Atopic dermatitis pathogenesis clinic treatment. Atopic dermatitis: etiology, pathogenesis, classification, therapy. Antifungal and antibacterial agents

Atopic dermatitis in infants is a chronic immune inflammation of the skin of a child, characterized by a certain form of rashes and their stages of appearance.

Children's and infant atopic dermatitis significantly reduces the quality of life of the whole family due to the need to strictly adhere to a special therapeutic diet and hypoallergenic life.

Major risk factors and causes of atopic dermatitis

The risk factor for atopic is often a hereditary burden of allergies and. Factors such as constitutional features, nutritional disorders, and insufficiently good child care are also unfavorable.

Knowledge about the pathogenesis of this allergic disease will help to understand what atopic dermatitis is and how to treat it.

Every year, the knowledge of scientists about the immunopathological processes occurring in the body in atopic nursery is increasing.

In the course of the disease, the physiological skin barrier is disturbed, Th2 lymphocytes are activated, and the immune defense decreases.

Understanding the skin barrier

Dr. Komarovsky, in his articles popular among young parents, touches on the topic of the characteristics of children's skin.

Komarovsky highlights The 3 main features that matter in breaking the skin barrier:

underdevelopment of sweat glands;
fragility of the stratum corneum of the children's epidermis;
high lipid content in the skin of newborns.

All these factors lead to a decrease in the protection of the skin of the baby.

Hereditary predisposition

Atopic dermatitis in infants can result from a filaggrin mutation, which changes the filaggrin protein, which ensures the structural integrity of the skin.

Atopic dermatitis is formed in children under one year of age due to a decrease in local skin immunity to the penetration of external allergens: biosystems of washing powder, epithelium and hair of pets, fragrances and preservatives contained in cosmetic products.

Antigenic loads in the form of toxicosis of pregnant women, taking a pregnant woman of medications, occupational hazards, highly allergenic nutrition - all this can provoke an exacerbation of an allergic disease in a newborn.

food;
professional;
household.

Prevention of allergies in infants can be the natural, maximum long-term, rational use of medicines, treatment of diseases of the digestive system.

Classification of atopic dermatitis

Atopic eczema is divided by age in three stages:

infant (from 1 month to 2 years);
children's (from 2 years old to 13);
teenage.

In newborns, the rash looks like redness with bubbles. The bubbles break open easily, forming a weeping surface. The baby is worried about itching. Children comb the rash.

Bloody-purulent crusts form in the field. Rashes often appear on the face, thighs, and legs. Doctors call this form of rash exudative.

In some cases, there are no signs of wetness. The rash looks like spots with slight peeling. The scalp and face are more often affected.

At 2 years of age in sick children, the skin is characterized by increased dryness, cracks appear. Rashes are localized in the knee and elbow fossa, on the hands.

This form of the disease is scientifically called "erythematous-squamous form with lichenization." In the lichenoid form, peeling is observed, mainly in the folds, in the elbow bends.

Facial skin lesions appear at an older age and are called "atopic face". There is pigmentation of the eyelids, peeling of the skin of the eyelids.

Diagnosis of atopic dermatitis in children

There are criteria for atopic dermatitis, thanks to which the correct diagnosis can be made.

Main criteria:

early onset of the disease in an infant;
itching of the skin, often manifested at night;
chronic continuous course with frequent severe exacerbations;
the exudative nature of the rash in newborns and lichenoid in older children;
the presence of close relatives suffering from allergic diseases;

Additional criteria:

dry skin;
positive skin tests on allergy testing;
white dermographism;
the presence of conjunctivitis;
pigmentation of the periorbital region;
central protrusion of the cornea - keratoconus;
eczematous lesions of the nipples;
strengthening of the skin pattern on the palms.

Laboratory diagnostic measures for severe atopic dermatitis are prescribed by a doctor after examination.

Complications of atopic dermatitis in children

A common complication in children is the addition of various kinds of infections. The open wound surface becomes a gateway for fungi of the genus Candida.

Prevention of infectious complications consists in following the recommendations of the allergist on the peculiarities of the use of emollients (moisturizers).

List of possible complications of atopic dermatitis:

folliculitis;
boils;
impetigo;
annular stomatitis;
oral mucosa candidiasis;
candidiasis of the skin;
Kaposi's herpetiformis eczema;
molluscum contagiosum;
genital warts.

Traditional treatment for atopic dermatitis

Therapy of atopic dermatitis in children begins with the development of a special hypoallergenic diet.

An allergist makes a special elimination diet for a mother with atopic dermatitis in a baby. Such a diet will help keep breastfeeding as long as possible.

Approximate elimination hypoallergenic diet for children under one year old with atopic dermatitis.

Menu:

breakfast. Dairy-free porridge: rice, buckwheat, oatmeal, butter, tea, bread;
lunch. Fruit puree from pears or apples;
dinner. Vegetable soup with meatballs. Mashed potatoes. Tea. Bread;
afternoon tea. Berry jelly with cookies;
dinner. Vegetable and cereal dish. Tea. Bread;
second supper. Milk mixture or.

The menu for a child, and especially for a child with atopic dermatitis, should not contain spicy, fried, salty foods, seasonings, canned food, fermented cheeses, chocolate, carbonated drinks. The menu for children with allergic symptoms is limited to semolina, cottage cheese, sweets, yoghurts with preservatives, chicken, bananas, onions, and garlic.

The mixtures based on the treatment of atopic dermatitis in a child will also help.

In case of hypersensitivity to cow's milk proteins, the World Organization of Allergists strongly discourages the use of products based on non-hydrolyzed goat milk protein, since these peptides have a similar antigenic composition.

Vitamin therapy

Patients with atopic dermatitis are not prescribed multivitamin preparations, which are dangerous from the point of view of the development of allergic reactions. Therefore, it is preferable to use monopreparations of vitamins - pyridoxine hydrochloride, calcium pathotenate, retinol.

Immunomodulators in the treatment of allergic dermatoses

Immunomodulators that affect the phagocytic link of immunity have proven themselves well in the treatment of allergic dermatoses:

Polyoxidonium has a direct effect on monocytes, increases the resistance of cell membranes, and is able to reduce the toxic effect of allergens. It is applied intramuscularly once a day with an interval of 2 days. The course is up to 15 injections.
Likopid. Enhances the activity of phagocytes. Available in 1 mg tablets. May cause an increase in body temperature.
Zinc preparations. They stimulate the restoration of damaged cells, enhance the action of enzymes, and are used for infectious complications. Zincteral is applied at 100 mg three times a day for a course of up to three months.

Hormonal creams and ointments for atopic dermatitis in children

It is not possible to treat severe atopic dermatitis in children without the use of local anti-inflammatory glucocorticosteroid therapy.

For atopic eczema in children, both hormonal creams and various forms of ointments are used.

Below are the basic recommendations for the use of hormonal ointments in children:

with severe exacerbation, treatment begins with the use of strong hormonal agents - Celestoderm, Kutiveyta;
to relieve the symptoms of dermatitis on the trunk and arms in children, the drugs Lokoid, Elokom, Advantan are used;
it is not recommended to use Sinaflan, Ftorocort, Flucinar in pediatric practice due to serious side effects.

Calcineurin blockers

Alternative to hormonal ointments. Can be used for facial skin, areas of natural folds. Preparations of Pimecrolimus and Tacrolimus (Elidel, Protopic) are recommended to be used in a thin layer on rashes.

You can not use these drugs in immunodeficiency states.

The course of treatment is long.

Antifungal and antibacterial agents

In case of infectious uncontrolled complications, it is necessary to use creams containing antifungal and antibacterial components - Triderm, Pimafukort.

The previously used and successful zinc ointment was replaced by a new, more effective analogue - activated zinc pyrithione, or Skin-cap. The drug can be used in a one-year-old child in the treatment of a rash with infectious complications.

With pronounced weeping, an aerosol is used.

Dr. Komarovsky writes in his articles that there is no more formidable enemy for a child's skin than dryness.

Komarovsky advises using moisturizers (emollients) to moisturize the skin and restore the skin barrier.

The Mustela program for children with atopic dermatitis offers a moisturizer in the form of a cream emulsion.

The Lipicar program of the La Roche-Posay laboratory includes Lipikar balm, which can be applied after hormonal ointments to prevent dry skin.

Treatment of atopic dermatitis with folk remedies

How to cure atopic dermatitis permanently? This is the question scientists and doctors around the world are asking themselves. The answer to this question has not yet been found. Therefore, many patients are increasingly resorting to homeopathy and traditional methods of traditional medicine.

Treatment with folk remedies sometimes brings good results, but it is better if this method of treatment is combined with traditional therapeutic measures.

When the skin becomes wet during a severe exacerbation of allergic dermatosis, folk remedies in the form of a lotion with a decoction of a string or oak bark help well. To prepare the broth, you can purchase a series of filter bags at the pharmacy. Brew in 100 ml of boiled water. With the resulting broth, apply lotions to the rashes three times during the day.

Spa treatment

Most Popular sanatoriums for children with manifestations of atopic dermatitis:

sanatorium them. Semashko, Kislovodsk;
sanatoriums "Rus", "DiLuch" in Anapa with a dry maritime climate;
Sol-Iletsk;
sanatorium "Klyuchi" of the Perm Territory.

limit the child's contact with all types of allergens as much as possible;
give preference to cotton clothes for the baby;
avoid emotional stress;
cut your child's nails short;
the temperature in the living room should be as comfortable as possible;
try to keep the humidity in the child's room at 40%.

What follows avoid with atopic dermatitis:

apply cosmetics for alcohol;
wash too often;
use hard washcloths;
take part in sports competitions.

Details

Atopic dermatitis (atopic eczema, constitutional eczema) - hereditary allergic dermatosis with a chronic recurrent course, manifests itself as an itchy erythematous-papular rash with symptoms of lichenification of the skin. One of the most common dermatoses, it develops from early childhood and persists into puberty and adulthood.

Etiology and pathogenesis of atopic dermatitis.

Etiol and PG - a gene predisposing (atopy) to allergies, hyperreactive status with a tendency of vessels to vasoconstriction, hyperimmunoglobulinemia £ (e-atopy) with a tendency to immunodeficiency, inherited disorders of neurohumor regulation (decreased adrenergic reception), genetic determinant of enzymopathy. He showed a zab in children of the causes of intoxication, toxicosis and inaccuracies in the mother's nutrition during breastfeeding and lactation, the art of feeding the child. + tank, vir or fungus inf, food, everyday life and production of allergens, psychoemotional load, + meteorologist f-ry (drops in t, insufficient insolation).

PG: a decrease in suppressor and killer activity of the T-system of immunity, an imbalance in serum Ig production, à stimulation of B-lymphocytes with overproduction of IgE and a decrease in IgA and IgG. a decrease in the f-th act of lymphocytes, inhibition of the chemotaxis of polymorphonuclear leukocytes and monocytes, an increased level of CEC, a decrease in complement activity, a violation of cytokine production, which aggravates general immunodeficiency.

Functional disorders of C and vegetative NS manifested disturbances in psychoemotional status, crusts of neurodynamics, changes in the f-th status of beta-adrenergic receptors of lymphocytes. Characterized by dysf of the gastrointestinal tract - the enzyme nedost, dysbiosis, discieia, malabsorption syndrome and disturbance of kallikrein-kinin systems with activation of kininogenesis, an increase in the permeability of skin vessels, the effect of kinins on blood coagulation and fibrinolysis, on the neuro-receptor apparatus.

Kilnika of atopic dermatitis.

Clinic in early childhood (2-3 months). Zab can last for years, remissions are mainly in the summer and relapses in the fall. There are several phases in the development of the process: infant (up to 3 years old), children (from 3 to 7 years old), puberty and adult (8 years old and older) . leading a fasting symptom - intense, fasting or paroxysmal itching. In the infant and child phases, focal erythematous-squamous rashes with a tendency to exudate with the formation of vesicles and wet areas on the skin of the face, buttocks, of course, which may correspond to an eczematous process (constitutional eczema). In the pubertal and adult phases, an erythematous-lichenoid eruption of weakly rose-colored with a tendency to bend on the folds of the ends and images in the elbow folds, popliteal hollows, on the neck of lichenization zones and papular skin infiltration of the neurodermatitis diffusion type. dryness, pallor with an earthy skin tone (hypocorticism), white persistent dermographism. Skin lesions are localized, widespread and universal (erythroderma). on the face, the symmetry is not acute erythematous-squamous foci with indistinct contours, mainly in the periorbital region, in the area of the nasolabial triangle, around the mouth. The eyelids are swollen, thickened, periorbital folds are expressed, the lips are dry with fine cracks, in the corners of the mouth there are seizures (atonic cheilitis). On the skin of the neck, chest, back, bend over the end of the sets, there are small papular (miliary) elements of pale pink color, some of them have pruriginous character (papules are covered in the center of the hemorrhage zone with a dotted crust) against the background of weakly expressed irregular foci of erythema. In the region of the side of the neck, elbow folds, wrist joints, popliteal depressions, papular infiltration and lichenization are expressed: the skin is rough, stagnant red, with an exaggerated skin pattern. In the foci of small lamellar lesions, peeling, cracks, excoriation. In severe cases, the persistence of the process, foci of lichenization are large areas, arising on the back of the hands, feet, legs, developing generalization of the lesion in the form of erythroderma with an increase in the periphery of the LU, subfebrile. often + piokokk and vir inf, combined with vulgar ichthyosis. Patients may develop cataracts early (Andogsky's syndrome). Patients with atopic dermatitis and their relatives often have other allergies (asthma, hay fever).

Diagnosis of atopic dermatitis.

Histology: in the epidermis acanthosis, parakeratosis, hyperkeratosis, spongiosis is poorly expressed. In the dermis - expansion of capillaries, around the vessels of the papillary layer - infiltrates from lymphocytes.

Lab analyzes: OAK, OAM, proteinogram, glycemic and glucosuric profile, immunogram, examination of intestinal microflora and enzyme activity of the gastrointestinal tract, examination of feces for eggs of worms, lamblia, amoeba, opisthorchia and other helminthiasis, examination of the f shield of the gland, adrenal glands, liver, pancreas ...

Dst at the clinic, medical history (zab, life, family) and examinations.

Dif Ds with pruritus, eczema, toxidermia.

Treatment of atopic dermatitis.

Treatment of a hypoallergenic diet, funds, directed to the elimination of allergens, immune complexes, toxic metabolites from the orgma: unloading days for adults, cleanses enemas, infusion therapy - hemodez, reopolyglucin IV cap, detox agents: unitiol, sodium thiosulfate, tyubazh with magnesium sulfate and min water. enterosorbents (activated carbon, enterodesis, hemospheres. In severe cases, plasmapheresis.antihistamine and antiserotonin drugs (suprastin, diphenhydramine, tavegil, fenkarol, etc.), replacing them to avoid addiction every 7-10 days, H 2 blockers - duovel, histodil once at night for a month.

Immunocorrective therapy is prescribed in accordance with the immunogram: on the T-cell link (taktivin, thymalin, thymogen intranasally), drugs that mainly affect the B-cell link of immunity - splenin, sodium nucleinate, glycyram, etymizole, methyluracil, as adaptogens and nonspecific immunocorrectors , histaglobulin. A set of measures is carried out to normalize the gastrointestinal tract and eliminate dysbiosis (bacteriophages, eubiotics, bifikol, bifidumbacterin, colibacterin, lactobacterin, enzymes, hepatoprotectors), sanitize the foci of HR inf. For effects on the central nervous system and vegetation NS sedatives (valerian, motherwort, peony), tranquilizers (nosepam, mezapam), periph alpha-adrenoblock (pyrroxan 0.015 g), N-cholinoblock (bellataminal, belioid). From physiotherapeutic agents, UFO, electrosleep, ultrasound and magnetotherapy, phonophoresis of drugs for lesions (dibunol, naphthalan), ozokerite and paraffin applications for skin lichenization foci are used.

Outwardly use ointments with papaverine (2%), naphthalan (2-10%), tar (2-5%), ASD-111 fractions (2-5%), Dibuno-la liniment, methyluracil ointment, in the acute period - KS ointment (Advantan, Lorinden C, Celestoderm, etc.). dispensary observation and sanatorium-resort to lay down in a warm southern climate (Crimea), in sanatoriums of a stomach-kish profile (KavMinVody).

More than 10 years ago, the term "atopic dermatitis" was adopted to replace a large group of diseases manifested by allergic skin rashes. This is not just a new formulation of diagnosis and transformation of medical vocabulary. The main purpose of the terminology change is to unite and coordinate the efforts of doctors of various specialties who supervise patients with atopic dermatitis. This disease is associated with other organ lesions and transforms depending on the patient's age. That is why, in addition to the dermatologist, pediatricians, allergists, gastroenterologists, otolaryngologists, and pulmonologists take part in his fate, in addition to the dermatologist. However, we must admit that we are still only on the way to the coordinated treatment of atopic dermatitis, to the formation of an interdisciplinary approach to solving this problem. That is why it is relevant to generalize the available theoretical information on the etiopathogenesis of dermatosis, understanding the experience and assessing our capabilities in the management of these patients.

Atopic dermatitis is an allergic skin disease with a hereditary predisposition, accompanied by itching and characterized by a chronic recurrent course.

The name of dermatosis has undergone numerous changes. It was designated as constitutional eczema, atopic eczema, diffuse or disseminated neurodermatitis, prurigo Benier. Domestic dermatologists still widely use the name "diffuse neurodermatitis", while the term "atopic dermatitis" has been established in foreign literature since the 30s of the last century.

Atopic dermatitis is one of the most common diseases found in all countries, in both sexes and in different age groups. According to numerous authors, the incidence varies from 6 to 20% per 1000 population; more often women are ill (65%), less often men (35%). The incidence of atopic dermatitis among residents of megalopolises is higher than among residents of rural areas. In children, atopic dermatitis occurs in 1-4% of cases (up to 10-15%) among the entire population, while in adults - in 0.2-0.5% of cases.

Atopic dermatitis is a polyetiological disease with a hereditary predisposition, and the inheritance is polygenic in nature with the presence of a leading gene that determines skin lesions and additional genes. It should be noted that it is not the disease as such that is inherited, but a combination of genetic factors that contribute to the formation of allergic pathology.

It has been shown that atopic dermatitis develops in 81% of children if both parents suffer from this disease, and in 56% - when only one parent is sick, and the risk increases if the mother is sick. In patients with atopic dermatitis, up to 28% of relatives suffer from airway atopy. In a study of twin pairs, it was found that the incidence of atopic dermatitis in homozygous twins is 80%, and in heterozygous twins - 20%.

It can be assumed that there is a main (leading) gene that is involved in the realization of hereditary predisposition, leading to the manifestation of the process under the influence of unfavorable external influences - environmental risk factors.

Exogenous factors contribute to the development of exacerbations and chronicity of the process. Susceptibility to environmental factors depends on the age of the patient and his constitutional characteristics (morphological and functional characteristics of the gastrointestinal tract, nervous, endocrine, immune systems).

Among the exogenous factors that provoke the onset and development of the skin process in persons with a genetic predisposition, food, inhalation allergens, external irritants of a physical nature, animal and plant origin, stress factors, meteorological effects, insolation are of the greatest importance.

The trigger mechanism for the development of atopic dermatitis is most likely food allergy, which manifests itself already in early childhood. Dietary proteins of both plant and animal origin are foreign to the human immune system. Proteins from food are broken down in the human gastrointestinal tract to polypeptides and amino acids. Polypeptitis partially retains immunogenicity and is able to stimulate the immune system. They are the triggers of childhood allergies. In some cases, food allergy is manifested by rare episodes of skin rashes. For many children, this process is resolved without outside interference; only in some small patients the process becomes chronic.

The pathogenesis of atopic dermatitis is based on chronic allergic inflammation of the skin. The leading role in the development of the disease is assigned to immune disorders.

The term “atopic dermatitis” introduced into official medicine reflects the immunological (allergic) concept of the pathogenesis of atopic dermatitis, based on the concept of atopy as a genetically determined ability of the body to produce high concentrations of general and specific immunoglobulins (Ig) E in response to environmental allergens.

The leading immunopathological mechanism is a two-phase change in T-helpers (Th 1 and Th 2). In the acute phase, Th 2 is activated, leading to the formation of IgE antibodies. The chronic phase of the disease is characterized by the predominance of Th1.

The role of an immune trigger is the interaction of allergens with IgE antibodies (reagins) on the surface of mast cells and basophils. Studies have shown the existence of two genes associated with the main immunological abnormality of atopy - the formation of IgE in response to environmental allergens.

However, as some authors believe, it is unlikely that a chronic recurrent disease such as atopic dermatitis is solely the result of an abnormal IgE response to surrounding allergens (atopenes). There is evidence of both systemic immunosuppression in patients with atopic dermatitis and reduced cell-mediated immunity in the skin itself. It has been proven that in the affected skin, strong atopenic immune reactions occur, partially mediated by Th 2 cells (in the early stages) and Th 1 (in the later stages, a complex interaction of cells is observed: keratinocytes, endothelial, mast, eosinophilic granulocytes).

Already existing allergic inflammation is supported by the release of inflammatory mediators (histamine, neuropeptides, cytokines). Researchers on the pathogenesis of atopic dermatitis are currently faced with the question: is the immune response and inflammation caused by microdoses of allergens present in the skin, or is there cross-reactivity with endogenous autoantibodies that share etiotropic specificity with atopic allergens?

According to modern concepts, there are four immunological types (variants) of atopic dermatitis. The first type is characterized by an increase in the number of CD8 + lymphocytes at a normal level of IgE; for the second - high and medium IgE content against the background of a normal number of CD4 + - and CD8 + - lymphocytes; for the third - variability of IgE concentrations and a high content of CD4 + lymphocytes; for the fourth, significant variations in IgE with a decrease in CD4 + and CD8 + lymphocytes. Immunological variants correlate with the clinical features of atopic dermatitis.

A distinctive pathogenetic feature of atopic dermatitis is dense colonization of the skin Staphylococcus (S.) aureus. Among other triggering mechanisms that trigger and maintain chronic skin damage and inflammation, colonization of S. aureus is considered to be the most significant. Sensitization to S. aureus correlates with the severity of atopic dermatitis. Studies published in recent years have confirmed an obvious pattern: the severity of the course of atopic dermatitis depends on the presence of staphylococcal enterotoxins in the skin. Enterotoxins of S. aureus were found in culture media of 75% of strains isolated from the skin of patients with atopic dermatitis. Enterotoxins are able to induce the production of IgE antibodies specific to them. In 57% of patients with atopic dermatitis, serum IgE antibodies to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB) and toxic shock syndrome toxin (TSST-1) were detected.

Studies have proven the highest reactogenicity of SEB: application of this enterotoxin to healthy skin of patients with atopic dermatitis and healthy individuals caused a pronounced inflammatory reaction. It was shown that the density of colonization of strains S. aureus, producing SEA and SEB is higher in children with atopic dermatitis sensitized to these enterotoxins than in non-sensitized children.

An important role in maintaining the chronic inflammatory process in the skin with atopic dermatitis is played by the fungal flora ( Malassezia furfur, mushrooms of the genus Candida, mycelial dermatophytes, Rhodotorula rubra). It is involved in the pathogenesis of the disease by inducing allergen-specific IgE, developing sensitization and additional activation of dermal lymphocytes.

Thus, the clinical manifestation of atopic dermatitis is the result of interactions between genetic factors, changes in the immune system, and adverse environmental influences.

Various classifications of atopic dermatitis have been created, which have separate general provisions.

1. The staging of the course and the division by age periods:

infant - up to 2 years;
children - from 2 to 7 years old;
teenage and adult.

In practice, for the first period, the conditional term "exudative diathesis" is most often used as a diagnosis, the term "children's eczema" is more appropriate for the second period, and only in the third period the disease acquires the typical features of "atopic dermatitis".

2. Phases of the course: acute, subacute, chronic.

3. Clinical forms:

erythematous-squamous;
vesicle-crusous;
erythematous-squamous with moderate lichenification;
lichenoid with pronounced lichenification (true prurigo Benier);
prurigid.

From a clinical point of view, the classic course of atopic dermatitis differs in a number of patterns. So, starting, as a rule, in early childhood, the disease proceeds for many years with an alternation of relapses and remissions, differing in the duration and intensity of the severity of symptoms. Over time, the severity of the disease weakens, and at the age of 30-40 years, most patients experience spontaneous cure or significant regression of symptoms. Clinical and statistical studies show that the diagnosis of atopic dermatitis in people over 40-45 years old is very rare.

The course of atopic dermatitis in different age periods is characterized by a certain localization and there are morphological features of skin rashes. The main differences regarding clinical manifestations are in the localization of lesions and the ratio of exudative and lichenoid elements of the rash. Itching is a persistent symptom, regardless of age.

A feature of the first age period is the predominance of rashes of exudative acute and subacute inflammatory nature with localization on the face, flexion and extensor surfaces of the limbs.

By the end of this period, the foci are localized mainly in the folds of large joints, wrists, and neck.

In the second age period, the process is in the nature of chronic inflammation, inflammatory and exudative phenomena are less pronounced. Cutaneous manifestations are represented by erythema, papules, desquamation, infiltration, lichenification, multiple cracks and excoriation. After the resolution of the rash, areas of hypo- and hyperpigmentation remain. An additional fold of the lower eyelid is formed (Danny Morgan sign).

In adolescence and in adults, infiltration, lichenization prevail, erythema has a bluish tint, papular infiltration is pronounced. The favorite localization of rashes is the upper half of the body, face, neck, upper limbs.

Pathomorphosis of the disease is expressed. The features of the clinical course of atopic dermatitis at the end of the twentieth century. are: earlier appearance of the first signs - from 1-2 months of age; more severe course with an increase in the area of skin lesions up to the development of erythroderma; an increase in the transition of acute forms to chronic, often severe, against the background of an increase in primary chronic pathology of internal organs, severe disorders of the nervous system, immunity disorders; an increase in the number of patients with a course resistant to therapy; early disability. The number of patients with the formation of respiratory atopy (allergic rhinitis, atopic bronchial asthma) and skin-respiratory manifestations of allergy (dermorespiratory syndrome) has increased, that is, there is an "atopic march" (progression of allergic pathology from skin symptoms to respiratory).

For severe forms of atopic dermatitis, the following clinical changes are characteristic: "multi-colored" coloration of the skin of the trunk with a brownish-brown tint, grayish-icteric component, wavy hypo- and hyperpigmentation of the skin of the neck, "marble" whiteness of the skin of the nose, pinpoint follicular keratosis, "marbling" of the skin limbs. The severity of the listed symptoms correlates depending on the severity of the course of atopic dermatitis, including due to the syndrome of endogenous intoxication.

One of the risk factors for the development of skin manifestations of atopic dermatitis, especially severe forms, is the unreasonable and often uncontrolled use of drugs or their combinations. On the one hand, this is due to insufficient qualifications and awareness of local specialists, on the other hand, it is due to the widespread use of self-medication, which, in turn, is associated with the availability of a large number of OTC pharmaceuticals on our market.

The antigenic properties of a drug depend on its ability to conjugate with serum and tissue proteins. As a rule, it is not the drugs themselves that are conjugated to proteins, but their metabolites. It was found that acid anhydrides, aromatic compounds, quinones, mercaptans, oxazolones, in particular the oxazolone of penicilloic acid (a metabolite of penicillin), which, by reacting with the amino group of the amino acid lysine of the carrier protein, form a stable bond and become highly antigenic, have this ability.

Observations show that with drug intolerance in patients with atopic dermatitis, the causative allergens are the antibiotic penicillin and its semisynthetic derivatives (in 87% of cases), non-steroidal anti-inflammatory drugs, and B vitamins.

The spectrum of clinical manifestations of atopic dermatitis is very diverse both in terms of the combination of various symptoms in each patient and in their severity. According to the frequency of occurrence of diagnostic signs, the clinical picture of atopic dermatitis can be presented in the form of two groups: obligatory and auxiliary (Rajka and Hanifin, 1980).

Mandatory signs:

"Flexion" or "folded" lichenization in adults, damage to the face and extensor surfaces of the limbs in infants,
beginning at an early age,
seasonality.

Auxiliary signs:

family atopic history,
psycho-emotional addiction,
food allergies,
general dryness of the skin,
periorbital hyperpigmentation,
tendency to skin infections,
Morgan fold,
eosinophilia of the blood,
an increased level of IgE in the blood,
white dermographism,
anterior subcapsular cataract.

To establish a diagnosis of atopic dermatitis, it is necessary to have all four mandatory signs and three to four auxiliary ones.

In practice, it is customary to distinguish mild, moderate and severe atopic dermatitis, however, for an objective assessment of the severity of the skin process and the dynamics of the course of the disease in 1994, the European Working Group on Atopic Dermatitis proposed the SCORAD scale ( scoring atopic dermatitis).

The SCORAD scale takes into account the following indicators:

A - the prevalence of skin lesions,

B - the intensity of clinical manifestations,

C - subjective symptoms.

The calculation of the area of skin lesions (A) is carried out according to the rule of "nines": head and neck - 9%, front and back surfaces of the body - 18% each, upper limbs - 9% each, lower limbs - 18% each, perineal area and genitals - 1%.

The intensity of clinical manifestations (B) is assessed by six symptoms:

erythema (hyperemia),
edema / papule formation,
oozing / crusting,
excoriation,
lichenification / desquamation,
general dryness of the skin.

The severity of each feature is assessed from 0 to 3 points: 0 - absence, 1 - poorly expressed, 2 - moderately expressed, 3 - sharply expressed.

Assessment of subjective symptoms (C) - the intensity of pruritus and the degree of sleep disturbance are assessed on a 10-point scale (by children over 7 years of age or by parents over the last 3 days and / or nights).

The total value of the SCORAD index is calculated using the formula SCORAD index = A / 5 + 7B / 2 + C.

Index values can range from 0 (no disease) to 103 (severe atopic dermatitis).

The clinical course of atopic dermatitis is distinguished by a true polymorphism of rashes, a combination of clinical forms, up to "invisible".

The erythematous-squamous form is characterized by the presence of an acute or subacute inflammatory nature of the foci, small flat and follicular miliary papules. The skin is dry, lichenified, covered with fine-lamellar scales. Severely itchy rashes are localized on the elbows, dorsum of the hands, posterolateral surfaces of the neck, popliteal fossa.

Lichenoid form is distinguished by dry, erythematous skin with an exaggerated pattern, edematous, infiltrated. Against the background of erythema, large, slightly shiny papules are located, merging in the center of the lesions and isolated along the periphery. Papules are covered with pityriasis scales. Linear and point excoriations are noted. Often, the process takes on a widespread nature, a secondary infection joins, which causes regional lymphadenitis. With this form, erythroderma often occurs.

The pruriginous form is characterized by scattered excoriation, excoriated follicular papules, sometimes with large, persistent, spherical follicular and pruriginous papules; lichenization is moderately expressed.

In the eczematous form, there are limited foci of skin lesions, mainly in the area of the hands, with the presence of papulovesicles, often "dry", infiltration, crusts, cracks. Along with this, there are foci of lichenification in the area of the elbow and popliteal folds. However, eczematous lesions are often the only manifestation of atopic dermatitis.

During remission, patients with atopic dermatitis may experience so-called "minor symptoms" of skin manifestations of atopic predisposition: dry skin, ichthyosiform peeling, hyperlinearity of the palms (folded palms), the skin of the trunk is covered with shiny, flesh-colored follicular papules. Horny papules are determined on the extensor surfaces of the upper limbs in the elbow bends. At an older age, skin dyschromia is noted. Often, in patients on the skin in the cheek area, whitish spots are determined, as well as folding of the skin of the anterior surface of the neck, reticular pigmentation - a symptom of a "dirty neck".

During the period of remission, minimal manifestations may be weakly scaly spots or cracks in the area of attachment of the auricle lobe, cheilitis, recurrent seizures, a median fissure of the lower lip, erythematous-squamous lesion of the upper eyelids. Knowledge of these symptoms allows timely identification of patients and the formation of high-risk groups.

Diagnosis of atopic dermatitis is based on a typical clinical picture, taking into account anamnestic data, mandatory and auxiliary signs. In terms of diagnostic phenomena, white dermographism should be noted, which is an almost constant characteristic of the functional state of the skin vessels in atopic dermatitis and is most pronounced during exacerbation. In some patients, during the period of remission, it can turn pink, which is often used by doctors as a prognostic sign.

Laboratory diagnostic methods do not have an absolute diagnostic value, since in some patients the indicators may be within normal levels. Often, in patients with atopic dermatitis, the serum IgE content is increased, which persists during the period of remission; eosinophilia is detected in the blood formula.

Despite the typical clinical picture of atopic dermatitis, in some cases there is a need for differential diagnosis. Differential diagnosis is carried out with seborrheic dermatitis, scabies, ichthyosis, limited neurodermatitis, microbial eczema, skin lymphoma in an early stage, Dühring's disease.

Seborrheic dermatitis is characterized by the presence of foci with clear boundaries in places of accumulation of sebaceous glands - "seborrheic zones" (forehead, face, nose, nasolabial fold, chest, back). Erythema is expressed slightly, yellowish scales. There is no seasonality of the disease and an increase in serum IgE concentration.

With scabies, multiple itchy papules, scabies, excoriation, crusts, a characteristic "night itch" are revealed at the same time in several family members. However, the presence of atopic dermatitis does not exclude the possibility of simultaneous infection with scabies.

Ichthyosis begins in infancy, is characterized by diffuse lesions of the skin in the form of dryness, peeling, follicular keratosis in the absence of itching, erythema, papules.

Limited neurodermatitis occurs more often in adolescence and in adults without atopic history and previous childhood phases. The lesions are more often located on the posterior and lateral surfaces of the neck, they are in the nature of single asymmetric foci of lichenization. White dermographism and increased IgE levels are absent.

In the case of a sharp exacerbation of atopic dermatitis with the development of eczematization with pronounced oozing in the foci, the clinical picture may resemble widespread eczema. Correctly collected anamnesis, revealing the onset of the disease in early childhood, family predisposition, typical sites of localization, white dermographism, allows differential diagnosis.

Persistent, widespread, excruciating itching with no less common moderately severe lichenification in persons over 50 years of age may make the debut of T-cell lymphoma. The patient's age, the absence of previous typical signs of atopic dermatitis, histological examination allow to verify the diagnosis.

For Duhring's disease, mainly vesicular, papular, urticarial rashes are characteristic, localized in groups on the extensor surfaces of the limbs. Gluten intolerance, eosinophilia in the blood and vesicle contents, determination of IgA during immunological research are noted.

Certain progress in understanding the mechanisms of the development of allergic inflammation opens up new opportunities in the development of pathogenetic methods of therapy for atopic dermatitis. The multifactorial concept of pathogenesis and the revealed disorders in the study of various organs and systems substantiate the use of a wide range of therapeutic measures in the therapy of patients, some of which have come to be called traditional: a hypoallergenic diet, the appointment of antihistamines, sedatives, detoxification therapy, and various external agents.

The main goals of organizing the treatment of a patient with atopic dermatitis:

primary prevention of patient sensitization (elimination therapy);
correction of concomitant diseases;
suppression of the inflammatory reaction in the skin or control over the state of allergic inflammation (basic therapy);
correction of immune disorders.

It is advisable to start treatment of atopic dermatitis with the elimination of allergens, which involves the use of elimination diets and protective regimens.

Diet therapy, based on the exclusion of intolerable foods from the patient's diet, as well as histaminoliberator products, is the basis for etiopathogenetic treatment of patients with atopic dermatitis, since it is known that genetically determined allergic manifestations can be prevented with the help of elimination measures that exclude contact with causally significant allergens.

Patients are advised to exclude easily digestible protein foods from their diet - milk, chicken, eggs, fish, citrus fruits; it is not recommended to use canned food, smoked meats, fried foods, coffee, chocolate, honey, nuts, limit the amount of sweets. The basis of the diet should be vegetables, dairy products, cereals, boiled meat. Advice on the correct selection of clothing for a patient with atopic dermatitis (preference should be given to cotton fabrics), frequent wet cleaning of premises using special cleaning systems based on the separation of dust in a water suspension are also important. The treatment of concomitant diseases and the rehabilitation of chronic foci of focal infection, which determine an additional irritating effect on the patient's immune system, are of great importance. First of all, we are talking about diseases of the gastrointestinal tract, ENT organs. Treating patients with appropriate specialists greatly improves the quality of dermatological treatment.

The appointment of therapy should be approached differentially, taking into account the age, period, severity of the disease, the severity of the inflammatory reaction, the prevalence of the lesion and the associated complications of local infection.

In the presence of single lesions with minimal clinical manifestations, mild itching can be limited to local treatment.

The assertion that the therapy of atopic dermatitis remains predominantly local with the use of external agents is difficult to refute. This approach, formulated decades ago, is still relevant today. At the same time, the arsenal of means and the possibilities of external therapy have undergone significant changes for the better: new classes of external drugs - immunosuppressants have appeared, the arsenal of glucocorticosteroid (GCS) drugs for external use has expanded; Qualitative changes have taken place in the market for skin care products for patients with atopic dermatitis.

The choice of specific corticosteroids for atopic dermatitis is carried out taking into account not only the form, stage and localization of clinical manifestations, but also the strength of the action of external corticosteroids (gradations with division into weak, medium strength, strong).

So, weak drugs are prescribed when the rash is localized on the face or in the folds, when treating children; medicines of moderate strength - with localization of rashes on different parts of the body; strong GCS - with lichenification, chronic inflammatory process.

With regard to the strength of the GCS, it can be noted that the principle of correspondence "strength of GCS-localization of the rash" is largely determined by the likelihood of side effects.

When choosing funds for external use, it is necessary to choose the right effective dosage form: for erythematous-squamous form of atopic dermatitis, it is advisable to use creams, lotions with the addition of keratolytics, with lichenoid - ointments, compresses with epithelial and antimicrobial additives, preferably under an occlusive dressing. With a pruriginous form, it is more expedient to prescribe suspensions, pastes with the addition of GCS, as well as aerosols, gels, creams; with eczematous - lotions, creams, gels.

In a state of remission of atopic dermatitis, medicinal cosmetics and hygienic care products in the form of emulsion and liquid creams, emulsions, gels, balms are preferred.

Local corticosteroids are prescribed intermittent courses with a gradual dose reduction to prevent withdrawal syndrome. If it is necessary to use drugs for a long time, it is advisable to use drugs with different chemical structures.

In childhood, treatment begins with weak GCS ointments (1% hydrocortisone), followed by a switch to drugs containing GCS: vitamin F-99 cream, glutamol. In pediatric practice, preference is given to the latest generation of drugs - methylprednisolone aceponate (Advantan), alclomethasone (afloderm), mometasone (elokom), hydrocortisone 17-butyrate (locoid). The optimism of foreign and Russian colleagues, caused by the emergence and already widespread distribution of a new class of external immunosuppressants - tacrolimus, pimecrolimus (elidel), is fully justified, the mechanism of action of which is associated with blockade of early cytokine transcription, suppression of T-lymphocyte activation.

In this case, it is necessary to take into account the minimum age from which the use of local GCS is allowed: Advantan, Afloderm, Locoid - from 6 months; elok - from 2 years old.

For adults, with pronounced skin changes, strong GCS are often applied to the affected areas for a short time (2-4 days) and quickly switch to medium-strength drugs (elokom, advantan, afloderm) against the background of antihistamine therapy.

Often, the course of atopic dermatitis is complicated by secondary bacterial and / or fungal infections.

In this case, it is necessary to use combined preparations containing components with anti-inflammatory, antibacterial and antifungal effects. The most optimal in this situation is the use of combined drugs: triderm, acriderm, acriderm genta, hyoxysone, oxycyclosol, oxycort ointment, aerosol, fucicort, fucidin G.

When prescribing general therapy, the leading role is given to antihistamines, which are prescribed permanent courses (from 2 weeks to 3-4 months), taking into account the possibility of combining antihistamines of different generations (diazolin in the morning / afternoon - tavegil at night). A special effect of ketotifen (zaditen, astafen), which has a stabilizing effect on the membranes of mast cells, has been noted. It should be noted that first generation antihistamines must be prescribed sequentially, alternating the drug used every 7-10 days. Convenient in practical use are zirtek and kestin, which have a prolonged action, providing the possibility of a single daily use.

Pharmacotherapy of moderate atopic dermatitis involves the administration of 0.005 g desloratadine inside for up to 1.5 months, loratadine 0.01 g 1 time per day for 7-10 days, clemastine 0.001 g 2-3 times a day for 7-10 days, chloropyramine 0.025 g 3 times a day for 7-10 days, ebastine 10 mg 1 time a day for 7-10 days. Perhaps parenteral administration of diphenhydramine (1% - 2 ml intramuscularly, No. 10-15), clemastine (0.1% - 2 ml intramuscularly, No. 10-15), chloropyramine (2% - 2 ml intramuscularly, No. 10-15).

Shown intravenous sodium thiosulfate (30% solution of 10 ml, 10-15 injections), isotonic sodium chloride solution (intravenous drip, 200-400 ml 2-3 times a week, No. 4-7), polyvidone (200-400 ml 2-3 times a week, No. 4-7).

An important role is played by sedative and psychotropic drugs, which are prescribed in courses of 2-4 weeks (tincture of peony, motherwort, valerian root, persen, relanium, phenazepam, mesapam). From the group of vitamin preparations, patients with atopic dermatitis are shown vitamin A, prescribed in the form of retinol acetate and retinol palmitate (capsules, drops). The appointment of other vitamin preparations should be approached with caution, since patients with atopic dermatitis often have hypersensitivity to certain vitamins, especially group B.

In severe, stubborn cases, with erythrodermic forms of atopic dermatitis, it becomes necessary to use GCS systemically. Prednisolone, dexamethasone, methylprednisolone are prescribed in medium starting doses (30-40 mg per day), taking into account the daily rhythm of the physiological production of steroids. To avoid the possible development of secondary infections, an alternating method of treatment is often used (double daily dose every other day). The appointment of GCS in high doses determines the need for corrective therapy (potassium preparations, antacids, anabolic steroids).

With a torpid course of atopic dermatitis, cyclosporine is prescribed in the form of capsules or a solution at a maximum dose of 5 mg / kg of body weight per day, followed by its decrease to the minimum maintenance. It should be borne in mind that if there is no effect against the background of using the maximum dose of the drug within 6 weeks, the use of this drug should be discontinued.

A course of extracorporeal detoxification, in particular in the form of plasmapheresis, may be useful in severe atopic dermatitis.

In some cases, it becomes necessary to use antibiotics due to the development of a secondary infection in the form of strepto- and staphyloderma. The most appropriate in these cases is the appointment of erythromycin (1 g per day for 5-7 days), josamycin (1-2 g per day for 7-10 days). Tetracyclines can be used as alternatives. When prescribing antibiotics, one should remember the need for traditional prevention of intestinal microbiocenosis disorders.

The most widely used physical treatment is ultraviolet light therapy. Different in duration (depending on indications) courses of ultraviolet irradiation with a conventional quartz lamp, PUVA therapy or selective phototherapy significantly suppress the processes of immune inflammation in the skin and reduce itching. It should not be forgotten that natural sunlight itself has an excellent therapeutic effect against atopic dermatitis, which makes patients feel much better in summer.

Electrotherapy methods use galvanization, electrosleep, darsonvalization. They improve the function of blood vessels of the skin, activate the adrenal cortex, stabilize the state of the nervous system, thereby increasing the effectiveness of the entire complex of therapeutic measures.

A worthy place in the therapy of atopic dermatitis is occupied by laser therapy (in the case of significant lichenification of foci, contributing to their accelerated resolution) and reflexology (acu-, laser- and electropuncture).

Climatotherapy deserves special attention as an effective therapeutic and prophylactic agent for atopic dermatitis. A patient's stay in a dry maritime climate (Crimea, Sea of Azov, Dead Sea, Adriatic Sea) often completely relieves him of inflammatory skin changes and itching, significantly lengthens remission, and reduces the intensity of exacerbation.

Determining the prognosis in atopic dermatitis is difficult, since the individual characteristics of the immune response, as well as concomitant diseases, are very diverse. In almost 50% of patients, the clinical signs of the disease disappear by the age of 15, in the rest (45-60%) they can persist throughout their lives.

At the end of the course of drug therapy, having achieved regression of the main manifestations of the disease, it is necessary to carry out long-term supportive therapy (restoration of the damaged lipid layer, corneotherapy). Hygienic (daily) care products also play an important role. Recently, in addition to the lanolin-based creams traditionally used for atopic dermatitis with the addition of salicylic acid, urea, new generation preparations for permanent use have appeared - products based on thermal waters of various foreign dermatocosmetic lines, among which the therapeutic cosmetics of Dermatological Laboratories Aven (Pierre Fabre, France). All products produced by these laboratories contain Aven thermal water.

Thermal water "Aven" has a neutral pH, slightly mineralized, contains a wide range of trace elements (iron, manganese, zinc, cobalt, copper, nickel, aluminum, bromine, selenium), as well as silicon, which forms a thin softening and protective film on the skin. The water does not contain surfactants, is characterized by a low concentration of sulphides and thiosulphates, and is completely devoid of hydrogen sulphide. It is distinguished by the balance of the cationic (Ca 2+ / Mg 2+) and anionic (C l- / SO4 2-) components.

Numerous scientific research works have proven the anti-inflammatory, trophic, antipruritic, softening, irritation-reducing effects of the Aven thermal water. Its properties observed in clinical practice have been confirmed experimentally in vitro at the cellular level. Its ability to suppress the process of degranulation of mast cells, to cause an increase in the synthesis of interferon γ, the production of interleukin-4 has been proven.

Among the remedies, the Tolerance Extrem cream stands out, which contains, along with the Aven thermal water, cartama oil, glycerin, liquid paraffin, perhydroxysqualene, and titanium dioxide. Thanks to the use of the cream, a feeling of comfort is quickly achieved; this remedy relieves skin irritation, improves the tolerance of drug treatment. The cream is applied to cleansed skin (usually the face) twice a day (1 mini-dose for 3 days).

The TriKzera line contains ingredients to control the three main symptoms of atopic dermatitis - xerosis (“lipid trio”), inflammation (Aven thermal water) and itchy skin (glycocol). The TriKzera cream contains Aven thermal water, ceramides, basic fatty acids (linoleic, linolenic), plant sterols, glycerin, glycocol. The active components of the cream contribute to the rapid restoration of the structure of the damaged epidermis and, as a consequence, the barrier function of the skin; inhibit the processes of peroxidation, providing a protective effect against the cell membranes of epidermal cells. The cream intensively softens and moisturizes the skin, has an antipruritic effect. "TriKzera" is applied to cleansed skin at least 2 times a day. The softening effect of TriKzera cream is enhanced by TriKzera softening bath - a balanced emulsion - water / oil / water containing the same main active ingredients. TriKzera softening bath protects from the effects of hard water during bathing, which is important not only for therapeutic, but also for daily hygienic care. Therapeutic care for dry atopic skin is assisted by the Cold Cream line. The cold cream contains Aven thermal water, white beeswax, paraffin oil. Cold cream reduces the sensitivity of the skin, restores the hydrolipid balance, reduces the feeling of skin tightness, reduces the intensity of erythema and peeling. Cold Cream is applied to cleansed skin several times a day (as needed). The composition of "Emulsions for the body with cold cream" includes thermal water "Aven", sesame oil, cartama, coconut, allantoin. Thanks to its light texture, "Body Emulsion with Cold Cream" is well distributed and absorbed, easy to apply on large skin surfaces. It is applied several times a day.

"Lip balm with cold cream", which has a regenerating and softening effect, is used for perioral dermatitis and cheilitis, which are a common manifestation of atopic dermatitis.

For hygienic care of dry and atopic skin, it is possible to use "Soap with cold cream" or "Gel with cold cream", which, gently cleansing the skin, moisturize and soften it, return a feeling of comfort.

Among the means of medical and hygienic care that improve the quality of life of patients with atopic dermatitis, we can mention the Lipikar series (Surgra, Sindat, bath oil, balm, emulsion), Hydranorm and Ceralip creams. In the A-Derma line, the Egzomega series (cream, milk) based on realba oats is popular. In case of the presence of foci of wetness, it is recommended to use the preparation of the Bioderma line - the cream "Atoderm RO Zinc".

To reduce the general dryness (xerosis) of the skin, for hygienic care, the bath oil "Balneum Hermal" is used, which is also a mild detergent that does not contain soap, and therefore there is no need to use additional detergents.

A new remedy for eliminating dry skin - cream-foam "Allpresan" - 1, 2, 3.

Caring for the scalp also requires attention, and the use of ointments and creams is excluded. The prescription of steroid-containing lotions ("Belosalik", "Diprosalik", "Elokom"), shampoos of the "Friderm" series (with zinc, neutral tar) is considered traditional.

During the period of remission, the use of revitalizing shampoos "Elution", "Extra-du", "Selezhel", "Kertiol", "Kertiol S", "Quelual DS" (Laboratory Ducre) is shown as a means of hygienic care for the scalp.

In complex care, it is advisable to use a nutritious mask "Lactocerate" 1-2 times a week, "Lactocerate - a nutritionally regenerating shampoo" and a protective spray.

When caring for the red border of the lips and corners of the mouth, Ceralip (restoring lip cream), Lipolevr (protective pencil), lip balm with Cold Cream (regenerating, protective, soothing, softening), Sicalfat ( antibacterial cream), "Kelian" (nourishing and regenerating lip cream), "Iktian" (protective and moisturizing lip stick).

During the period of solar activity, it is advisable to use photoprotective agents of the "Photoscreen" series (cream, milk, spray, gel-cream), Antihelios.

Thus, the modern arsenal of means of various nature and direction of action allows a balanced and rational approach to the management of patients with atopic dermatitis, taking into account the pathogenesis, course of the disease, as well as the capabilities of the doctor and patient. By combining the joint efforts of various specialists, long-known methods and new approaches to the therapy of patients, by positively changing the patient's attitude, we will be able to come closer to solving the complex medical and social problem of treating atopic dermatitis.

Literature

Balabolkin I.I., Grebenyuk V.I. Atopic dermatitis in children. M .: Medicine, 1999.238 p.
Atopic dermatitis: approaches to prevention and external therapy / ed. prof. Yu. V. Sergeeva. M., 2006.
Filatova T.A., Revyakina V.A., Kondyurina E.G. Parlazin in the treatment of atopic dermatitis in children // Questions of modern pediatrics. 2005. T. 4. No. 2. S. 109-112.
Kudryavtseva E.V., Karaulov A.V. Locoid and modern approaches to external therapy of atopic dermatitis // Immunology, Allergology, Infectology. 2003. No. 4. S. 57-62.<
Fedenko E.S.Atopic dermatitis: justification of a phased approach to therapy // Consilium medicum. 2001. T. 3. No. 4. S. 176-183.
Atopic dermatitis: recommendations for practitioners / under the general. ed. R. M. Khaitov and A. A. Kubanova. M., 2003.
Kochergin N.G., Potekaev I.S. Cyclosporin A in atopic dermatitis (mechanisms of immunosuppression and clinical efficacy). M., 1999.
Pytskiy V.I., Adrianova N.V., Artomasova A.R. Allergic diseases. M., 1999.470 p.
Suvorova K.N., Antoniev A.A., Dovzhansky S.I., Pisarenko M.F. Atopic dermatitis. Saratov: Saratov University Press, 1989.
Kochergin N.G. Atopic dermatitis // Russian Journal of Skin and Venereal Diseases. 1998. No. 5. S. 59-65.

E. N. Volkova, Doctor of Medical Sciences, Professor
Russian State Medical University, Moscow

Atopic dermatitis (AD) - Chronic allergic skin disease that develops in individuals with a genetic predisposition to atopy.

Recurrent course, characterized by exudative and / or lichenoid eruptions, increased serum IgE levels and hypersensitivity to specific and nonspecific stimuli.

Etiology. 1) heredity

2) allergens. (house dust, epidermal, pollen, fungal, bacterial and vaccine allergens)

3) non-allergenic causal (psycho-emotional stress; changes in the meteorological situation; food additives; pollutants; xenobiotics.)

Pathogenesis. immunological pathogenesis:

Langerhans cells (perform the function of antigen-presenting) inside the epidermis form a uniform network between keratinocytes in the intercellular space. → On their surface there is R for an IgE molecule. → In contact with antigen → move to distal and proximally located tissue layers. → interact with ThO-lymphocytes which differentiate into Thl and Th2 cells. Th2 cells promote the formation of specific IgE antibodies by B lymphocytes and their fixation on mast cells and basophils.

Repeated contact with the allergen leads to mast cell degranulation and the development of an immediate phase of the allergic reaction. It is followed by the IgE-dependent late phase of the reaction, characterized by tissue infiltration with lymphocytes, eosinophils, mast cells, neutrophils, macrophages.

Further, the inflammatory process becomes chronic. Itching of the skin, which is a constant symptom of AD, leads to the formation of an itching-combing cycle: keratocytes damaged by scratching release cytokines and mediators that attract inflammatory cells to the lesion.

Almost 90% of patients with AD have skin colonization Staph, aureus, capable of exacerbating or maintaining skin inflammation through the secretion of superantigens toxins that stimulate T cells and macrophages. About half of children with AD produce IgE antibodies to staphylococcal toxins.

The clinical picture. various manifestations - papules, small epidermal vesicles, erythematous spots, peeling, scabs, cracks, erosion and lichenification. A characteristic symptom is severe itching.

In infants(infant form - up to 3 years) elements are located mainly on the face, trunk, extensor surfaces, scalp.

Ages 3-12(children's form) - on the extensor surfaces of the limbs, face, in the ulnar and popliteal fossa.

In adolescence(12-18 years old) the neck, flexion surfaces of the limbs, wrists, and upper chest are affected.

Have young people - neck, back of the hands.

Often → areas of hypopigmentation on the face and shoulders (lichen white); a characteristic fold along the edge of the lower eyelid (Denier-Morgan line); strengthening of the line pattern of the palm (atopic palms); white dermographism.

The severity of blood pressure is determined by the international SCORAD system, taking into account objective symptoms, area of skin lesions, assessment of subjective signs (itching and sleep disturbance).

AD is often complicated by secondary bacterial (staphylococcus and streptococci) infections.

Diagnostics. 1) anamnesis (onset of neglect at an early age; heredity; itching; typical morphology of skin rashes; typical localization of skin rashes; chronic recurrent course;

2) high level of total IgE and allergen-specific IgE antigens in serum.

3) Prick test or skin scarification tests

4) in vitro diagnostics.

5) elimination and provocative tests with food.

Differential diagnosis carried out with seborrheic dermatitis; Wiskott-Aldrich syndrome, hyperimmunoglobulinemia E syndrome, microbial eczema;

Treatment.

1) diet therapy... elimination diet (exclusion of provocative foods, limitation of sugar, salt, broths, spicy, salty and fried foods,

2)elimination of household allergens.

3)Systemic treatment →antihistamines I, II and III generations (zyrtec, claritin, ketotifen, telfast).

→membrane stabilizing drugs ( ketotifen, xidiphon, antioxidants, nalcrom. Vitamins)

→calcium preparations(gluconate, lactate, glycerophosphate 0.25-0.5 orally 2-3 times a day)

→ herbal medicine (licorice root, which stimulates the function of the adrenal glands and its preparation glycyram, etc.).

→digestive enzymes(festal, digestal, pancreatin, etc.),

→ With severe pyoderma → antibacterial therapy(macrolides, I and II generation cephalosporins, lincomycin.)

4) External therapy:

→ The child's fingernails should be cut short,

→ indifferent pastes, ointments, talkers containing anti-inflammatory, keratolytic and keratoplastic agents. Burov's liquid (aluminum acetate solution), 1% tannin solution, etc.

→ With severe manifestations → glucocorticosteroids (elokom (cream, ointment, lotion), advantan (emulsion, cream, ointment).

→external antibacterial drugs(bactroban, 3-5% paste with erythromycin, lincomycin). → treated with fucorcin, a solution of brilliant green, methylene blue.

Forecast. Complete clinical recovery occurs in 17-30% of patients.

3. Obesity. Obesity is a heterogeneous disease caused by the accumulation of triglycerides in fat cells and manifested by excessive fat deposition. The frequency is 5%, it is more common in girls.

Etiology and pathogenesis. Excess fat deposition arises as a result of the discrepancy between the balance of food intake and energy consumption towards the prevalence of the former. Predisposition factors - congenitally caused an increase in the content of fat cells (adipocytes) in the body, especially fat metabolism with the predominance of lipogenesis processes over lipolysis; endocrine disorders (hypothyroidism, hypogonadism, hypercortisolism, etc.); damage to the hypothalamus (birth trauma, infections, brain hypoxia, etc.).

Clinic. Obesity - excess body weight exceeding 10% of the required body weight, excess db is due to the fatty component of the soma, and not muscle and bone. For a more accurate assessment of the degree of excess adipose tissue in the body, the measurement of skin folds with a caliper is used.

The most common is the constitutionally exogenous (simple) form of obesity, accounting for up to 90% of all forms of overnutrition in children. The presence of obesity from childhood creates the prerequisites for the formation of such diseases in the future as: atherosclerosis, hypertension, type II diabetes mellitus, cholelithiasis, etc. also forms of obesity - hypothalamic, itsenko-Cushing's syndrome, pubertal hypothalamic syndrome.

Treatment of the constitutional-exogenous form of obesity. The main method of treatment is diet therapy. With moderate obesity, the calorie content of the diet is reduced by 0-30%, with pronounced obesity - by 45-50%, the energy intensity of food decreases mainly due to easily digestible carbohydrates, partly fats. The amount of protein in the daily diet should correspond to the needs of a healthy child of the same age. The daily calorie intake of a severely obese schoolchild is usually about 500 kcal. Physical therapy, the patient's psychological attitude (motivation) is of great importance.

Prevention. A rational daily regimen and nutrition of a pregnant woman, as well as at an early age of a child, are of great importance in the prevention of a simple form of obesity, since overeating of a pregnant woman and irrational feeding (carbohydrate overfeeding) of a child in the first year of life leads to an increase in the number of fat cells in the body of the latter, which creates preconditions for the development of obesity in him in the future.

Ticket 30

ANEMIA

Anemia is a condition characterized by a decrease in the number of red blood cells below 3.5 * 10 12 / l and / or a decrease in the level of hemoglobin per unit of blood volume below 110 g / l for young children and 120 g / l for preschool and older children.

Classification of anemias.

I. Deficiency anemia 1. Iron deficiency; 2. Protein deficient; 3. Vitamin deficiency

II. Post-hemorrhagic anemias 1. Acute; 2. Chronic

III. Hypo- and aplastic anemias A. Congenital forms 1. With lesions of erythro-, leuko-, and thrombocytopoiesis: a) with congenital malformations (Fanconi type); b) without congenital anomalies (type Estren - Damesek); 2. With partial lesions of hematopoiesis: a) selective erythroid dysplasia (Blackfem-Diamond type) B. Acquired forms 1. With lesions of erythro-, leuko-, and thrombocytopoiesis: a) acute aplastic; b) subacute hypoplastic; c) chronic hypoplastic with a hemolytic component. 2. Partial hypoplastic anemia with selective damage to erythropoiesis.

IV. Hemolytic anemias

A. Hereditary 1. Membranopathies (microspherocytosis, elliptocytosis, stomatocytosis, paroxysmal nocturnal hemoglobinuria); 2. Fermentopathy (violations of the glycolytic pathway, pentose phosphate cycle, nucleotide exchange); 3. Defects in the structure and synthesis of hemoglobin (sickle cell anemia, thalassemia, methemoglobinemia);

B. Acquired 1. Immunopathological (isoimmune - transfusion of incompatible blood, hemolytic disease of newborns, autoimmune, haptenic medication); 2. Infectious (cytomegalovirus and other viral, bacterial); 3. Toxic (due to heavy metal poisoning); 4. Caused by increased destruction of erythrocytes (with hypersplenism, microangiopathy); 5. DIC syndrome.

According to the color index, anemias are divided into hypochromic (less than 0.85), normochromic (0.85-1.0) and hyperchromic (over 1.0). According to the functional state of erythropoiesis - into hyperregenerative (reticulocytosis over 50% o), regenerative (more than 5% o) and hyporegenerative. By the average volume of erythrocytes - into microcytic (50-78 fl), normocytic (80-94 fl), macrocytic (95-150 fl).

With hypochromia and microcytosis, iron deficiency anemias, sideroblastic (chronic infections, systemic and oncological diseases), hemoglobinopathies usually occur. With normochromic-normocytic indicators - aplastic anemia, myelodysplasia (bone marrow dysplasia), hypoproliferation (renal, endocrine diseases, protein deficiency). With macrocytosis B12-, folate deficiency, dyserythropoietic, congenital and acquired aplastic anemias in the early stages, anemia with hypothyroidism and liver pathology.

Iron-deficiency anemia. Iron deficiency anemia (IDA) is the most common type of anemia in childhood. Its frequency varies widely and depends on social conditions. IDA is most often observed at an early age, preceded by a period of latent iron deficiency.

Etiology and pathogenesis. The main reason is the depletion of iron stores at a time when the requirements for increasing blood volume and mass of red blood cells exceed food intake and absorption. A full-term newborn has a total amount of iron in the body of about 240 mg, 75% of which is hemoglobin. At the age of one year, the iron reserve is already 400 mg. The concentration of iron in human milk is about 1.5 mg / l. 13-19% of iron is absorbed from animal food, thus, exclusive breastfeeding (without timely introduction of complementary foods) cannot fully meet the needs of a growing body in iron.

The main predisposing factors :) alimentary iron deficiency (with late introduction of complementary foods, improper feeding);) insufficient supply of it (prematurity, multiple pregnancy, mother's anemia during pregnancy); 3) disorders of iron absorption (dyspepsia, intestinal infections, chronic diseases); 4) increased iron losses (blood loss, helminthiasis); 5) increased requirements for iron (frequent infectious diseases).

Hemolytic anemias. Hemolytic anemias are characterized by a reduction in the life span of erythrocytes, indirect hyper-bilirubinemia, activation of erythropoiesis, manifested by reticulocytosis. The consequence of compensatory hyperplasia of the bone marrow are changes in the skeleton.

Classification. A. Hereditary 1. Membranopathies (microspherocytosis, elliptocytosis, stomatocytosis, paroxysmal nocturnal hemoglobinuria); 2. Fermentopathy (disorders of the glycolytic pathway, pentose phosphate cycle, nucleotide exchange); 3. Defects in the structure and synthesis of hemoglobin (sickle cell anemia, thalassemia, methemoglobinemia); B. Acquired 1. Immunopathological (isoimmune - transfusion of incompatible blood, hemolytic disease of newborns, autoimmune, haptenic medication); 2. Infectious (cytomegalovirus and other viral, bacterial); 3. Toxic (due to heavy metal poisoning); 4. Caused by increased destruction of erythrocytes (with hypersplenism, microangiopathy); 5. DIC syndrome.

2.Vitamin D-deficiency rickets. Vitamin D-deficient rickets is a disease of a fast-growing organism caused by a deficiency of many substances, but mainly vitamin D, which leads to disruption of calcium and phosphorus homeostasis, which is manifested by the defeat of many systems, but most pronounced - bone and nervous.

Specific for lesions of the skeletal system in this disease are changes in the growth zones - the metaepiphyseal parts of the bones. Therefore, rickets is an exclusively pediatric concept. When a pronounced vitamin D deficiency occurs in an adult, only signs of osteomalacia (demineralization of the bone without its structural restructuring) and osteoporosis (demineralization of the bone with restructuring of its structure) appear in the bone system. In this regard, the clinical manifestations of hypovitaminosis D in an adult patient is called osteomalacia.

Etiology.

Risk factors: prenatal (violation of the regime, nutrition, physical activity; gestosis, somatic pathology; multiple pregnancy, prematurity), postnatal (artificial feeding with unadapted mixtures, frequent diseases of the child, low physical activity, individual constitutional predisposition).

Result: insufficient depot of vitamin D, calcium, phosphorus, vitamins and minerals.

1.exogenous rickets: insufficient solar insolation.

2. alimentary factor:

Late introduction of animal food into the diet, vegetarianism (phytin and lignin in large quantities interfere with the absorption of calcium, phosphorus, exogenous vitamin D);

Lack of specific prevention of rickets;

Feeding a premature baby with artificial formula not enriched with phosphates.

3.endogenous rickets:

Syndrome of maldigestion and malabsorption (malabsorption of vit. D),

Damage to the hepatobiliary system (impaired hydroxylation of provitamin D),

Insufficient bile secretion (impaired absorption and breakdown of fats (vitamin D is a fat-soluble vitamin).

Severe parenchymal kidney disease, with the involvement of tubulointerstitium (violation of hydroxylation, reduced reabsorption of minerals).

The syndrome of massive protein loss (exudative enteropathy, nephrotic syndrome, burn disease) is eliminated by a-globulins-carriers together with active metabolites of D.

Drugs: anticonvulsants, glucocorticoids, etc. - inactivation of vitamins D. Long-term use of these drugs by young children requires the appointment of a prophylactic dose of vitamin D.

Pathogenesis. The pathogenesis of vitamin D-deficient rickets can be represented in the form of a simplified scheme: Deficiency of 1,25- (OH) 2-D → Enterocyte (↓ synthesis of Ca-binding protein) → Small intestine (↓ absorption of Ca ++, H2PO-, HPO4) → Blood flow ( ↓ Ca ++) → Parathyroid glands (PTH): 1) kidneys (1,25- (OH) 2-D); 2) bones (bone resorption) → an act of a rickety process.