With allergic contact dermatitis on nickel. Professional allergic contact dermatitis is more inherent in the defeat of the hands and environmental process. With an allergic contact dermatitis caused by artificial resins, erythematous rashes are observed, often with an edema. During sensitization associated with Ursol and Schipidar, there are mainly erythematous-bullous elements, in many cases professional eczema, for example. With the "cement eczema", sensitizing to the chromium ions or nickel scabes with allergies to nickel, such symptoms as microwetylation, mocking, itching are dominated in the clinical picture.
Depending on the clinical picture and the severity of the inflammatory process, it has sharp, subacute and chronic forms. The acute form of the disease is characterized by erythema, the formation of small vesiculous elements, subsequently dried into thin, easily spinning crusts. There may be swelling, urctaria, bubbles. Clinical picture Subighteous dermatitis is the same, but inflammatory changes are expressed to a lesser extent. The chronic form of the disease develops with long constant contact with an allergising substance, for example. In terms of activity. This is the so-called professional allergic contact dermatitis, or professional eczema. Clinical picture at this state of polymorphic; The clarity of the boundaries of the pathological process is lost, the lesion foci is beginning to occur on other areas of the skin, not in contact with the allergen.
Drug allergic contact dermatitis is induced by various drugs when skin contact; The development of anaphylaxis for drug contact is celebrated extremely rarely. Causeous factors are medicines commonly used as part of ointments with local treatment of skin diseases: antibiotics, especially neomycin and streptomycin, etc. Antibacterial drugs, anesthetic substances, novocaine, glucocorticosteroid drugs. The identification of the sensitizing drug is difficult, as ointments are often used in dermatology with complex composition, for example. Antibiotics and glucocorticosteroid preparations, antibiotics and anesthetic drugs. Of particular importance is the background on which these drugs are prescribed, since, on the one hand, the impaired integrity of the epithelium with lesion of the skin creates conditions for the rapid penetration of the medication, and with Dr.-testifies to the existing inferiority of the immunocompetent function of the skin, which contributes to the formation of a drug allergic contact dermatitis. The disease can also develop in healthy individuals on unchanged skin using various creams in which there are substances such as para-aminobenzoic acid, ethylenediamine in small quantities as stabilizers. Hormonal creams can also cause a disease. Such a process is quickly cured after the abolition of the resulting disease of the cream. The most often drug allergic contact dermatitis occurs in persons related by the type of activity with medicinal substances: employees of the pharmaceutical industry, pharmacists, medical staff. Such allergic contact dermatitis is characterized by a chronic flow with a transition to a professional field. The cessation of contact with sensitizing substances does not always lead to recovery, since often the disease is complicated by autoimmune processes.
The course of the disease changes if the sensitizing agent enters the body orally, parenterally or other, in such cases there is an eccentification of the process, itching sebum, which takes generalized character.
Differential diagnosis It is carried out with dermatitis atonic, eczema true and eczema microbial and mycotic.

Treatment of allergic contact dermatitis

Treatment must be carried out in two directions: preventing further contact with the agent caused; Treatment of the pathological process. The first direction includes the establishment of the cause with the help of allergological diagnostic samples of the skin applications and elimination of allergen. Common events are to use protective clothing, automation of production processes, improvement of ventilation, replacing high-caloric substances less allergenic (hypoallergenic cosmetics, etc.), the use of protective creams, decrease in trauma. Drug allergic contact dermatitis is often associated with the use of ointments containing sensitizing agents, especially when local treatment of skin diseases. Therefore, it is better to use oil creams in which there are no preventive substances. It is necessary to carefully assign masses based on Lanolin, as it can have sensitizing properties, ointments with complex compositions, since it often does not indicate the substances contained in these mixtures in small quantities, namely they may have allergenic properties.
In some cases, the disease is enough to eliminate the sensitizing agent to cure the patient. However, this is not always possible, since many substances are common in everyday life, industry, nature.
Local therapy includes the following medical events. In the first few minutes after contact with sensitizing agents, for example. juice of plants, it is necessary to rinse the skin thoroughly. In the treatment of moderate severity, hormonal ointments are used, the best fluorine-containing. These ointments should be carefully used on the face (the danger of the occurrence of acne, and in the field of skin folds (skin atrophy). Applying such ointments can be seen six or seven times a day, carefully rubbing into the inflamed skin. An occlusive dressings for 6-10 hours are recommended for improving penetration. It is necessary to avoid ointments of other composition, not to assign ointment with anesthetics, as they can enhance sensitization and besides themselves are sensitizers. The local purpose of antihistamine drugs may worsen the course of the disease. When the secondary infection is connected, the system antibiotics are recommended, and the locally hormonal ointments, but not ointment with the combined composition (antibiotic - glucocorticosteroid drug). IN acute cases Heavy allergic contact dermatitis local treatment consists only of indifferent binding - salt, aqueous or mortar of the Burov. The use of criminal ointments on vesiculous and wet stages is not shown. With pronounced itching should be used cold water or ice.
General therapy includes the following medical measures: systemic glucocorticosteroid drugs are used only at the acute stage of heavy allergic contact dermatitis with bubbles, swelling and mocking. Domestic dermatologists recommend low doses of hormonal drugs (prednisone 10-15 mg or other. Means in an equivalent dose within 10-12 days with a gradual decline in dose), foreign on high doses preference for the following schemes:I - the first four days 40 mg of prednisolone or other drug in the equivalent dose, the following four - 20, the last four days 10 mg and cancellation; II - the shock dose is the first 24 hours of acute state (60-100 mg of prednisolone, preferably in one reception), then reduced dose for two to three weeks.

Atopic dermatitis

Atopic dermatitis - chronic recurrent skin disease, the main signs of which are sebum and liquidification itching.
The term "Topic dermatitis" was introduced by Schulzberger, Kok and Cook in 1923. Previously, the disease was called neurodermatitis. However, atopic dermatitis is not quite correctly identified with the neurodermitite diffuse, since this concept is broader and includes those forms of true, especially children's, eczema and diffuse neurodermitis, which occur most often in childhood, in individuals with allergic predisposition and impaired immunity. Atopic dermatitis is 2-5% of skin diseases, combined or alternate with other atopic diseases - asthma bronchial, pollinosis, rinitis allergic.

Etiology of atopic dermatitis

In most cases, especially in childhood, allergens of food - eggs, flour, milk, etc. are assumed as etiological factors of atopic dermatitis. This is confirmed as follows: communication between use in food of some products and exacerbation of the disease; improving after elimination of suspected foods in childhood; The first appearance of the symptoms of atopic dermatitis after administration in the diet of the supplies - vegetables, fruits, eggs, meat; positively allergic diagnostic samples of skin on one or more allergens in most patients with atopic dermatitis; detecting antibodies related to immunoglobulin E, against various allergens. At an older age and in adults, it is assumed with allergic to allergens to household, allergens microbial, epidermal and mite. However, a clear correlation between contact with the allergen and the development of atopic dermatitis is not always detected: the elimination of the intended food allergen, in particular milk, does not always lead to the remission of the disease; The intensity of the skin samples with suspected allergens and the content of antibodies belonging to immunoglobulin e, serum does not correlate with the prevalence and weight of the process.
Hereditary predisposition to the development of atopic dermatitis is an autosomal dominant type of inheritance. There is a link between the frequency of development of the disease and the presence of HLA-A9 histocompativity antigens, HLA - A3.

Pathogenesis of atopic dermatitis

There are two theories of pathogenesis of atopic dermatitis The first associates the disease with impaired immunological mechanisms and sensitization to various allergens. The second assumes a vegetative imbalance in the skin structures (blockade of adrenergic in receptors). Immunological theory is based on numerous facts of changes in cellular and humoral immunity with atopic dermatitis. Features of humoral immunity with atopic dermatitis are as follows: Improving the level of immunoglobulin E parallel to the severity of the disease and reduced it after a long remission (at least a year); detection of antibodies related to immunoglobulin E, against various allergens; correlation between an increase in nonspecific immunoglobulin E and antibodies related to immunoglobulin E; an increase in the amount of lymphocytes in the immunoglobulin e; Identification of patients with atopic dermatitis of fat cells with immunoglobulin E fixed on them; Increased in serum of non-specific immunoglobulin G and high-speed anaphylaxis antibodies related to G4 immunoglobulins; Reducing the level of immunoglobulin A in serum in 7% of children suffering from atopic dermatitis; Providing immunoglobulin deficiency A majority of patients in the first three - six months of life.
Features of cellular immunity with atopic dermatitis are as follows: Reducing the number and functional activity of lymphocytes r; increased tendency to the emergence of infectious diseases disseminated vaccine, simpleness, warts, contagious mollusk and chronic fungal infections, i.e., clinical signs of cell immunity disorders; negative samples for tuberculin and candidal antigen; The shortage of circulating T-suppressors induced by Con-A and Timozin. With a serious flow of atopic dermatitis with signs of secondary infection, a decrease in phagocytosis and chemotaxis of neutrophils is often noted. Immunological theory is based on these facts and assumes that the pathogenesis of atopic dermatitis is associated with the dysfunction of regulatory cells, in particular with the deficiency of T-suppressors, as a result of which, in first, autocytotoxic cells appear (T, macrophages), capable of damaging the cells of the epidermis, secondly, synthesized increased quantity Antibodies related to immunoglobulin E, which can react with antigen on target cells - basophils, fat cells, monocytes, macrophages. In addition, the possibility of participation in the pathogenesis of the atopic dermatitis of late reactions, dependent on Immunoglobulin E. The question of the value of autoimmune processes during atopic dermatitis is not resolved.
The theory of vegetative imbalance is based on the following: patients have a white dermographism, narrowing of vessels in response to acetylcholine and cold, reducing the response to histamine, violation in cyclic nucleotide system. The facts accumulated in recent years, the regulation of immunological homeostasis, in particular the synthesis of immunoglobulin E, through the cyclic nucleotide system and the role of vegetative regulation in this process, allow you to associate immunological and vegetative theory of the development of atopic dermatitis.

Patomorphology of atopic dermatitis

Shock tissue with atopic dermatitis are vessels of the epidermis. With atopic dermatitis, their expansion occur, an increase in the vascular permeability, the output of cell elements to the surrounding tissues, swelling, resulting in spongiosis, erythema, papules and vesicles. Acute atopic dermatitis is manifested by spongiosis (intracellular swelling) and intapidermal vesicles containing lymphocytes, eosinophils and neutrophils; Paraperatosis is observed (incomplete keratinization with the presence of nuclei in the horn layer of the epidermis); In the upper layer of dermis, swelling, extension of vessels, perivascular infiltration by leukocytes are noted. The subacute form is characterized by intapidermal vesicles, acanthosis (thickening of Malpigiyev layer), paracratosis and less pronounced spongiosis; With this form, inflammatory infiltration of the dermis lymphocytes is observed. In chronic atopic dermatitis, acanthosis is formed, the expansion of capillaries is revealed with the thickening of their walls in the upper part of the dermis, perivascular infiltration lymphocytes, eosinophils, histiocytes. In the foci of liquidification, the epidermis hyperplasia with a small swelling, pronounced thickening of the papillars of the dermis, an increase in the number of monocytes, macrophages and fat cells.

Clinic atopic dermatitis

Atopic dermatitis occurs mainly in childhood and continues until 25-40 years. Features of the clinical picture, the course and outcome of the disease depends on age. In all phases, the atopic dermatitis marks the intense sebum, especially expressed in breast and childhood. As a result, the itch appears and most often - liquidification appears, which is a pronounced strengthening of the visible normal pattern of the skin, especially on the neck, in the patellied fumes, elbow bends associated with constant itching and thickening of the epidermis. Children often in the process are involved thumbs, dorsal and ventral surfaces, especially in winter. Atopical dermatitis are inherent in the amplification of the skin pattern on the palms - "Atopic palms", lacquered nails, line of Denis (characteristic fold on the edge of the lower eyelid), dark color of the eyelid, transverse fold between the upper lip and nose (with a combination of atopic dermatitis and allergic rhinitis), assumed Autosomal dominant inheritance of this feature. In patients, white dermographism is determined, severe skin dryness, as in ichthyosis, there are changes in neurological status, which creates a special psychosomatic state - "Atopic personality". Atopic dermatitis can be complicated by contact allergies to topically used substances, in such cases the condition is interpreted as "mixed dermatitis", i.e. atopic dermatitis and dermatitis allergic contact. Mixed dermatitis are often observed in women - "eczema owners" - with characteristic localization in hand. In the overwhelming bread of such cases, an allergic predisposition in the family is detected. In severe forms of atopic dermatitis, it is often complicated by infection. The course of the disease is chronic recurrent. The chronic process is characterized by the thickening of the epithelial layer, dryness, liquidification, impaired pigmentation. The aggravation is often manifested by eczematous rashes with mocking. With age, there is a complete disappearance of atopic dermatitis and the appearance of bronchial asthma, half aulinosis, allergic rhinitis.
With atopic dermatitis, an increased sensitivity to viral infections is noted: the occurrence of eczema vaccinatum and herpeticum generated by vaccinations characterized by the development of grouped vesicles and empty, mainly in the places of existing eczematous foci, increase temperatures up to 39 ° C, intoxication. Progressive vaccines in children with atopic dermatitis is associated with a defect (or) in-systems of immunity. In adults with atopic dermatitis, medicinal contact dermatitis on neomycin, ethylenediamine, etc. The heavy form of atopic dermatitis is often complicated by skin infectious processes (impetigo, folliculites, abscesses, "cold abscesses of the skin"),
In the clinical picture of atopic dermatitis, a number of features were allocated, a combination of which makes it possible to diagnose the disease.
The forecast is favorable at an earlier beginning of atopic dermatitis (up to six months), limited to the localization of the process, the effect of glucocorticosteroid drugs and antihistamine preparations, less favorable during the dissemination of the process in early childhood, dislocid form of erythema; Detect the current of atopic dermatitis negative emotional factors.

Differential diagnosis of atopic dermatitis

In the chest and early childhood, the atopic dermatitis is differentiated with seborrheic dermatitis, scabies, immunodeficient diseases - Wording - Oldrich syndrome, coaxy-teleangectasia, hypermumunoglobulinemia syndromes E and hypogammaglobulinemia, selective deficiency of immunoglobulin M, chronic granulomatosis, chronic, red flat, deprive. Atopic dermatitis in adults should be differentiated with scabies, microbial and mycotic, contact dermatitis.

Treatment of atopic dermatitis

atopic dermatitis is difficult to amenable to therapy. The diet constraint is not always effective, with suspected connection with the allergy of the food, an eliminational diet is needed. Recommended the elimination of high-caliped products, spices, carbohydrate limit, in some cases - milk elimination. The diet should be rich in vitamins. Patients should avoid overeating. Local treatment in the acute exudative stage is to apply a baruric solution (1: 40) and hypertonic, binding solutions, suitable forms with the infusion of chamomile. Between the change of gauze bandages, glucocorticosteroids and creams can be used (1% hydrocortisone or 0.025% triamcinolone). Application of glucocorticosteroidal ointments is most effective in chronic stage. Better resorption is achieved when using an occlusal dressing. The danger of developing complications from the use of glucocorticosteroid drugs should be taken into account, especially when treating the disseminated form of atopic dermatitis in early childhood. In the chronic stage of atopic dermatitis, especially with ichthyosis, the use of softening creams is shown. For phenomena of liquidification and hyperkeratosis, the use of targeting ointments should be very careful - in the hollow
fresh photoermatosis. General therapy is the appropriate purpose of antihistamine drugs in order to reduce itching, edema, erythema; Oral glucocorticosteroid drugs should be prescribed only in severe cases, a short rate, when other measures are not effective; With pronounced itching, tranquilizers are shown. Recently, attempts at the treatment of atopic dermatitis with immunomodulators - transfer factor, decaris, thymosin. The results are not unambiguous. Specific hyposensibilization is shown in the combination of atopic dermatitis with asthma bronchial atopic, pollinosis, allergic rhinitis. In case of bacterial complications, the use of oral antibiotics is preferable, since ointment with antibiotics worsen the state. For the treatment of ecstheree vaccinatum and herpeticum, complicating atopic dermatitis, preparations of V-globulin, immunostimulants are used. № 2, 2001 - »» Skin diseases: diagnosis, treatment, prevention

Yu.V. Sergeev, Academician Raen, Doctor of Medical Sciences, Professor Modern approaches to diagnosis, therapy and prevention

The problem of atopic dermatitis (blood pressure) is becoming increasingly important in modern medicine. The growth of morbidity in the last decade, chronic, with frequent relapses, the current, insufficient effectiveness of existing treatment methods and prevention today put this disease in a number of the most pressing problems of medicine.

According to modern ideas, atopic dermatitis is a genetically determined, chronic, recurrent skin disease, clinically manifested by the primary itching itching, lichenoid papulas (in infancy Papuloseclasses) and liquidification. The basis of the pathogenesis of blood pressure is the altered reactivity of the body, due to immunological and non-immunological mechanisms. The disease is often found in combination with a personal or family history of allergic rhinitis, asthma or half anconde.

The term "atopia" (from Greek. ATOPOS - unusual, alien) Introduced A.F. Sosa in 1922 to determine the hereditary forms of increased sensitivity of the body to various impacts of the external environment.

According to modern ideas, under the term "ATOPIA" understand the hereditary form of allergies, which is characterized by the presence of reactive antibodies. The reasons for atopic dermatitis are unknown, and this is reflected in the absence of generally accepted terminology. "Atopic dermatitis" is the term most common in world literature. Its synonyms are also used - a constitutional eczema, Purigo Bempnia and constitutional neurodermatitis.

Etiology and pathogenesis of atopic dermatitis Largely remain unclear. The theory of allergic genesis of atopic dermatitis, which binds the appearance of a disease with congenital sensibylazation and the ability to form the formation of reactive (Ig) antibodies is widespread. In patients with atopic dermatitis, the content of total immunoglobulin E has sharply increased, including both antigen-specific IgE antibodies to various allergens and IGE molecules. The role of the starting mechanism play penetrating through the mucous membrane is universally common allergens.

Among the etiological factors leading to the development of the disease, indicate sensitization to food allergens, especially in childhood. This is due to congenital and acquired disorders of the functions of the digestive tract, improper feeding, early administration to the diet of high-caliped products, intestinal dysbiosis , a violation of a cytoprotic barrier, etc., which contributes to the penetration of antigens from food casher through the mucous membrane into the inner medium of the body and the formation of sensitization to food products.

Sensitization to pollen, domestic, epidermal and bacterial allergens is more characteristic at high age.

However, the reactive type of allergic reaction is not the only one in the pathogenesis of atopic dermatitis. In recent years, the greatest interest in recent years is attracted in a cell-mediated immunity link. It is shown that patients have an imbalance of TH1 / TH2-lymphocytes, a violation of phagocytosis, other non-specific immunity factors, barrier properties of the skin. This explains the exposure to patients with various infections of viral, bacterial and fungal genesis.

Immunogenesis of blood pressure is determined by the peculiarities of a genetically programmed immune response to an antigen under the influence of various provoking factors. Long-term exposure of antigen, stimulation of TH2 cells, the products of allergenceless IGE antibodies, degranulation of fat cells, eosinophilic infiltration and inflammation, enhanced by damage to keratinocytes due to combs, all this leads to chronic inflammation in the skin with blood pressure, which plays a crucial role in the pathogenesis of skin hyperreactivity.

Causes an interest and hypothesis on intradermal suction of staphylococcal antigens, which cause a slow, supporting exemption from histamine fat cells or directly, or through immune mechanisms. A large role in pathogenesis can play violations in vegetative nervous system.

White dermatitis characteristic of atopic dermatitis are white dermatitis and perverted reaction to intradermal administration of acetylcholine. For these changes, the skin lies, obviously, the main biochemical defect, the essence of which is not very clear. In patients with atopic dermatitis, 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 impairment in the synthesis of cyclic adenosine monophosphate (CAMF) was noted.

Endocrinopathies are given to an essential place in the pathogenesis of atopic dermatitis, various types Violations of exchange. Great role central nervous systemWhat was recognized and recognized at the present time and is reflected in the neuro-allergic theory of origin of atopic dermatitis.

All outlined explains why atopic dermatitis develops against the background of various and interdependent immunological, psychological, biochemical and many other factors.

Clinical manifestations Atopic dermatitis is extremely diverse and depend mainly on age in which the disease is manifested. Starting in infancy, atopic dermatitis, often with remissions of various duration, can last to puberty, and sometimes it does not pass until the end of life. The disease is developing by attacks that occur often seasonally, with the improvement or disappearance of manifestations in the summer. In severe cases, atopic dermatitis flows without remission, giving a picture similar to erythrodermia.

Skin status of asymptomatic atopic patient The skin of the suffering atopic dermatitis, especially during remission or the "dormant flow", is distinguished by dryness and ichthiosiforous peeling. The frequency of vulgar ichthyosis in atopic dermatitis varies from 1.6 to 6%, respectively, various phases of the disease. Hyperlinearity of the palms (folded palms) is observed when combined with vulgar ichthyosis.

The skin of the body and the exclusive surfaces of the limbs are covered with shiny, bodily color by follicular papulas. On the side surfaces of the shoulders, elbows, sometimes horny papules are defined in the shoulder joints area, usually regarded as Keratosis Pilaris. At older age, the skin is distinguished by dischromic varnish with the presence of pigmentation and secondary leukoderma. Often in patients in the field of cheeks are determined by whitish spots Pityriasis Alba.

During the remission, the only minimal manifestations of atopic dermatitis can be barely peeling, weakly infiltrated stains or even cracks in the field of the lower edge of the attachment of the um of the ears. In addition, such signs may be Haylit, recurring snacks, the middle crack of the lower lip, as well as the eryymoskummous lesions upper eyelids. Periorbital darkening, the pallor of the skin of the face with the earthly tint may be important indicators of the atopic personality.

Knowledge of small symptoms of skin manifestations of atopic predisposition is of great practical importance, because it can serve as a basis for the formation of increased risk groups.

Phases of atopic dermatitis

During atopic dermatitis, depending on clinical features In various age periods, it is possible to distinguish three phases of the disease - infant, children's and adult. The phases are characterized by the originality of reactions to the stimulus and are distinguished by the change of localization of clinical manifestations and a gradual weakening of the signs of acute inflammation.

Infant phase Usually begins with the 7-8th week of the child's life. Throughout this phase, leather damage is acute eczematosis.

The rashes are localized mainly on the face, hitting the skin of the cheeks and forehead, leaving a free nasolabial triangle. At the same time, changes are gradually the changes on the extensive surface of the shins, shoulders and forearms. It is often amazed by the skin of the buttocks and torso.

The disease in the infant phase may be complicated by a pyrogen infection, as well as yeast lesions, which often accompanies lymphadenitis. Atopic dermatitis takes a chronic recurrent course and exacerbates with a violation of the function of the gastrointestinal tract, teething, respiratory infections and emotional factors. In this phase, the disease can be spontaneously cured. However, more often atopic dermatitis goes to the next, children's phase of the disease.

Children's phase Begins after 18 months of age and continues to the puberty period.

The rashes of atopic dermatitis in the early stages of this phase are represented by erythematous, edema papulas, prone to the formation of solid lesions. Later in the clinical picture, libheneed papules and foci of liquidification begin to prevail. As a result, the combing foci of lesions are covered by excoriations and hemorrhagic crusts. The rashes are localized mainly in the elbow and populated bends, on the side surfaces of the neck, top of the chest and brushes. Over time, most children are cleaned with rashes, and only patellied and elbow sibiba remain affected.

Adult phase It comes in a publ of the clinical symptomatics approaching rashes in late childhood.

The lesions are represented by Lenoid Papulas and Foci of Lichenification. Mocking is only occasionally.

The favorite localization is the top of the body, neck, forehead, the skin around the mouth, the bending surface of the forearm and wrists. In severe process, the process can take a common, diffuse character.

Selecting the phases of atopic dermatitis, it is necessary to emphasize that not all disease occurs with the natural alternation of clinical manifestations, it can begin with the second or third phase. But whenever the disease manifested itself, each age period is characterized by its morphological features presented in the form of three classical phases.

Table 1. Main clinical signs of atopic dermatitis

• itching skin;
• typical morphology and rash location;
• tendency to chronic recurrent flow;
• personal or family history of the atopic disease;
• white dermographism

Related diseases and complications

Other manifestations of atopy, for example, such as respiratory allergy , detected in most patients with atopic dermatitis. Cases of combination of respiratory allergies with atopic dermatitis are highlighted as a skin-respiratory syndrome, a large atopic syndrome, etc.

Drug allergies, reaction to insect bites and population bits, nutritional allergies, urticaria most often pursue patients hell.

Skin infections. Sick atopic dermatitis are subject to infectious diseases of the skin: pyodermia, viral and fungal infection. This feature reflects an immunodeficiency state characteristic of patients with atopic dermatitis.

From a clinical point of view, pyodermia has the greatest value. More than 90% of patients with atopic dermatitis have skin saming with golden staphylococcus, and its density is most pronounced in location places of lesions. Piodemia is usually represented by pustules localizing the limbs and torso. In childhood, a piococcal infection can manifest itself in the form of otites and sinusitis.

Patients with atopic dermatitis regardless of the sharpness of the process are inclined to affect viral infection, more often than a virus of a simple herpes. In rare cases, a generalized "Herpenetiform Eczema" (Caposhi vario-forming rash) is developing, reflecting the insufficiency of cellular immunity.

Older persons (after 20 years) are susceptible to fungal infection, as a rule, Trichophyton Rubrum. In childhood, the defeat of the mushrooms of the genus Candida prevails.

The diagnosis of "Atopic dermatitis" in typical cases does not submit significant difficulties (see Table 1). In addition to the main diagnostic signs of atopic dermatitis, more accommodation in diagnostics have additional features, which can be attributed to the above-described skin status of asymptomatic atopic patient (xerosis, ichthyosis, palm hyperlinearity, Haylit, Saint, Keratosis Pilaris, Pityriasis Alba, Pallor of the face, periorubital darkening and Dr.), eye complications and tendency to infectious diseases of the skin.

On this basis, international diagnostic diagnostic criteria have been developed, including the allocation of basic (mandatory) and additional diagnostic signs. Their different combination (for example, three basic and three additional) is sufficient for diagnosis. However, our experience shows that the diagnosis, especially in the early stages and with a hidden course, must be put on the basis of minimal signs and to confirm its modern methods of laboratory diagnostics. This allows preventive measures in a timely manner and not to give a disease to manifest itself in extreme forms.

To assess the severity of the skin process and the dynamics of the disease, the SCORAD coefficient is currently developed. This coefficient unites the area of \u200b\u200baffected skin and the severity of objective and subjective symptoms. It became widely used by practical doctors and researchers.

Essential assistance in diagnostics play special methods of further reasons requiring, however, special interpretation. Among them, the most important to be called a specific allergological examination, study of immune status, feces analysis on dysbacteriosis. Other methods of surveys are carried out depending on the accompanying diseases in the patient.

Specific allergological examination. In most patients with atopic dermatitis, sensitization is detected to a wide range of allergens tested. Skin testing allows you to identify suspected Allergen and carry out preventive measures. However, the involvement in the process of skin does not always allow this examination, difficulties may arise both with the conduct of such reactions and in the interpretation of the results obtained. In this regard, immunological studies were widely distributed, allowing blood testing to determine sensitization to one or another allergens.

Immunological examination. IgE antibodies. The serum concentration of Ig is increased more than 80% of patients with atopic dermatitis and is more often higher than in respiratory diseases. The degree of increasing the total IGE correlates with the severity (prevalence) of the skin disease. At the same time, high levels of Ig are determined in patients with atopic dermatitis, when the disease is in the remission. The pathogenetic value of the total IGE in the inflammatory response remains unclear, since about 20% of patients with typical manifestations of atopic dermatitis have a normal level of Ig. Thus, the definition in the level of general IGE helps the diagnosis, but it is impossible to fully focus on the diagnosis, the forecast and the signation of patients with atopic dermatitis.

PACT (Radioallergosorbent test), Mast, IFA methods to determine the content of specific IgE antibodies in vitro.

Our experience of using these methods with ad shows their high diagnostic significance. The effective preventive program is based on them (see Table 2).

Table 2. The etiological structure of allergies in patients with atopic dermatitis [according to RAST)

		Allergens (Allergen code "Pharmacia")	number positive Rast,%
Pollen
q.	1	Wound trivy	31,3
	3	Cocksfoot	40,9
	4	Oatman meadow	40,0
	5	Rai Grasse	34,7
	6	Timothy grass	40,0
	8	Matlik meadow	40,5
	12	Rye sowing	20,2
w.	1	Ambrosia	5,26
	5	Wormwood	37,8
	6	Wormwood ordinary	36,0
	7	Daisy	24,3
	8	Dandelion	27,7
	9	Plantain	10,4
	10	Mary Weary	8,33
	15	Quinoa	0
f.	1	Maple	12,8
	2	Alder	39,3
	3	Birch	44
	4	Hazel	29,8
	7	Oak	21,5
	12	Iva goat	16,2
	14	Poplar	8,7
	15	Ash	9,7
	16	Pine	3,3
Household
d.	1	Dermatophag. Pteron.	14,1
	2	Dermatophag. Farinae.	10,3
h.	1	Home dust N1.	26
	2	Home dust N2.	30
	3	Home dust N3.	25
Epidermal
e.	1	Epidermis Cats	33,3
	2	Epidermis dog	15
	3	Epidermis Horses	10,8
	4	Epidermis cow	12,3
	10	Feather Goose	1,85
	70	Feather Goose	1,7
	85	Pooh chicken	3,2
	86	Feather Duck	5,4
Food
f.	1	Egg white	7,8
	2	Milk	2,2
	3	Cod fish)	13,8
	4	Wheat	24,4
	5	Rye sowing	22
	6	Barley	14,8
	7	Oats.	14,3
	9	Fig	11,4
	11	Buckwheat	17,1
	12	Peas	10,1
	20	Almond	2,6
	23	Crabs	0
	25	Tomatoes	7,7
	26	Pork	9,3
	31	Carrot	11,4
	33	Oranges	6,7
	35	Potatoes	13,9
	47	Garlic	12,3
	48	Onion	7,8
511	(75)	Egg yolk	5,5
530		Cheese "Cheddar"	1,4
531		Rocfort Cheese	3,3
Fungal
m.	1	Mold Penicill	26,8
	2	ClapPorium	24,4
	3	Aspergillus	24,4
	4	Mork Rakeozus	21,1
	5	Candy Olba	22,5
	6	Alternaria Alterna	26,3
Fungal
r	1	Askarida	12,5
	2	Echinococci	0
	3	Saintosomes	8,7

The study of cellular immunity allows to differentiate the immuno-dependent form of atopic dermatitis from immune-dependent and carry out an in-depth reduction in order to clarify the pathogenetic mechanism. Evaluation of the immune status makes it possible to identify immunodeficient states, carry out controlled immunocorrorizing therapy. In the series of studies we conducted, the existence of four clinical and immunological versions of the flow of blood flow is proved, which makes it possible to carry out immunocorrorizing therapy, taking into account the peculiarities of the immune response of a particular patient.

Treatment

Getting Started at the treatment of atopic dermatitis, one should consider the age stage, clinical manifestations and related pathology. Clinical and laboratory examination of the patient allows you to establish a leading pathogenetic mechanism, reveal the risk factors, challenge the treatment and preventive measures. In the plan it is necessary to provide for the stages of the course treatment, the change of drugs, fixing the treatment and prevention of relapses.

In cases where atopic dermatitis is a manifestation of atopic syndrome (accompanying asthma, rhinitis, etc.) or caused by a violation of other organs and systems, it is necessary to correct the revealed concomitant diseases. For example, in childhood, the dysfunctions of the gastrointestinal tract play a major role, in puberty - endocrine dysfunction, etc.

Dietherapy can bring significant improvement, including preventing strong exacerbations.

Types of dietherapy

Elimination diet, that is, a diet aimed at eliminating diagnosed allergens, is usually not difficult for older children and adults. As the first step of the dietary regime, it is recommended to exclude eggs and cow's milk, regardless of whether they were a provoking factor. It is essential that the patients with atopic dermatitis often does not often have a correlation between the skin tests (or the PACT) and the food anamnesis.

When appropriate, during the exacerbation period, the hypo-timer diet must first eliminate extractive nitrogen substances: meat and fish broths, fried meat, fish, vegetables, etc. Completely excluded from the douse chocolate, cocoa, citrus, strawberries, black currant, melon, honey, grenades, nuts, mushrooms, caviar. Also exclude spices, smoked, canned and other products containing additives of preservatives and dyes having a high sensitizing ability.

A hypochloride diet (but not less than 3 g sodium chloride per day) plays a special role in atopic dermatitis.

In connection with the reports of violation of fatty acid metabolism in patients with atopic dermatitis, they recommend a dietary supplement containing fatty acids. It is advisable to add to the food diet of vegetable oil (sunflower, olive, etc.) to 30 g per day in the form of seasoning to salads. Vitamin F-99 is prescribed, containing a combination of linoleic and linolenic acids, or in high doses (4 capsules 2 times a day), or in the middle (1-2 capsules 2 times a day). The drug is especially effective in adults.

General treatment. Medicia treatment It should be carried out strictly individually and may include tranquilizers, anti-allergic, anti-inflammatory and disinfectants. It should be noted that in the treatment of atopic dermatitis, a large number of methods and means (corticosteroids, cytostatics, intortal, allergoglobulin, specific GPSENSIBILIZATION, PUVA-therapy, plasmapheresis, acupuncture, unloading and diet therapy, etc.) were proposed. However, the greatest importance in the practice of medicines that have anti-face effect - antihistamines and tranquilizers.

Antihistamines are an integral part of the pharmacotherapy of atopic dermatitis. Preparations of this group are prescribed to remove the symptoms of itching and swelling at skin manifestations, as well as atopic syndrome (asthma, rhinitis).

Conduring treatment with antihistamine preparations of the first generation (Supratin, Tuequil, diazoline, Fercarol), it is necessary to remember that it develops rapid addiction. Therefore, drugs should be changed every 5-7 days. In addition, it must be borne in mind that many of them have a pronounced anticholinergic (atropine-like) action. As a result, contraindications under glaucoma, prostate adenoma, bronchial asthma (increase in sputum viscosity). Penetrating through the blood-generation barrier, the first-generation preparations cause a sedative effect, so they should not be appointed with students, drivers and all those who should lead an active lifestyle, as the concentration of attention is reduced and the coordination of movements is reduced.

Currently accumulated significant application experience antihistamine drugs second generation - Laratodine (Claritin), Asthemisol, Ebostin, Cetirizin, Fexofenadine. Tachofilaxia (addiction) does not develop to the preparations of the second generation, during the reception there is no atropine-like side effect. Nevertheless, Claritine is given a special place in therapy. To date, this is the safest and most effective antihistamine drug, which is most often appointed in the world. This is due to the fact that Claritin is not only deprived of the side effects of the first-generation ag-drugs, but even with a significant (up to 16 times), an increase in the daily dose does not cause virtually no side effects characteristic of a number of second-generation ag-drugs (a slight sedative effect, Increase the Qt interval, ventricular flicker, etc.). Our many years of experience in the use of Claritin showed it high efficiency and tolerance.

The systemic administration of corticosteroids is applied limited and with common processes, as well as unbearable, painful itch, not bubbling other means. Corticosteroids (better methipred or triamcinolone) are given for several days to remove the sharpness of the attack with a gradual decline in the dose.

Intensive therapy using infusion agents (hemodez, refooliglucin, polyyonic solution, saline, etc.) is used in the prevalence of the process and phenomena of intoxication. The methods of extracorporeal disinfection (hemosorption and plasmapheresis) have proven well.

Ultraviolet irradiation. In the treatment of persistent atopic dermatitis, a very useful auxiliary method may be light therapy . Ultraviolet light requires only 3-4 procedures per week and, with the exception of erythema, has little side effects.

At the joining of secondary infection, antibiotics apply wide spectrum. Erythromycin, rondomycin, vibramicin for 6-7 days are appointed. In childhood, tetracycline drugs are prescribed from 9 years. Complication of blood pressure with herpetic infection is an indication for the appointment of acyclovir or Famvira in standard dosages.

Recurrent pyodermia viral infection, Mycosis is indications of immunomodulating / immunostimulating therapy (tactual, diucifon, levamizol, sodium nucleicate, isoprinozin, etc.). Moreover, immunocorrorizing therapy should be carried out under the strict control of immunological indicators.

In general therapy of patients, hell must be included, especially in children, enzyme preparations (Abomin, Festal, Mezim-Forte, Panzinorm) and various chisubiots (bifidbacteris, baktisubyl, Linex, etc.). Eubiotics are better assigned by the results of a microbiological structure of the feces on dysbacteriosis.

In general, for children, patients with blood pressure, we are always recommended a medical and preventive triad admin - membrane-stabilizing drugs (shitting), enzymes and eubiotics.

Good effect has a destination antioxidants , especially Aevit and Varon.

Outdoor treatment It is carried out taking into account the acuteness of the inflammatory response, the prevalence of defeat, age and the accompanying complications of the local infection.

In the acute stage, accompanied by mock and crusts, bonds containing anti-inflammatory, disinfecting drugs are used (for example, drilling fluid, chamomile infusion, tea). After removing the phenomena of acute inflammation, creams, ointments and pastes are used, containing brine and anti-inflammatory substances (naphthalan oil 2-10%, tar 1-2%, ichthyol 2-5%, sulfur, etc.).

Corticosteroid preparations were widely used in external therapy. The main, basic corticosteroids in the treatment of blood pressure continues to remain drugs such as the celenerrms (cream, ointment), the sake-dealerm with Garamcin and trieders (cream, ointment) - includes anti-inflammatory, antibacterial and antifungal components.

In recent years, new neurinedic corticosteroids of local use has been presented in the pharmaceutical market. These should include Elokom and Advantan.

Currently, the greatest experience of applying in dermatology among new drugs is accumulated on Elokom (Mometazone Furoate 0.1%) both around the world and in the practice of Russian doctors. In this regard, I would like to highlight some of the features of the elocom. The unique structure of mometazone with the presence of a furious ring provides high anti-inflammatory efficiency, not inferior to fluorine-containing GKS. A long anti-inflammatory effect allows you to assign 1 times a day to eloc. Low systemic absorption of elocoma (0.4-0.7%) gives confidence to doctors in the absence of systemic complications (of course, subject to the main rules for using GCS). It is known that for all the time of using elocoma in medical practice, and this is more than 13 years old, there are no cases of complications from the System System. At the same time, the absence of a fluorine molecule in the structure of the elocoma provides high local safety of the drug (after all, it is the use of fluorinated and especially twice fluorinated drugs increases the risk of skin atrophy). These international studies indicate that the level of safety of the elocoma corresponds to the hydrocortisone acetate 1%. Ello and Advantan preparations are recommended by the Ministry of Health of the Russian Federation and the Russian People's Union for the treatment of atopic dermatitis in children as a sectoral standard. An important advantage of elocoma is also the presence of three dosage forms - ointment, cream and lotion. This allows you to apply eloc at different stages of atopic dermatitis, on different skin sections and young children (from two years).

Ultraviolet irradiation. In the treatment of persistent atopic dermatitis, light therapy may be a very useful auxiliary method. Ultraviolet light requires only 3-4 procedures per week and, with the exception of erythema, has little side effects.

Prevention

Primary prevention. Activities for the prevention of atopic dermatitis must be carried out before the child's birth - in the antenatal period (antenatal prevention) and continue in the first year of life (postnatal prevention).

Antenatal prevention should be carried out in conjunction with an allergist, the doctors of the gynecological department and children's clinic. Significantly increase the risk of the formation of an allergic disease. High antigenous loads (toxicosis of pregnant women, massive drug therapy for pregnant women, effect on it professional allergens, one-sided carbohydrate nutrition, abuse of bonded food allergens, etc.).

In the early postnatal period, it is necessary to try to avoid excessive drug therapy, early artificial feeding, which lead to the stimulation of the synthesis of immunoglobulin. A strict diet concerns not only a child, but also nursing mother's breasts. If there is a risk factor in atopic dermatitis, the correct care for the skin of the newborn, the normalization of the gastrointestinal tract is necessary.

Secondary prophylaxis. In all cases, an anti-inflicted program for atopic dermatitis should be built with the factors similar to that with rehabilitation: drug, physical, mental, professional and social. The proportion of each aspect of the secondary prevention of non-etinakov at different phases of the disease. The prevention program must be drawn up taking into account the integrated assessment of the condition of the patient and continuity with the preceding treatment.

The correction of identified concomitant diseases, as well as leading pathogenetic mechanisms is an important part of anti-inflicted treatment.

Patients should be prevented about the need to comply with preventive measures that exclude the impact of provoking factors (biological, physical, chemical, mental), on compliance with the prophylactic elimination-hypoallergenic diet, etc. The preventable pharmacotherapy and applying preventable pharmacotherapy with the use of membrane-stabilizing drugs (shitty, ketotifenis, intort) is effective. Preventive (preventive) their appointment during periods of expected exacerbation of blood pressure (spring, autumn) long-term 3-month courses makes it possible to prevent recurrences.

At the rapid anti-lucid therapy of atopic dermatitis, spa treatment is recommended in the Crimea, on the Black Sea coast of the Caucasus and the Mediterranean.

Socio-household adaptation, professional aspects, psychotherapy and autotreating are also of great importance.

An important role is assigned to cooperation between the patient or his parents and the attending physician. There should be conversations about the essence of the disease, allergens causing exacerbations, possible complications, joins of respiratory allergies, the need to prevent exacerbations and many other things. In general, these events are held in the form of special training programs (trainings).

Atopic dermatitis, bronchial asthma etiology pathogenesis Clinical picture laboratory and instrumental diagnostics Treatment Care Prevention

Atopic dermatitis

Atopic dermatitis is a chronic allergic inflammatory skin disease characterized by age characteristics of clinical manifestations and recurrent flow.

The term "atopic dermatitis" has many synonyms (children's eczema, allergic eczema, atopic neurodermatitis, etc.).

Atopic dermatitis is one of the most frequent allergic diseases. His prevalence among children increased significantly in recent decades and ranges from 6% to 15%. At the same time, there is a clear tendency to increase the specific gravity of patients with severe diseases and continuously recurrent flow.

Atopic dermatitis is a significant risk factor for the development of bronchial asthma, since the emerging sensitization is accompanied not only by inflammation of the skin, but also the general immune response with the involvement of various respiratory tract departments.

Etiology.The disease in most cases is developing in persons with hereditary predisposition. It was established that if both parents suffer allergies, then atopic dermatitis occurs in 82% of children, unless one parent has an allergic pathology - 56%. Atopic dermatitis is often combined with such allergic diseases as bronchial asthma, allergic rhinitis, allergic conjunctivitis, food allergies.

Food allergens, microscopic pits of home dust, disputes of some fungi, epidermal pets are played a major role in the etiology of the disease. From food allergens to the main one belongs to the cow's milk.

Some patients with causative allergens are pollen trees, cereal plants, various herbs. The etiological role of bacterial allergens (intestinal wand, pyrogen and golden staphylococcus) has been proven. Drugs, especially antibiotics (penicillins), sulfanimamides are also sensitizing effects. Most children with atopic dermatitis detects polyvalent allergies.

Pathogenesis.Two forms of atopic dermatitis are isolated: immune and non-immune. In imperative form, there is an inherited ability when meeting with allergens, produce a high level of antibodies attributable to the IGE class, and therefore allergic inflammation develops. Currently, genes controlling IGE products are identified.

Most children with a non-immune form of atopic dermatitis have adrenal dysfunction: the insufficiency of glucocorticoid secretion and hyperproduction of mineralificoids.

Clinical picture.Depending on the age, the infant stage of atopic dermatitis is distinguished (from 1 month to 2 years); Children's (from 2 to 13 years old) and teenage (over 13 years old).

The disease may proceed in the form of several clinical forms: exudative (eczematous), erythematoscope, erythematoscope with liquidization (mixed) and lynching.

The prevalence of the process on the skin is distinguished by limited atopic dermatitis (the pathological process is localized mainly on the face and symmetrically at the hands of the hands, the skin lesion area is no more than 5-10%), common (in the process are involved with elbow and populated bends, grinding and ray joint joints, The front surface of the neck, the lesion area is 10-50%) and diffuse (extensive lesions of the skin of the face, body and limbs area of \u200b\u200bmore than 50%).

Usually the disease begins on 2 ^ 1st month of the child's life after translating it to artificial feeding. In the infant stage, hyperemia and infiltration of skin appear on the face in the cheek area, forehead and chin, multiple rashes in the form of papules and microwaves with serous contents. Veinsicles are quickly revealed with separation of serous exudate, as a result of which abundant mocking (exudative form) arise. The process can spread to the skin of the body and limbs and is accompanied by a pronounced itch.

In 30% of patients, the infant stage of atopic dermatitis proceeds in the form of an erytemmatomic-eyed form. It is accompanied by hyperemia, infiltration and peeling of the skin, the appearance of erythematous spots and papules. Rash first appear on the cheeks, forehead, the scalp. Exudation is absent.

At the children's stage, exudative foci, characteristic of infant atopic dermatitis, are less pronounced. The skin is significantly hypersmirmed, dry, its folds are thickened, the hyperkeratosis is noted. On the skin there are foci of liquidation (underlined skin pattern) and linghenda papules. They are most often in elbow, poned and ray-tailed folds, the back surface of the neck, brushes and stop (erytemmatoscopsy form with liquidization).

In the future, the number of ductoid papules increases, multiple comb and cracks appear on the skin (a lifting form).

The face of the patient acquires a characteristic species, defined as an "atopic face": eyelids are hyperpigmented, their skin flakes, there is an emphasis of the skin folds and combing eyebrows.

The teenage stage is accompanied by sharply pronounced liquidation, dryness and peeling of the skin. The rashes are represented by dry, peeling erythematous papulas and a large number of defective plaques. It is mostly affected by the skin on the face, neck, shoulders, back, flexion surfaces of the limbs in the field of natural folds, back surfaces of brushes, stop, fingers and legs.

Teenagers may have an adult form of atopic dermatitis, which is characterized by strong itch and multiple follicular papulas. They have a spherical shape, dense consistency, numerous scattered excorities are located on their surface. Rash are combined with pronounced liquidization.

With the easiest course of atopic dermatitis, limited skin lesions, minor erythema or leasing, weak itching of the skin, rare exacerbations are 1-2 times a year.

With a moderate course, there is a common nature of skin lesion with moderate exudation, hyperemia and / or liquidization, moderate itching, more frequent exacerbations - 3-4 times a year.

The difficult course is characterized by a diffuse character of lesion of skin, hyperemia and / or liquidation, constant itching and almost continuous recurrent flow.

To assess the severity of atopic dermatitis in allergology, the International SCORAD system applies. It is estimated in several parameters.

Parameter A. - the prevalence of the skin process, i.e. Skin lesion area (%). To estimate, you can use the palm rule (the area of \u200b\u200bthe palm surface of the brush is taken equal to 1% of the entire body surface).

Parameter B. - Intensity of clinical symptoms. To do this, the severity of 6 signs (erythema, edema / papule, peel / mocking, excitations, liquidification, dry skin) are calculated. Each characteristic is estimated from 0 to 3 points: 0 - absent, 1 - weakly expressed, 2 - moderately expressed, 3 - is expressed sharply. Evaluation of symptoms is carried out on the skin area where defeats are most pronounced.

Parameter C. - Subjective signs (itching, sleep disorder). Rated from 0 to 10 points.

The Scorad \u003d A / 5 + 7B / 2 + C index of it may be from 0 (there is no skin damage) to 103 points (the maximum expressed manifestations of the disease). Easy shape of the flow on Scorad - less than 20 points, medium-heavy - 20-40 points; Heavy form - more than 40 points.

Atopic dermatitis can occur in the form of several clinical and etiological options (Table 14).

Laboratory diagnostics.In general blood test, eosinophilia is noted, with the addition of secondary infection on the skin - leukocytosis, accelerated ESP. The immunogram is determined elevated level IgE. To identify causal allergen outside the exacerbation of the skin, a specific allergological diagnosis is carried out (skin samples with allergens). If necessary, resort to an eliminational-provocative diet, which is particularly informative in children of the first years of life.

Treatment.Therapeutic activities should be complex and include hypoallergenic life, diet, drug therapy in the form of local and systemic treatment.

In the apartment where a child lives with atopic dermatitis needs, it is necessary to maintain the air temperature not higher than +20 ... +22 ° C and relative humidity 50-60% (overheating enhances the itching of the skin).

Table. fourteen. Clinical and etiological options atronic dermatitisw. children

With prevailing food sensitization	With predominant tick sensitization	With predominant fungal sensitization
Communication of exacerbation with the reception of certain foods; Early start when moving to artificial or mixed feeding	Exacerbations: a) year-round, continuously recurring current; b) when contacting home dust; c) Strengthening of the skin of the skin at night	Exacerbations: a) when taking products containing mushrooms (kefir, kvass, dough and dr.); b) in rawroom facilities, in crude weather, in the autumn-winter season; c) when appointing antibiotics, especially penicillin row
Positive clinical dynamics when appointing an elible diet	The inefficiency of the elibinal diet. Positive effect when changing the place of residence	Efficiency of targeted eliminate events and diet
Identification of sensitization to food allergens (positive skin samples to food allergens, high content of allers-gene-spectric IGE antibodies in blood serum)	Identification of sensitization to allergens of tick-level dust and complex home dust allergen (positive skin samples, high content of allers-spectric IGE antibodies in serum)	Detection of sensitization to fungal allergens (positive skin samples, high content of allergen-specific IGE antibodies in blood serum)

Much attention should be paid to the creation of hypoallergenic life with elimination of causal and potential allergens and non-specific stimuli. To this end, it is necessary to take measures to eliminate the sources of accumulation of homemade dust, in which ticks are allergens: make wet cleaning daily, remove carpets, curtains, books, if possible, use acaricides.

It should not be kept in the apartment of pets, birds, fish, growing houseplants, as animal wool, bird feathers, dry fish food, as well as spores of mushrooms that are in flower pots belong to Allsrgen. Contact with plants forming pollen should be eliminated.

No less significant decrease in the influence of the child of nonspecific stimuli (the elimination of smoking in the house, the use of drawing in the kitchen, the lack of contact with the means of household chemicals).

The most important element of the complex treatment of atopic dermatitis is a diet. From the edible diet, products are eliminated by causal allergens (Table 15). They are detected on the basis of the poll of the parents and the child, these special allergic examination, taking into account the analysis of the food diary.

Table. fifteen. Classification of foods according to the degree of allergizing activity

Medicase therapy of atopic dermatitis includes local and general treatment.

Currently, a stepped disease therapy is applied.

I step (dry skin): moisturizing agents, elimination activities;

Stage II (light or moderately pronounced symptoms of the disease): local glucocorticosteroids of low and medium activity, antihistamines 2nd generation antihistamines, calcineurine inhibitors (local immunomodulators);

III step (moderate and pronounced symptoms of the disease): local glucocorticosteroids of medium and high activity, antihistamines 2nd generation antihistamines, calcineurine inhibitors;

IV Stage (heavy atopic dermatitis, non-treatable): immunosuppressors, antihistamines of the 2nd generation, phototherapy.

Local treatment - mandatory part complex therapy Atopic dermatitis. It should be differentiated taking into account the pathological changes of the skin.

Preparations of starting therapy with median and severe forms of the disease are local glucocorticoids (MGC). Taking into account concentration active substance There are several MHC classes (Table 16).

Table. sixteen. Classification of local glucocorticoids by degree

activity

With the light and moderate the course of atopic dermatitis, MHC I and II class are used. In case of severe disease, treatment is starting with class III drugs. In children under 14, it should not be resorted to the IV class MHC. MGK have limited use on sensitive skin areas: on face, neck, genitalia, in skin folds.

Powerful drugs are prescribed by a short rate for 3 days, weak - for 7 days. With a decrease in clinical manifestations of the disease in the case of its wave-like flow, it is possible to continue the treatment of MHC by an intermittent course (usually 2 times a week) in combination with nutritional means.

Preparations are applied to the skin 1 time per day. Inappropriate their breeding indifferent ointments, as it is accompanied by a significant decrease in the therapeutic activity of drugs.

Local glucocorticoids should not be used for a long time, as they cause the development of local side effects, such as stria, skin atrophy, telegangectasia.

The minimum side effects have nephlated MHCs ( elokom, Advantan). Of these, Elokom has an advantage in efficiency compared to Advanta.

With atopic dermatitis complicated bacterial infection On the skin, combined preparations containing corticosteroids and antibiotics are recommended: hydrocortisone with oxytetracycline, betamythasone with gentamicin.In recent years, the combination of a wide range of action is widely used - fusidic acid with breastplate (Futsikort) or with hydrocortisone (futsidin d).

With fungal lesions, a combination of MGC with antifungal agents is shown ( mikonazole.). Triple action (anti-allergic, antimicrobial, antimicotic) have combined drugs containing glucocorticoid, antibiotic and anti-grab agent (Betamethason + gentamicin + Clotrimazole).

Local immunomodulators are used for local treatment of atopic dermatitis at the light and medium-duration of the disease. They prevent disease progression, reduce the frequency and severity of exacerbations, reduce the need for MHK. These include nonsteroidal drugs. pimekrolimus and tacrolimus In the form of 1% cream. They are used for a long time, for 1.5-3 months and more on all areas of the skin.

In some cases, an alternative to MHC and local immunomodulators can serve degty preparations. However, they are currently practically not applied due to the slow development of anti-inflammatory action, a pronounced cosmetic defect and possible carcinogenic risk.

It has an anti-inflammatory effect and restores the structure of the damaged epithelium Dr. Panthenol. It can be used from the first week of child's life on any skin area.

As preparations that improve the regeneration of the skin and restoring damaged epithelium, can be applied bepanten, Salkoeril.

Pronounced anti-face action 5-10% Benzocaine solution, 0.5-2% Menthol solution, 5% Zimanin solution.

The modern standard of local therapy of atopic dermatitis includes nutritious and moisturizing agents. They are applied daily, their action is retained about 6 hours, so applying them to the skin must be regular, including after each washing or bathing (the skin should remain soft all day). They are shown both during the exacerbation of the disease and during the remission.

Mazi and creams more effectively restore damaged epithelium than lotions. Everyone 3-4 The weeks need a change of nutritious and moisturizing agents.

Traditional care products, especially based on lanoline and vegetable oils, have a number of flaws: they create an impenetrable film and often cause allergic reactions. In addition, their effectiveness is low.

More promising the use of modern means of therapeutic dermatological cosmetics (Table 17). The most common is the special dermatological laboratory "Bioderma" (the program "Atoderm"), the Laboratory "Udazh" (program for dry and atopic skin), Aven Lab (program for atopic skin).

To purify the skin, it is advisable to carry out daily cool baths (+32 ... + 35 ° C) for a duration of 10 minutes. The use of baths are preferable to the soul. Baths are carried out with means having a soft detergent (pH 5.5), not containing alkali. For the same purpose, the means of therapeutic dermatological cosmetics are recommended. After bathing, the skin is just rushing, without wiping dryness.

The means of basic therapy of the overall treatment of atopic dermatitis are antihistamines (Table 18).

Antihistamines of the 1st-generation drugs have a number of significant drawbacks: to achieve the desired therapeutic effect requires their appointment in large doses. In addition, they cause lethargy, drowsiness, reduce attention. In this regard, they should not be used for a long time and apply when aggravating the process with short courses overnight.

Table. 17. Tools of dermatological cosmetics for skin care during atopic dermatitis

Program		Moisturizing		Anti-inflammatory
The "Atoderm" program (Laboratory "Bioderma")	copper - zinc gel copper - zinc	atoderm RR Cream Hydrabio Thermal Water Ureage (Spray) Cream Hydrole - Pidik	atoderm RR Cream Emotrint Cream Estrom	Cream Atoderm Spray Copper - Zinc Cream Copper - Zinc Cream Gel Gel Graduate
Program for dry and atopic skin (URYAZH laboratory)	copper - zinc gel copper - zinc	Thermal URYAZH (spray) Cream Hydrole Pidik	Emotron Cream Extreme Cream	Spray Copper - Zinc Cream Copper - Zinc Cream grade Gel greedy

Table. eighteen. Modern Aitigistamiy drugs

Antihistamines of the 2nd generation antihistamines are more effective. They can be used in the daytime.

In order to stabilize the membranes of the fat cells, Kromons are prescribed - nascar Membrane-stabilizing drugs: ketotifen, vitamin E, Dimphosbon, Xidipon, Antioxidants ( vitamins A, C, polyunsaturated fatty acids), vitamins and B.15, zinc, iron preparations. Effective anti-leukotriene preparations ( montelukast, Zafirlukast and etc.).

To normalize the function of the gastrointestinal tract and biocenosis of the intestine, enzyme preparations are shown ( feed, Mezim-Forte, Poletrath, Creon) and factors contributing to intestinal colonization normal microfloraoy (probiotics - lactobacterin, bifidobacteria, enterol, bakyubyl and etc.; Prebiotics - inulin, fructoligosachary, galactoligosaccharides; Synbiotics - fructoligosacheri + bifidobacteria, lactiol + lactobacilli, etc.).

For sorption of food allergens systematically use enterosorbents: activated coal, smect, polypesman, Belosorb.

Systemic glucocorticoids and immunosuppressive therapy are used in severe flow and insufficient effectiveness of all other methods of treatment.

Prevention.Primary prophylaxis It must be carried out during the period of intrauterine development and continue after the child's birth.

Significantly increase the risk of formation of atopic dermatitis in a child High antigenic loads during pregnancy (the abuse of high-allergy products, one-sided carbohydrate nutrition, an irredising drug, gestosis, effects of professional allergens).

In the first year of the child's life, its breastfeeding, rational nutrition of a nursing mother, the correct introduction of a doctor, hypoallergenic life.

The primary prevention of atopic dermatitis also provides for the prevention of smoking during pregnancy and in the house where the child is located, eliminating the contact of a pregnant woman and child with pets, a decrease in the contact of children with chemicals in everyday life.

Secondary prophylaxis It is to prevent recurrence. In breastfeeding, it is essential to significantly reduce the severity of the course of the disease may comply with the mother of a hypoallergenic diet, receiving probiotics. It matters their use in the child. If it is impossible to breastfeeding, the use of hypoallergenic mixtures is recommended. In the future, the basic principle of diet and therapy remains an exception from the edible diet of the causing allergen.

In the system of prophylactic measures, the hygienic content of the room is very important (the use of air conditioner in hot weather, use during harvesting vacuum vacuum cleaner, etc.), providing hypoallergenic life, child learning and family.

The essential link of secondary prevention is skin care (the correct use of nutrient and moisturizing agents and therapeutic drugs, applying sunscreen sunscreen, daily reception of the cool shower, use for washing of stuffing fabric, not allowing intensive skin friction, wearing cotton fabrics , silk, flax, exclusion from the wardrobe of products from wool and animal fur, regular change of bed linen, use for bedding with synthetic fillers. During the aggravation, the child shows a dream in cotton gloves and socks, a short nail coloring, applying for washing liquid detergents.