home Audience 5 Atopic dermatitis pathogenesis clinic treatment. Atopic dermatitis: Skin diseases: diagnosis, treatment, prevention. Differential diagnosis of atopic dermatitis

Atopic dermatitis pathogenesis clinic treatment. Atopic dermatitis: Skin diseases: diagnosis, treatment, prevention. Differential diagnosis of atopic dermatitis

Atopic dermatitis (AD) is a multifactorial inflammatory skin disease characterized by itching, a chronic relapsing course and age-related features of the localization and morphology of lesions.

Etiology and epidemiology

In the pathogenesis of AD, hereditary determination plays an important role, leading to disruption of the skin barrier, defects of the immune system (stimulation of Th2 cells followed by hyperproduction of IgE), hypersensitivity to allergens and nonspecific irritants, colonization by pathogenic microorganisms (Staphylococcus aureus, Malassezia furfur), as well as imbalance of the autonomic nervous system with increased production of inflammatory mediators. Atopic dermatitis is one of the most common diseases (from 20% to 40% in the structure of skin diseases), occurring in all countries, in people of both sexes and in different age groups.

The incidence of AD over the past 16 years has increased 2.1 times. The prevalence of AD among children is up to 20%, among adults – 1–3%.

Atopic dermatitis develops in 80% of children whose both parents suffer from this disease, and in more than 50% of children when only one parent is sick, while the risk of developing the disease increases by one and a half times if the mother is sick.

Early formation of atopic dermatitis (between the ages of 2 and 6 months) is observed in 45% of patients, during the first year of life – in 60% of patients. By 7 years of age, 65% of children, and by 16 years of age, 74% of children with atopic dermatitis experience spontaneous remission of the disease. 20–43% of children with atopic dermatitis subsequently develop bronchial asthma and twice as often allergic rhinitis.

Classification

There is no generally accepted classification.

Symptoms of atopic dermatitis

Age periods
Age-related features of the localization and morphology of skin elements distinguish atopic dermatitis from other eczematous and lichenoid skin diseases. The main differences in clinical manifestations by age are the localization of lesions and the ratio of exudative and lichenoid components.

Itching is a constant symptom of the disease in all age periods.

The infancy period of AD usually begins at 2–3 months of a child’s life. During this period, the exudative form of the disease predominates, in which inflammation is acute or subacute. The clinical picture is represented by erythematous spots, papules and vesicles on the cheeks, forehead and/or scalp, accompanied by intense itching, swelling, and weeping. Dermographism is usually red. The initial manifestations of the disease are also localized on the extensor and flexion surfaces of the limbs. By the end of this period, the lesions persist mainly in the folds of large joints (knees and elbows), as well as in the wrists and neck. The course of the disease is largely associated with nutritional factors. The infant period of AD usually ends by the second year of the child’s life with recovery (in 50% of patients) or moves into the next period (childhood).

The childhood period of AD is characterized by rashes that are less exudative than in infancy and are represented by inflammatory miliary and/or lenticular papules, papulovesicles and erythematous-squamous elements localized on the skin of the upper and lower extremities, in the wrists, forearms, elbow and popliteal folds, ankle joints and feet. Dermographism becomes mixed or white. Pigmentation of the eyelids, dyschromia, and often angular cheilitis appear. The condition of the skin is less dependent on nutritional factors. There is a seasonality in the course of the disease with exacerbations in spring and autumn.

The adolescent and adult period of AD is characterized by rashes mainly on the flexor surface of the extremities (in the elbow and popliteal folds, flexor surfaces of the ankle and wrist joints), on the back of the neck, and in the behind-the-ear areas. The rashes are represented by erythema, papules, desquamation, infiltration, lichenification, multiple excoriations and fissures. In areas where the rash resolves, areas of hypo- or hyperpigmentation remain in the lesions. Over time, in most patients the skin clears of the rashes, only the popliteal and elbow folds remain affected.

Most patients by the age of 30 experience incomplete remission of the disease (dry skin remains, its increased sensitivity to irritants, moderate seasonal exacerbations are possible).

Stages of the disease

The stage of exacerbation or pronounced clinical manifestations is characterized by the presence of erythema, papules, microvesicles, oozing, multiple excoriations, crusts, peeling; itching of varying degrees of intensity.

Stages of remission:

with incomplete remission, there is a significant decrease in the symptoms of the disease with the preservation of infiltration, lichenification, dryness and flaking of the skin, hyper- or hypopigmentation in the lesions;
complete remission is characterized by the absence of all clinical symptoms of the disease.

Prevalence of the skin process

With a limited localized process, the affected area does not exceed 10% of the skin.

In a widespread process, the affected area is more than 10% of the skin.

Severity of the process

The mild course of the disease is characterized by predominantly limited-localized manifestations of the skin process, minor skin itching, rare exacerbations (less than 1-2 times a year), and a relapse duration of up to 1 month, mainly in the cold season. The duration of remission is 8–10 months or more. There is a good effect from the therapy.

In moderate cases, the lesion is widespread. The frequency of exacerbations is 3–4 times a year with increasing duration. The duration of remission is 2–3 months. The process takes on a persistent, torpid course with little effect from the therapy.

In severe cases of the disease, the skin process is widespread or diffuse, with long-term exacerbations, rare and short-term remissions (frequency of exacerbations - 5 times a year or more, duration of remission 1-1.5 months). Treatment brings short-term and minor improvement. There is severe itching, leading to sleep disturbances.

Clinical forms

The exudative form is observed mainly in infants, characterized by symmetrical erythematous, papulovesicular rashes on the skin of the face and scalp, exudation with the formation of scaly crusts is noted. Subsequently, the rash spreads to the skin of the outer surface of the legs, forearms, torso and buttocks, and can also appear in natural folds of the skin. Dermographism is red or mixed. Subjectively, itching of the skin of varying intensity is noted.

The erythematous-squamous form is more often observed in children aged 1.5 to 3 years, characterized by the presence of itchy nodules, erosions and excoriations, as well as slight erythema and infiltration in the area of rashes on the skin of the trunk, upper and lower extremities, less often on the skin of the face . Dermographism pink or mixed.

The erythematous-squamous form with lichenification is observed in children aged 3 years and older and adults, characterized by erythematous-squamous and papular foci. The skin is dry, lichenified, with a large number of excoriations and small lamellar scales. The rashes are localized mainly on the flexor surface of the limbs, the dorsum of the hands, and the anterior and lateral surfaces of the neck. Hyperpigmentation of the skin of the periorbital area and the appearance of a fold under the lower eyelid (Denis-Morgan lines) are observed. There is increased dryness of the skin. Dermographism is white, persistent or mixed. The itching is pronounced, constant, less often paroxysmal.

The lichenoid form is observed most often in adolescents and is characterized by dryness, a pronounced pattern, swelling and infiltration of the skin. There are large confluent foci of skin lichenification. The itching is persistent, persistent.

The pruriginous form is observed relatively rarely, more often in adults and is characterized by rashes in the form of multiple isolated dense edematous papules, on top of which small blisters may appear. Lesions may be widespread, with a predominant localization on the skin of the extremities. Dermographism pronounced white persistent.

The most severe manifestation of AD is erythroderma, which is characterized by universal damage to the skin in the form of erythema, infiltration, lichenification, peeling and is accompanied by symptoms of intoxication and impaired thermoregulation (hyperthermia, chills, lymphadenopathy).

Complicated forms of AD

The course of AD is often complicated by the addition of a secondary infection (bacterial, mycotic or viral). This feature reflects the violation of anti-infective protection characteristic of patients with AD.

The most common infectious complication of AD is the addition of a secondary bacterial infection. It occurs in the form of strepto- and/or staphyloderma with characteristic skin manifestations against the background of exacerbation of AD. Pyococcal complications manifest themselves in the form of various forms of pyoderma: ostiofolliculitis, folliculitis, vulgar impetigo, less commonly streptococcal impetigo, and sometimes boils.

A variety of mycotic infections (dermatophytes, yeast-like, mold and other types of fungi) also often complicate the course of AD, leading to a longer course of exacerbations, lack of improvement or worsening of the condition. The course of the disease becomes persistent. The presence of a mycotic infection can change the clinical picture of AD: lesions with clear scalloped, slightly raised edges appear, seizures and cheilitis often recur, and lesions of the postauricular, inguinal folds, nail bed, and genitalia are noted.

Patients with AD, regardless of the severity of the process, are prone to viral infection (usually herpes simplex virus, human papillomavirus). Herpetic superinfection can lead to a rare but serious complication - Kaposi's herpetic eczema. The disease is characterized by widespread rashes, severe itching, fever, and rapid onset of pyococcal infection. Possible damage to the central nervous system, eyes, and the development of sepsis.

Benign lymphadenopathy is usually associated with exacerbations of AD and manifests itself as enlarged lymph nodes in the cervical, axillary, groin and femoral areas. The size of the nodes can vary, they are mobile, elastic in consistency, and painless. Benign lymphadenopathy goes away on its own or with treatment. Severe enlargement of lymph nodes that persists despite a decrease in disease activity requires a diagnostic biopsy to exclude a lymphoproliferative disease.

Complications of AD from the eyes manifest themselves in the form of recurrent conjunctivitis, accompanied by itching. In severe cases, chronic conjunctivitis can progress to ectropion and cause constant watery eyes.

Diagnosis of atopic dermatitis

The diagnosis of AD is established on the basis of anamnestic data and a characteristic clinical picture.

Diagnostic criteria for AD

Main diagnostic criteria:

skin itching;
skin lesions: in children of the first years of life - rashes on the face and extensor surfaces of the limbs, in older children and adults - lichenification and scratching in the bends of the limbs;
chronic relapsing course;
the presence of atopic diseases in the patient or his relatives;
onset of the disease in early childhood (up to 2 years).

Additional diagnostic criteria:

seasonality of exacerbations (worsening in the cold season and improvement in the summer);
exacerbation of the process under the influence of provoking factors (allergens, irritants (irritants), foods, emotional stress, etc.);
increased levels of total and specific IgE in blood serum;
peripheral blood eosinophilia;
hyperlinearity of the palms (“folded”) and soles;
follicular hyperkeratosis (“horny” papules on the lateral surfaces of the shoulders, forearms, elbows);
itching with increased sweating;
dry skin (xerosis);
white dermographism;
tendency to skin infections;
localization of the skin process on the hands and feet;
nipple eczema;
recurrent conjunctivitis;
hyperpigmentation of the skin of the periorbital area;
folds on the front of the neck;
Dennie-Morgan sign (additional fold of the lower eyelid);
cheilitis.

To make a diagnosis of AD, a combination of three main and at least three additional criteria is necessary.

To assess the severity of AD, semi-quantitative scales are used, of which the SCORAD (Scoring of Atopic Dermatitis) scale is the most widely used. SCORAD provides a score for six objective symptoms: erythema, edema/papular features, crusting/wetting, excoriation, lichenification/desquamation, and dry skin. The intensity of each sign is assessed on a 4-level scale: 0 – absent, 1 – weak, 2 – moderate, 3 – strong. When assessing the area of skin damage, you should use the rule of nine, in which the unit of measurement is the surface area of the patient’s palm, equivalent to one percent of the entire skin surface. The numbers indicate the area value for patients over the age of 2 years, and in brackets - for children under the age of 2 years. Assessment of subjective symptoms (itching, sleep disturbance) is carried out in children over 7 years of age and adults; in young children, subjective symptoms are assessed with the help of parents, who are first explained the principle of assessment.

Mandatory laboratory tests:

Clinical blood test.
Clinical urine analysis.
Biochemical blood test

Additional laboratory tests:

Determination of the level of total IgE in blood serum using enzyme immunoassay.
Allergy testing of blood serum - determination of specific IgE to food, household antigens, antigens of plant, animal and chemical origin.

According to indications, consultations with other specialists are prescribed, antibodies to Giardia antigens, roundworms, opisthorchis, and toxocara are determined in the blood serum.

In difficult cases, when making a differential diagnosis, histological examination of skin biopsies is possible.

Differential diagnosis

Atopic dermatitis is differentiated from the following diseases:

Seborrheic dermatitis, allergic contact dermatitis, diaper dermatitis, psoriasis vulgaris, ichthyosis vulgaris, microbial eczema, dermatophytosis, mycosis fungoides (early stages), limited neurodermatitis (lichen Vidal), actinic reticuloid, phenylketonuria, acrodermatitis enteropathica, Wiskott-Aldrich syndrome.

Treatment of atopic dermatitis

Treatment Goals

achieving clinical remission of the disease;
elimination or reduction of inflammation and skin itching, prevention and elimination of secondary infection, moisturizing and softening the skin, restoring its protective properties;
prevention of the development of severe forms of AD and complications;
improving the quality of life of patients.

General notes on therapy

Fundamentally important in the treatment of patients with AD is the elimination of trigger factors (psycho-emotional stress, house dust mites, mold, changes in climatic zones, environmental distress, violation of the dietary regime, violation of the rules and regimen of skin care, irrational use of synthetic detergents, as well as shampoos , soaps, lotions with a high pH value, tobacco smoke, etc.).

When collecting anamnesis, analyzing the characteristics of the clinical manifestations of the disease and examination data, the significance of certain factors for a particular patient is assessed and elimination measures are carried out. Sanitation of foci of chronic infection, normalization of the gastrointestinal tract and biliary tract are also important.

All patients with atopic dermatitis, regardless of the severity, prevalence, severity of the skin process, the presence or absence of complications, are prescribed basic skin care products.

In case of limited skin damage, in mild to moderate cases of AD, during exacerbations of the disease, predominantly external therapy is prescribed: glucocorticosteroid drugs for external use of strong or moderate activity and/or topical calcineurin blockers, not excluding basic therapy.

After the exacerbation has stopped, topical glucocorticosteroids (TCS) and calcineurin blockers are discontinued, and the patient continues to use only basic therapy.

In case of moderate atopic dermatitis during the period of exacerbation, phototherapy and, if indicated, detoxification agents may be additionally prescribed.

Therapy for patients with severe atopic dermatitis includes, in addition to external agents, systemic drug therapy or phototherapy. As a systemic treatment, cyclosporine and/or systemic glucocorticosteroid drugs can be prescribed for a short course. Basic external therapy is continued regardless of the chosen treatment method.

Regardless of the stage and severity of atopic dermatitis, if necessary, additional treatment methods are used, which include antihistamines, antibacterial, antiviral, and antimycotic agents. At all stages of patient management, it is recommended to implement training programs with a psychorehabilitation focus.

Patients with atopic dermatitis require dynamic monitoring with regular assessment of the severity, severity and extent of the skin process during each visit to the doctor. Therapy can change either with intensification (transition to a higher level of treatment) when clinical manifestations become more severe, or with the use of more gentle methods of therapy (lowering the level of treatment) in the case of positive dynamics of the disease.

In the treatment of children with atopic dermatitis, one should use only those means and methods of therapy that are approved for use in pediatric practice in accordance with the child’s age. Preferred are dosage forms in the form of a cream and monocomponent external agents: topical glucocorticosteroid drugs, calcineurin inhibitors. Combined glucocorticosteroid drugs containing antibacterial and/or antimycotic components are indicated only with clinical and/or laboratory confirmation of a bacterial and/or fungal infection. Unreasonable use of multicomponent external agents may contribute to the development of additional sensitization in children.

Indications for hospitalization

lack of effect from treatment on an outpatient basis;
severe AD requiring systemic therapy;
the addition of a secondary infection that cannot be controlled on an outpatient basis;
development of a viral infection (Kaposi's herpetic eczema).

Treatment regimens for atopic dermatitis:

In the treatment of patients with atopic dermatitis, a stepwise approach has been widely used to select adequate therapy:

each subsequent stage of treatment is a complement to the previous one;
in case of infection, it is necessary to add antiseptic / antibacterial drugs to treatment;
if therapy is ineffective, it is necessary to exclude compliance violations and clarify the diagnosis

External therapy.

The effectiveness of topical therapy depends on three basic principles: sufficient strength of the drug, sufficient dose and correct application. External medications should be applied to moistened skin.

External anti-inflammatory drugs are applied directly to skin lesions and discontinue use if the process resolves. Recently, a proactive treatment method has been recommended: long-term use of small doses of topical anti-inflammatory drugs on the affected areas of the skin in combination with the use of emollients on the entire skin and regular visits to a dermatologist to assess the condition of the skin process.

The amount of topical preparation for external use is measured according to the “finger tip length” rule (FTU, FingerTipUnit), with one FTU corresponding to a column of ointment with a diameter of 5 mm and a length equal to the distal phalanx of the index finger, which corresponds to a mass of about 0.5 g. This The dose of the topical agent is sufficient to apply to the skin of two adult palms, which is about 2% of the total body surface area.

In accordance with the clinical manifestations of the disease and the localization of lesions, the following dosage forms can be used: aqueous solutions, emulsions, lotions, aerosols, pastes, creams, ointments.

Extemporaneous ointments, pastes, lotions containing salicylic acid, petroleum jelly, petroleum jelly, methyluracil, lanolin. naphthalan, ichthyol, dermatol, zinc, starch, bismuth, talc, boric acid, iodine, olive oil, have a complex anti-inflammatory, keratolytic, keratoplasty, disinfectant, drying effect.

Topical glucocorticosteroid drugs

Topical glucocorticosteroids (TCCS) are the first choice for local anti-inflammatory therapy and have a significant effect on the skin process compared with the placebo effect, especially when used with wet-to-dry dressings (A). Proactive therapy with tGCs (use 2 times a week under supervision for a long time) helps reduce the likelihood of exacerbation of AD tGCS can be recommended in the initial stage of exacerbation of AD to reduce itching.

The use of tGCs is indicated for severe inflammation, significant itching and lack of effect from the use of other external therapy. TGCS should be applied only to the affected areas of the skin, without affecting healthy skin.

THCS are classified according to the composition of active ingredients (simple and combined), as well as the strength of anti-inflammatory activity

When prescribing tGCS, it is necessary to take into account the degree of activity of the drug and the dosage form.
It is not recommended to mix topical glucocorticosteroid drugs with other external therapy drugs.
External glucocorticosteroid drugs are applied to the affected areas of the skin 1 to 3 times a day, depending on the drug chosen and the severity of the inflammatory process. For mild atopic dermatitis, a small amount of corticosteroids 2-3 times a week in combination with the use of emollients is sufficient.
It is necessary to avoid the use of high-potency corticosteroids on the face, genital area and intertriginous areas. For these areas, corticosteroids with minimal atrophogenic effect (mometasone furoate, methylprednisolone aceponate, hydrocortisone-17-butyrate) are usually recommended.
To avoid a sharp exacerbation of the disease, the dose of corticosteroids should be reduced gradually. This is possible by switching to TGCS of a lower level of activity while maintaining daily use, or by continuing to use strong TGCS, but with a decrease in the frequency of applications (intermittent mode).
Itching can be considered as a key symptom when assessing the effectiveness of therapy, so the dose of corticosteroids should not be reduced until itching disappears in patients with atopic dermatitis.

Contraindications/restrictions to the use of topical glucocorticosteroid drugs:

bacterial, fungal, viral skin infections;
rosacea, perioral dermatitis, acne;
local reactions to vaccination;
hypersensitivity;
significant trophic changes in the skin.

Side effects when using topical glucocorticosteroid drugs.

Side effects occur in cases of uncontrolled long-term use of glucocorticosteroid drugs without taking into account the localization of lesions and manifest themselves in the form of local changes (skin atrophy, stretch marks, steroid acne, hirsutism, infectious complications, perioral dermatitis, rosacea, telangiectasia, pigmentation disorders), and when applied to over large areas of skin, a systemic effect is observed in the form of suppression of the function of the hypothalamus-pituitary-adrenal axis as a result of transdermal absorption of drugs.

Special situations

Pregnancy/teratogenicity/lactation

Topical glucocorticosteroid drugs do not have a teratogenic effect and are prescribed in short courses during exacerbation of atopic dermatitis in pregnant women. Drugs with the lowest bioavailability should be used to minimize the risk of systemic effects. It should be taken into account that the use of high-potency corticosteroids on large areas of the skin for a long time during pregnancy can lead to intrauterine growth retardation and the threat of suppression of the function of the fetal adrenal cortex.

Calcineurin inhibitors for external use

Calcineurin inhibitors for external use are an alternative to topical glucocorticosteroid drugs and are the drugs of choice in the treatment of atopic dermatitis on sensitive areas of the body (face, neck, skin folds). The use of these drugs is also recommended in cases where the patient has no effect from external therapy using glucocorticosteroids.

Pimecrolimus is used in the topical treatment of mild to moderate atopic dermatitis on lesions for a short time or for a long time in adults, adolescents and children over 3 months of age.

Tacrolimus is used to treat patients with moderate to severe atopic dermatitis as second-line therapy when other treatments are ineffective.

Topical calcineurin inhibitors are non-steroidal immunomodulators and have a pronounced effect compared to placebo for both short-term and long-term use, and are especially indicated for use in problem areas (face, folds, anogenital area). Proactive therapy using tacrolimus ointment 2 times a week reduces the likelihood of exacerbation of the disease. Topical calcineurin inhibitors may be recommended to reduce pruritus in patients with AD.

Tacrolimus is used as 0.03% and 0.1% ointment in adults and 0.03% ointment in children.

Contraindications/restrictions to the use of topical calcineurin inhibitors:

hypersensitivity;
children's age (for pimecrolimus - up to 3 months, for tacrolimus - up to 2 years);
acute viral, bacterial and fungal skin infections;
Given the possible risk of increased systemic absorption of the drug, calcineurin inhibitors are not recommended for use in patients with Netherton's syndrome or atopic erythroderma;
It is not recommended to apply the vaccine to the area where the vaccine was administered until local manifestations of the post-vaccination reaction have completely disappeared.

Adverse reactions when using topical calcineurin inhibitors.

The most common adverse reactions are symptoms of skin irritation (burning and itching sensation, redness) at the application sites. These phenomena occur in the first days of treatment, 5 minutes after application, last up to 1 hour and, as a rule, significantly decrease or disappear by the end of the first week.

In patients using topical calcineurin inhibitors, sometimes (less than 1% of cases) there is a worsening of atopic dermatitis, the development of a viral (herpes simplex, molluscum contagiosum, papillomas) or bacterial infection (folliculitis, boils), as well as local reactions (pain, paresthesia, peeling, dryness).

Special situations

Pregnancy and lactation

There is insufficient data on the use of topical calcineurin inhibitors during pregnancy and lactation. Pimecrolimus is used with caution during these periods (completely excluding application to the mammary gland area during breastfeeding). Tacrolimus is currently not recommended during pregnancy and lactation.

Features of the use of topical calcineurin inhibitors in children.

According to the instructions for medical use registered in the Russian Federation, pimecrolimus can be prescribed to children from 3 months of age (in the USA and EU countries there is a limit of 2 years). Tacrolimus (0.03% ointment) is approved for use from 2 years of age.
Treatment with tacrolimus should be started by applying 0.03% ointment 2 times a day. The duration of treatment under this regimen should not exceed three weeks. Subsequently, the frequency of use is reduced to once a day, treatment continues until complete regression of the lesions.
If there is no positive dynamics within 14 days, a repeated consultation with a doctor is necessary to clarify further treatment tactics.
After 12 months of maintenance therapy (using tacrolimus twice a week), the drug should be temporarily discontinued and then the need for continued maintenance therapy should be considered.

Activated zinc pyrithione

Activated Zinc Pyrithione (0.2% aerosol, 0.2% cream and 1% shampoo)

Other external agents.

Currently, in the treatment of patients with atopic dermatitis, naphthalan, tar, and ichthyol preparations are used in various dosage forms: pastes, creams, ointments, which can be used in a hospital setting as symptomatic treatment. The concentration of the active substance depends on the severity and severity of the clinical manifestations of the disease. There is no evidence of the effectiveness of this group of drugs, and there is no information about the effectiveness of treatment.

Phototherapy.

Several methods of ultraviolet therapy (A) are used to treat atopic dermatitis:

narrowband mid-wave ultraviolet therapy 311 nm (UVB range, wavelength 310–315 nm with emission maximum 311 nm);
ultraviolet therapy of the far long-wave range (UVA-1 range, wavelength 340-400 nm);
selective phototherapy (broadband mid-wave ultraviolet therapy (UVB range with a wavelength of 280–320 nm).

Average doses of UVA-1 therapy are as effective as narrowband UVB(A). High doses of UVA1 are preferably used during exacerbation of AD

Phototherapy is carried out both in inpatient and outpatient settings as monotherapy or in combination with drug treatment.

All of these methods of ultraviolet therapy can be prescribed to adults; Children over 7 years of age may be prescribed narrowband phototherapy.

Before prescribing treatment, to identify contraindications, a clinical examination of the patient and a set of laboratory tests are carried out: a thorough history taking, clinical blood and urine tests, a biochemical blood test (including liver and kidney function indicators in the study), if indicated, a consultation with a therapist, ophthalmologist, endocrinologist, gynecologist and other specialists.
The initial radiation dose is prescribed based on the patient's individual sensitivity to phototherapy or depending on skin type (according to the Fitzpatrick classification).
In the progressive stage of the disease, phototherapy should be prescribed after the resolution of acute inflammatory phenomena, with caution increasing subsequent single doses.
When carrying out phototherapy, external agents should be used no later than 2 hours before and no earlier than 2-3 hours after the phototherapy procedure.
During the entire course of treatment, patients should avoid exposure to the sun and protect the skin of exposed areas of the body from sunlight with clothing or photoprotective cream.
During a phototherapy session, it is necessary to use photoprotective glasses with side protection, the use of which will avoid the development of keratitis, conjunctivitis and cataracts.
Lips, ears, nipples, as well as areas exposed to chronic sun exposure (face, neck, back of the hands), if there are no rashes on them, are recommended to be protected during procedures with clothing or photoprotective agents.
The use of photosensitizing drugs should be excluded or limited: tetracycline, griseofulvin, sulfonamides, thiazide diuretics, nalidixic acid, phenothiazines, coumarin anticoagulants, sulfonylurea derivatives, methylene blue, antibacterial and deodorizing agents, aromatic oils, etc.

Contraindications/limitations to the use of phototherapy:

intolerance to ultraviolet radiation;
the presence of photosensitive diseases: albinism, dermatomyositis, xeroderma pigmentosum, systemic lupus erythematosus, Gorlin syndrome, Bloom syndrome, Cockayne syndrome, trichothiodystrophy, porphyria, pemphigus, bullous pemphigoid;
a history or at the time of treatment of melanoma or other precancerous and cancerous skin diseases, dysplastic melanocytic nevi;
concomitant immunosuppressive therapy (including cyclosporine);
use of photosensitizing drugs and products (including food and cosmetics);
past treatment with arsenic or ionizing radiation;
concomitant diseases for which physiotherapy methods are contraindicated.

Adverse reactions when using phototherapy

The main early adverse reactions of phototherapy are: erythema of varying severity, itching, dryness and hyperpigmentation of the skin. Some other complications of phototherapy have been described (blistering rashes, folliculitis, keratitis, conjunctivitis, etc.), but in practice they are relatively rare.

Long-term side effects of phototherapy have not been fully established: long-term phototherapy can cause premature aging of the skin, information about the possibility of its carcinogenic effect is contradictory.

Systemic therapy.

Cyclosporine

Cyclosporine is prescribed for severe AD in adults.

Contraindications/restrictions for the use of cyclosporine

Hypersensitivity (including to polyoxyethylene castor oil), malignant neoplasms, precancerous skin diseases, pregnancy, lactation.

Adverse reactions when using cyclosporine

When treated with cyclosporine, the following may be observed: gingival hyperplasia, loss of appetite, nausea, vomiting, diarrhea, abdominal pain, hepatotoxicity (increased activity of transaminases, bilirubin), hyperlipidemia, increased blood pressure (often asymptomatic), nephropathy (often asymptomatic; interstitial fibrosis with glomerular atrophy, hematuria), hypomagnesemia, hyperkalemia, edema, hypertrichosis, tremor, headache, paresthesia, myopathy, increased feeling of fatigue, burning in the hands and feet, menstrual irregularities in women, anaphylactic reactions.

Due to the development of possible side effects, in particular nephrotoxicity, the use of cyclosporine should be limited in patients with severe concomitant diseases.

When treated with cyclosporine, the risk of developing lymphoproliferative diseases and other malignant tumors, especially of the skin, increases. The frequency of their development primarily depends on the degree and duration of concomitant and previous immunosuppression (for example, phototherapy).

Special situations

Features of use in children

Cyclosporine is rarely prescribed to children, in cases of severe atopic dermatitis and the ineffectiveness of other treatment methods.

Systemic glucocorticosteroid drugs.

Systemic glucocorticosteroid drugs are used in the treatment of patients with atopic dermatitis only to relieve exacerbations in severe cases of the disease in adults and extremely rarely in children. This prescribing tactic is associated, first of all, with the possibility of developing an exacerbation of the disease after discontinuation of the drug. Also, with long-term use of systemic glucocorticosteroid drugs, the likelihood of developing side effects increases.

Antihistamines.

The effectiveness of this group of drugs for AD is not high. The therapeutic value of first-generation antihistamines lies mainly in their sedative properties by normalizing night sleep and reducing the intensity of itching

Basic therapy

Basic therapy includes regular use of emollients and moisturizers, eliminating (if possible) the effects of provoking factors.

Training programs

They are highly effective and are conducted in many countries as part of the “Schools for Patients with Atopic Dermatitis”

Emollients/Moisturizers

Emollients exist in the form of lotions, creams, ointments, cleansers, and bath products. The specific drug and its dosage form are selected individually based on the patient’s preferences, individual skin characteristics, season, climatic conditions, and time of day. General recommendations for the use of moisturizers and emollients:

Side effects when using emollients are rare, but cases of contact dermatitis and occlusive folliculitis have been described. Some lotions and creams may be irritating due to the presence of preservatives, solvents and fragrances. Lotions containing water may cause dryness due to the effect of evaporation.

Elimination of provoking factors.
Elimination of house dust mites and mountain climate improve the condition of AD patients
Patients with AD should follow a diet that excludes those foods that cause an early or late clinical reaction in controlled challenge studies.

Treatment of atopic dermatitis complicated by secondary infection

Systemic antibacterial therapy is prescribed for widespread secondary infection of lesions in AD

Signs of a bacterial infection include:

the appearance of serous-purulent crusts, pustulization;
enlarged, painful lymph nodes;
sudden deterioration in the patient's general condition.

Antibacterial drugs for external use

Antibacterial drugs for external use are used to treat localized forms of secondary infection.

Topical combination preparations containing glucocorticosteroids in combination with antibacterial, antiseptic, and antifungal drugs can be used in short courses (usually within 1 week) if there are signs of secondary skin infection.

Antimicrobial drugs for external use are applied to the affected areas of the skin 1–4 times a day for up to 2 weeks, taking into account clinical manifestations.

In order to prevent and eliminate secondary infection at sites of excoriation and cracks, especially in children, aniline dyes are used: fucorcin, 1–2% aqueous solution of methylene blue (methylthioninium chloride).

Systemic antibacterial drugs

Indications for prescribing systemic antibacterial therapy:

increased body temperature;
regional lymphadenitis;
presence of an immunodeficiency state;
common forms of secondary infection.

General principles for prescribing systemic antibacterial therapy:

Systemic antibacterial drugs are used to treat recurrent or widespread bacterial infections.
Before prescribing systemic antibacterial drugs, it is recommended to conduct a microbiological study to identify the pathogen and determine sensitivity to antibacterial drugs.
Before receiving the results of a microbiological study, in most cases, treatment is started with broad-spectrum antibacterial drugs that are active against the most common pathogens, primarily S.aureus.
Inhibitor-protected penicillins, first or second generation cephalosporins, macrolides, and in adults - fluoroquinolones are used with high efficiency.
The duration of systemic antibiotic therapy is 7–10 days.
It is unacceptable to carry out maintenance therapy with systemic antibacterial drugs due to the possibility of development of resistance of microorganisms to antibacterial drugs.

Systemic antivirals

One of the severe and life-threatening complications of atopic dermatitis is the development of Kaposi's herpetic eczema when the skin is infected with herpes simplex virus type I, which requires the administration of systemic antiviral therapy using acyclovir or other antiviral drugs.

Features of therapy with systemic antiviral drugs in children

For the treatment of Kaposi's herpetic eczema in children, it is recommended to prescribe a systemic antiviral drug, acyclovir.
In the case of a disseminated process, accompanied by general symptoms (fever, severe intoxication), it is necessary to hospitalize the child in a hospital with a boxed ward. In a hospital setting, intravenous administration of acyclovir is recommended. External therapy consists of using antiseptics (fucorcin, 1% aqueous solution of methylene blue, etc.).
In case of eye damage, it is recommended to use acyclovir eye ointment, which is placed in the lower conjunctival sac 5 times a day. Treatment is continued for at least 3 days after symptoms have subsided.

Measures to prevent secondary infection:

avoid long-term use of antibacterial drugs for external use in order to avoid the development of bacterial resistance;
Avoid contamination of topical preparations:
tubes of ointments should not be stored open;
When applying creams, it is necessary to follow hygienic procedures - use clean sponges, remove cream residues from the surface of the jar.

Requirements for treatment results

clinical remission of the disease;
restoration of lost ability to work;
improving the quality of life of patients with AD.

Tactics in the absence of treatment effect

Additional examination to confirm the correctness of the diagnosis and identify the most significant trigger factors for the patient.

Prevention of atopic dermatitis

regular basic skin care;
elimination of provoking factors;
prescribing probiotics in addition to the main diet of mothers with a burdened allergic history (in the last weeks of pregnancy) and/or newborns at risk of developing atopy during the first months of life.

If you have any questions about this disease, please contact dermatovenerologist Adaev Kh.M:

Email: [email protected]

Instagram @dermatolog_95

For quotation: Butov Yu.S., Podolich O.A. Atopic dermatitis: issues of etiology, pathogenesis, methods of diagnosis, prevention and treatment // Breast cancer. 2002. No. 4. P. 176

General information

Atopic dermatitis (AD) is a common, persistent dermatosis, occupying 50-60% of the structure of allergic diseases, and this figure is steadily growing (Balabolkin I.I., Grebenyuk V.N., Williams H.C. et al. 1994) For the first time the term “ “atopic dermatitis” was proposed by Sulzbeger in 1923 for skin lesions accompanied by increased sensitivity to various allergens, manifested by instability of the cell membranes of skin vessels, combination with other atopic diseases (bronchial asthma, hay fever, rhinitis, etc.).

Currently, blood pressure is considered as independent nosological form , clearly different from contact allergic dermatitis, microbial and seborrheic eczema, limited neurodermatitis. AD occurs most often in early childhood against the background of exudative diathesis, eczematous process, often with complicated heredity due to poor nutrition, intoxication, metabolic disorders, disorders of the nervous and endocrine systems (hypofunction of the adrenal cortex, gonads, hyperfunction of the thyroid gland), but can also form in adulthood.

Leading signs of atopy are severe itching, chronic recurrent course, white dermographism, increased levels of IgE in the blood serum, a decrease in IgM and IgA, a sharp increase in IgG, indirectly indicating delayed-type hyperreactivity (Samsonov V.A. 1985, Suvorova K.N. 1998, Sanford A.J. 1995 ). The impact of unfavorable, exogenous (physical, chemical, biological) and endogenous (genetic predisposition, immune disorders) factors aggravate the clinical picture of the disease. However, the etiology remains unclear, the pathogenesis has not been fully studied, and a clear classification has not been developed.

Pathogenesis

Psychosomatic disorders play a certain role in the development of AD. Severe itching, irritability, restless shallow sleep, inappropriate reactions, white dermographism are classic manifestations of psychosomatic pathology. When assessing the psychosomatic status of patients, a high degree of anxiety, the development of reactive depression, and asthenovegetative syndrome were revealed. (Revyakina V.A., Ivanov O.L., Belousova T.A. 2000).

It has been shown that the main substrate in psychoneuroimmune interaction is neuropeptides (substance P, calcitonin gene-like peptide), which ensure the relationship between nerve fibers, mast cells and blood vessels. Under the influence of the “axon reflex,” vasodilation develops, manifested by erythema. Substance P ensures the release of histamine from skin mast cells and has a direct effect on blood vessels, increasing their permeability, which may explain the poor effectiveness, in some cases, of antihistamines. Thus, a direct relationship is visible between the central and autonomic parts of the nervous system. Improvement in psycho-emotional status under the influence of therapy was correlated with the positive dynamics of the skin process. (Ivanov O.L., Belousova T.A. 2000).

Hereditary predisposition in the pathogenesis of atopic dermatitis is confirmed by the high frequency of occurrence of the association of HLA antigens: A3, A9, B7.8, B12, B40. Clinical data also indicate the role of heredity in the transmission of pathological symptoms from parents to children. Thus, from an allergic father, signs of atopy develop in a child in 40 - 50% of cases, from a mother - in 60 - 70%. If both parents are carriers of atopy, then the incidence of the disease in the child reaches 80%. (Mazitov L.P. 2001).

Research by Toropova N.P. the possibility of transplantental transfer of ready-made antibodies from mother to fetus and its hypersensitization is shown, this apparently explains the development of allergic reactions to mother's milk in the first months of life. Such mothers are recommended to follow a strict diet, limiting the consumption of nitrogenous extractives, chlorides, and proteins.

A certain number of children develop latent sensitization, which manifests itself in the form of allergic reactions at the age of 19-20 years. It is not the disease that is inherited, but a set of genetic factors that contribute to the formation of an allergic factor in the body (Fedenko E.S. 2001).

The functional state of the gastrointestinal tract is of great importance in the formation of blood pressure. Dysfunction of the gastrin regulation link was revealed, consisting of imperfect parietal digestion, insufficient activity of enzymes in the processing of chyme, accumulation in the lumen of the small intestine of a huge amount of protein allergenic complexes, their free absorption and the creation of preconditions for sensitization and aggressive course of the skin process. (Toropova N.P., Sinyavskaya O.A. 1993).

The risk of developing food allergies increases due to non-compliance with the diet of a pregnant woman, children in the first months of life who are bottle-fed, as well as the use of food additives containing xenobiotics. Thus, in children of the first year of life, chicken eggs, cow's milk proteins, and cereals are common causes of AD. The course of AD is aggravated by the development of dysbiosis, due to the often uncontrolled use of antibiotics, corticosteroids, the presence of foci of chronic infection, allergic diseases (asthma, rhinitis), dysmetabolic nephropathies, and helminth infections. The waste products of the latter activate immunocompetent cells that carry out the synthesis of IgE and immune complexes.

In the development of exacerbation of blood pressure, inhaled allergens play an important role. The possibility of forming complex associations with bacterial, fungal, viral and drug allergens has been shown, causing the formation of polyvalent sensitization (Maksimova A.E. 1997).

According to Fedenko E.S. (2001) the causally significant allergen in the development of exacerbation of blood pressure are non-steroidal anti-inflammatory drugs, sulfonamides, B vitamins. We also observed the development of allergic reactions such as toxicoderma, urticaria, to B vitamins in patients with diffuse neurodermatitis, true eczema (Zheltakov M.M. ., Skripkin Yu.K., Somov B.A., Butov Yu.S. 1969).

Considerable attention has recently been paid to the polygenic type of inheritance, the characteristic features of which are immune disorders at the level of differentiation of the T-lymphocyte subpopulation. It has been established that null T helper cells (Th 0) under the influence of antigens differentiate into T helper cells of the first type (Th 1) or T helper cells of the second type (Th 2), which differ from each other in the secretion of cytokines, PGE. The first type controls apoptosis of mutated cells through a-TNF, and g-IFN inhibits the development of viruses. The second type provides protection against bacterial allergens and activates antibody formation due to IL-4, IL-5 and IL-13.

In AD, lymphocyte differentiation proceeds through Th2, activating b-cells and the synthesis of allergic IgE antibodies. The process of sensitization occurs with the participation of mast cells with the release of histamine, serotonin, kinins and other biologically active substances, which corresponds to the early phase of the hyperergic reaction. This is followed by an IgE-dependent late phase, characterized by infiltration of T-lymphocytes into the skin, determining the chronicity of the allergic process.

It has been shown that the development of the inflammatory process in patients with AD occurs in the presence of dendritic cells, Langerhans cells with a constantly high level of eosinophils, IgE, cytokines and mediators. The ability of eosinophils to live long and produce neurotoxins and enzymes in the tissue ensures a chronic process accompanied by severe itching, damage to keratinocytes and an even greater release of cytokines and inflammatory mediators, creating conditions for a “vicious circle”.

Thus, the analysis shows that exogenous (physical, chemical and biological) and endogenous (the role of the nervous system, gastrointestinal tract, genetic predisposition and immune disorders) factors take part in the development of AD.

Clinical aspects of blood pressure

Typical clinical picture of blood pressure characterized by: itching of the skin, persistent hyperemia or transient erythema, papulovesicular rashes, exudation, dry skin, peeling, excoriation, lichenification, widespread or limited in nature. The disease usually begins in the first months of life, then taking a recurrent course with the possibility of complete or incomplete remission of varying frequency and duration.

Atopic reactions in childhood occur:

often in the form of acute inflammatory exudative reactions;
localized on the face, in folds, outer surfaces of the limbs;
there is a clear relationship with nutritional factors;
followed by a chronic, wave-like course of inflammation, vegetative dystonia and lichenification.
At subsequent stages, patients develop:
persistent lechinization;
less significant reactions to allergenic stimuli;
less clear seasonality.

Possible clinical forms of manifestation:

Erythematous-squamous;

Vesiculocrustic;

Erythematous-squamous with weak or moderate lichenification in the elbow and popliteal folds;

Lichenoid with a large number of lichenoid papules;

Prurigo-like (Suvorova K.N. 1998).

Based on studies conducted in children with AD, Korotky N.G. identified a number of clinical and pathogenetic options for the development and course of the disease:

1. True, allergic variant AD with a predominance of a specific IgE-mediated immune mechanism

2. Mixed version of blood pressure , where both specific and nonspecific mechanisms are expressed.

3. Pseudo-allergic variant with a predominance of nonspecific mechanisms.

In true, allergic and mixed variants of AD, the severity of the process depends not only on skin damage, which may not always be significant, but also on other organ manifestations of atopy, in particular, bronchial asthma and gastrointestinal pathology. In the pseudoallergic variant of AD, the leading place in the development of the pathological process is given to neurovegetative and microcirculatory disorders.

Diet therapy

Due to severe dysfunction of the gastrointestinal tract, timely and adequately prescribed diet therapy, in most cases, promotes remission of the disease or even complete recovery. The elimination diet is based on the reliably proven sensitizing role of certain foods in the development of exacerbations of blood pressure and their exclusion.

From the diet of patients suffering from AD, products containing food additives (dyes, preservatives, emulsifiers), as well as strong meat broths, fried foods, spices, spicy, salted, smoked, canned foods, liver, fish, caviar, eggs are excluded. , cheeses, coffee, honey, chocolate and citrus fruits.

The diet should include fermented milk products, cereals (oatmeal, buckwheat, pearl barley), boiled vegetables and meat. The developed diets must be optimal in protein and vitamin content and are compiled in close cooperation with an allergist and nutritionist.

Drug therapy

When choosing a systemic drug, the patient’s age, period of illness, and the presence of concomitant diseases are taken into account.

In the treatment of blood pressure, to reduce neurotic reactions, it is prescribed with nutritional and psychotropic drugs . Among herbal preparations, it is preferable to use tincture of peony, motherwort and valerian root, novo-passit. Antidepressants are also used in therapy. Amitriptyline 0.025-0.05 g is prescribed orally; nialamide orally 0.025-0.01 g. Of tranquilizers used diazepam 0.005-0.015 g per day, lorazepam 0.001-0.0025 g per day.

Indications for use antihistamines justified by the critical role of histamine in the mechanism of skin itching and the development of inflammation in AD. Due to the presence of a sedative effect, 1st generation antihistamines are not advisable to prescribe to school-age children. For planned long-term use, it is more rational to choose any 2nd generation antihistamine (loratadine, terfenadine, cetirizine, ebastine). Ebastine (Kestin) does not cause pronounced anticholinergic and sedative effects, is prescribed in a daily dose of 10 mg, and if symptoms are severe, the dose can be increased to 20 mg. Cetirizine prescribed in tablets of 0.01 g for 7 days, at a rate of 0.25 mg/kg 1-2 times a day. 2nd generation drugs are currently not used in children under 2 years of age.

Diazolin, chloropyramine, clemastine It is preferable to use during periods of severe skin itching, for 7-15 days, if not only an antipruritic, but also a sedative effect is required. Cyproheptadine has antiserotonin activity, which expands the scope of its application. Clemastine from 6 to 12 years, 0.5 - 1.0 mg, over 12 years, 1 mg 2 times a day. Chloropyramine is prescribed to children under 1 year old, 6.25 mg (1/4 tablet), from 1 to 6 years old, 8.3 mg. (1/3 tablet), from 6 to 14 years, 12.5 mg. 2-3 times a day. In therapy, it is often necessary to combine the use of 1st and 2nd generation drugs.

Membrane stabilizing agents . From this group, they are used in the treatment of blood pressure. ketotifen And sodium cromoglycate . They stabilize mast cell membranes, antagonize H1-histamine receptors, inhibit the development of the allergic process and can act as a calcium channel blocker. The therapeutic effect appears after 2-4 weeks. Sodium cromoglycate additionally affects the gastrointestinal mucosa, preventing the development of allergic reactions at this level. The drug is prescribed in the acute and subacute period of blood pressure in combination with antihistamines. Children from 1 year to 3 years at a dose of 100 mg (1 capsule) 3-4 times a day; from 4 to 6 years - 100 mg 4 times a day; from 7 to 14 years - 200 mg 4 times a day. The duration of the course of therapy is on average from 1.5 to 6 months.

Suitable purpose drugs that improve digestion , to correct the breakdown of allergenic food substances (Festal, Mezim-Forte, Hilak-Forte).

Demonstrated effectiveness enzyme preparations , taking into account violations of the enzyme systems of the gastrointestinal tract in patients. (Korotky N.G. 2000). Dysbacteriosis is an indication for the full use of probiotics, which normalize the microbial landscape of the intestine.

Increasing the effectiveness of treatment is facilitated by prescribing vitamin preparations . Of the B vitamins, preference is given to calcium pantothenate (B 15), which is prescribed at 0.05-0.1 g 2 times a day for a month, and pyridoxal phosphate (B 6), which is prescribed at 0.1-0.2 g per day. It is advisable to administer b-carotene; it increases the resistance of lysosome and mitochondrial membranes to the action of metabolic toxins, stimulates the immune system and regulates lipid peroxidation.

Immunomodulatory therapy is carried out in cases where blood pressure occurs in combination with clinical signs of immunological deficiency and the presence of defects in the immunogram. In the form of a decrease in the B-cell level, phagocytic cells, an increase in IgE, an imbalance of Th 1 -Th 2 cells. Clinical signs include: the presence of foci of pyogenic infection; frequent exacerbations of the skin process; frequent acute respiratory viral infections with low-grade fever and lymphadenopathy; lack of clinical effect from adequate standard therapy for blood pressure.

Application systemic antibiotics appropriate for low-grade fever and lymphadenitis. With preliminary determination of microflora sensitivity to antibiotics. In empirical therapy, preference is given to the use of macrolides and 2-3rd generation cephalosporins.

Systemic glucocorticosteroids (GCS) are most often prescribed in particularly severe, persistent cases of blood pressure, used in a hospital setting and in short courses under the cover of antacid drugs (Almagel) and calcium supplements (calcium gluconate, calcium glycerophosphate). Prednisolone and dexamethasone 20-25 mg per day are used; adults are prescribed betamethasone injections. The mechanism of the anti-inflammatory activity of GCS is to block the activity of phospholipase A, inhibit the synthesis of leukotrienes and prostaglandins, reduce the activity of hyaluronidase and lysosomal enzymes, and activate the synthesis of histaminase (Grebenyuk V.N., Balabolkin I.I. 1998).

External therapy is an integral part of the complex treatment of blood pressure, occupying a leading place in it. With the help of local treatment, a number of effects are achieved: suppression of signs of skin inflammation; eliminating dryness; restoration of damaged epithelium; improving skin barrier functions.

The choice of drug is determined by the stage of the disease, the phase of inflammation and the severity of skin manifestations. In order to achieve success, it is necessary to follow a certain sequence in the administration of local treatment. For acute weeping processes, lotions and dermatological pastes are used. As the inflammation subsides, non-fluorinated corticosteroids are prescribed in the form of a cream or ointment. Ointments have a more pronounced anti-inflammatory effect and are prescribed for the treatment of subacute and chronic skin lesions. Creams are the form of choice for acute processes.

In cases of pyoderma, erythromycin, lincomycin, geoxyzone ointments, and aniline dyes are prescribed. Among other anti-inflammatory drugs that have long been used in the treatment of blood pressure, one should mention products containing tar, naphthalan, and sulfur.

Forecast The course of blood pressure and the quality of life of the patient and his family largely depend on the reliable knowledge he has received about the causes of the development of skin rashes, itching, and on the careful implementation of all doctor’s recommendations and prevention.

Main directions prevention - this is compliance with the diet, especially for pregnant and nursing mothers, breastfeeding children. Particular attention should be paid to limiting exposure to inhalant allergens, reducing exposure to household chemicals, preventing colds and infectious diseases, and prescribing antibiotics accordingly.

Literature:

1. Balabolkin I.I., Grebenyuk V.N., Williams H.C. et al.

2. Vorontsov I.M. Atopic dermatitis in children. M.-p.263.

3. Grebenyuk V.N. Balabolkin I.I. Progress of external corticosteroid therapy for AD//Pediatrics -1998. No. 5 p.88-91.

4. Zheltakov M.M. Skripkin Yu.K. Somov B.A. Butov Yu.S. Allergic reactions caused by B vitamins. VDV 1969, No. 1, p. 62-65

5. Korotky N.G. Pathogenetic role of disturbances in hormonal regulation of cavity digestion and absorption in hypertension and correction with enzyme preparations. Russian Journal of Skin and Venereal Diseases. 2000 - No. 1 - pp. 12-17.

6. Yazdovsky V.V. HLA and allergic diseases. Pulmonology 1994, 4, 6-9.

7. Maksimova A.E. Features of skin microflora in patients with AD. Author. diss. Ph.D. 1997.

8. Mazitov L.P. Modern aspects of pathogenesis and treatment of allergic dermatoses in children. Russian medical journal 2001 v.9. No. 11 p. 457-459.

9. Naumov Yu.N., Kotenkov V.I., Alekseev L.P. Structure of human HLA genes and antigens of classes 1-2./ Immunology 1994,2,4-8.

10. Revyakina V.A. The role of etiologically significant allergens in the development of AD in children // Allergology-1998 No. 4 p. 13-14.

12. Samsonov V.A. Neurodermatitis and bacterial allergies. Abstract. Doctor of Medical Sciences M. 1984.

13. Skripkin Yu.K. Somov B.A. Butov Yu.S. Allergic dermatoses. M.1975. 234 p.

14. Smirnova G.I. Allergic dermatoses in children//M.BUK, ltd. 1998, p.299.

15. Suvorova K.N. Atopic dermatitis: immunopathogenesis and immunotherapy strategy. Russian honey magazine. 1998, vol.6, 368-367.

16. Toropova N.P. Sinyavskaya O.A. Eczema and neurodermatitis in children. Ekaterenburg. 1993, 147 p.

17. Fedenko E.S. - Atopic dermatitis: Rationale for a step-by-step approach to therapy. Consilium medicum 2001 vol.3 no.4 p.176-183.

18. Khaitov R.M., Luss L.V., Aripova T.U. Prevalence of symptoms of asthma, AR and AD in children. /Allergy, asthma and clinical immunology. - 1998. - No. 9. - pp. 58-69.

19. Leung D.Y.M. Role of IgE in atopic dermatitis//Curr. Opinion Immunol-1993-Vol.5-P.956.

20. Sanford A.J. “Genetic map of cromosome llg, including the atopy locus. Eur Hum Genet 1995, no. 3 p. 188.

21. Casale T.B., Bowman S. Induction of human cutaneous mast cell degranulation by opiates peptides//Immunol-1984-Vol.73.

Atopic dermatitis (AD) - chronic allergic skin disease, which develops in individuals with a genetic predisposition to atopy.

A recurrent course is characterized by exudative and/or lichenoid rashes, increased serum IgE levels and hypersensitivity to specific and nonspecific irritants.

Etiology. 1) heredity

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

3) non-allergenic causative (psycho-emotional stress; changes in weather conditions; 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 R for the IgE molecule. → Upon contact with antigen → move to the distal and proximal 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 degranulation of the mast cell and the development of the immediate phase of the allergic reaction. This is followed by an IgE-dependent late phase of the reaction, characterized by tissue infiltration by lymphocytes, eosinophils, mast cells, neutrophils, and macrophages.

Further, the inflammatory process becomes chronic. Itching of the skin, which is a constant symptom of AD, leads to the formation of an itch-scratch 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 superantigen toxins that stimulate T cells and macrophages. About half of children with AD produce IgE antibodies to staphylococcal toxins.

Clinical picture. Various manifestations - papules, small epidermal vesicles, erythematous macules, desquamation, scabs, fissures, erosions and lichenification. A characteristic sign is severe itching.

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

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

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

U young people - neck, dorsum of hands.

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

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

AD is often complicated by secondary bacterial (staphylo and streptococcus) infections.

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

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

3) Prick test or skin prick tests

4) in vitro diagnostics.

5) elimination-provocative tests with food products.

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, xidifon, antioxidants, nalcrom. Vitamins)

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

→ herbal medicine (licorice root, which stimulates adrenal function and its drug glycyram, etc.).

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

→For severe pyoderma → antibacterial therapy(macrolides, 1st and 2nd generation cephalosporins, lincomycin.)

4) External therapy:

→ The child’s fingernails should be cut short,

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

→ For 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 disease of heterogeneous origin caused by the accumulation of triglycerides in fat cells and manifested by excess fat deposition. Frequency - 5%, occurs more often in girls.

Etiology and pathogenesis. Excess fat storage occurs as a result of a discrepancy between the balance of food intake and energy expenditure in the direction of predominance of the former. Predisposition factors are innately responsible for an increase in the content of fat cells (adipocytes) in the body, features of fat metabolism with a predominance of the processes of lipogenesis over lipolysis; endocrine disorders (hypothyroidism, hypogonadism, hypercortisolism, etc.); damage to the hypothalamus (birth trauma, infections, cerebral hypoxia, etc.).

Clinic. Obesity is an excess of body weight exceeding 10% of the body weight; the excess is caused by the fat component of the soma, and not by the muscle and bone components. To more accurately assess the degree of excess adipose tissue in the body, skin folds are measured with a caliper.

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

Treatment of 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 severe obesity - by 45-50%, the energy content of food is reduced 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 student suffering from severe obesity is usually about 500 kcal. Physical therapy and the patient’s psychological attitude (motivation) are of great importance.

Prevention. A rational daily regimen and nutrition for a pregnant woman, as well as at an early age for a child, are of great importance in the prevention of simple forms 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 latter’s body, which creates prerequisites for his further development of obesity.

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 volume of blood below 110 g / l for young children and 120 g / l for preschool and older children.

Classification of anemia.

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

II. Posthemorrhagic anemia 1. Acute; 2. Chronic

III. Hypo- and aplastic anemia A. Congenital forms 1. With damage to erythro-, leuko-, and thrombocytopoiesis: a) with congenital developmental anomalies (Fanconi type); b) without congenital anomalies (Estren-Dameshek type); 2. With partial damage to hematopoiesis: a) selective erythroid dysplasia (Blackpham-Diamond type) B. Acquired forms 1. With damage to 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 anemia

A. Hereditary 1. Membranopathy (microspherocytosis, elliptocytosis, stomatocytosis, paroxysmal nocturnal hemoglobinuria); 2. Enzymopathies (disorders of the glycolytic pathway, pentose phosphate cycle, nucleotide metabolism); 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, hapten medications); 2. Infectious (cytomegalovirus and other viral, bacterial); 3. Toxic (caused by heavy metal poisoning); 4. Caused by increased destruction of red blood cells (with hypersplenism, microangiopathy); 5. DIC syndrome.

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

Iron deficiency anemia, sideroblastic anemia (chronic infections, systemic and oncological diseases), and hemoglobinopathies usually occur with hypochromia and microcytosis. 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 anemia 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 and is 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 demand for it in increasing blood volume and red blood cell mass exceeds dietary 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, so exclusive breastfeeding (without timely introduction of complementary foods) cannot fully meet the iron needs of a growing body.

The main predisposing factors:) nutritional deficiency of iron (with untimely introduction of complementary foods, improper feeding);) insufficient supply (prematurity, multiple pregnancies, maternal anemia during pregnancy); 3) iron absorption disorders (dyspepsia, intestinal infections, chronic diseases); 4) increased iron loss (blood loss, helminthiasis); 5) increased needs for iron (frequent infectious diseases).

Hemolytic anemia. Hemolytic anemia is characterized by a reduction in the lifespan of erythrocytes, indirect hyperbilirubinemia, and activation of erythropoiesis, manifested by reticulocytosis. The consequence of compensatory bone marrow hyperplasia is skeletal changes.

Classification. A. Hereditary 1. Membranopathies (microspherocytosis, elliptocytosis, stomatocytosis, paroxysmal nocturnal hemoglobinuria); 2. Enzymopathies (disorders of the glycolytic pathway, pentose phosphate cycle, nucleotide metabolism); 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, hapten medications); 2. Infectious (cytomegalovirus and other viral, bacterial); 3. Toxic (caused by heavy metal poisoning); 4. Caused by increased destruction of red blood cells (with hypersplenism, microangiopathy); 5. DIC syndrome.

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

Specific to the damage to 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 severe vitamin D deficiency occurs in an adult, only signs of osteomalacia (demineralization of bone without structural restructuring) and osteoporosis (demineralization of bone with restructuring of its structure) appear in his skeletal system. In this regard, the clinical manifestations of hypovitaminosis D in an adult patient are called osteomalacia.

Etiology.

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

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

1. exogenous rickets: insufficient solar insolation.

2. nutritional factor:

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

Lack of specific prevention of rickets;

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

3. endogenous rickets:

Maldigestion and malabsorption syndrome (malabsorption of vitamin 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 diseases, with involvement of the tubulointerstitium (impaired hydroxylation, decreased reabsorption of minerals).

Massive protein loss syndrome (exudative enteropathy, nephrotic syndrome, burn disease) is eliminated by a-globulin carriers together with active metabolites D.

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

Pathogenesis. The pathogenesis of vitamin D deficiency rickets can be presented in the form of a simplified diagram: 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) → act of rachitic process.

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 the diagnosis and a transformation of medical vocabulary. The main goal of changing terminology is to unite and coordinate the efforts of doctors of various specialties supervising 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 life, sequentially or simultaneously. However, we must admit that we are still only on the way to a coordinated treatment of atopic dermatitis, to the formation of an interdisciplinary approach to solving this problem. That is why it seems relevant to summarize the available theoretical information on the etiopathogenesis of dermatosis, comprehend the experience and assess 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 relapsing course.

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

Atopic dermatitis is one of the most common diseases found in all countries, in people of both sexes and in different age groups. According to numerous authors, the incidence varies from 6 to 20% per 1000 population; Women are more likely to get sick (65%), men are less likely to get sick (35%). The incidence of atopic dermatitis in residents of megacities is higher than in 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 inheritance is polygenic in nature with the presence of a leading gene that determines skin damage 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 have the disease, and in 56% when only one parent is sick, with the risk increasing if the mother is sick. In patients with atopic dermatitis, up to 28% of relatives suffer from atopy of the respiratory tract. 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 implementation 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 (morphofunctional characteristics of the gastrointestinal tract, nervous, endocrine, immune systems).

Among the exogenous factors that have a provoking effect on the occurrence and development of the skin process in persons with a genetic predisposition, the most important are food products, inhalation allergens, external irritants of a physical nature, animal and plant origin, stress factors, meteorological influences, and insolation.

The trigger for the development of atopic dermatitis is most likely food allergy, which manifests itself in early childhood. Food proteins of both plant and animal origin are foreign to the human immune system. Proteins supplied with food are broken down in the human gastrointestinal tract into polypeptides and amino acids. Polypeptides partially retain immunogenicity and are able to stimulate the immune system. They are the triggers of allergies in childhood. In some cases, food allergies manifest as rare episodes of skin rashes. For many children, this process resolves without outside intervention; only in some young patients the process becomes chronic.

The pathogenesis of atopic dermatitis is based on chronic allergic inflammation of the skin. Immune disorders play a leading role in the development of the disease.

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 total and specific immunoglobulins (Ig) E in response to the action of environmental allergens.

The leading immunopathological mechanism is a biphasic change in T helper cells (Th 1 and Th 2). In the acute phase, Th 2 activation occurs, leading to the formation of IgE antibodies. The chronic phase of the disease is characterized by a predominance of Th1.

The role of the immune trigger is the interaction of allergens with IgE antibodies (reagins) on the surface of mast cells and basophils. Research has proven the existence of two genes related to the main immunological abnormality of atopy - the formation of IgE in response to environmental allergens.

However, as some authors believe, it is unlikely that such a chronic relapsing disease as atopic dermatitis is only the result of the presence of an abnormal IgE response to environmental 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 strong atopenia-directed immune reactions occur in the affected skin, partially mediated by Th 2 (in the early stages) and Th 1 cells (in the later stages, a complex interaction of cells is observed: keratinocytes, endothelial, mast, eosinophilic granulocytes).

Already existing allergic inflammation is maintained due to the release of inflammatory mediators (histamine, neuropeptides, cytokines). The question currently facing researchers in the pathogenesis of atopic dermatitis is: are 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 with a normal IgE level; for the second - high and medium IgE content against the background of a normal number of CD4 + - and CD8 + - lymphocytes; for the third - variability in 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 trigger mechanisms that initiate and maintain chronic skin damage and inflammation, colonization with S. aureus is considered 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 atopic dermatitis depends on the presence of staphylococcal enterotoxins in the skin. S. aureus enterotoxins were found in the culture media of 75% of strains isolated from the skin of patients with atopic dermatitis. Enterotoxins are capable of inducing the production of IgE antibodies specific to them. In 57% of patients with atopic dermatitis, IgE antibodies to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB) and toxic shock syndrome toxin (TSST-1) were detected in the blood serum.

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

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 through the induction of allergen-specific IgE, the development of sensitization and additional activation of dermal lymphocytes.

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

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

1. Staged course and division by age periods:

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

In practice, for the first period, the conditional term “exudative diathesis” is most often used as a diagnosis; for the second period, the term “childhood eczema” is more appropriate, and only in the third period does the disease acquire the typical features of “atopic dermatitis”.

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

3. Clinical forms:

erythematous-squamous;
vesiculocrustosis;
erythematous-squamous with moderate lichenification;
lichenoid with pronounced lichenification (true Besnier prurigo);
prurigiform.

From a clinical point of view, the classic course of atopic dermatitis is distinguished by a number of patterns. Thus, starting, as a rule, in early childhood, the disease proceeds for many years with alternating relapses and remissions, varying in duration and intensity of symptoms. Over time, the severity of the disease weakens, and at the age of 30-40 years, most patients experience spontaneous recovery or significant regression of symptoms. Clinical and statistical studies show that the diagnosis of atopic dermatitis in people over 40-45 years of age 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 the localization of lesions and the ratio of exudative and lichenoid elements of the rash. Itching is a constant symptom, regardless of age.

A feature of the first age period is the predominance of exudative acute and subacute inflammatory rashes localized on the face, flexor and extensor surfaces of the extremities.

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

In the second age period, the process is of the nature of chronic inflammation, inflammatory and exudative phenomena are less pronounced. Skin manifestations include erythema, papules, desquamation, infiltration, lichenification, multiple fissures and excoriations. After the rash resolves, areas of hypo- and hyperpigmentation remain. An additional fold of the lower eyelid is formed (Denny-Morgan sign).

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

The pathomorphosis of the disease is pronounced. 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; a more severe course with an increase in the area of skin damage up to the development of erythroderma; an increase in cases of transition of acute forms into chronic, often severe, against the background of an increase in primary chronic pathology of internal organs, severe disorders of the nervous system, and immunity disorders; an increase in the number of patients with a treatment-resistant course; early disability. The number of patients with the formation of respiratory atopy (allergic rhinitis, atopic bronchial asthma) and skin and respiratory manifestations of allergies (dermorespiratory syndrome) has increased, i.e., an “atopic march” is noted (the progression of allergic pathology from skin to respiratory symptoms).

Severe forms of atopic dermatitis are characterized by the following clinical changes: “multi-colored” coloration of the skin of the body with a brownish-brown tint, a grayish-icteric component, wavy hypo- and hyperpigmentation of the skin of the neck, “marbled” whiteness of the skin of the nose, punctate keratosis pilaris, “marbling” of the skin limbs. The severity of the listed symptoms correlates depending on the severity 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 the lack of 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 over-the-counter pharmacological drugs on our market.

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

Observations show that in case of drug intolerance in patients with atopic dermatitis, the causal 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 the combination of various signs 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:

“flexor” or “folded” lichenification in adults, damage to the face and extensor surfaces of the limbs in infants,
onset at an early age
seasonality.

Auxiliary signs:

To establish a diagnosis of atopic dermatitis, the presence of all four mandatory signs and three or four auxiliary signs is necessary.

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 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 - prevalence of skin lesions,

B - intensity of clinical manifestations,

C - subjective symptoms.

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 extremities - 9%, lower extremities - 18%, perineal area and genitals - 1%.

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

The severity of each sign is assessed from 0 to 3 points: 0 - absent, 1 - mildly expressed, 2 - moderately expressed, 3 - severely expressed.

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

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

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

The clinical course of atopic dermatitis is distinguished by true polymorphism of rashes, a combination of clinical forms, even “invisible”.

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

The lichenoid form is distinguished by dry, erythematous skin with an exaggerated pattern, edematous, infiltrated. Against the background of erythema, there are large, slightly shiny papules, 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 becomes widespread and a secondary infection occurs, which causes regional lymphadenitis. With this form, erythroderma often occurs.

The pruriginous form is characterized by scattered excoriations, 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”, infiltrates, crusts, and 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 the period of 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 body is covered with shiny, flesh-colored follicular papules. Horny papules are identified on the extensor surfaces of the upper extremities in the elbow bends. At older ages, skin dyschromia is noted. Often, patients have whitish spots on the skin in the cheek area, as well as folding of the skin on the front surface of the neck, reticular pigmentation - a symptom of a “dirty neck”.

During the period of remission, minimal manifestations may be slightly flaky spots or cracks in the area of attachment of the earlobe, cheilitis, recurrent seizures, a median fissure of the lower lip, erythematous-squamous lesions of the upper eyelids. Knowledge of these symptoms allows for 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, it should be noted white dermographism, which is an almost constant characteristic of the functional state of skin vessels in atopic dermatitis and is most pronounced during exacerbation. In some patients, during the period of remission, it may become pink, which is often used by doctors as a prognostic sign.

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

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

Seborrheic dermatitis is characterized by the presence of lesions with clear boundaries in places where sebaceous glands accumulate - “seborrheic zones” (forehead, face, nose, nasolabial fold, chest, back). The erythema is slightly expressed, the scales are yellowish. There is no seasonality of the disease and no increase in the concentration of IgE in the blood serum.

With scabies, multiple itchy papules, scabies burrows, excoriations, crusts, and a characteristic “night itch” are detected simultaneously in several family members. However, the presence of atopic dermatitis does not exclude the possibility of simultaneous infection with scabies.

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

Limited neurodermatitis occurs more often in adolescence and in adults without an atopic history and previous childhood phases. The lesions are most often located on the back and lateral surfaces of the neck and are in the nature of single asymmetrical foci of lichenification. 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 weeping in the lesions, the clinical picture may resemble widespread eczema. A correctly collected anamnesis, revealing the onset of the disease in early childhood, family predisposition, typical sites of localization, white dermographism, allows for differential diagnosis.

Persistent widespread painful itching with no less common moderately severe lichenification in people over 50 years of age may constitute the debut of T-cell lymphoma. The patient’s age, the absence of previous typical signs of atopic dermatitis, and histological examination allow the diagnosis to be verified.

Dühring's disease is characterized by predominantly vesicular, papular, urticarial rashes, localized in groups on the extensor surfaces of the extremities. There is gluten intolerance, eosinophilia in the blood and the contents of the vesicle, determination of IgA in an immunological study.

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

The main goals of organizing treatment for 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 of the state of allergic inflammation (basic therapy);
correction of immune disorders.

It is advisable to begin 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 intolerant foods from the patient’s diet, as well as histamine-releasing foods, is the basis for the 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 eat canned food, smoked meats, fried foods, coffee, chocolate, honey, nuts, and limit the amount of sweets. The basis of the diet should be vegetables, dairy products, cereal dishes, and boiled meat. Equally important is 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 dust separation in a water suspension. Of great importance are 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. First of all, we are talking about diseases of the gastrointestinal tract and ENT organs. Treatment of patients by appropriate specialists significantly improves the quality of dermatological treatment.

The prescription of therapy must be approached differentially, taking into account age, period, severity of the disease, severity of the inflammatory reaction, extent of the lesion and associated complications due to local infection.

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

The statement that therapy for atopic dermatitis remains predominantly local using topical agents is difficult to refute. This approach, formulated decades ago, is still relevant today. At the same time, the arsenal of means and possibilities of external therapy have undergone significant changes for the better: new classes of external drugs - immunosuppressants - have appeared, the arsenal of glucocorticosteroid (GCS) agents for external use has expanded; qualitative changes have occurred 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 action of external corticosteroids (gradations divided into weak, medium, strong).

Thus, weak drugs are prescribed when the rash is localized on the face or in the folds, when treating children; medications of moderate strength - for localization of rashes in different parts of the body; strong corticosteroids - during lichenification, a chronic inflammatory process.

With regard to the strength of the action of GCS, it can be noted that the principle of correspondence “strength of GCS - localization of the rash” is largely determined by the likelihood of a side effect.

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

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

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

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

In this case, it is necessary to take into account the minimum age from which the use of local corticosteroids is permitted: Advantan, Afloderm, Lokoid - from 6 months; elocom - from 2 years old.

Adults with pronounced skin changes often apply strong corticosteroids to the affected areas for a short period of time (2-4 days) and quickly switch to medium-strength drugs (Elocom, 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 combination drugs containing components with anti-inflammatory, antibacterial and antifungal effects. The most optimal in this situation is the use of combination drugs: triderm, acriderm, acriderm genta, hyoxyzone, oxycyclosol, oxycort ointment, aerosol, fucicort, fucidin G.

When prescribing general therapy, the leading role is given to antihistamines, which are prescribed in 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 mast cell membranes, has been noted. It should be noted that first-generation antihistamines must be prescribed sequentially, alternating the drug used every 7-10 days. Convenient for practical use are Zyrtec and Kestin, which have a prolonged effect, allowing for one-time daily use.

Pharmacotherapy of moderate atopic dermatitis involves the administration of desloratadine 0.005 g orally for up to 1.5 months, loratadine 0.01 g once a 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. 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) is possible.

Intravenous administration of sodium thiosulfate (30% solution, 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 each) is indicated. ml 2-3 times a week, No. 4-7).

An important role is given to sedative and psychotropic drugs, which are prescribed in courses of 2-4 weeks (tincture of peony, motherwort, valerian root, persen, relanium, phenazepam, mezapam). 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 prescription of other vitamin preparations must be approached with caution, since patients with atopic dermatitis often experience hypersensitivity to certain vitamins, especially group B.

In severe, persistent cases, with erythrodermic forms of atopic dermatitis, there is a need for systemic use of GCS. Prednisolone, dexamethasone, methylprednisolone are prescribed in average 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 administration of GCS in increased doses determines the need for corrective therapy (potassium supplements, antacids, anabolic steroids).

In the torpid course of atopic dermatitis, cyclosporine is prescribed in the form of capsules or solution at a maximum dose of 5 mg/kg body weight per day, followed by its reduction to the minimum maintenance dose. It must be taken into account that if there is no effect after using the maximum dose of the drug for 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 for severe atopic dermatitis.

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

Of the physical methods of treatment, phototherapy with ultraviolet rays is the most widely used. Courses of ultraviolet irradiation of varying duration (depending on indications) with a conventional quartz lamp, PUVA therapy or selective phototherapy significantly suppress the processes of immune inflammation in the skin and reduce itching. We should not forget that natural sunlight itself has an excellent therapeutic effect against atopic dermatitis, making patients feel much better in the summer.

Electrotherapy methods include galvanization, electrosleep, and darsonvalization. They improve the function of skin blood vessels, 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 treatment of atopic dermatitis is occupied by laser therapy (in the case of significant lichenification of lesions, contributing to their accelerated resolution) and reflexology (acoustic, laser and electropuncture).

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

Determining the prognosis for 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, clinical signs of the disease disappear by the age of 15; in the rest (45-60%), they can persist throughout life.

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 maintenance therapy (restoration of the damaged lipid layer, corneotherapy). Hygienic (daily) care products also play an important role. Recently, in addition to lanolin-based creams traditionally used for atopic dermatitis with the addition of salicylic acid and urea, new generation preparations for permanent use have appeared - products based on thermal waters of various foreign dermatocosmetic lines, among which the medicinal cosmetics of the Aven Dermatological Laboratories (Pierre concern) stand out Fabre, France). All products produced by these laboratories contain Aven thermal water.

Thermal water "Aven" has a neutral pH, is slightly mineralized, contains a wide range of microelements (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 sulfides and thiosulfates, and is completely free of hydrogen sulfide. It is distinguished by the balance of cationic (Ca 2+ /Mg 2+) and anionic (C l- /SO4 2-) components.

Numerous scientific research studies have proven the anti-inflammatory, trophic, antipruritic, softening, and irritation-reducing effects of 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, cause an increase in the synthesis of interferon γ, and the production of interleukin-4 has been proven.

Among the therapeutic care products, the Tolerance Extreme cream stands out, which contains, along with 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 product relieves skin irritation and improves the tolerability of drug treatment. The cream is applied to cleansed skin (usually the face) twice a day (1 mini-dose for 3 days).

The TriXera line contains ingredients to control the three main symptoms of atopic dermatitis - xerosis (lipid trio), inflammation (Aven thermal water) and skin itching (glycocol). The TriKzera cream contains Aven thermal water, ceramides, essential fatty acids (linoleic, linolenic), plant sterols, glycerin, glycol. The active components of the cream contribute to the rapid restoration of the structure of the damaged epidermis and, as a result, the barrier function of the skin; inhibit peroxidation processes, providing a protective effect on the cell membranes of epidermocytes. The cream intensively softens and moisturizes the skin and has an antipruritic effect. TriXera is applied to cleansed skin at least 2 times a day. The softening effect of the TriKzera cream is enhanced by the TriKzera softening bath - a balanced emulsion - water / oil / water, containing the same main active ingredients. "TriKzera softening bath" protects against 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 helped by a line with Cold Cream. Cold cream contains Aven thermal water, white beeswax, paraffin oil. Cold cream reduces skin sensitivity, restores 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 body emulsion with cold cream contains Aven thermal water, sesame oil, cartama oil, coconut oil, and allantoin. Thanks to its light texture, “Body Emulsion with Cold Cream” is well distributed and absorbed, convenient for application to large surfaces of the skin. Apply 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, by carefully cleansing the skin, moisturize and soften it, returning a feeling of comfort.

Among the therapeutic and hygienic care products that improve the quality of life of patients with atopic dermatitis, we can note the Lipikar series (Surgra, Syndet, bath oil, balm, emulsion), Hydranorm and Ceralip creams. In the A-Derma line, the Egzomega series (cream, milk) based on realba oats is popular. If there are areas of weeping, it is recommended to use a product from the Bioderma line - Atoderm R.O. Zinc cream.

To reduce overall dryness (xerosis) of the skin and hygienic care, “Balneum Hermal” bath oil 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 product for eliminating dry skin - cream-foam "Allpresan" - 1, 2, 3.

Caring for the skin of the scalp also requires attention, and the use of ointments and creams is excluded. It is considered traditional to prescribe steroid-containing lotions (“Belosalik”, “Diprosalik”, “Elokom”), and shampoos of the “Friderm” series (with zinc, neutral tar).

During the period of remission, the use of healing shampoos “Elusion”, “Extra-du”, “Selezhel”, “Kertiol”, “Kertiol S”, “Kelual DS” (Ducret Laboratory) is recommended as a means of hygienic care for the scalp.

In complex care, it is advisable to use the nourishing mask “Lactocerate” 1-2 times a week, “Lactocerate - nourishing and restorative shampoo” and a protective spray.

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

During periods of solar activity, it is advisable to use photoprotective products from the “Photoscreen” series (cream, milk, spray, gel cream), Antihelios.

Thus, the modern arsenal of means of different nature and direction of action allows for 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 the patient. By combining the joint efforts of various specialists, long-known methods and new approaches to the treatment of patients, by positively changing the patient’s mood, 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., Kondurina E. G. Parlazin in the treatment of atopic dermatitis in children // Issues of modern pediatrics. 2005. T. 4. No. 2. P. 109-112.
Kudryavtseva E.V., Karaulov A.V. Lokoid and modern approaches to external therapy of atopic dermatitis // Immunology, allergology, infectology. 2003. No. 4. P. 57-62.<
Fedenko E. S. Atopic dermatitis: rationale for a step-by-step approach to therapy // Consilium medicum. 2001. T. 3. No. 4. P. 176-183.
Atopic dermatitis: recommendations for practicing physicians / under general. ed. R. M. Khaitov and A. A. Kubanova. M., 2003.
Kochergin N. G., Potekaev I. S. Cyclosporin A for atopic dermatitis (mechanisms of immunosuppression and clinical effectiveness). M., 1999.
Pytsky V. I., Adrianova N. V., Artomasova A. R. Allergic diseases. M., 1999. 470 p.
Suvorova K. N., Antonev A. A., Dovzhansky S. I., Pisarenko M. F. Atopic dermatitis. Saratov: Saratov University Publishing House, 1989.
Kochergin N. G. Atopic dermatitis // Russian Journal of Skin and Venereal Diseases. 1998. No. 5. P. 59-65.

E. N. Volkova, Doctor of Medical Sciences, Professor
RGMU, Moscow

Details

Atopic dermatitis (atopic eczema, constitutional eczema) - hereditary allergic dermatosis with a chronic recurrent course, manifested by an itchy erythematous-papular rash with symptoms of skin lichenification. 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 - genet predisposition (atopy) to allergies, hyperreactive status with a tendency of blood vessels to vasoconstriction, hyperimmunoglobulinemia £ (e-atopy) with a tendency to immunodeficiency, inheritance of neurohumor regulation disorder (decreased adrenoreception), genet determinant of enzymeopathy. He showed concern in children about the effects of intoxication, toxicosis and poor nutrition of the mother during breastfeeding and lactation, and the art of feeding the child. + tank, virus or fungus info, food, everyday life and production allergens, psycho-emotional stress, + meteorologist factors (changes in t, lack of insolation).

PG: decrease in suppressor and killer activity of the T-immune system, imbalance of Ig serum production, à stimulation of B-lymphocytes with hyperproduction of IgE and decrease in IgA and IgG. decreased f activity of lymphocytes, inhibition of chemotaxis of polymorphonuclear leukocytes and monocytes, increased level of CEC, decreased complement activity, impaired production of cytokines, aggravating general immunodeficiency.

Functional disorders of the central nervous system and autonomic system have manifested disturbances in the psychoemotional state, cortical neurodynamics, and changes in the composition of beta-adrenergic receptors of lymphocytes. The gastrointestinal tract is characterized by dysf - enzyme deficiency, dysbacteriosis, dyskiezia, malabsorption syndrome and disruption of the kallikrein-kinin system with activation of kininogenesis, an increase in the permeability of skin vessels, the effects of kinins on blood coagulation and fibrinolysis, on the neuroreceptor apparatus.

Kilnika of atopic dermatitis.

Clinic in early childhood (2-3 months). Zab can continue for years, remissions are mainly in the summer and relapses in the fall. There are several phases of development of the process: infant (up to 3 years), childhood (from 3 to 7 years), puberty and adult (8 years and older) . The leading symptom of fasting is intense, fasting or paroxysmal itching. In the infant and childhood phases, focal erythematous-squamous rashes with a tendency to exudate with the formation of vesicles and areas of weeping on the skin of the face, buttocks, of course, which may correspond to an eczematous process (constitutional eczema). In the pubertal and adult phases, erythematous-lichenoid rashes are faintly pink in color with a tendency to disintegrate on the flexure of the extremities and appear in the elbow bends, popliteal cavities, on the neck, zones of lichenification and papular infiltration of the skin according to the type of diffuse neurodermatitis. dryness, pallor with a sallow skin tone (hypocortisolism), white persistent dermographism. Skin lesions are localized, widespread and universal (erythroderma). on the face, the symmetry is not sharp, there are erythematous-squamous lesions with unclear contours, mainly in the periorbital region, in the area of the nasolabial triangle, around the mouth. The eyelids are swollen, thickened, periorbital folding is pronounced, the lips are dry with fine cracks, and there are pockets in the corners of the mouth (atonic cheilitis). On the skin of the neck, chest, back, folded surfaces, there are numerous small papular (miliary) elements of pale pink color, some of them are pruriginous (papules are covered in the center of the hemorrhagic zone with a punctate crust) against a background of weakly uneven foci of erythema. In the area of the back of the neck, elbow bends, wrist joint, popliteal cavities, papular infiltration and lichenification are expressed: the skin is rough, stagnant-red in color, with an exaggerated skin pattern. In the lesions there are small plates of peeling, cracks, and excoriation. In severe cases, the persistence of the process, large areas of lichenification, appearing on the back of the hands, feet, legs, developing generalized lesions in the form of erythroderma with an increase in the periphery of lymph nodes, low-grade fever. often + pyococcus and vir inf, combined with vulgar ichthyosis. Patients may develop cataracts early (Andogsky syndrome). People 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 mild. In the dermis there is dilation of the capillaries, around the vessels of the papillary layer there are infiltrates of lymphocytes.

Lab tests: CBC, OAM, proteinogram, glycemic and glucosuric profile, immunogram, examination of intestinal microflora and enzyme activity of the gastrointestinal tract, examination of stool for eggs of worms, lamblia, amoeba, opisthorchia and other helminth infections, examination of the f shield gland, adrenal glands, liver, pancreas .

Dst on the clinic, medical history (health, life, family) and examinations.

Diff Ds with pruritus, eczema, toxicoderma.

Treatment of atopic dermatitis.

Treatment is a hypoallergenic diet, products aimed at eliminating allergens from the body, immune complexes, toxic metabolites: fasting days for adults, cleansing enemas, infusion therapy - hemodez, rheopolyglucin IV drip, detox agents: unithiol, sodium thiosulfate, tubages with magnesium sulfate and min water. enterosorbents (activir charcoal, enterodes, hemosphere. In severe cases, plasmapheresis. antihistamine and antiserotonin drugs (suprastin, diphenhydramine, tavegil, fenkarol, etc.), changing 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: for the T-cell link (tactivin, thymalin, thymogen intranasally), drugs that mainly affect the B-cell link of immunity - splenin, sodium nucleinate, glycyram, etimizol, methyluracil, as adaptogens and nonspecific immunocorrectors , histaglobulin. A set of measures is carried out to normalize the gastrointestinal tract and eliminate dysbacteriosis (bacteriophages, eubiotics, bificol, bifidumbacterin, colibacterin, lactobacterin, enzymes, hepatoprotectors), sanitize foci of chronic infection. For effects on the central nervous system and vegetative nervous system, a sedative (valerian, motherwort, peony), tranquilizers (nozepam, mezapam), perif alpha-adrenergic block (pyrroxan 0.015 g), N-cholin block (bellataminal, belioid). Physiotherapeutic agents include ultraviolet irradiation, electrosleep, ultrasound and magnetic therapy, phonophoresis, lek drugs on lesions (dibunol, naftalan), ozokerite and paraffin applications on lesions of skin lichenification.

Externally use ointments with papaverine (2%), naphthalan (2-10%), tar (2-5%), ASD-111 fractions (2-5%), dibunol liniment, methyluracil ointment, in the acute period - KS ointment (advantan, lorinden S, celestoderm, etc.). dispensary observation and sanatorium-resort treatment in the warm southern climate (Crimea), in sanatoriums of the Zhelud-Kish profile (KavMinVody).