Atopic dermatitis (AD) has recently received much attention from specialists and doctors. general practice. This is due to the fact that, despite the great successes achieved in studying the pathogenetic basis of this disease, the development of new treatment methods, including the use of modern external glucocorticosteroids, immunosuppressive drugs, external cosmetics, new antihistamines, it is not possible to stop the increase in incidence and prevent development of severe forms of atopic dermatitis.

The current classification of atopic dermatitis has been criticized because it does not reflect all possible options its flow. Factors leading to complications of the disease are often not taken into account, which reduces the effectiveness of the therapy. Algorithms for the treatment of severe atopic dermatitis have not been developed. All this causes the formation of severe forms of atopic dermatitis, distrust of the patient and his parents in the actions of doctors and, ultimately, social maladjustment of the child and a decrease in the quality of life of the patient and his family.

Atopic dermatitis is a chronic allergic disease of the skin, which most often manifests itself in early childhood and can subsequently acquire characteristic features chronically current inflammatory process with rare remissions or frequent exacerbations.

Recently, there have been trends all over the world towards an increase in the prevalence of atopic dermatitis, the development of its severe forms and the disability of patients. IN Russian Federation More than 7 thousand children are recognized annually as disabled due to diseases of the skin and subcutaneous tissue; atopic dermatitis accounts for over 80% of cases. According to domestic data literary sources, greatest number disabled children are defined in the age group from 8 to 17 years, girls predominate among them.

Often parents various reasons Children are not given disability status. In this regard, with an increase in the number of patients with severe atopic dermatitis hospitalized in specialized departments, the percentage of disabled children does not increase significantly.
The classification of atopic dermatitis in Russia today has not been established. The classification approach proposed in the scientific and practical programs of 2000 and 2004 has been criticized, since it does not allow covering all variants of the clinical course of atopic dermatitis (Fig. 1).

Dermatologists and allergists are seriously discussing the possibility of distinguishing variants of the course of atopic dermatitis within the nosology. This is due to the fact that in some patients with clinical manifestations of atopic dermatitis, high levels IgE in the blood and there are no signs of sensitization of the body, which is one of the diagnostic criteria for the disease.

We use the classification proposed by I. I. Balabolkin and V. N. Grebenyuk (1999), according to which atopic dermatitis is divided into five main clinical variants. Each option has its own characteristic features, and with any of them a severe course of atopic dermatitis is possible (Fig. 2-5).

The clinical and morphological forms of the disease described below may not be limited by age. For example, one child at the age of five may suffer from an erythematosquamous form of atopic dermatitis, another from an erythematosquamous form with lichenification, characterized by localized foci of lichenification with severe dryness, excoriations and cracks.


Western experts also debated whether the IgE-independent variant of the disease (the so-called internal type) should be classified as atopic dermatitis or not. The last point in the controversy was set World Organization on allergy IAACI (WA0) (World Allergy Organization) in 2003: the term “eczema” was decided to be used to describe a skin disease with a typical clinical picture of atopic dermatitis without signs of atopic sensitization (internal type), and atopic dermatitis / atopic eczema to be registered as a form of atopic dermatitis with IgE-dependent sensitization (external type). Criteria for distinguishing two variants of the course of atopic dermatitis were determined, based on data from scientific research in recent years (Table 1).


It should be noted, however, that this division is not entirely accurate: firstly, sometimes patients with IgE-independent dermatitis may have diagnosed bronchial asthma and/or allergic rhinitis(traditionally, these diseases with an IgE-dependent course are classified as the atopic triad); secondly, with age, as the duration of atopic dermatitis increases due to the expansion of the spectrum of sensitization in patients with eczema, positive skin tests with allergens to which they were not previously sensitive can be obtained, which allows them to be transferred to the group of patients with atopic dermatitis and regard eczema as the first stage in the formation of allergic pathology. Probably, with the advent of new knowledge about possible reasons development of atopic dermatitis, answers to questions that currently remain open will be obtained.

Causes and symptoms of atopic dermatitis in children

Atopic dermatitis develops on initially changed skin. The skin of patients is usually dry, with increased transepidermal moisture loss. Changes in the skin barrier are often associated with disorders that arise when inherited characteristics of metabolic processes occurring in the skin are transmitted from parents. Many non-immune mechanisms leading to these changes are trigger factor in the development of immune disorders, since they do not limit the penetration of substances into the skin, leading to sensitization of the body and the launch of many immune reactions.

Among the non-immune factors in the development of atopic dermatitis are:

An important pathogenetic factor of immune disorders in atopic dermatitis is the involvement of T-lymphocytes, fibrocytes, Langerhans cells, mast cells and epidermal keratinocytes. Modern research allowed us to understand the immune mechanisms involved in the pathogenesis of atopic dermatitis. The basis of allergic inflammation in atopic dermatitis is activation of the immune system, namely T-lymphocytes located in the skin, induction of keratinocyte apoptosis, IgE synthesis, and involvement of eosinophils.

Penetration of allergens into the skin is possible due to a violation of the skin barrier due to increased dryness of the skin and the absence of a natural protective hydrolipid film that prevents direct contact of antigens from environment with the stratum corneum. Allergens that penetrate the skin are captured by Langerhans cells, which present them to T lymphocytes.

Allergens can penetrate through inhalation and through the gastrointestinal tract. Their absorption by dendritic cells of the mucous membrane respiratory tract and digestive tract and the subsequent launch of the process of sensitization of the body are especially pronounced in children of the first years of life, preschool and primary school age. The immaturity of the barrier function of the mucous membrane of the respiratory and digestive tract, the insufficiency of secretory IgA production also contribute to sensitization of the body.

The interaction of allergens with specific IgE fixed on the surface of Langerhans cells leads to activation of these cells, manifested by the production of proinflammatory cytokines. The involvement of CD4+ T cells in atopic dermatitis is not questioned. Various allergens can lead to activation of T-lymphocytes: food, aeroallergens, superantigens and autoallergens. Recently, the role of aeroallergens, which can induce allergic reactions of both immediate and delayed types, has been intensively studied.

Increased IgE levels and eosinophilia in atopic dermatitis depend on the expression of receptors for cytokines produced by Th2 cells (Fig. 6). As is known, Th1 lymphocytes produce IL-2, IL-12, IFN-γ and TNF-α, which activate macrophages, causing delayed hypersensitization. Th2 lymphocytes secrete IL-4, IL-5, IL-6, IL-10 and IL-13, which activate B cells.


IN normal conditions there is a balance between two subpopulations of T cells, which have an inhibitory effect on each other. IL-12, synthesized by Langerhans cells, keratinocytes and eosinophils, stimulates the formation of the Th2 phenotype. IL-4 and IL-10 produced by Th2 lymphocytes, as well as prostaglandin E2, inhibit the expression of IL-12 by macrophages and the production of IFN-γ, thereby suppressing the formation of the Th1 phenotype. Thus, in the case of the development of atopic dermatitis, the number of Th2 prevails; in such patients, the production of IL-4 increases and the synthesis of IFN-γ decreases, which contributes to an increase in the production of IgE by B lymphocytes.

The role of mast cells in the pathogenesis of atopic dermatitis has long been described and is associated with the early and late phases of immediate-type allergies. Delayed-type hypersensitivity is characteristic of the chronic, continuously relapsing course of atopic dermatitis and can be observed in children with severe disease. It is shown that in chronic stage In atopic dermatitis, the immune response switches from Th2 to Th1 type with pronounced expression of IFN-γ by infiltrate cells, which is preceded by a peak of IL-12 expression.

IN latest research A concept has been proposed for the participation of T-regulatory cells in the allergic immune response, which are capable of exerting a suppressive effect on Th0/Th1 and Th2 lymphocytes and on the effector cells of allergic inflammation: mast cells, basophils and eosinophils. In addition, they can influence B lymphocytes by suppressing IgE production. CD8+ T cells, dendritic cells, IL-10-producing B cells, and natural killer cells can also exert a suppressive effect through T-regulatory cells.

Special attention is paid to patients with typical clinical manifestations of atopic dermatitis who have normal values Ig class E without detection of specific IgE in the blood serum, which are combined into the group of patients with non-atopic (atopiform) dermatitis. Studies reveal similar mechanisms of dermatitis pathogenesis, with the exception of IgE hyperproduction.

T cells similar in nature are found in the skin, however, the production of cytokines in this form differs from that in the allergic form of the disease: T cells produce the same amount of IL-5 and IFN-γ and less IL-4 and IL-13, which induce IgE synthesis. Recent studies, for example, have demonstrated that in the IgE-independent variant, increased skin sensitivity to allergens such as Dermatophagoides pteronyssinus and birch pollen may be associated with the fixation of IgG antibodies on cells, which are also associated with an allergic response.

Diagnosis of atopic dermatitis in children

Currently, in Russia, to make a diagnosis of atopic dermatitis, it is customary to use the criteria of J. M. Hanifin and G. Rajka, published in 1980.

Mandatory features include:

Auxiliary features include:

Each patient with atopic dermatitis with to varying degrees the severity of the disease must have at least three mandatory signs. Auxiliary signs are recorded in at least 1/3 of patients.

The severity of exacerbation of the disease is assessed using the semi-quantitative SCORAD scale, which takes into account:

The prevalence of skin lesions (A) is calculated using the "rule of nines": head and neck - 9%; upper limbs - 9% each; anterior and posterior surfaces of the body - 18% each; lower extremities - 18% each; perineal area and genitals - 1%.

The intensity of clinical manifestations (B) is assessed by six symptoms: 1. erythema (hyperemia); 2. swelling/papulosis; 3. weeping/crusting; 4. excoriation; 5. lichenification/desquamation; 6. general dry skin. Depending on the severity, each symptom is given a score from 0 to 3 points: 0 - absence; 1 - weakly expressed; 2 - moderately expressed; 3 - pronounced.

Assessment of subjective symptoms (C) - the intensity of skin itching and the degree of sleep disturbance - is carried out on a 10-point scale by children over 7 years of age or parents. The average indicator for the last 3 days and/or nights is determined. The final value of the SCORAD index is calculated using the formula: SCORAD Index = A/5 + 7B/2 + C. An exacerbation is considered mild when the SCORAD index is from 0 to 30, moderate - from 30 to 60, severe - over 60.

The severity of atopic dermatitis is determined based on the following criteria: number of relapses per year, average duration relapses, prevalence of skin lesions (Table 2).


Among the diseases treated differential diagnosis atopic dermatitis includes scabies, psoriatic lesions, seborrheic dermatitis, microbial eczema, Vidal's simplex (limited neurodermatitis), urticaria, contact dermatitis.

When examining children with atopic dermatitis, special attention is paid to collecting allergy history; Skin testing is carried out during clinical remission of the disease. Often in children with severe clinical manifestations of atopic dermatitis, the only possible method To identify causally significant allergens, allergy diagnostics in vitro remains; in hospital settings, provocative tests with allergens are used, and a general clinical examination is carried out.

Severe atopic dermatitis is often associated with the development of pathological conditions that arise against the background of an acute inflammatory process both on the skin and in the intestines. Thus, the gastrointestinal form of food allergy, which often accompanies the course of atopic dermatitis, can contribute to the development of malabsorption syndrome.

When studying biopsies of the mucous membrane of the stomach and jejunum of children with atopic dermatitis, an increase in the number of degranulated mast cells, edema, eosinophilic and lymphoplasmacytic infiltration of the lamina propria of the mucous membrane, and lymphangiectasia are noted. These changes lead to disturbances in metabolic processes due to the occurrence of tissue hypoxia with an increase in the process of glycolysis, as well as to a decrease in the activity of tissue respiration enzymes and disruption of microcirculation. Inhibition of the absorption capacity of the jejunum causes the development of malabsorption syndrome in children in the first year of life. Underestimation of the possibility of developing this complication leads to inadequate therapy and weight loss, which is especially dangerous for children early age.


Factors such as the addition of a secondary infection, the development of malabsorption syndrome, relative enzymatic deficiency, concomitant somatic pathology and, unfortunately, inadequate therapy for the patient’s condition can lead to a more severe course of atopic dermatitis.

In children with atopic dermatitis, changes in the intestinal microbiocenosis are often detected. The question of the role of the intestinal biocenosis in this disease remains controversial. The studies of S. G. Makarova (2009) demonstrated a direct relationship between the severity of skin lesions and the severity of dysbiotic abnormalities.

In the group of children with severe skin manifestations, grades III and IV dysbiotic abnormalities predominated; significantly more often than in children with mild and moderate manifestations of dermatitis, an imbalance of the aerobic group of the biocenosis was determined (increase in the total amount of Escherichia coli, dominance of coccal flora); in a greater number of cases, flora with signs of aggression was detected (hemolyzing coli, hemolysing enterococcus); Staphylococcus aureus, fungi of the genus Candida, and associations of several opportunistic microorganisms were more often detected.

The identified patterns confirmed the relationship between two pathological conditions - atopic dermatitis and intestinal dysbiosis - while the question of the primacy of one of them remained relevant in both theoretical and practical aspects.

Currently intestinal biocenosis play an important role in the development of intestinal immune function and the formation of food tolerance. It is even assumed that disturbances in the composition of the intestinal microflora can trigger the entire cascade of immune reactions leading to the development of atopic dermatitis.

However, at the stage of an already formed allergic process, the leading pathogenetic significance apparently still belongs to food allergy. This is confirmed by the absence of any effect from the correction of dysbiotic abnormalities, carried out without treating the underlying disease.

Treatment of atopic dermatitis in children

Therapy for atopic dermatitis is aimed at eliminating specific and nonspecific trigger factors, resolving allergic inflammation of the skin, normalizing the gastrointestinal tract, combating dry skin, restoring the damaged lipid layer and is based on the following plan:
The basis of diet therapy is:

The basis of treatment of severe forms of atopic dermatitis is pharmacotherapy of acute conditions. The importance of anti-inflammatory treatment with systemic glucocorticosteroids (GCS), relief of itching with antihistamines, and normalization of the gastrointestinal tract is dictated by the severity of the disease and the development of pathological conditions that require active interventions.

External therapy certainly plays an important role in resolving the inflammatory process of the skin, however, without systemic pharmacological control, its use leads to the progression of atopic dermatitis and deterioration of the patient’s condition. The absence in Russia of clear, agreed upon treatment regimens for severe forms of the disease determines low efficiency treatment of atopic dermatitis, the occurrence of severe side effects of therapy and sharp decline quality of life of the child.

Systemic glucocorticosteroids (GCS) have a strong anti-inflammatory and immunosuppressive effect, helping to resolve allergic inflammation and relieve itching (Fig. 7). Despite the lack of long-term controlled studies, the positive effects of GCS are not disputed by anyone. Over a long period of time, positive experience has been accumulated in the use of GCS in patients with atopic dermatitis. Glucocorticosteroids (GCS) for atopic dermatitis are prescribed in a short course due to the risk of developing serious side effects: growth retardation, suppression of the function of the hypothalamic-pituitary-adrenal system, arterial hypertension, cataracts, osteoporosis, etc.


Both in our country and abroad, a dose not exceeding 1.5 mg/kg/day is recommended. (for prednisolone), parenterally (intramuscularly) 1 time a day for 5-7 days. In some situations, oral administration of GCS at a dose of 1 mg/kg/day is possible. followed by a rapid reduction in the dose of the drug until complete withdrawal, the course of treatment is 7-14 days.

Intravenous administration of glucocorticosteroids (GCS) to children with atopic dermatitis is not indicated, especially since there is no doubt about the fact that the skin of patients is colonized by Staphylococcus aureus, which has enterotoxigenic properties. There are not isolated cases of the development of infectious complications associated with catheter-associated infection in children.

The prescription of antihistamines for atopic dermatitis is pathogenetically justified (Fig. 8). The advantages of first generation drugs are the ability parenteral administration and the presence of a sedative effect, which helps improve the sleep of a child suffering from intense itching. Only drugs of this group have, along with antihistamine, also antiserotonin activity, an anabolic-like effect and are approved for use in children starting from the first month of life. Second-generation drugs that do not cause drowsiness, do not affect psychomotor function and cognitive abilities, are also often used in the treatment of atopic dermatitis. Their use in many cases is limited by the age of the patient.


Systemic antibacterial therapy is carried out consistently only in case of complicated atopic dermatitis. More often we're talking about about infection with Staphylococcus aureus. The drugs of choice include first or second generation cephalosporins or semisynthetic penicillins. Usually a course of treatment of 7-10 days is effective. Recently, due to the increasing frequency of detection of methicillin-resistant strains, macrolides are not prescribed. In cases of drug allergies to the above antibiotics, clindamycin is used.

The basis for external treatment of severe forms of atopic dermatitis are anti-inflammatory drugs containing glucocorticosteroids (GCS). In Russia, when prescribing therapy, it is proposed to be guided by the phase of the disease (acute, chronic), the age of the child and to begin therapy with strong corticosteroids (based on the European classification of J. A. Miller and D. D. Munro).

Rules external therapy GKS:

The combination drugs include glucocorticosteroids (GCS):
  1. with antiseptics: group I: Dermozolon (clioquinol)., group III: Lorinden S (clioquinol);
  2. with antibiotics: group I: Hyoxysone (oxytetracycline), oxycort (oxytetracycline), fucidin G (fusidic acid)., group III: Polcortolone TS (tetracycline), fucicort (fusidic acid), celestoderm B with garamicin (gentamicin), flucinar N ( neomycin);
  3. with antibiotics and antifungal drugs: group III: Triderm (gentamicin, clotrimazole), acriderm GK (gentamicin, clotrimazole);
  4. with salicylic acid: group III: Belosalik, Lorinden A, Akriderm SK, Diprosalik, Elokom S.

When prescribing combined glucocorticosteroids (GCS) to patients with complicated atopic dermatitis, they are guided by the composition of the drug (the presence of an antibacterial or antifungal agent). It is important to remember that many drugs are classified as III group By biological activity and are not recommended for use in young children, as they may have a systemic effect, being absorbed through the child’s damaged skin. In young children, the use of occlusive dressings is also limited to prevent the risk of systemic side effects.


Recently, the possibilities of external therapy for atopic dermatitis have expanded significantly. This is primarily due to the introduction to the pharmaceutical market of drugs approved for use in young children, with the emergence of new dosage forms, with the accumulation of experience in treatment with external glucocorticosteroids (GCS).

New ones are being successfully developed medicines for the treatment of atopic dermatitis. One of them is non-steroidal anti-inflammatory drugs (NSAIDs) for external use - pimecrolimus (cream 1%) and tacrolimus (ointment 0.03 and 0.1%), which, along with glucocorticosteroids (GCS), are already included in the group of main anti-inflammatory drugs .

Pimecrolimus inhibits Th1 and Th2 cell activation through suppression of the production of proinflammatory and immunomodulatory cytokines, IL-2, IL-4, IL-8, TNF-a, IFN-y and GM-CSF and, in addition, regulates the levels of IL-5, IL-10 and IL-13 in CD4+ and CD8+ lymphocytes. Its effect on the apoptosis of T lymphocytes and keratinocytes (but not Langerhans cells) and on the inhibition of mast cells and basophils with the prevention of the release of histamine and tryptase was noted.

However, there is still ongoing debate about the safety of using these drugs, especially in young children and long-term therapy, which is associated with the risk of lymphoma and UV-induced skin cancer during immunosuppressive treatment. Studies conducted on large groups of patients did not reveal cases of development oncological diseases.

However, when treating patients with severe atopic dermatitis, the risk may still increase. In the USA, Europe and Russia, topical calcineurin inhibitors are widely used in pediatric practice. Extensive experience in their use has been accumulated. On the Russian pharmaceutical market there is pimecrolimus (cream 1%), recommended as a second line of therapy and approved for use in children from 3 months of age (in the USA and Europe - from 2 years). Tacrolimus (0.03 and 0.1% ointment) is not registered in Russia.

The effectiveness of specific immunotherapy is still debated. In Russia at severe course This treatment method is not recommended for atopic dermatitis.

The use of immunosuppressive treatment aimed at restoring the normal ratio of Th1 and Th2 lymphocytes eliminates the imbalance in the production of IL-4 and IFN-γ by T lymphocytes, leading to a significant increase in IgE levels (Fig. 10). Therapy with cyclosporine A (CsA) is carried out only in cases of refractory disease under the supervision of specialists who can control the risk of side effects.


Cyclosporine A (CsA) belongs to a group of drugs for which the correct choice of drug dose is critical. This is due to the low therapeutic index of CsA, at which the therapeutic concentration of the drug is close to toxic. Even a slight increase in the concentration of cyclosporine A (CsA) in the blood with inadequate treatment leads to side effects that threaten the patient’s life. At the same time, low doses of the drug do not have a sufficient therapeutic effect, which may discredit this method of treatment.

Due to multiple interactions with drugs that can reduce and increase the concentration of CsA in the blood, competing for metabolic pathways in the liver, the physician must constantly monitor any additional therapeutic interventions, assessing the possible risks of treatment.

The initial dose of cyclosporine A (CsA) is 2.5-5 mg/kg/day. and is divided into 2 doses, the recommended course of treatment is from 6 weeks to 12 months. During CsA therapy, it is necessary to exclude grapefruit juice and drugs metabolized through cytochrome P450 from the diet. Contraindications to the use of cyclosporine A (CsA) are concomitant bacterial and viral infections, liver and kidney damage.

The main side effects of treatment with cyclosporine A (CsA) are nephrotoxicity and increased blood pressure. The risk of undesirable consequences of immunosuppressive treatment increases when high doses are prescribed and the duration of therapy increases. At the same time, when using CsA, growth retardation is not observed; the drug is devoid of many life-threatening side effects such as skin cancer and hepatotoxicity that are common with other treatments for severe forms of atopic dermatitis.

According to our data, the use of immunosuppressive treatment with cyclosporine A (CsA) is effective in patients with severe atopic dermatitis, resistant to treatment. traditional therapy(Table 3). Of the side effects, transient hypoisosthenuria, paresthesia and headache were noted in only 2 cases.


The time for the onset of the most pronounced positive clinical effect for different clinical and morphological forms of atopic dermatitis varied. Thus, with the erythematosquamous form of atopic dermatitis, positive dynamics during treatment were noted earlier than with the erythematosquamous form with lichenification and the lichenoid form. Long-term administration of cyclosporine A (CsA) made it possible to prolong the period of clinical remission of the disease and optimize the treatment of atopic dermatitis. During treatment, the levels of circulating immune complexes, eosinophils and peripheral blood lymphocytes significantly decreased, which could be an objective criterion for the effectiveness of the therapy.

Plasmapheresis is rarely used due to the risk of developing anaphylactic shock when administering protein solutions. It is recommended to remove 30-40% of the volume of circulating plasma per session, conduct a course of plasmapheresis of 3 sessions with a frequency of 1 session every 4 days, and replace the plasma with protein solutions.

Physiotherapeutic treatment methods are often carried out in a sanatorium and include electrotherapy (electrosleep, electrophoresis), magnetotherapy, phototherapy, hydrotherapy, heat therapy and aeroion therapy.

Anti-relapse treatment is performed after completion of the main course of treatment. The importance of these therapeutic activities associated with frequent relapses illness due to cessation of treatment and resumption of symptoms of the disease. The basis of treatment is:
Thus, the treatment of severe forms of atopic dermatitis should be comprehensive, including the elimination of specific and nonspecific trigger factors, diet therapy, systemic and external anti-inflammatory therapy, the prescription of antihistamines and, to prevent exacerbation of the disease, the use of anti-relapse treatment agents. It is important to remember that the task of successful treatment of atopic dermatitis, especially its severe forms, can be solved only with the adequate use of pathogenetically based treatment, ultimately aimed at improving the quality of life of the patient and his family.

© Kudryavtseva A. V.

The origins of a problem such as atopic dermatitis in children should be sought in infancy. Unreasonably early transfer of the baby to milk formulas for feeding and their constant change in search of the best one provokes the development of food allergies in the baby. In the case of contact allergic dermatitis, skin contact with substances (objects) comes to the fore, due to contact with which the child exhibits a negative reaction.

Dermatitis is an inflammatory skin disease that occurs under the influence of some unfavorable factor.

Children most often experience so-called atopic dermatitis, which is a chronic allergic skin disease.

Atopic dermatitis is a multifactorial dermatosis with a hereditary predisposition, developing in 80–85% of children in the first year of life, characterized by: functional disorders nervous system, itchy skin lesions with the presence of polymorphism.

Why does atopic dermatitis appear in children: causes

In atopic dermatitis, the trigger is food allergy, which manifests itself in early childhood. For a child’s immune system, food proteins are foreign. In the child's gastrointestinal tract, proteins are converted into polypeptides and amino acids. Polypeptides are the cause of allergies in early childhood, but not all of them cause allergic reactions. In some cases, food allergies manifest as rare episodes of skin rashes. Only in a small percentage the process occurs chronically.

Atopy translated from Greek means “unusual, strange.” Another reason why dermatitis appears in children is allergic diseases of the parents. At hereditary predisposition allergic antibodies are produced in increased quantities and react to a variety of irritants - food, medicinal, pollen, fungal, epidermal, house dust mites, etc.

Such children are ready for allergies from birth, but the disease can manifest itself only after prolonged contact with the allergen. At the first contacts, memory cells remember the allergen, and with repeated contacts, specific antibodies, immunoglobulins E (IgE), begin to be produced, which cause hypersensitivity. And subsequent encounters with the allergen cause the development of an allergic disease. Mast cells (those cells that produce specific antibodies) are found in the skin, respiratory tract, and gastrointestinal tract (GIT). Normal condition These tissues limit the entry of allergen into the body, preventing the development of clinical manifestations. Accordingly, diseases of the skin, respiratory tract, and gastrointestinal tract provoke the appearance of various allergic reactions.

Atopic families may produce healthy children, but their offspring (third generation) may suffer from allergic diseases.

Atopic dermatitis in an infant is the first and earliest manifestation of the disease, often leading to the development of bronchial asthma. The development of atopic dermatitis can occur when using any product in a baby’s diet. The allergic reaction depends on the nature of the antigen, its dose, frequency of administration, and individual tolerance.

Causes of atopic dermatitis and allergies in infants

Milk is considered the most common cause of atopic dermatitis in children. In fact, an allergy to milk is quite rare, and the causes of dermatitis (skin rashes) in infants in 85% of cases are:

These causes of atopic dermatitis in children are not associated with allergies, but only with the fact that the little person does not have time to adapt to a new and difficult life. Weakened by excessive stress, the child’s organs work worse, leading to changes in blood tests, stool tests for carbohydrates, coprology, etc.

If you start changing or eliminating foods, formulas, complementary foods, or prescribing a diet for a nursing mother, instead of helping the child heal minor disorders in the immune system and pancreas, then the situation will only get worse, since new product– this is a new burden on the already weak systems of a sick child.

Searching for an allergen using a blood test or skin tests in this case will not give a clear picture: some slightly suspicious products, plants, etc. may be found, but worms or giardia, of course, will not be found, which means they will continue to live in the child’s body, breaking his immunity and poisoning the body.

The causes of atopic dermatitis in children can vary, but for most it occurs as follows. Usually, infants are introduced to complementary foods drop by drop, a few grams, 1/4 teaspoon, between feedings or before them. And even if no serious mistakes are made, when a child is given a large amount of new food at once or a product is introduced that is not appropriate for his age (for example, baby kefir at 1 month, when the package says “from 6 months”), the child breaks out in a rash.

No one is to blame - parents followed advice from decent books, pediatricians - instructions and textbooks. Is this an allergy? Most likely not. Books, textbooks and instructions were written a long time ago, and since then, due to the deterioration of the environment and human lifestyle, newborn children have become a little different.

Now we need to introduce new foods to children under one year of age much more carefully than our grandmothers or even you did with older children.

A more careful introduction of complementary foods will not harm your child at all; he will not experience any lack of food, vitamins, etc. But you will minimize the risk of developing it, and subsequently, perhaps, avoid allergies and other diseases, even.

Diathesis as a reaction to the introduction of complementary foods occurs when the child’s body and its enzymatic systems are not ready to digest a new product. Not knowing how to digest an apple, porridge or kefir, the pancreas “strains”, trying to produce the necessary enzymes in the required quantity. This leads to a slight “inflammation” of the pancreas (on ultrasound it is usually enlarged in such children). The child’s immune system must respond to any inflammation and heal it, but the baby’s systems are still immature and unformed, so an inadequate reaction of the immune system appears on the skin in the form of diathesis.

The best nutrition for an infant is mother's milk. But there are situations when it is necessary to introduce additional nutrition - an adapted milk formula. As mentioned above, the introduction of supplementary feeding is necessary when there is a shortage of breast milk, when the baby does not get enough to eat, requires breastfeeding earlier than 2.5 hours after the end of the previous feeding, and does not gain weight well. Another indication for introducing the mixture is the prescription of therapy to the mother that is incompatible with natural feeding (treatment of cancer, serious hormone therapy). Another reason may be group or Rh conflict. In exceptional cases, it is recommended to abolish breast milk and introduce formula when the mother is prescribed antibiotics (but in most cases this situation does not require the abolition of breastfeeding), as well as for very severe decompensated lactase deficiency (most often in these cases, treatment is carried out without stopping breast milk, but sometimes it is necessary to introduce a medicinal formula and switch to mixed feeding).

The child may react to the introduction of the mixture with a deterioration in general condition, skin rashes, abdominal pain, changes in the nature of the stool (greens, mucus, constipation). Late regurgitation or “fountain” regurgitation may occur. Sometimes problems that existed before the introduction of supplementary feeding intensify, or new symptoms of existing diseases appear. Deterioration occurs due to the immaturity of the baby’s adaptation systems up to 4 months, so any change in nutrition at this age can lead to breakdowns.

Sometimes the reason for the deterioration of the condition is the baby’s individual immunity to a particular mixture. To assess the individual reaction to the mixture, you need to track changes in condition from the initial one according to the following criteria: skin, stool, behavior (restlessness, regurgitation). That is, before introducing the mixture, you need to remember or write down all the problems that the baby has, and, when you start giving the mixture, track the changes. If deterioration occurs, do not remove the mixture immediately, but continue to give it in the amount at which the problems began.

If the deterioration is associated with difficulties in adaptation, then within 2-3 days the reactions will end and the child’s condition will return to its original level. If the deterioration is significant and does not go away within 4 days, this means that this mixture is not suitable for the child and you need to try another one. So don't buy right away large number a mixture that the child has not tried before.

To avoid the development of dermatitis in infants, the mixture must be introduced gradually, starting with 5-10 g of the finished mixture (no more than 30 g, which corresponds to a scoop of dry formula), after breastfeeding. On the first day, you can give a small amount of the mixture at each feeding or at some. On the second day and beyond, the amount of formula can be increased by adding a measuring spoon or less per feeding. The less the better – even just a pinch. If the formula is introduced for supplementary feeding (if there is a lack of breast milk), then the feedings can be mixed (both breast and formula in one feeding, but breast first). Gradual introduction of the mixture reduces the risk of reactions. If the mixture suits the child, that is, does not cause any reactions, then it is better not to change it (you can only change the number - the level of the mixture according to age, but you can not change the level either). Also change the mixture of one stage to the same mixture of the next stage gradually: replace within 5–7 days in the amount of one scoop at each feeding.

Adaptation is the totality of the work of the immune and digestive systems. In young children, the process of getting used to new food usually lasts up to 7-14 days. It is during this period that reactions to the introduction of a new mixture may occur. If the adaptation process has passed, the baby has been eating some kind of formula for a long time and suddenly he begins to have problems with the skin or tummy, then the mixture and nutrition in general (hereinafter juices, cereals, purees) have nothing to do with it: the problem must be looked for in the work of the gastrointestinal tract. intestinal tract, other organs and systems, but do not change nutrition.

The risk of a child’s illness increases when exposed to unfavorable external factors, which can be not only artificial feeding, but also eating foods rich in substances that can cause allergies. Allergens can also include particles of hair and dander from pets, mites, cockroaches, molds, house dust, medications (for example, antibiotics), food additives, and preservatives.

In young children, one of the first allergens is cow's milk, which contains about 15–20 antigens, of which the most allergenic are: β-lactoglobulin, α-lactoalbumin, casein, bovine serum albumin. 85–90% of children with atopic dermatitis are allergic to cow's milk proteins.

Most often, allergic reactions occur to the following products: whole milk, eggs, fish and seafood, wheat, rye, carrots, tomatoes, peppers, strawberries, wild strawberries, raspberries, citrus fruits, pineapples, persimmons, melon, coffee, cocoa, chocolate, mushrooms, nuts, honey

Dermatitis in children can be caused by food additives containing preservatives, flavorings, flavorings, and emulsifiers. These dyes include E-102 - tartrazine, which colors food products in yellow. The development of allergic reactions can be facilitated by sulfur additives in the form of metabisulfate, sulfur compounds (E-220-227), and sweeteners.

Risk factors for atopic dermatitis and allergies in children

Factors contributing to the manifestation of obvious allergies may be obvious allergens:

Non-allergenic risk factors for atopic dermatitis in children:

What do the manifestations of atopic dermatitis look like in children (with photos and videos)

Signs of the disease may appear in the 2-3rd month of a baby’s life, but most often they occur after he is transferred to artificial feeding.

At the initial stage, symptoms of atopic dermatitis in children appear, such as redness and swelling of the skin of the cheeks. Then yellow crusts and cracks form on the changed skin. The skin on the head, buttocks, elbow and knee bends, and wrists can also be affected.

The development of dermatitis is facilitated by exposure of the skin to cold or elevated temperatures, sun exposure, contact with chemicals, as well as wearing irritating clothes (rough fabrics, synthetics, thick internal seams).

In areas where children's skin is affected, a manifestation of dermatitis occurs, such as itchy skin, which can be so severe that it disturbs the baby's sleep. The skin thickens, becomes dry, covered with scales, and flakes off. In such places, cracks form and heal with great difficulty.

See what atopic dermatitis looks like in children in these photos:

The child loses weight, becomes restless, irritable, and tearful.

The disease lasts a long time, characterized by alternating periods of severe inflammation and subsidence of the process. Dietary disorders and psycho-emotional stress can provoke an exacerbation.

The disease may continue for many years. Exacerbations of atopic dermatitis are observed mainly in autumn period year. In the infant and childhood phases, focal patchy-scaly rashes are observed with a tendency to form blisters and areas of weeping on the skin of the face, buttocks, and limbs. In the pubertal and adult periods, nodular rashes of a faint pink color dominate, which are located mainly on the flexor surfaces of the limbs, especially in the elbows, popliteal cavities, and on the neck in the form of a characteristic pattern. Atopic dermatitis is characterized by dry, pale skin with an earthy tint. Skin lesions can be localized, widespread and affect the entire skin. In a typical case, skin lesions are expressed on the face, where there are spotty-scaly lesions with unclear contours, mainly in the periorbital region, in the area of ​​the nasolabial triangle, and around the mouth. The patient's eyelids are swollen, thickened, lips are dry, with small cracks. On the skin of the neck, chest, back, and limbs there are numerous small nodular elements of a pale pink color, some of them are covered in the central zone with a hemorrhagic crust. In the area of ​​the lateral surfaces of the neck, elbow bends, wrist joints, popliteal cavities, the skin is rough, stagnant red in color, with an enhanced skin pattern. The lesions show peeling, cracks, and abrasions. In severe cases, the process is persistent, the lesions cover large areas, they also appear on the back of the hands, feet, legs and other areas, the lymph nodes enlarge, and the temperature may rise.

These photos show what dermatitis looks like in children:

At older ages in children, the main manifestations of atopic dermatitis are:

Additional signs are:

Watch the video “Atopic dermatitis in children”, which shows all the manifestations of this disease:

Causes of contact dermatitis in children

Contact dermatitis most often develops as a result of skin contact with chemicals: acids, alkalis, salts of chromium, nickel, mercury.

In addition, medications, physical, biological, climatic and other influences can cause manifestations of dermatitis in schoolchildren.

The characteristics of the course of dermatitis and the severity of its clinical manifestations depend on the properties of the irritating factor itself, the duration of its influence and the state of reactivity of the body.

A characteristic feature of dermatitis is a fairly rapid reverse development after the irritant is eliminated.

The causes of contact dermatitis are often direct long-term or repeated exposure to the skin of chemicals (acids, alkalis in high concentrations, etc.), mechanical (abrasions, friction tight clothes, shoes, plaster casts, pressure from instruments, etc.), physical (high and low temperatures, ultraviolet (actinic dermatitis), x-rays, radioactive isotopes, as well as contact with biological irritants and plants (such as buttercup, spurge, shore grasses, primrose, etc.).

In everyday life, simple (contact) dermatitis in schoolchildren can be triggered by shampoos, caustic soaps, cosmetics, detergents, citrus juice and a number of topical medications.

Dermatitis localized around the mouth occurs in children who have the habit of licking their lips.

Contact dermatitis occurs at the site of exposure to the irritant and, as a rule, does not spread beyond its boundaries.

The predisposition to the development of contact dermatitis varies among schoolchildren. Thus, in some children the disease occurs with minimal exposure to the irritant. Symptoms of contact dermatitis in children are the appearance of erythema, swelling, and then blisters, papules and pustules on the skin. Skin changes are accompanied by burning and pain in the affected areas.

With the development of contact dermatitis from exposure to X-rays, high temperature and some other irritants, the lesions subsequently ulcerate and scar.

Simple (contact) dermatitis resolves quite quickly (within a few days) after eliminating contact with the irritant.

Plantar dermatitis is caused by wearing tight synthetic shoes. The disease occurs mainly in schoolchildren during the prepubertal period.

The lesions are localized on supporting surfaces and have a glassy appearance. Cracks may appear. Skin changes are accompanied by pain.

To treat this disease, changing shoes using temporary local applications of emollients is sufficient.

Types of allergic contact dermatitis in children

Allergic contact dermatitis in children also occurs as a result of exposure to external irritants, however, unlike simple contact dermatitis, it is based on an allergic restructuring of the body.

Allergic dermatitis can be caused by substances such as chromium salts, formalin, phenol-formaldehyde and other artificial resins that are part of varnishes, adhesives, plastics, etc. Also, pronounced allergenic properties are inherent in penicillin and its derivatives, mercury salts.

Some children are extremely sensitive to nickel. Allergic dermatitis in this case can occur from contact with nickel-containing fasteners on clothing or jewelry. Nickel contact dermatitis is often localized to the earlobes.

Shoe dermatitis can be caused by antioxidants in shoe lubricants or by tanning agents and chromium salts in the leather used to make the shoes. When you sweat profusely, these substances tend to leach out.

Allergic dermatitis from shoes usually develops back side feet and toes, without affecting the interdigital spaces. Unlike simple contact dermatitis, it rarely affects the palmar and plantar surfaces. In typical cases, symmetry of the lesions is observed.

Dermatitis from clothing develops through contact with the following allergens: factory dyes, elastic fabric fibers, resins, fabric mordants. Dyes, resins and mordants in fabrics may not adhere well and may subsequently leach out when the garment is worn.

Allergic dermatitis on the face can be caused by all types of cosmetics (especially often on the eyelids). Unexpectedly, allergic dermatitis may develop when using topical medicinal products, especially when used to treat pre-existing dermatitis. Such allergens include local antihistamines, anesthetics, neomycin, merthiolate and ethylene diamide, which is present in many ointments.

Allergic contact dermatitis can occur in 2 forms - acute and chronic, prone to exacerbations. Once hypersensitivity to a particular allergen occurs, it usually persists for many years.

Skin symptoms in allergic contact dermatitis in children resemble the morphological elements of simple contact dermatitis, with the difference that in allergic dermatitis the inflammatory process spreads beyond the lesion and manifests itself as eczema-type weeping.

Diagnosis of this disease is carried out by performing skin tests with minimal concentrations of the relevant allergens.

The most common toxic-allergic dermatitis of drug origin in schoolchildren occurs when taking medications. The disease is caused by both allergic and toxic components of the drug.

Drug-induced toxic-allergic dermatitis develops with long-term repeated, less often short-term, intake of the medication orally or when administered parenterally.

The combination of allergic and toxic effects of the irritant, varying in severity and strength, causes the development of the so-called medicinal disease, in which, in addition to lesions of the skin and mucous membranes, the tissues of the nervous, vascular systems and internal organs are involved in the inflammatory process.

Toxicity forecast allergic dermatitis drug origin depends on the severity of general clinical and allergic reactions. The most severe consequences, often leading to death, are observed with Lyell's syndrome.

Children with atopic dermatitis may later develop other allergic diseases (bronchial asthma, allergic rhinitis, urticaria, etc.).

Methods for diagnosing atopic dermatitis in children

The diagnosis of atopic dermatitis based on the existing signs will be considered reliable if the patient has three main and three or more additional signs. However, the main clinical signs are: skin itching and increased skin reactivity. Itching is characterized by its persistence throughout the day, as well as its intensification in the morning and at night. Itching disrupts the child's sleep, irritability appears, quality of life is disrupted, especially in adolescents, and learning difficulties appear. Skin manifestations of atopic dermatitis are characterized by severe itching, erythematous papules against a background of hyperemic skin, which are accompanied by scratching and serous exudate. This is typical for acute dermatitis.

Diagnosis of atopic dermatitis in children is based on complaints, information clearly indicating the connection between exacerbation of the disease and a causally significant allergen, determination clinical symptoms dermatitis, the presence of factors that provoke exacerbation of the disease - allergenic and non-allergenic. For diagnosis, a special allergological examination is carried out, which includes analysis of anamnestic data, determination of specific antibodies to the allergen as part of IgE, and skin testing.

The level of immunoglobulin E to various allergens is determined in the blood using an enzyme-linked immunosorbent or radioimmune method. Results are expressed in points from zero to four. An increase in the level of IgE to the allergen by two points or more confirms the presence of sensitization.

The main method for diagnosing atopic and allergic dermatitis in infants and older children is elimination-provocative tests. In practice, an open test is used, in which the product is given to the patient and the reaction is observed.

Contraindications to provocative tests may include:

Provocative tests are carried out outside the exacerbation of the disease.

If a child has problems such as skin rashes First of all, you need to examine the gastrointestinal tract, because almost 90% of skin rashes are of intestinal origin. Necessary studies include stool tests for dysbacteriosis and scatology; ultrasound of the abdominal organs often provides useful information. For these tests, you need to contact a pediatric gastroenterologist or immunologist, because the gastrointestinal tract is not only digestive organ, but also the largest organ of the immune system. If necessary, additional studies may be prescribed: skin tests(not recommended up to 3 years) or blood tests to detect allergy antibodies - IgE (not recommended up to 1 year). The presence of “allergic” antibodies in very high concentrations is a sign of true allergy - the highest degree of immune dysfunction. As a rule, with such an allergy, allergists are involved in the treatment of the child. But this form of allergy is much less common than “pseudo-allergic” reactions against the background of impaired adaptation to nutrition, in which the blood test will show specific antibodies to “allergens” in low and medium concentrations (and this will not be the basis for a diagnosis of “allergy”, on the contrary – this will prove the absence of allergies).

To find the cause of complaints, additional tests may also be prescribed to identify infections that can cause allergies, such as chronic viral infections, chlamydial infection, mycoplasma infection, giardiasis, and helminthic infestations. A dermatologist may recommend topical remedies for food allergies, but in general atopic dermatitis is not a dermatological problem.

Among the therapeutic measures for atopic dermatitis, one can single out treatment aimed at eliminating the causes of allergies (immunocorrection, treatment of dysbacteriosis, restoration normal functioning gastrointestinal tract, removal of foci of chronic infection), as well as symptomatic therapy - primarily, elimination of itching. Symptomatic remedies include antihistamines and external agents. Among external remedies, hormonal ointments can be prescribed. It is advisable to use them when severe exacerbations when other means do not help, but no more than 10 days.

If symptoms of dermatitis occur in children, treatment should be started immediately.

Diet recommendations for allergic and atopic dermatitis in children

Treatment of atopic and allergic dermatitis in children is carried out comprehensively. Dermatitis should be treated in the early stages, otherwise the disease progresses and becomes chronic. It is necessary first of all to eliminate contact with the allergen.

In the first place is the elimination of causally significant allergens, which is carried out based on the results of an allergological examination. There is no standard elimination diet for allergic dermatitis in children. In this regard, when a patient’s hypersensitivity to certain foods is detected, a specific elimination diet is prescribed. If there is no positive dynamics within ten days, reconsider the diet. For children, an elimination diet is prescribed at 6-8 months, then it is revised, as sensitivity to allergens changes with age.

In the diet of children under one and a half years old, the most allergenic foods are excluded, such as eggs, fish, seafood, peas, nuts, and millet.

Dairy-free formulas are prescribed if the child is allergic to cow's milk. Mixtures based on protein hydrolyzate are prescribed. The child must be breastfed for at least six months. A nursing mother is obliged to exclude from her diet foods to which the child is hypersensitive. Complementary feeding is prescribed to children no earlier than 6 months.

The allergenicity of some products can be reduced through long-term heat treatment.

It is important not to include in your diet foods with added dyes, fruit essences, vanilla, or smoked foods. Meat broths It is better to replace with vegetable soups. Strictly contraindicated chewing gum. Sugar can be replaced with fructose.

If the child is bottle-fed, it is necessary to use a special formula for children with allergies. If the baby is breastfed, it is necessary to adjust the mother's diet for the entire feeding period. When introducing complementary foods, preference is given to green vegetables - cabbage, zucchini and dairy-free cereals.

But when following a diet, it is necessary to remember that excessive restrictions can lead to deficiency. nutrients in the child’s diet and disruption of his physical development.

When treating allergic dermatitis in children, to monitor correct adherence to the diet, you can conduct food diary. In it, make a daily record of what time and what foods your child consumed, and also record the occurrence or exacerbation of symptoms of dermatitis. This way you can establish a connection between the use of a particular product and the disease. This will allow you to individually choose a diet for your child. Show the diary to the doctor.

How can you get rid of atopic dermatitis in a child?

Before you begin to treat atopic dermatitis in a child, avoid contact of the baby’s skin with irritants such as wool, synthetic fabrics, and metal objects, including beads, bracelets, and chains.

Contact of a child with household chemicals is extremely undesirable. Symptoms of dermatitis can be provoked by washing powders, soaps, shampoos, and various cosmetics. All of them should be intended for children.

Make sure your child does not scratch the affected skin. Trim your baby's nails often and put him to bed in a long-sleeved shirt. Scratching the skin can lead to the development of an infectious process. Treat all abrasions with a slightly pink solution of potassium permanganate or a solution of brilliant green. It is important to follow skin care rules.

To get rid of atopic dermatitis in a child as quickly as possible, you need to bathe your baby daily and use medicated cosmetics and ointments for skin care. Conventional cosmetics are not suitable in this case; your doctor will help you choose them. To bathe a child, you can use a decoction of string and chamomile.

In severe cases, hormonal ointments are used for treatment.

They provide quick effect and significantly alleviate the child’s condition, but they are allowed to be used only under the supervision of a doctor.

Antiallergic drugs are also prescribed (antihistamines - tavegil, suprastin, ketotifen, calcium preparations), usually in the form of tablets. Modern drugs have a minimum of side effects and last a long time.

What should you do in case of atopic dermatitis in a child based on house dust? In this case, the following activities are carried out:

  1. regular wet cleaning;
  2. mattresses and pillows are covered with plastic zippered envelopes;
  3. bed linen is washed weekly in hot water;
  4. pillows must have synthetic filling and be covered with two pillowcases;
  5. furniture in the apartment should be made of wood, leather, vinyl;
  6. patients are not allowed to be present when cleaning the premises;
  7. When using air conditioners, the temperature should be regular; humidifiers and evaporators should not be used without controlling the humidity in the room.

In case of allergy to mold fungi, the following elimination measures are carried out:

  1. When cleaning the bathroom, it is necessary to use products that prevent mold growth at least once a month;
  2. a hood is installed in the kitchen to remove moisture during cooking;
  3. Patients are not allowed to mow the grass or remove leaves.

Measures to prevent epidermal sensitization in dermatitis:

  1. It is not recommended to wear clothes containing wool or natural fur;
  2. It is recommended to avoid visiting the zoo, circus, apartments where there are pets;
  3. If an animal enters the premises, it is necessary to carry out wet cleaning repeatedly after removing it.

For pollen allergies, the following measures are taken:

  1. When flowering, close windows and doors tightly;
  2. walking is limited;
  3. during the period of dusting, the place of residence changes;
  4. It is prohibited to use herbal cosmetics;
  5. Treatment with herbal preparations is not recommended.

Below we describe how to treat dermatitis in a child using medications.

What to do with atopic dermatitis in a child: how and how to treat the disease

For symptoms of atopic dermatitis in children, effective drugs that block individual parts of allergic reactions are used for treatment:

  1. antihistamines;
  2. membranotropic drugs;
  3. glucocorticoids.

In complex treatment enterosorbitols are used, sedatives, drugs that improve or restore digestive function, physiotherapy.

When treating atopic and atopic dermatitis in children, symptoms, age, stage of the disease, features of the clinical picture, severity, prevalence of the pathological process, complications and concomitant pathologies are taken into account.

Antihistamines. The main mechanism of action of antihistamines is the blockade of the inflammatory process caused by the binding of IgE antibodies to the allergen. Antihistamines block histamine H1 receptors, which reduces the severity of swelling, hyperemia, and itching. The last symptom, itching, does not always disappear with this therapy. When prescribing antihistamines, the peculiarities of their mechanism of action are taken into account. Thus, first-generation drugs have a sedative effect. In this regard, they are not prescribed to school-age children due to the fact that their use reduces concentration and the ability to concentrate. Due to the decrease in the effectiveness of first-generation drugs with long-term use, it is recommended to change them every 7-10 days or prescribe second-generation drugs. In the chronic course of the process, with severe eosinophilia, cetirizine and claritin (long-acting second-generation H1-blockers) are prescribed. They have high specificity, begin to act within 30 minutes, the main effect lasts up to 24 hours, do not affect other types of receptors, and they do not penetrate the hepatoencephalic barrier.

Use of corticosteroids. The use of oral glucocorticoids is indicated for extremely severe allergic dermatitis. They are prescribed in these cases locally. When applied topically, corticosteroids suppress the components of allergic inflammation, the release of mediators, and the migration of cells into the area of ​​skin lesions; they cause vasoconstriction and reduce swelling. They relieve the symptoms of dermatitis in acute and chronic periods.

Currently, a series of drugs have been developed that are safe enough for use in children: in the form of lotions, creams, and ointments. It is recommended to use such products as advantan and others. It is used from 4 months and in various types. Elok is effective. It does not cause systemic effects and can be used once a day; its effect is detected already in the first days.

When choosing corticosteroid drugs, it is necessary to strive to eliminate acute symptoms atopic and allergic dermatitis in children in short terms. Despite the risk of side effects, corticosteroid drugs are the mainstay of treatment for atopic dermatitis.

How else can you cure atopic dermatitis in a child?

To cure atopic dermatitis in a child as quickly as possible, it is recommended to use β-methasone-containing ointments, the use of which for a long time is not recommended. Acriderm is one of these products. Akriderm and Akriderm GC have a moisturizing effect and prevent drying of the skin. Akriderm C contains salicylic acid, which softens and exfoliates the scales of the epidermis. The combined drug Akriderm GK contains gentamicin (an antibiotic) and an antifungal agent. It has an antibacterial and antifungal effect.

In the treatment of atopic dermatitis in children, anti-inflammatory external agents are also used: sulfur, tar, LSD-3, Peruvian balsam, clay.

It is necessary to wash the child with cool water (long bathing and hot water are not recommended, use special shampoos such as Friederm tar, Friederm zinc, Friederm pH balance.

For secondary skin infections, pastes containing 3–5% erythromycin are used in the form of ointments. Skin treatment with solutions of brilliant green and methylene blue.

For fungal infections, creams Nizoral, Clotrimazole, etc. are prescribed.

A lasting clinical effect in atopic dermatitis occurs with the correct combination of allergen elimination, taking into account all factors in the mechanism of disease development, the use of local glucocorticosteroids, and correction of neurovegetative dysfunctions.

Methods of treatment and prevention of atopic dermatitis in children

Many doctors are confident that atopic dermatitis in a child can be cured, and there are four ways to do this.

Most common– Prescribe and change antihistamines all the time. The method firmly and permanently connects the patient with the doctor, but does not bring permanent and final relief. It’s hard to even call it quality treatment.

Second option– block the immune response using mast cell membrane stabilizers for the duration of the allergen’s action in the hope that the immune system, developing with the child, will wean itself from a hyperreaction to the allergen. Treatment is long-term and can only be effective against pollen allergens. The doctor and parents wait until the child “outgrows” the allergy as a result of hormonal changes in the body. Sometimes it works.

Third way– elimination of the allergen, that is, the creation of conditions under which the child will not encounter the allergen. For example, you don’t have fish or pets, don’t give certain products, you are leaving for distant countries during the allergen bloom. The hope is the same as in the second option. Sometimes it works too.

Fourth method– desensitization – the introduction of minimal, close to homeopathic, doses of the allergen into the child’s body. It works like this. Although for the emergence of true allergic reaction A microscopic amount of the allergen is enough, however, the doctor can reduce this amount tens or hundreds of times. By introducing such a dose into the body, it begins to teach it not to react to the allergen. It is very important to know what exactly the child is allergic to. They learn about this based on the results of tests to identify the allergen.

It is necessary to avoid errors in the mother's nutrition during pregnancy and lactation, and to treat the mother's chronic diseases before and during childbirth. To prevent outbreaks of atopic dermatitis in children and adults, it is recommended spa treatment in a warm southern climate, in gastrointestinal sanatoriums.

The prognosis in most cases in young children is favorable, subject to proper nutrition and therapeutic measures aimed at normalizing the functioning of the gastrointestinal tract and adaptation systems. Most often, food allergies go away without a trace and without consequences. But you should not expect that the child will “outgrow” the disease on his own and do nothing.

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Determination of specific immunoglobulins G to allergens in vitro. During remission

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IN medical practice under eosinophilia understand the condition of the blood in which there is an increase in the level of special blood cells - eosinophils. In this case, infiltration (impregnation) of other tissues with eosinophils is also observed. For example, with an allergic rhinitis, eosinophils can be found in nasal secretions, with bronchial asthma with bronchitis - in sputum, with accumulation of blood in the lungs or pleural tumors - in pulmonary fluid.

In an adult, the number of eosinophils in the blood is considered normal from 0.02 x 10 9 / l to 0.3 x 10 9 / l.

The following degrees of eosinophilia are distinguished:
1. Small - up to 10% of the total number of leukocytes.
2. Moderate – 10-20%.
3. High – over 20%.

Persistent eosinophilia is most often a sign of helminthic infections, allergic reactions, and some leukemias.

Eosinophilia - a symptom or a disease?

Eosinophilia is not an independent disease, but a sign (symptom) of many infectious, autoimmune, allergic and other diseases. Their list is quite wide.

4. Symptoms of gastrointestinal diseases.
Since many diseases digestive systems lead to disruption of the intestinal microflora, the process of cleansing the body of toxins slows down, which leads to increased content eosinophils. With such dysbiosis, the patient may be bothered by vomiting and nausea after eating, pain in umbilical region, diarrhea, cramps, signs of hepatitis (jaundice, liver enlargement and pain).
5. Blood diseases.
Systemic histiocytosis against the background of eosinophilia is characterized by frequent infectious diseases, enlarged liver and spleen, damage to the lymph nodes, cough, cyanosis of the skin (blue discoloration), dyspnea (difficulty breathing).
Along with eosinophilia, with lymphogranulomatosis there is fever, pain in the bones and joints, weakness, itching over most of the skin surface, lymphadenopathy, enlargement of the liver and spleen, and there may be a cough.
Eosinophilia in non-Hodgkin's lymphoma is also accompanied by fever, weakness, loss of body weight and motor activity, as well as symptoms characteristic of damage to certain areas. Thus, when a tumor appears in the abdominal area, symptoms such as thirst, abdominal enlargement, and intestinal obstruction are noted. From the central nervous system - headaches, paralysis and paresis, decreased vision and hearing. Chest pain, cough, facial swelling, and difficulty swallowing may occur.

Pulmonary eosinophilia

This term refers to infiltration (impregnation) lung tissue eosinophils. This is the most common tissue localization of eosinophils.

The disease combines the following conditions:
1. Eosinophilic granulomas.
2. Pulmonary infiltrates (volatile).
3. Eosinophilic pulmonary vasculitis caused by various causes.
4. Eosinophilic

Some aspects of the epidemiology, pathogenesis and conservative treatment of allergic rhinitis: allergic inflammation

Fungal sensitization in allergic lung diseases in children: children, fungal sensitization, allergic bronchitis, allergic bronchopulmonary aspergillosis, exogenous allergic alveolitis, bronchial asthma.

Eosinophilic skin diseases

Eosinophilic skin diseases: (1)

Working version of the classification of cytomegalovirus infection in children: children, allergies, atopy, atopic dermatitis, pathogenesis.

Mechanisms of development of atopic dermatitis in children (literature review): children, allergies, atopy, atopic dermatitis, pathogenesis.

Atopic dermatitis: heterogeneity of clinical forms and diversity of pathogenesis mechanisms: dendritic cells, Langerans cells

Atopic dermatitis: heterogeneity of clinical forms and diversity of pathogenesis mechanisms: pathogenesis of atopic dermatitis

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Eosinophils and their role in the pathogenesis of allergic diseases

V.B. Dzhalchinova, G.M. Chistyakov

Key words:

eosinophils of different densities, allergies.

In the late 70s and early 80s, reports appeared that not only mast cells, but also other cells possess IgE receptors. It turned out that the most important in this regard are eosinophils, capable of producing mediators responsible for the development of cell and tissue damage.

Clinicians, both therapists and pediatricians, in everyday practice very often have to deal with eosinophilia, which is observed in various diseases, but mainly in atopic forms of allergic diseases. Judgments about the significance of eosinophilia in blood and tissues until recently were controversial. A position has been put forward about its protective role, motivated by the fact that eosinophils supposedly produce arylsulfatase, an anti-leukotriene enzyme. However, the results of further studies did not confirm this concept. Most researchers agree on the damaging effects of eosinophilia and, especially, hypereosinophilia. To understand the mechanism of this damaging effect, it is necessary to have an idea, at least in general terms, of the morphology and function of these cells.

Most authors indicate that the damaging effect is inherent mainly in low-density eosinophils, since their activation occurs to a much greater extent. Tissue damage seen with bronchial asthma(ciliostasis, desquamation of epithelial cells of the mucous membranes, thickening basement membranes cells bronchopulmonary system) turned out to be similar to that observed in the experiment when the trachea comes into contact with low-density eosinophil proteins. Using the immunofluorescence method, a cationic protein was detected in bronchial tissue in bronchial asthma, in the skin in recurrent urticaria and atopic dermatitis. If previously the influx of activated eosinophils into the inflammatory focus was considered as a passive reaction, now tissue eosinophilia appears to be an active phenomenon, “responsible” for some pathological processes and, first of all, for allergic inflammation.

The significance of eosinophilia in allergic reactions is especially demonstrative when considering the connection of eosinophils with platelet activating factor. It is known that this factor is secreted by various types of cells, especially alveolar and peritoneal macrophages, monocytes, platelets, and polynuclear neutrophils. It has also been proven that it is also released by eosinophils. In vitro studies have shown that, under the influence of an ionophore, eosinophils with low density secrete platelet activating factor in much greater quantities than those with normal density. It is of interest that there is a reciprocal relationship between eosinophils and platelet activating factor. On the one hand, eosinophils produce this factor, and on the other, the latter activates eosinophils, which, as already mentioned, secrete the proteins contained in the granules, especially peroxidase. In addition, under the influence of platelet aggregation factor, along with other stimuli, in particular under the influence of a calcium ionophore, low-density eosinophils are able to synthesize and release leukotriene C, although in small quantities. Platelet aggregation factor has the most pronounced chemotactic activity against eosinophils, and also promotes their adhesion to endothelial cells, which was shown in in vitro experiments. Apparently, in vivo, the transformation of eosinophils with normal density into cells with reduced density also occurs with the participation of this factor. The number of the latter increases in damaged tissues. Thus, in pulmonary diseases in the pleural fluid the number of low-density eosinophils reaches 80-100%, in bronchoalveolar lavage - 60%.

An essential feature of eosinophils, which is directly related to the purely clinical aspects of eosinophilia, is the presence on these cells, as mentioned above, of receptors for corticosteroid hormones. The work of many researchers has revealed varying degrees of expression of these receptors. This was especially demonstrably revealed when studying blood eosinophils of patients suffering from hypereosinophilic syndrome. This syndrome is heterogeneous in its genesis. It can be observed with helminthic infestation, with atopy, and be a “harbinger” of the development of various diseases, including malignant diseases - T lymphoma, lymphogranulomatosis, histiocytosis, Crohn's disease, Whipple's disease, cancer, necrotizing angiitis (Churg-Strauss disease). The decrease or disappearance of hypereosinophilia under the influence of corticosteroid therapy is evidence of the pronounced activity of glucocorticoid receptors of eosinophils. In such situations, the eosinopenic effect when using corticosteroid hormones is explained by the inhibition of eosinophil migration, as well as inhibition of eosinophilopoiesis. It is also reported that a decrease in the number of peripheral blood eosinophils under the influence of corticosteroid therapy occurs due to cells with normal density, while the number of cells with low density remains little changed. This finding suggests that the expression of glucocorticoid receptors is greater in eosinophils with normal density compared to cells with reduced density. A similar phenomenon occurs in hypereosinophilic syndrome of atopic origin, the prognosis of which is generally favorable. At the same time, there is evidence that the predominance of low-density eosinophils in hypereosinophilic syndrome in the absence of any visible manifestations can serve as a “harbinger” various kinds visceral lesions. Therefore, some clinicians recommend prescribing for hypereosinophilic syndrome as a prophylaxis for manifest forms. pathological process prednisolone at the rate of 0.5-1 mg per 1 kg of body weight per day. However, the effect of such an effect is not always achieved, since due to the weak expression of glucocorticoid receptors by low-density eosinophils, the latter turn out to be corticosteroid-resistant.

Of significant interest is the study of the total number of eosinophils and especially the number of their subpopulations in such a classic allergic disease as atopic dermatitis. The dependence of the studied parameters on the volume of skin lesions and the severity of the disease as a whole was revealed. It turned out that in severe forms in the peripheral blood the number of low-density eosinophils decreases, which is explained by their migration into the tissue of the “shock” organ, where their pathogenic effect occurs.

Most of the works devoted to the study of the role of eosinophils in the pathological process concern bronchial asthma. A significant increase in the number of these cells in the blood, sputum and lung tissue in patients suffering from this disease is indicated. A significant contribution to the study of the role of eosinophils in bronchial asthma was the work to determine the morphometric parameters of these cells in the blood and sputum in the dynamics of the disease, taking into account therapeutic effects. Using computer morphometric analysis, the sizes of the areas of the cell, cytoplasm, and nucleus were determined. The nuclear-cytoplasmic ratio was calculated. It was found that during the period of attacks, the studied indicators changed upward compared to the control ones. Under the influence of complex treatment, positive dynamics of the studied indicators were noted, but their complete normalization did not occur. At the same time, a correlation was observed between changes in the morphometric parameters of blood and sputum eosinophils both before and during therapy. Assessing the results obtained as a whole, the authors conclude that the process of eosinophilopoiesis is enhanced in bronchial asthma. Other authors have also reported the important role of eosinophils in the development of allergic inflammation in bronchial asthma.

Thus, the above data indicate that the eosinophil is an effector cell, the activity of which is manifested in various diseases and pathological conditions, but mainly in atopic forms of allergic diseases. At the same time, as mentioned above, the pathogenic effect is inherent mainly in eosinophils with reduced density, since it is these cells that release active proteins that have a damaging effect on the tissue of the “shock” organ. The role of eosinophils has been studied to a greater extent in bronchial asthma, to a lesser extent in atopic dermatitis, and then mainly in adult patients. Currently, thanks to the significant expansion of laboratory research methods and their widespread use in clinical practice, it has become possible to study in detail the morphometric and morphological characteristics of eosinophils and their density characteristics. Of particular importance is the determination of the quantitative ratio of subpopulations of cells of different densities, which will contribute to the objective determination of the activity of allergic inflammation, in particular with atopic dermatitis in children, both in isolated form and combined with various visceral lesions, and to determine the most rational ways of therapeutic intervention.

Russian Bulletin of Perinatology and Pediatrics, N5-1999, p.42-45

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