Atopic dermatitis (AD) has recently received much attention from specialists and doctors. general practice. This is due to the fact that, despite the great success achieved in the study of the pathogenetic foundations of this disease, the development of new methods of treatment, including the use of modern external glucocorticosteroids, immunosuppressive drugs, external cosmetics, new antihistamines, fails to stop the growth of the disease and prevent development of severe forms of atopic dermatitis.

The modern classification of atopic dermatitis is criticized because it does not reflect all options its currents. Often the factors leading to the complication of the disease are not taken into account, which reduces the effectiveness of the therapy. Algorithms for the treatment of severe atopic dermatitis have not been worked out. All this leads to the formation of severe forms of atopic dermatitis, distrust of the patient and his parents to the actions of doctors and, ultimately, the 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 skin disease that most often manifests in early childhood and may further develop character traits chronically current inflammatory process with rare remissions or frequent exacerbations.

Recently, there have been trends around the world to increase the prevalence of atopic dermatitis, the development of its severe forms and the disability of patients. IN Russian Federation More than 7,000 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 national literary sources, the largest number children with disabilities is defined in the age group from 8 to 17 years, girls predominate among them.

Often, parents various reasons do not issue children with disabilities. 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 has not yet been established. The classification approach proposed in the scientific and practical programs of 2000 and 2004 is 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 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 variant has its own characteristics, 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. So, for example, one child at the age of five may suffer from an erythematosquamous form of atopic dermatitis, another - an erythematosquamous form with lichenification, characterized by localized foci of lichenification with severe dryness, excoriations and cracks.


Western experts have also argued about whether to attribute the IgE-independent variant of the course of the disease (the so-called internal type) to atopic dermatitis or not. The final point in the controversy was World Organization IAACI (WA0) (World Allergy Organization) in 2003: the term "eczema" was decided to refer to 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 the difference between the two variants of the course of atopic dermatitis were determined, based on the data of scientific studies of recent years (Table 1).


It should be noted, however, that this division is not entirely accurate: first, sometimes patients with IgE-independent dermatitis may have diagnosed bronchial asthma and/or allergic rhinitis(traditionally, these diseases in the IgE-dependent variant of the course are referred to as the atopic triad); secondly, with age, with an increase in the duration of atopic dermatitis due to the expansion of the spectrum of sensitization in patients with eczema, positive skin tests with allergens to which they had no sensitivity before 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 will provide answers to questions that are currently open.

Causes and symptoms of atopic dermatitis in children

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

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

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

The 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 the inhalation and through the gastrointestinal tract. Absorption by mucosal dendritic cells respiratory tract and the digestive tract and the subsequent start 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 lack of production of secretory IgA also contribute to the sensitization of the body.

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

An increase in the level of IgE 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-y and TNF-a, which activates 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 that 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 amount of Th2 prevails, in such patients the production of IL-4 increases and the synthesis of IFN-y 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 allergy. Delayed-type hypersensitivity is characteristic of a chronic, continuously relapsing course of atopic dermatitis and can be traced in children with a severe course of the disease. It is shown that in chronic stage atopic dermatitis, the immune response switches from Th2 to Th1 with a pronounced expression of IFN-y by the cells of the infiltrate, which is preceded by a peak in the expression of IL-12.

IN latest research the concept of participation in the allergic immune response of T-regulatory cells, 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, is proposed. In addition, they can affect B-lymphocytes by suppressing the production of IgE. CD8+ T cells, dendritic cells, IL-10-producing B cells, and natural killer cells may also exert a suppressive effect through regulatory T 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 a group of patients with non-atopic (atopiform) dermatitis. In studies, they reveal similar mechanisms of the pathogenesis of dermatitis, with the exception of hyperproduction of IgE.

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. In recent studies, for example, it has been demonstrated that in an 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, for the 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 varying degrees the severity of the disease must be at least three mandatory signs. Auxiliary signs are recorded in at least 1/3 of patients.

The severity of the exacerbation of the disease is assessed using the SCORAD semi-quantitative 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; front and back surface of the body - 18% each; lower limbs - 18% each; perineum and genitals - 1%.

The intensity of clinical manifestations (B) is assessed by six symptoms: 1. erythema (hyperemia); 2. edema/papules; 3. wetting/peeling; 4. excoriation; 5. lichenification/desquamation; 6. general dryness of the skin. Depending on the severity, each sign is given a score from 0 to 3 points: 0 - absence; 1 - weakly expressed; 2 - moderately pronounced; 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 by parents. The average indicator for the last 3 days and/or nights is determined. The final value of the SCORAD index is calculated by 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 the course of atopic dermatitis is determined based on the following criteria: the number of relapses per year, average duration relapses, the prevalence of skin lesions (Table 2).


In the range of diseases with which it is carried out differential diagnosis atopic dermatitis include scabies, psoriatic lesions, seborrheic dermatitis, microbial eczema, Vidal's lichen simplex (limited neurodermatitis), urticaria, contact dermatitis.

When examining children with atopic dermatitis, special attention is paid to the collection allergic history; skin testing is carried out during the period of clinical remission of the disease. Often in children with severe clinical manifestations of atopic dermatitis, the only possible method to identify causally significant allergens, allergodiagnostics in vitro remains, in a hospital setting, provocative tests with allergens are used, and a general clinical examination is carried out.

The severe course of atopic dermatitis is often associated with the development of pathological conditions that occur 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 biopsy specimens 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, and lymphangiectasia are noted. These changes lead to disturbances in metabolic processes due to the occurrence of tissue hypoxia with increased glycolysis, as well as to a decrease in the activity of tissue respiration enzymes, and microcirculation disorders. Inhibition of the suction capacity of the jejunum causes the development of malabsorption syndrome in children of 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.


A more severe course of atopic dermatitis can be caused by such factors 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.

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

In the group of children with severe skin manifestations, III and IV degrees of dysbiotic deviations prevailed; Significantly more often than in children with mild and moderate manifestations of dermatitis, an imbalance in the aerobic group of the biocenosis was determined (an increase in the total number of Escherichia coli, the dominance of coccal flora); in more cases, flora with signs of aggression (hemolyzing coli, hemolyzing enterococcus); Staphylococcus aureus, fungi of the genus Candida, associations of several conditionally pathogenic microorganisms were found more often.

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

Currently intestinal biocenosis play an important role in the formation of the immune function of the intestine 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 allergies. This is confirmed by the absence of any effect from the correction of dysbiotic deviations, carried out without treatment of the underlying disease.

Treatment of atopic dermatitis in children

Therapy of atopic dermatitis is aimed at eliminating specific and non-specific trigger factors, resolving allergic inflammation of the skin, normalizing the functioning of the gastrointestinal tract, combating dry skin, restoring the damaged lipid layer and is built according to the following plan:
The basis of diet therapy is:

The basis for the treatment of severe forms of atopic dermatitis is the pharmacotherapy of acute conditions. The importance of anti-inflammatory treatment with systemic glucocorticosteroids (GCS), relief of itching with antihistamines, 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, of course, plays an important role in resolving the inflammatory process of the skin, but without systemic pharmacological control, its use leads to the progression of atopic dermatitis and the deterioration of the patient's condition. The absence in Russia of clear agreed treatment regimens for severe forms of the disease causes low efficiency treatment of atopic dermatitis, the appearance of severe side effects of therapy and a sharp decline child's quality of life.

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 gained in the use of corticosteroids in patients with atopic dermatitis. Glucocorticosteroids (GCS) in atopic dermatitis are prescribed in a short course because of 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. (according to prednisolone), parenterally (intramuscularly) 1 time per 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 decrease 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 the fact of colonization of the skin of patients with Staphylococcus aureus, which has enterotoxigenic properties, is beyond doubt. There are not isolated cases of development of infectious complications in children associated with catheter-associated infection.

The appointment of antihistamines in atopic dermatitis is pathogenetically justified (Fig. 8). The advantages of first generation drugs are the possibility parenteral administration and the presence of a sedative effect, which helps to improve the sleep of a child suffering from intense itching. Only drugs of this group have, along with antihistamine and also antiserotonin activity, anabolic-like action and are approved for use in children 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 antibiotic therapy is consistently carried out only in the complicated course of atopic dermatitis. More often we are talking about infection with Staphylococcus aureus. The drugs of choice include first or second generation cephalosporins or semisynthetic penicillins. The course of treatment is usually effective from 7-10 days. Recently, due to an increase in the frequency of detection of methicillin-resistant strains, macrolides are not prescribed. In cases of drug allergy to the above antibiotics, clindamycin is used.

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

Rules for holding external therapy GKS:

The combination drugs include glucocorticosteroids (GCS):
  1. with antiseptics: group I: Dermozolon (clioquinol), group III: Lorinden C (clioquinol);
  2. with antibiotics: group I: Hyoxysone (oxytetracycline), oxycort (oxytetracycline), fucidin G (fusidic acid). neomycin);
  3. with antibiotics and antifungal drugs: group III: Triderm (gentamicin, clotrimazole), akriderm 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 a complicated course of atopic dermatitis, they are guided by the composition of the drug (presence of an antibacterial or antifungal agent). It is important to remember that many drugs are 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 of 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 advent of new dosage forms, with the accumulation of experience in the treatment of external glucocorticosteroids (GCS).

Successfully developing new medicines for the treatment of atopic dermatitis. One of them are 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), have already entered the group of main anti-inflammatory drugs .

Pimecrolimus inhibits Th1 and Th2 cell activation through the suppression of the production of pro-inflammatory 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 apoptosis of T-lymphocytes and keratinocytes (but not Langerhans cells) and on the inhibition of mast cells and basophils with the prevention of histamine and tryptase release has been noted.

However, disputes about the safety of the use of these drugs have not subsided so far, especially in young children and with long-term therapy, which is associated with the risk of developing 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. We have accumulated a lot of experience in their application. The Russian pharmaceutical market has pimecrolimus (1% cream) recommended as a second line of therapy and approved for use in children from 3 months of age (in the US and Europe - from 2 years). Tacrolimus (ointment 0.03 and 0.1%) is not registered in Russia.

The question of the effectiveness of the use of specific immunotherapy is still being discussed. In Russia with severe course atopic dermatitis, this method of treatment is not recommended.

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


Cyclosporine A (CsA) belongs to the group of drugs for which the correct choice of the 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 life of the patient. At the same time, low doses of the drug do not have a sufficient therapeutic effect, which can discredit this method of treatment.

In view of the multiple interactions with drugs that can decrease 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, grapefruit juice and drugs metabolized by cytochrome P450 should be excluded from food. Contraindications to the use of cyclosporine A (CsA) are concomitant bacterial and viral infections, liver and kidney damage.

The main side effects of cyclosporine A (CsA) treatment are nephrotoxicity and increased blood pressure. The risk of undesirable consequences of immunosuppressive treatment increases with the appointment of high doses and with an increase in the duration of therapy. At the same time, with the use of CsA, growth retardation is not observed, the drug is devoid of many life threatening side effects such as skin cancer and hepatotoxicity associated with other treatments for severe 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 traditional therapy(Table 3). Of the side effects, transient hypoisostenuria, paresthesia and headache were noted in only 2 cases.


The time of onset of the most pronounced positive clinical effect in different clinical and morphological forms of atopic dermatitis varied. Thus, in the erythematosquamous form of atopic dermatitis, positive dynamics during treatment was noted earlier than in the erythematosquamous form with lichenification and 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 with the introduction of protein solutions. It is recommended to remove 30-40% of the volume of circulating plasma per session, to conduct a course of plasmapheresis of 3 sessions with a frequency of 1 session in 4 days, and to replace the plasma with protein solutions.

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

Anti-relapse treatment is performed after the completion of the main course of treatment. The importance of these therapeutic measures associated with frequent relapses disease due to discontinuation of treatment and the 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 appointment of antihistamines, and the use of anti-relapse treatment to prevent exacerbation of the disease. 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 sound treatment, ultimately aimed at improving the quality of life of the patient and his family.

© A. V. Kudryavtseva

The origins of such a problem as atopic dermatitis in children should be sought in infancy. The unreasonably early transfer of the baby to milk formulas for feeding and their constant change in search of the best provoke 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 has a negative reaction.

Dermatitis is an inflammatory skin disease that occurs under the influence of any adverse factor.

In children, the so-called atopic dermatitis is most often observed, which is a chronic allergic skin disease.

Atopic dermatitis is a multifactorial dermatosis with a hereditary predisposition that develops 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 a food allergy, which manifests itself in early childhood. For the child's immune system, food proteins are foreign. In the gastrointestinal tract of a child, proteins are converted into polypeptides and amino acids. Polypeptides are the cause of allergies in early childhood, but not all cause allergic reactions. In some cases, food allergies are manifested by rare episodes of skin rashes. Only a small percentage of the process is chronic.

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

Readiness for allergies in such children is present from birth, but the disease can manifest itself only after prolonged contact with the allergen. At the first contact, memory cells remember the allergen, and upon repeated contact, specific antibodies, immunoglobulins E (IgE), begin to be produced, which cause hypersensitivity. And subsequent meetings 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 limits the intake of the allergen into the body, preventing the development of clinical manifestations. Accordingly, diseases of the skin, respiratory tract, gastrointestinal tract provoke the appearance of various allergic reactions.

Healthy children can also be born in atopic families, but their offspring (the third generation) may already 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 with the use of any product in the baby's diet. An 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 the most common cause of atopic dermatitis in children. In fact, milk allergy 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 man 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, feces "for carbohydrates", coprology, etc.

If you start changing or canceling foods, formulas, complementary foods, prescribing a diet for a nursing mother, instead of helping the child heal minor disorders in the immune system, pancreas, then the situation will only worsen, since New Product- this is a new load on the already weak systems of a sick child.

The search for an allergen by blood test or skin tests in this case will not give a clear picture: some slightly suspicious foods, 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 be different, but in most it occurs as follows. Usually, infants begin to introduce complementary foods drop by drop, a few grams, 1/4 teaspoon, between feedings or before them. And even if gross mistakes are not made, when a child is immediately given a large amount of new food or a product is introduced that is not age-appropriate (for example, baby kefir at 1 month, when the package says “from 6 months”), the child is covered with a rash.

No one is to blame - parents followed the advice from decent books, pediatricians - instructions and textbooks. Is it an allergy? Most likely no. Books, textbooks and instructions were written a long time ago, and since then, due to the deterioration of the environment, the way of life of a person, newborn children have become a little different.

Now it is necessary to introduce new products 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 in any way, he will not experience any lack of food, vitamins, etc. But you will minimize the risk of developing it, and subsequently, you may avoid allergies, and other diseases, up to.

Diathesis as a reaction to the introduction of complementary foods occurs when the child's body, its enzymatic systems are not ready to digest a new product. Not knowing how to digest an apple, porridge or kefir, the pancreas “tenses up”, trying to produce the necessary enzymes in the right amount. 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, unformed, so an inadequate reaction of the immune system appears on the skin in the form of diathesis.

The best food for a baby is mother's milk. But there are situations when you need 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 child does not eat up, requires breasts earlier than 2.5 hours after the end of the previous feeding, and is not gaining weight well. Another indication for the introduction of the mixture is the appointment of mother therapy that is incompatible with breastfeeding (treatment of cancer, serious hormone therapy). Another reason may be a group or Rhesus conflict. In exceptional cases, it is recommended to cancel breast milk and introduce a mixture when antibiotics are prescribed to the mother (but in most cases this situation does not require the abolition of breastfeeding), as well as in very severe decompensated lactase deficiency (most often in these cases, treatment is carried out without canceling breast milk, but sometimes the introduction of a therapeutic mixture and the transition to mixed feeding are required).

The child may react to the introduction of the mixture with a deterioration in the general condition, skin rashes, abdominal pain, changes in the nature of the stool (greens, mucus, constipation). Late regurgitation or regurgitation with a "fountain" may appear. Sometimes the problems that were before the introduction of supplementary feeding are exacerbated, 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 individual immunity of the baby to a particular mixture. To assess the individual response to the mixture, it is necessary to track changes in the state from the initial one according to the following criteria: skin, stool, behavior (anxiety, regurgitation). That is, before the introduction of the mixture, you need to remember or write down all the problems that the baby has, and, starting to give the mixture, track the changes. If deterioration occurs, do not immediately remove the mixture, but continue to give in the amount at which the problems began.

If the deterioration is associated with the difficulties of 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 in 4 days, then this means that this mixture is not suitable for the child and you need to try another one. So don't buy right now. a large number of the mixture that the child has not tried before.

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

Adaptation is a combination of the work of the immune and digestive systems. In young children, the process of getting used to a 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 eats some kind of mixture for a long time and suddenly he starts having problems with the skin or tummy, then the mixture and nutrition in general (hereinafter - juices, cereals, mashed potatoes) have nothing to do with it: the problem must be sought in the work of the gastrointestinal tract. intestinal tract, other organs and systems, and do not change the diet.

The risk of a child's illness increases when exposed to adverse external factors, which can be not only artificial feeding, but also eating foods rich in substances that can cause allergies. In the role of allergens, particles of pet hair and dander, mites, cockroaches, mold fungi, house dust, drugs (for example, antibiotics), food additives, preservatives can also act.

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.

The most common allergic reactions occur on the following products: whole milk, eggs, fish and seafood, wheat, rye, carrots, tomatoes, peppers, strawberries, strawberries, raspberries, citrus fruits, pineapples, persimmons, melons, coffee, cocoa, chocolate, mushrooms, nuts, honey

Disease dermatitis in children can cause food additives containing preservatives, flavors, flavors, 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), sweeteners.

Risk factors for atopic dermatitis and allergies in children

Factors contributing to the manifestation of overt allergies can be overt allergens:

Non-allergenic risk factors for atopic dermatitis in children:

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

Signs of the disease may appear on the 2-3rd month of a baby's life, but most often they occur after transferring him to artificial feeding.

At the initial stage, there are such symptoms of atopic dermatitis in children 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, in the area of ​​the elbow and knee folds, and wrists can also be affected.

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

At the sites of skin lesions in children, a manifestation of dermatitis occurs, such as skin itching, which is so pronounced that it disturbs the baby's sleep. The skin thickens, becomes dry, covered with scales, peels off. In such places, cracks are formed, healing with great difficulty.

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

The child loses weight, becomes restless, irritable, whiny.

The disease proceeds for a long time, characterized by alternating periods of pronounced inflammation and remission of the process. Violations of the diet, psycho-emotional stress can provoke an exacerbation.

The disease may continue long years. Exacerbations of atopic dermatitis are observed mainly in autumn period of the year. In the infant and child phases, focal spotty-scaly rashes are observed with a tendency to form bubbles and areas of weeping on the skin of the face, buttocks, and extremities. In the pubertal and adult periods, nodular rashes of a slightly pink color dominate, which are located mainly on the flexion surfaces of the limbs, especially in the elbows, popliteal cavities, 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, the skin lesion is expressed on the face, where there are spotty-scaly lesions with fuzzy contours, mainly in the periorbital region, in the area of ​​the nasolabial triangle, around the mouth. The eyelids of the patient are edematous, thickened, the lips are dry, with small cracks. On the skin of the neck, chest, back, limbs there are abundant 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. Peeling, cracks, abrasions are expressed in the lesions. In severe cases, the process is persistent, the lesions cover large areas, they also occur on the back of the hands, feet, legs and other areas, the lymph nodes increase, the temperature may rise.

These photos show what dermatitis looks like in children:

In older children, the main manifestations of atopic dermatitis are:

Additional features 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, chromium salts, nickel, mercury.

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

Features 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 exposure and the state of the organism's reactivity.

A characteristic feature of dermatitis is a rather rapid regression after the removal of the irritant.

The causes of contact dermatitis are often direct prolonged or repeated exposure to the skin of chemicals (acids, alkalis in high concentrations, etc.), mechanical (abrasion, friction tight clothes, shoes, plaster casts, pressure 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, coastal 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 drugs.

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

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

The predisposition to the development of contact dermatitis in schoolchildren is different. So, in some children, the disease occurs with minimal exposure to the stimulus. Symptoms of contact dermatitis in children are the appearance on the skin of erythema, swelling, and then vesicles, papules and pustules. Skin changes are accompanied by burning and soreness in the lesions.

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 fairly quickly (within a few days) after contact with the irritant is eliminated.

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

Lesions are localized on the supporting surfaces and have a vitreous appearance. Cracks may appear. Skin changes are accompanied by soreness.

For the treatment of this disease, a change of shoes with the use of 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 stimuli, 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 may occur upon contact with nickel-containing fasteners on clothing or jewelry. The nickel type of contact dermatitis is often localized on the earlobes.

Shoe dermatitis can be caused by antioxidants found in shoe lubricants, or by tannins and chromium salts in the leather the shoes are made from. With profuse sweating, these substances are usually leached out.

Allergic dermatitis from shoes usually develops on back side feet and fingers, without affecting the interdigital spaces. Unlike simple contact dermatitis, it rarely affects the palms and soles. In typical cases, the lesions are symmetrical.

Clothing dermatitis develops in contact with the following allergens: factory dyes, elastic fibers of fabrics, resins, fabric mordants. Dyes, resins, and fabric mordants can be poorly fixed and leach out when the garment is worn.

Allergic dermatitis on the face can be caused by all kinds of cosmetics (especially often on the eyelids). Unexpectedly, allergic dermatitis can develop with the use of topical medicinal products especially when used to treat pre-existing dermatitis. These allergens include local antihistamines, anesthetics, neomycin, merthiolate, and ethylenediamide, 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 extends beyond the lesion and manifests itself as weeping like eczema.

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

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

Drug toxic-allergic dermatitis develops with prolonged repeated, less often - short-term administration of the drug orally or when administered parenterally.

The combination of the allergic and toxic effects of the irritant, which is different 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, tissues of the nervous, vascular systems and internal organs are involved in the inflammatory process.

Forecast toxico- allergic dermatitis drug origin depends on the severity of general clinical and allergic reactions. The most severe consequences, often leading to death, are observed in 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 on the basis of the available signs will be considered reliable if the patient has three main and three or more additional signs. However, the main clinical signs are: pruritus and increased skin reactivity. Itching is characterized by its persistence during the day, as well as its intensification in the morning and at night. Itching disturbs the child's sleep, irritability appears, the quality of life is disturbed, especially in adolescents, and learning difficulties appear. Skin manifestations in atopic dermatitis are characterized by severe itching, erythematous papules on the 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 relationship of exacerbation of the disease with a causally significant allergen, determination clinical symptoms dermatitis, the presence of factors that provoke an exacerbation of the disease - allergenic and non-allergenic. For diagnosis, a special allergological examination is carried out, which includes the analysis of anamnestic data, the determination of specific antibodies to the allergen in the composition of IgE, and the setting of skin tests.

The level of immunoglobulin E to various allergens is determined in the blood using an enzyme immunoassay or radioimmunoassay 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 babies are elimination-provocation tests. In practice, an open test is used, in which the product is given to the patient and the reaction is observed.

Contraindications to the production of provocative tests may be:

Provocative tests are carried out without exacerbation of the disease.

When a child has problems in the form of skin rashes First of all, you need to examine the gastrointestinal tract, because almost 90% of skin rashes are of intestinal origin. Necessary studies are stool tests for dysbacteriosis and coprology, often useful information is provided by ultrasound of the abdominal organs. With 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 assigned: skin tests(not recommended before 3 years) or blood tests to detect allergy antibodies - IgE (not recommended until 1 year). The presence of "allergic" antibodies in a very high concentration is a sign of true allergy - the highest degree of immune dysfunction. As a rule, with such an allergy, allergists are connected to the treatment of a 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 contain specific antibodies to "allergens" in low and medium concentrations (and this will not be the basis for the diagnosis of "allergy", on the contrary - this will be proof of the absence of allergies).

To search for 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 treatments 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, dysbacteriosis therapy, recovery normal functioning gastrointestinal tract, removal of foci of chronic infection), as well as symptomatic therapy - primarily the elimination of itching. Symptomatic agents include antihistamines and topical agents. Among external agents, hormonal ointments can be prescribed. It is advisable to use them when severe exacerbations when other means do not help, but not 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 in a complex manner. It is necessary to start treating dermatitis 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 are the elimination of causally significant allergens, which is carried out on the basis of 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 certain elimination diet is prescribed. In the absence of positive dynamics within ten days, the diet should be reviewed. 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, millet.

Dairy-free mixtures are prescribed in cases where 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 hypersensitivity in a child has been identified. Complementary foods for children are prescribed no earlier than 6 months.

To reduce the allergenicity of some products, you can use long-term heat treatment.

It is important not to include foods with the addition of dyes, fruit essences, vanilla, and smoked products in the diet. Meat broths It is better to replace vegetable soups. Strictly contraindicated chewing gums. Sugar can be replaced with fructose.

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

But when following a diet, it must be remembered that excessive restrictions can lead to a lack nutrients in the diet of the child and the violation of his physical development.

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

How to get rid of atopic dermatitis in a child

Before you start treating atopic dermatitis in a child, exclude contact of the baby's skin with irritants such as wool, synthetic fabrics, and metal objects, including beads, bracelets, chains.

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

Make sure that the child does not scratch the affected skin. Cut your baby's nails often, 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 potassium permanganate solution or brilliant green solution. It is important to follow the rules of skin care.

To get rid of atopic dermatitis in a child as quickly as possible, it is necessary to bathe the baby daily and use medical cosmetics and ointments for skin care. Ordinary cosmetics in this case are not suitable, the doctor will help you choose them. For bathing a child, you can use a decoction of a string, chamomile.

In severe cases, hormonal ointments are used for treatment.

They render quick effect and greatly facilitate the condition of the child, but they are allowed to be used only under the supervision of a doctor.

Of the drugs, 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 act for a long time.

And what to do with atopic dermatitis in a child on house dust? In this case, the following activities are carried out:

  1. regular wet cleaning;
  2. mattresses and pillows are covered with plastic envelopes with a zipper;
  3. bed linen is washed weekly in hot water;
  4. pillows should 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 during the cleaning of 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 anti-mold products at least once a month;
  2. an extractor hood is installed in the kitchen to remove moisture during cooking;
  3. sick people are not allowed to mow the grass, remove the leaves.

Measures to prevent epidermal sensitization in dermatitis:

  1. it is not recommended to wear clothes that include wool, 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 its removal.

With pollen allergies, the following activities are carried out:

  1. when flowering tightly close windows and doors;
  2. walks are limited;
  3. for the period of dusting, the place of residence changes;
  4. it is forbidden to use herbal cosmetics;
  5. it is not recommended to carry out treatment with herbal preparations.

The following describes how to treat dermatitis in a child using medicines.

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

With symptoms of atopic dermatitis in children, effective remedies are used for treatment that block individual links of allergic reactions:

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

In complex treatment, enterosorbites are used, sedatives, drugs that improve or restore the function of digestion, physiotherapy.

In the treatment of atopic and atopic dermatitis in children, symptoms, age, stage of the disease, clinical features, severity, prevalence of the pathological process, complications and comorbidities 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 edema, hyperemia, and itching. The last symptom, itching, does not always disappear with this therapy. When prescribing antihistamines, the features of the mechanism of their action are taken into account. So, first-generation drugs have a sedative effect. In this regard, they are not assigned to school-age children due to the fact that when they are used, concentration of attention and the ability to concentrate are reduced. Due to the decrease in the effectiveness of first-generation drugs with their 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, claritin are prescribed (drugs of prolonged action H1-blockers of the second generation). They have high specificity, begin to act after 30 minutes, the main effect lasts up to 24 hours, do not affect other types of receptors, and they do not penetrate the hepato-brain barrier.

The use of corticosteroids. The use of glucocorticoids orally is indicated for extremely severe allergic dermatitis. They are appointed in these cases locally. When applied topically, corticosteroids suppress the components of allergic inflammation, the release of mediators, cell migration to the area of ​​skin lesions, they cause vasoconstriction, and reduce swelling. They remove the phenomena of dermatitis in the acute and chronic periods.

Currently, a series of preparations has been developed that are safe enough for use in children: in the form of lotions, creams, and ointments. The use of such agents as advantan and others is recommended. It is used from 4 months and in various types. Elocom is effective. It does not cause a systemic effect, and it can be used once a day, its effect is detected already in the first days.

The choice of corticosteroid agents should seek to eliminate acute symptoms atopic and allergic dermatitis in children short time. Despite the risk of side effects, corticosteroid drugs are the mainstay in the treatment of 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 is not recommended for a long time. These funds include akriderm. Akriderm and Akriderm GK 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 (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 baths and hot water are not recommended, use special shampoos such as Friderm tar, Friderm zinc, Friderm pH balance.

In case of secondary infection of the skin, pastes containing 3-5% erythromycin are used in the form of ointments. Skin treatment with solutions of brilliant green, methylene blue.

With a fungal infection, Nizoral, Clotrimazole, etc. creams are prescribed.

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

Methods of treatment and prevention of atopic dermatitis in a child

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

The most common- Always prescribe and change antihistamines. The method firmly and permanently connects the patient with the doctor, but does not bring permanent and final relief. It is even difficult to call quality treatment.

Second option- block the immune response with mast cell membrane stabilizers for the duration of the allergen in the hope that the immune system, developing with the child, will wean itself from overreaction to the allergen. Treatment is long and can only be effective against pollen allergens. The doctor and parents are waiting for the child to “outgrow” the allergy as a result of hormonal changes in the body. Sometimes it works out.

Third way- elimination of the allergen, that is, the creation of conditions under which the child will not meet with the allergen. For example, you do not keep fish or pets, do not give certain products, you leave for the time of flowering of the allergen to distant countries. Hope is the same as in the second option. It also works sometimes.

Fourth way- 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 by tens and hundreds of times. By injecting such a dose into the body, he begins to teach him 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 maternal nutrition during pregnancy and lactation, to treat chronic diseases of the mother before and during childbirth. For the prevention of outbreaks of atopic dermatitis in children and adults, it is recommended Spa treatment in a warm southern climate, in sanatoriums of the gastrointestinal profile.

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 himself will "outgrow" the disease, and do nothing.

Article read 7,084 times.

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

Thank you

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. At the same time, 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 the lung fluid.

In an adult, the number of eosinophils in the blood is considered normal from 0.02x10 9 / l to 0.3x10 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 lesions, allergic reactions, and some leukemias.

Eosinophilia - symptom or 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.
Because many diseases digestive systems s lead to a violation of the intestinal microflora, the process of cleansing the body of toxins slows down, which leads to elevated content eosinophils. With such dysbacteriosis, the patient may be disturbed by vomiting and nausea after eating, pain in umbilical region, diarrhea, convulsions, signs of hepatitis (jaundice, enlarged liver and its soreness).
5. Blood diseases.
For systemic histiocytosis against the background of eosinophilia, frequent infectious diseases, enlargement of the liver and spleen, damage to the lymph nodes, cough, cyanosis of the skin (cyanotic staining), dyspnea (difficulty breathing) are characteristic.
Along with eosinophilia, with lymphogranulomatosis, fever, pain in the bones and joints, weakness, itching on most of the surface of the skin, lymphadenopathy, enlargement of the liver and spleen, and there may be a cough are noted.
Eosinophilia in non-Hodgkin's lymphomas is also accompanied by fever, weakness, decreased body weight and motor activity, as well as symptoms characteristic of the defeat of certain areas. So, when a tumor appears in the abdominal region, symptoms such as thirst, an increase in the abdomen, and intestinal obstruction are noted. From the side of the central nervous system - headaches, paralysis and paresis, decreased vision and hearing. There may be pain behind the sternum, cough, swelling of the face, impaired swallowing.

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 vasculitis of the lungs 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)

A 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, allergy, atopy, atopic dermatitis, pathogenesis.

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

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

Neuropeptides and other neurohumoral regulators in the pathogenesis of bronchial asthma in children: picfirst

Modern clinical and immunological features of scabies and new approaches to its diagnosis and therapy

Eosinophils and their role in the pathogenesis of allergic diseases

V.B. Dzhalchinov, G.M. Chistyakov

Keywords:

eosinophils of different density, allergy.

In the late 1970s and early 1980s, there were reports that not only mast cells, but also other cells have receptors for IgE. It turned out that eosinophils, which are capable of producing mediators responsible for the development of cell and tissue damage, are of the greatest importance in this regard.

Clinicians, both internists and pediatricians, in their daily 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 the blood and tissues were controversial until recently. A statement was made about its protective role, motivated by the fact that supposedly eosinophils produce arylsulfatase, an anti-leukotrienzyme enzyme. However, the results of further studies did not confirm this concept. Most researchers agree on the damaging effect of eosinophilia and, especially, hypereosinophilia. To understand the mechanism of this damaging action, it is necessary to have an idea, at least in general terms, about 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 mucosal epithelial cells, 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 earlier the influx of activated eosinophils into the inflammatory focus was considered as a passive reaction, then at present 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 demonstratively manifested when considering the relationship 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 shown to be released by eosinophils. The results of in vitro studies have shown that under the influence of the ionophore, low density eosinophils secrete platelet activating factor in much greater quantities than those with normal density. Of interest is the fact that there is a reciprocal relationship between eosinophils and platelet activating factor. On the one hand, eosinophils produce this factor, and on the other hand, 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 calcium ionophore, low density eosinophils are able to synthesize and release leukotriene C, albeit in a small amount. 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 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. So, 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 already mentioned above, of receptors for corticosteroid hormones. The works of many researchers have revealed different degrees of expression of these receptors. This was especially demonstratively revealed in the study of blood eosinophils in patients suffering from hypereosinophilic syndrome. This syndrome is heterogeneous in its genesis. It can be observed with helminthic invasion, with atopy, be a "harbinger" of the development of various, including malignant diseases - T lymphoma, Hodgkin's disease, 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 a 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 the inhibition of eosinophilopoiesis. It is also reported that the decrease in the number of peripheral blood eosinophils under the influence of corticosteroid therapy occurs at the expense of cells with normal density, while the number of cells with low density remains unchanged. This position indicates that the expression of glucocorticoid receptors is more pronounced in eosinophils with normal density compared to cells of low 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 of it can serve as a "harbinger" various kinds visceral lesions. Therefore, some clinicians recommend prescribing manifest forms as a prophylaxis for hypereosinophilic syndrome. pathological process prednisolone at the rate of 0.5-1 mg per 1 kg of body weight per day. However, the effect of such exposure is not always achieved, because due to the weak expression of glucocorticoid receptors by low density eosinophils, the latter are 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 a severe form 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 is carried out.

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 on determining the morphometric parameters of these cells in the blood and sputum in the dynamics of the disease, taking into account therapeutic effects. With the help of 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 seizures, the studied indicators changed upwards compared to the control ones. Under the influence of complex treatment, a positive dynamics of the studied parameters was 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 the therapy. Assessing the results obtained in general, the authors conclude that the process of eosinophilopoiesis is enhanced in bronchial asthma. Other authors also report on the important role of eosinophils in the development of allergic inflammation in bronchial asthma.

Thus, these 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 mainly inherent in eosinophils with reduced density, since it is these cells that release active proteins that have a damaging effect on the tissues 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. At present, thanks to a significant expansion of laboratory research methods and their extensive use in clinical practice, it has become possible to study in detail the morphometric and morphological features 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 an objective statement of the activity of allergic inflammation, in particular in atopic dermatitis in children, both in an isolated form and combined with various visceral lesions, and to determine the most rational ways of therapeutic action.

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

Literature

1. Capron M., Gruart V. L "eosinophile: recepteurs et médiateurs. Rev Fr Allergol 1990; 30: 2: 71-75.

2. Gleich G., Adolphson C.R. The eosinophilic leukocyte. Adv Immunol 1986; 39:177-253.

3. Bletry O. De l "hypereosinophilie au syndrome hypereosinophilique. Rev Fr Allergol 1990; 30: 2: 87-90.

4. Capron M., Spiegelberg H.L., Prin L. Role of IgE receptors in effectors function of human eosinophils. J Immunol 1984; 232:462-468.

5. Rotenberg M.E., Owen W.F., Silberstein D.S. Eosinophils cocultured with endothelial alls have increased survival and functional properties. Science 1987; 237:645-647.

6. Bletry O., Bodemer C., Godeau P. Syndrome hyperosinophilique: aspects cliniques. Rev Med Interne 1987; 8:292-301.

7. Gruartv, Balloul J.M., Prin L. Variations in protein expression related to human eosinophil heterogeneity. J Immunol 1989; 142:4416-4421.

8. Prin L., Capron M., Gosset P. Eosinophilic lung disease: immunological studies of blood and alveolar eosinophils. Clinexp Immunol 1986; 63:242-257.

9. Buttervorth A.E., Sturrock R.F. Eosinophils as mediators antibody dependent damage to schistosomula. Nature 1975; 256:727-729.

10. Capron M., Granette C", Torpier G. The second receptor for IgE in eosinophil effector function. Chem Immunol 1989; 47: 128-178.

11. Prin L., Capron M., Tonnel A.B. Heterogenety of human peripheral blood eosinophils: variability in cell density and cytotoxic ability in relation to the level and the origin of hipereosinophilia. Int Arch Allergy appl Immunol 1983; 72:336-346.

12. Fukuda T., Gleich G.J. Heterogeneity of human eosinophils. J Clin Immunol 1989; 83:369-373.

13. Arnoux B., Denjean A., Page C.P. Accumulation of platelets and eosinophils in baboon lung after PAF-acether challenge. Inhibition by ketotifen. Am Rev Respir Dis 1988; l37: 855-860.

14. Bruynzeel P.L.B., Koenderman L. Platelet-activating factor (PAF-acether) induces leukotriene C4 formation and luminol dependent chemiluminescence by human eosinophils. Pharmacol Res Commun 1986; l8:61-69.

15. De Monchy J.G.R., Kauffman H.F. Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions. Am Rev Respir Dis 1985; l31:373-379.

16. Prin L., Lefebvre P., Gruart V. Polinucliare eosinophile et recepteur glucocorticoide. Rev fr Allergol 1990; 30:2:83-85.

17. Bush R.K., Geller M., Busse W.W. Response to corticosteroids in the hypereosinophilic syndrome. Arch Intern Med 1978; l38:l244.

18. Butterfield J.H., Askerman S.J. Effects of glucocorticoids on eosinophil colony growth. J Allergyclin Immunol 1986; 78:450.

19. Bletry O., Scheable C. Manifestations cardiaques du sindrome hypereosinophilique. Interet de l "exograrhie lidimensionnelle (12 observations). Arch Mal Coeur 1984; 6: 633-641.

20. Prin L., Bletry O., Tonnel A.B. Lesion visceralis des hyperosinophilies. Presse med 1987; l6:945-949.

21. Menshikov A.A., Popova D.S., Nosko E.Yu. Population characteristics of eosinophilic granulocytes in patients with atopic dermatitis. Act on dermatology. Yekaterinburg 1993; 35-40.

22. Anaev E.Kh., Chernyaev A.L., Tatarsky A.R., Voronina L.M. Structural and functional characteristics and the role of eosinophils in the pathogenesis and treatment of bronchial asthma. Pulmonology 1994; 4:82-86.

23. Anaev E.Kh., Samsonova M.V., Chernyaev A.L., Chuchalin A.G. Morphometric characteristics of blood and sputum eosinophils in patients with bronchial asthma. Ter archive 1997; 3:23-25.

24. Fassakhov R.S., Boychuk S.V., Rakhmatulin I.M. The role of eosinophils in bronchial asthma. Ter archive 1992; 64:1:147-151.

25. Thomas L.H., Warner J.A. The eosinophil and its role in asthma. Gen Pharmacol 1996; 27:4:593-597.

CATEGORIES

POPULAR ARTICLES

2023 "kingad.ru" - ultrasound examination of human organs