What are atopic diseases and atopic skin? What does the word atopic mean in the name of the disease? Treatment of atopic and allergic conditions

Atopic dermatitis (AD) is one of the most common types of dermatosis, the manifestation of which is inflammation of the skin associated with an allergic reaction. Chronic disease in 90% of cases develops in people prone to atopy. The disease has a relapsing course and is characterized by the formation of lichenoid and exudative rashes, as well as hyperreactivity of the skin to specific and nonspecific irritants.

Atopic skin occurs as a complication of low-grade allergic inflammation. The pathogenesis of the disease, although multifactorial, is largely associated with immune disorders. With the development of AD, a change in the Th1/Th2 (lymphocytes) ratio is observed towards an increase in the number of Th2 helper cells. As a result, a restructuring of the cytokine profile occurs, which promotes the synthesis of IgE antibodies.

A sharp increase in the concentration of immunoglobulin E in the body, which contains antigen-specific antibodies, helps trigger the mechanisms of interaction of allergens with IgE agents. As a result, trigger factors significantly increase allergic inflammation. This reaction is caused by the release of the main inflammatory mediators, which include cytokines and histamines.

The etiological factors leading to the occurrence of atopic skin type include:

  • genetic predisposition;
  • psycho-emotional stress;
  • intestinal dysbiosis;
  • disruptions in the functioning of the endocrine system;
  • reduced adhesion at the cellular level;
  • hypersecretion of cytokines;
  • secondary immunodeficiency.

Against the background of the development of AD, there may be side diseases associated with functional disorders of the autonomic and central nervous systems. Therefore, if you notice symptoms of the disease, you should consult a doctor.

Clinical picture

As can be seen in the photo, the signs of atopic skin are very diverse and are largely determined by the age of the patient, as well as the severity of the disease. The pathology has a clear seasonal dependence: in the summer there is complete or partial remission, and in winter period– exacerbations and relapses. A typical symptomatic picture during the development of dermatosis is characterized by the appearance of the following signs:

  • cracking of the skin on the feet;
  • hyperemia of the feet;
  • swelling of the affected areas of the body;
  • itching and flaking of the skin;
  • formation of folds on the neck;
  • increased sweating;
  • dark circles under the eyes;
  • thinning hair on the head;
  • irritation in the bends of the legs and arms;
  • dermatitis of the breast nipples;
  • scaly papules on the wings of the nose;
  • ulcers on the face.

The main symptom of AD is thickening of the skin. Atopic facial skin at the initial stages of development of the pathology is characterized by an intensification of the skin pattern, as well as a doubling of folds on the lower eyelids.

The appearance of such signs is a direct indication for seeking help from a dermatologist.

Phases of atopic dermatitis

In 60% of cases, the first signs of dermatosis development appear in the first year, in 20% in the fifth year of life, and in another 20% in adulthood. Pathology is one of the chronic diseases Therefore, periods of exacerbation and remission will be observed in those suffering from AD throughout their lives.

In medical practice, it is customary to divide it into 4 main phases:

Signs of atopic skin diseases are more pronounced in childhood, which is due to weakened immunity and disruptions in the gastrointestinal tract. With absence adequate treatment The child may experience complications such as false croup, chronic rhinitis, conjunctivitis, etc.

Principles of treatment

Treatment of dermatitis is carried out taking into account the severity symptomatic picture and age phase. Therapy for dermatological diseases is aimed at:

  • exclusion of allergens;
  • eliminating itching;
  • correction of manifestations of concomitant pathologies;
  • detoxification of the body;
  • liquidation inflammatory processes;
  • prevention of relapses and complications.

Treatment of atopic skin should be comprehensive, therefore, in the process of eliminating dermatosis, several main directions are used, namely:

  1. elimination therapy – aimed at eliminating itching and swelling of the skin;
  2. basic therapy – stimulates the process of epithelization of affected tissues;
  3. immunocorrective therapy – helps to increase the reactivity of the immune system.

The principles of treatment and the necessary medications are selected exclusively by a specialist. It is important to adhere to the dosage and duration of therapy recommended by your doctor.

Interrupting the course of treatment is fraught with relapses and complications.

Groups of medicines

The clinical manifestations of AD are based on chronic allergies, which is caused by the effect of certain allergens on the patient’s sensitized body. Therefore, to eliminate the symptoms of dermatosis, I use drugs that have pronounced antiphlogistic and antiallergic properties. They influence the main links in the pathogenesis of skin inflammation, as well as the elimination of swelling of the affected tissues.

The most effective treatments for atopic skin include the following types of drugs:

  • antihistamines - block receptors of the main mediator of inflammatory processes, which helps eliminate swelling and dilation of peripheral blood capillaries;
  • antibacterial - eliminate pathogenic microbes that provoke the formation of ulcers on the skin;
  • calcineurin inhibitors are anti-inflammatory liniments that have a local immunosuppressive effect on areas of inflammation;
  • corticosteroids are the strongest antiphlogistic drugs that are used to treat severe forms of AD;
  • glucocorticosteroids - relieve inflammation and swelling of tissues without causing adverse reactions, which is due to the inability to be absorbed into the general bloodstream;
  • probiotics – normalize intestinal microflora, helping to restore activity beneficial bacteria Gastrointestinal tract.

Topical anti-inflammatory drugs

When the first signs of dermatosis occur, experts recommend the use of anti-inflammatory drugs local action. However, it should be taken into account that monotherapy using exclusively gels, ointments and liniments will be ineffective and will temporarily relieve the symptoms of the disease. What products can be used to care for atopic skin?

Atypical skin is characterized by the formation of foci of inflammation and purulent exudates on the surface of the affected areas of the body. To relieve the symptoms of dermatosis, antihistamine and anti-inflammatory drugs are used. They help reduce tissue swelling and speed up regeneration.

Doctors define atopic dermatitis as a chronic inflammatory skin disease accompanied by itching. AD has a pronounced seasonality: for example, in the autumn-winter period the probability of relapse is much higher than in spring and summer.

If you notice one of the following signs in your child, he may be suffering from dermatitis and needs to consult a specialist:

Constant dry skin

Regular inflammation of the skin, which is accompanied by itching,

Thickening, thickening, spots or scales on certain areas of the skin.

Parents suffering from asthma or allergic rhinitis should pay special attention to monitoring the condition of their children's skin. The hereditary factor plays a big role!

Those who have experienced atopic dermatitis know that a child’s skin needs special care, but not everyone knows that this care should be constant, at any stage of AD (exacerbation or remission).

Our task is not just to reduce the manifestations of atopic dermatitis, but to direct all our actions towards restoring the normal state of the skin. Following the basic rules of care can help here:

Eliminating (or limiting, as far as possible) exposure of the child’s skin to major irritating factors.

Elimination of dry skin and restoration of damaged lipid layer of the skin.

In order to confirm or dispel your fears, you need to consult a doctor; only a doctor, based on the results of the examination and (if necessary) test results, will be able to make an accurate diagnosis. Confirming the diagnosis of atopic dermatitis is not a death sentence! With proper rational care, you can help your baby more easily tolerate the manifestations of the disease.

Three secrets that will save your skin with atopic dermatitis

What is it atopic skin dermatitis? This is a skin disease of an allergic nature. Is one of the most serious illnesses. Most often it manifests itself in children early age.With atopic dermatitis, the skin is very dry and sensitive, which causes severe itching. Very often, irritation is caused by external factors such as sun, water, cosmetics. MedicForum found out how to deal with this disease.

Improper care can lead to dire consequences, which will be difficult to get rid of.

Signs of atopic skin

Severe itching is one of the very first signs; a person is constantly itching, even in his sleep,

Dry skin - sometimes very dry, can crack, peel, hurt, ulcers form,

Localization - usually appears in bend areas: elbows, knees, wrists. Children have a so-called diathesis on their cheeks.

The main cause of atopic dermatitis is genes. It is impossible to cure completely, but with proper care, nutrition and treatment it can lead to long-term remission.

Proper skin care for atopic dermatitis

Important in care is skin hydration. Dry skin worsens the condition and the protective barrier is broken. So, the most important thing a person suffering from atopic dermatitis should remember is:

1. Shower instead of a bath - the tap water is chlorinated, chlorine has a negative effect on the skin during atopic inflammation, it dries it out, so lying in the bath for a long time is not recommended. The best way out of the situation is to quickly rinse in the shower; you can buy special filters that purify the water. The water should not be hot.

2.Moisturizing the skin after a shower is one of the main tasks. There are special cosmetics designed for this type of skin. Can be bought at a pharmacy.

3. Soap that dries the skin - contains regular soap There may be substances that negatively affect the skin, damaging the hydrolipid layer. Instead, you can use oils, emulsions, and shower gels designed for this problem.

4. Facial cosmetics - facial care is also very important; you need to choose creams designed for dry and allergy-prone skin.

Most cosmetic products contain chemical substances, which have a bad effect on the condition of the skin. Something to keep in mind is SLS and SLES. Cosmetics for allergy-prone skin should not contain these substances, but before purchasing, be sure to familiarize yourself with what is included in the cream.

What are the contraindications?

Atopic skin does not like to be used the following means and actions:

Most types of soaps, balms and perfumes,

Scrubs and peelings,

Sudden changes in temperature,

Sweaty feet and palms,

Review of cosmetics

Cosmetics for atopic skin care They usually contain substances such as allantoin, panthenol, vitamins, glycerin, and oils.

1. AA Help cosmetics are 100% safe, without parabens, allergens and dyes. This is a fairly wide line of cosmetics including: creams, tonics, makeup remover milk, balms, cream-gel for face washing. The use of this cosmetics guarantees hydration, protection, and restoration of water balance. It has a beneficial effect on the skin, reduces itching, discomfort, and regulates the regeneration of the epidermis.

2. Shea butter is very healthy, has a beneficial effect on the skin: moisturizes, protects, restores. Oil is extracted in Africa from the fruits of the Shea tree. It also has an anti-inflammatory effect; vitamins A and E contained in the oil help in wound healing.

3. Emolium products - cosmetics from this company are intended for preventive care of dry and allergenic skin. Emolium is an emollient that restores the skin. 100% safe product, can only be purchased at the pharmacy. Effectively nourishes, moisturizes, and has an antibacterial effect. Suitable for people with very dry, atopic skin.

4. Atoperal cosmetic product is a cosmetic line from BlauFarma designed for the care of atopic, dry and sensitive skin. This company produces not only creams, but also shampoos for everyday care of scalp prone to allergies. The shampoo not only cleanses the scalp well, but also nourishes and moisturizes. 100% safe cosmetics.

5.Marseille soap - its homeland is France. Soap is made from natural oils. Ideal for caring for dry and sensitive skin. This soap is great for caring for atopic skin. There are no chemicals in the composition. Unlike classic soap, Marseilles does not dry out, but moisturizes, nourishes and cares for the skin.

Does proper diet matter for atopic dermatitis?

There is a specific list of foods whose consumption increases the risk of allergic reactions. Anyone who suffers from atopic dermatitis should know this.

Products that should not be consumed during treatment:

Red fruits and berries, citrus fruits,

Canned food and sausages,

Dairy products, milk,

You should eat foods rich in vitamin A, which has a protective function. The main foods that contain vitamin A are:

Lettuce, spinach,

Liver and fish oil.

Vitamins B and E are also useful. They restore protective layer skin, have antioxidant properties, increase immunity. It has long been known that all diseases come from the intestines and are a consequence poor nutrition. So:

1. Eat plenty of vegetables and fruits every day,

2.Drink plenty of water

3.You can’t smoke or drink alcohol,

4.Salads should be included in the diet with added olive oil,

5. Breakfast is an important component

6.You should limit sweets and salt,

At balanced diet, proper care and treatment, all symptoms will subside and possibly disappear forever.

Previously, experts told how to save yourself from skin cancer.

Question to the expert: How to care for skin with atopic dermatitis

Text: Anastasia Andreeva

ANSWERS TO MOST QUESTIONS THAT CONCERN US We are used to searching online. In a new series of materials, we ask exactly these questions: burning, unexpected or common ones - to professionals in a variety of fields.

Peeling spots on the folds of the arms and inflammation on the cheeks - it would seem that these are ghosts from childhood. But even in adults, atopic dermatitis can manifest itself to one degree or another. The disease can cause a lot of inconvenience: unpleasant itching and peeling, the foci of which are not so easy to eliminate.

Atopic dermatitis is a chronic non-contagious inflammatory lesion skin. The exact reasons for its occurrence are unknown, but it is believed that it is based on a hereditary factor, that is, genetics. In general, atopy is something like the body’s readiness to produce an allergic reaction (another example of an atopic disease is bronchial asthma). Perhaps the modern lifestyle and living in big cities also increases the risk; according to various hypotheses, this may be due to an “excess” of hygiene compared to the past or to increased stress levels. Of course, with the existing skin reaction The condition of the skin will also be affected by external influences on it.

We asked a cosmetologist about the reasons for the development of dermatitis and whether it can be masked with foundation. We also figured out how to properly care for atopic skin and what procedures and cosmetic ingredients should be avoided.

Anastasia Stepko

cosmetologist and head of the SOVA beauty workshop

Cosmetic procedures for patients with atopic dermatitis on the face solve, in addition to issues of care, also the tasks of preventing relapses of dermatosis and increasing the effectiveness of treatment. The products used should be targeted at atopic skin and have softening, moisturizing, and protective properties. Regular use of emollients, which contain lipids, urea, glycerin and other biologically active compounds, is necessary. The task of such ingredients is to provide long-lasting hydration of the skin, restore the hydrolipid film, and maintain water balance. Cosmetics should not contain alcohol or fragrances.

With atopy, proper cleansing of the skin is very important. It is necessary to select products with an acidic pH, and use them not only for the face, but also for the hands - to prevent dermatitis on the hands. It is better to choose special series for hypersensitive or atopic skin. For cleansing, you should absolutely not use products with a neutral or alkaline pH level, since they destroy the hydrolipid mantle of skin with dermatitis, aggravate its dryness and, therefore, can provoke an exacerbation of the disease. Procedures associated with damage to the stratum corneum of the skin, such as medium chemical peels or dermabrasion, should also be excluded from the care program.

During periods without exacerbations, physiotherapeutic procedures can be performed: laser therapy, treatment with light, ultraviolet rays, magnetic therapy. As for injections, it is better to choose drugs with hyaluronic acid and remember that atopic skin is prone to the formation of hematomas and has a low sensitivity threshold. For chemical superficial peels, a gel form of glycolic or lactic acid is recommended. The time the peel remains on the skin should be minimal, and the procedures should not be repeated more than once every ten days. People with atopic skin are not suitable for injections with collagen, peptides and protein components. Remember that any cosmetic procedures for dermatitis can be carried out only during a period of prolonged absence of exacerbations and relapses.

5 tools that may come in handy

Avène Trixera Nutritio Nourishing Cleansing Gel

Atopic skin needs the most gentle cleansing of the possible. As for facial skin, it is better to use water to a minimum. However, if you do wash your face with water, then only with a special product. Avène gel is designed specifically for very dry skin with atopic dermatitis and helps restore its protective barrier. If the price is too high, you can pay attention to La Roche-Posay products from the special Lipikar series, where you can also find a suitable shower gel.

Uriage Bariéderm Cica-Gel Nettoyant au Cu-Zn Cleansing Gel

Another cleansing product that is more suitable for periods of exacerbation. There is zinc here, which is often included in medicinal ointments that are prescribed for atopic dermatitis. The product can be used for both the face and body. To even out skin tone, citric acid was also included in the composition.

Uriage Xémose Crème Relipidante Anti-Irritations

In another specialized Uriage line, you can find a lipid-restoring cream for the face and body, which intensively nourishes the skin and helps relieve irritation and itching. The jar contains 400 milliliters - enough for a long time. At the same time, the product is absorbed quite quickly, which allows you to use it without any problems in the morning before leaving the house.

Bioderma Atoderm Intensive Baume Balm

Bioderma also has its own line for atopic skin. Particular attention is paid to cream with zinc, which is good for the skin during periods of exacerbation. The balm will also help prolong remission.

Embryolisse Lait-Crème Сoncentré cream concentrate

Embryolisse milk is suitable for very dry and atopic skin as a waterless cleansing option. It can also be used as a night cream or to soothe sensitive skin after shaving.

Atopic dermatitis cream

Regular skin care will help maintain its youth and aesthetic appearance for many years. Problematic skin requires special attention and careful selection of care products. For these purposes, special masks and lotions with a nourishing, moisturizing or restorative effect are intended. The cream for atopic dermatitis of the skin provides daily use, and its goals are to eliminate symptoms and protect the skin from harmful effects environment.

Atopic skin: what is it?

Atopy is characterized as a genetic condition in which the body is susceptible to a deficiency of cellular immunity, the development of atopic dermatitis and other allergic pathologies. With this condition, people often suffer from allergies to foods, as well as inhaled substances (pollen, dust, chemical fragrances, etc.). Atopic skin is essentially atopic dermatitis. The disease is caused by hypersensitivity of the skin to the environment and is accompanied by symptoms that worsen the quality of life.

Reasons for development

Atopic skin in an infant is usually a genetic predisposition. In adults, pathology can result from:

  • severe intestinal dysbiosis,
  • frequent psycho-emotional stress,
  • failure of metabolic functions in the body,
  • dysfunction of the endocrine system,
  • disorders of the central nervous system (CNS).

Young children, adolescents and young adults are most susceptible to pathology. If the disease appears in a newborn, then often, as the child grows, atopic dermatitis goes away on its own due to hormonal changes in the body. However, there are cases when pathology develops into chronic stage and worries patients already at a more mature age.

Note. In case of genetic predisposition, it is necessary to adhere to the recommendations of doctors and visit a medical facility as often as possible for the purpose of preventive examination. This will help to diagnose the pathology in time and prevent it from becoming chronic.

Main symptoms

The disease makes itself felt in the early stages of development and is accompanied by characteristic symptoms:

  • hyperemia of the feet (overflow of blood vessels),
  • dryness and flaking of the skin in the nose area,
  • skin rashes on the folds of the arms and legs,
  • ulcers on the skin of the face,
  • hyperhidrosis (excessive sweating),
  • dark circles under the eyes,
  • the appearance of folds in the neck area,
  • dryness, burning, cracks or rash on the breast nipples,
  • swelling of the affected areas on the skin,
  • recurring conjunctivitis.

In addition, rashes, itching and peeling can occur in any part of the body, and the skin with atopic dermatitis can crack, thicken and become overly vulnerable. Symptoms most often intensify during the cold season, when increased sweating and at night.

Diagnostics

To make an accurate diagnosis, visual inspection won't be enough. To determine pathology, doctors prescribe a number of diagnostic measures:

  • general urine analysis,
  • biochemical and general tests blood,
  • enzyme immunoassay (blood test for immunodeficiency),
  • blood test to determine the allergen that caused the pathology.

If these procedures are not enough, then a consultation with highly specialized specialists is prescribed, histological examination(taking a tissue sample), stool analysis for dysbacteriosis, ultrasound of the abdominal cavity, as well as a scarification test (test to identify allergens).

Therapeutic measures are prescribed by the doctor after making an accurate diagnosis. Treatment is based on:

  • eliminating symptoms,
  • eliminating allergens,
  • removing harmful substances from the body,
  • suppression of inflammatory processes,
  • decreased sensitivity to allergen,
  • preventing the development of complications.

To quickly relieve concomitant symptoms, topical agents are prescribed. The most popular and effective ones are presented in the table:

Also, depending on the course of the disease and the symptoms present, the following groups of drugs are prescribed:

In addition to these medications, medications are prescribed to support intestinal microflora, painkillers and other medications, depending on the clinical picture and the patient's condition.

Important! Pathology involves complex treatment, but only a doctor can correctly draw up a plan and select medications. Independent selection of medications is strictly prohibited, as this entails a lot of negative consequences.

With atopic dermatitis, it is important to monitor your lifestyle and adhere to some recommendations:

  1. You cannot stop prescribed medications on your own.
  2. To maintain the skin in good condition, it is necessary to regularly use topical products (moisturizing and nourishing creams, lotions, etc.).
  3. Include in diet whole grains, meat is not fatty varieties, fats plant origin, fermented milk products, rye bread.
  4. Avoid eating chocolate, alcoholic and coffee drinks, fatty fish and meats, honey, mushrooms, confectionery and other products that cause allergies.
  5. During an exacerbation, avoid contact with aggressive allergens (pollen, fluff).
  6. In hot weather, use medicated antiperspirants.
  7. Wear comfortable clothes made from natural fabrics.
  8. Use shampoos, gels and other products with a moisturizing or nourishing effect as hygiene products.

You should also limit excessive exercise, as it increases sweating, and this can cause the disease to reappear.

Folk recipes

Folk remedies for atopic skin do not belong to the main therapy, but help to alleviate the patient’s well-being and eliminate symptoms. Most often used:

  1. Soothing compress. Peel the potatoes (2 pieces), chop them using a grater, let them brew for 20-30 minutes. Then squeeze out the excess juice, place the mixture on gauze and apply a compress to the affected areas of the skin for 3-4 hours (with the potatoes facing the body). For children, if necessary, after the compress, special creams for the child’s atopic skin and moisturizing lotions based on thermal water are applied.
  2. Healing tincture. Mix 1 tbsp. l of crushed valerian root, chopped green peony, place the mixture in a prepared container and pour 400 ml of vodka into it. The remedy is infused for three weeks, take one teaspoon three times a day. It is better to take the medicine before or during meals.
  3. Healing lotion. Place one tablespoon of veronica in a glass and pour 200 ml of boiling water. Next, the product is infused for two hours and filtered. Treat the affected areas of the skin with the prepared lotion no less than 4-5 times throughout the day.

Prognosis for atopic dermatitis depends on how quickly the patient sees a doctor. The sooner the course of treatment begins, the more favorable the outcome will be. If you start the disease, it will progress, and the symptoms will worsen. Chronic pathology cannot be cured, so timely measures to eliminate the disease will help quickly get rid of side effects and improve the patient’s quality of life.

The most common allergic diseases include atopic skin; not everyone knows what it is. This disease occurs mainly in children. A characteristic symptom of atopic dermatitis is constant itching, which intensifies in the evening and at night. Depending on age, changes in the skin are located in different places. Treatment of atopic dermatitis includes the use of local and systemic drugs.

Causes of allergic dermatitis

Atopic dermatitis is an example of a skin allergy. Skin allergy is a hypersensitivity reaction to immunological mechanisms. Hypersensitivity consists of the appearance of symptoms such as itching, burning and erythematous changes on the skin in response to a specific irritant (allergen) that is tolerated by healthy people.

Approximately 10-20% of people have a hereditary tendency to allergies, which consists of excessive production of immunoglobulin IgE. IgE antibodies bind to the allergen molecule, then transmit information to mast cells (mast cells), which secrete substances responsible for the occurrence of allergy symptoms.

Children with atopic dermatitis are at high risk of developing allergic asthma And allergic rhinitis in future.

Atopic dermatitis is associated with genetic predisposition. It occurs more often in children whose parents also suffer from this disease. However, it has not yet been discovered how skin atopy is inherited. It is likely that more than one gene is responsible for the characteristic symptoms of the disease.

The structure of the skin is of great importance in the occurrence of the disease. The patient's skin loses water faster, which means it is more susceptible to excessive dryness. This occurs due to a decrease in the amount of ceramides, lipids that are found in the stratum corneum of the epidermis. Damage to the stratum corneum allows microorganisms to penetrate into the skin, which aggravate the course of the disease.

Main symptoms

The dominant symptom of atopic dermatitis is itching. The mechanism of itching is not fully known, but, of course, it is enhanced by significant skin dryness and irritation. Itchy skin Occurs throughout the day, but tends to get worse in the evening and at night, which can cause sleep disturbances and, in extreme cases, can even lead to depression.

Itching occurs in any form of the disease, and other symptoms vary depending on the age at which the disease occurs.

Atopic skin - what is it? There are 3 forms of the disease:

  • atopic skin in infants;
  • atopic dermatitis in children;
  • atopy in adolescents and adults.

Atopic dermatitis in infants is characterized by:

  • the occurrence of exudative changes, localized mainly on the skin of the face, which then dry out, forming crusts;
  • this often results in a bacterial infection that is associated with scratching of the skin;
  • the disease affects the cheeks and forehead, and the skin on the nose, lips and chin, as a rule, does not respond to change;
  • changes may appear on the body and the inner sides of the limbs;
  • When the scalp is damaged, the hair becomes dry and brittle.

For atopic dermatitis in children:

  • changes occur mainly in the folds knee joints, elbows, wrists, arms, legs and neck;
  • if they are located on the face, this is usually around the eyes and mouth;
  • erythematous lesions, severe dry skin and peeling appear;
  • Significant itching occurs, which is most severe at night.

For atopic dermatitis in adults and adolescents:

  • the disease affects the bends of the limbs, wrists, fingers and toes, shoulders, back, area around the eyes and mouth;
  • may affect the perineal area, which causes very unpleasant pain for the patient;
  • changes in the skin have the character of lupus, with peeling of the epidermis, irritation and scabs resulting from scratching.

Etiological factors

Symptoms of atopic dermatitis may appear or worsen in response to various antigens:

  1. 1. Food allergens - protein allergy cow's milk and/or chicken egg affects the severity of the disease in infants, but it has not been proven that stopping the intake of foods containing these proteins reduces the severity of the disease.
  2. 2. Inhalant allergens such as pollen, mites house dust, animal hair can increase the symptoms of atopic dermatitis.
  3. 3. Microbes - most patients with atopic dermatitis experience the presence of staphylococci on the skin, which aggravate the course of the disease. Some patients have antibodies against fungi that cause pityriasis versicolor and fungal skin infections.

There are a number of factors that enhance the course of the disease:

  • frequent washing;
  • dry air;
  • rapid changes in ambient temperature;
  • exposure to inhalation, food, and contact allergens;
  • infections, especially Staphylococcus aureus;
  • contact with irritating factors, such as detergents, cosmetics, cleaning products;
  • severe stress.

Diagnostic methods

The diagnosis of atopic dermatitis is made on the basis of chronic skin atopy with frequent relapses. Studies of the concentration of IgE and eosinophils in the blood are useful in diagnosis.

A positive result on this test means there are antibodies directed against a specific group of allergens, such as inhalant allergens, or against a single allergen, such as animal dander.

Eosinophils in the blood - elevated levels may indicate an allergy.

Skin tests are also used to make the correct diagnosis. Spot tests rely on placing drops of a solution containing the allergen on the skin of the forearm or back.

Intradermal tests are used if spot tests are negative. The allergen is administered by injecting a solution intradermally. Used in a concentration 100-1000 times less than for spot testing.

Spot test results and subcutaneous injection can be seen after about 15-20 minutes in the form of blisters on the skin.

In exceptional cases, a biopsy may be performed, mainly to rule out other diseases that may cause similar symptoms.

Glucocorticoids are also used orally for atopic dermatitis. Antihistamines are used for exacerbations of the disease, which are accompanied by severe itching. Phototherapy can be used after 12 years of age.

For atopic dermatitis, the doctor will definitely recommend suitable skin care, mainly the use of hypoallergenic cosmetics. This will ensure that all layers of the epidermis are sufficiently moisturized and the natural protective layer of the skin is strengthened. In addition, it is important to avoid products that cause new skin changes or worsen existing ones.

  • Chapter 1. General doctrine of illness 92
  • Chapter 6. Pathological physiology of peripheral (organ) circulation 705
  • Chapter 12. Pathological physiology 1247
  • 2.1.5. Violation of the electrical stability of the lipid layer
  • 2.2. General body reactions to damage
  • 2.2.1. General adaptation syndrome (stress)
  • 2.2.2. Activation of proteolytic systems of blood plasma
  • I Hagemann Factor Kallikrein j I Prekallikrein
  • 2.2.4. Coma
  • 2.2.5. Acute phase response
  • 2.2.5.2. Main mediators of the acute phase response
  • 3.1. Body reactivity
  • 3.2. Types of reactivity
  • 3.5. Resistance
  • 3.6. Factors influencing reactivity
  • 3.7. The role of heredity
  • Hydroxyphenyl grape acid
  • Phenylpyrogratic acid
  • Homogeneous antisinic acid
  • Homogentisine oxidase (alkaptonuria)
  • 4.1. Basic ideas about the structure
  • 4.2. General strategy of immune defense
  • 4.3. Immunodeficiency conditions
  • 4.3.1. Primary immunodeficiencies
  • 4.3.2. Secondary immunodeficiencies
  • 4.4. Autoimmune processes
  • 4.5. Lymphoproliferative processes
  • 5.1. The relationship between allergies and immunity
  • 5.3. Specific allergic reactions
  • 5.3.1. Allergic reactions type I (anaphylactic)
  • 5.3.2. Allergic reactions type II
  • 5.3.3. Allergic reactions type III
  • 5.3.4. Allergic reactions type IV
  • Characteristics of immediate and delayed types of hypersensitivity
  • 5.4. Atopy. Atonic and pseudoatopic diseases
  • 5.4.1. Development mechanisms
  • 5.4.2. Mechanisms of reversible airway obstruction
  • 5.5. Pseudoallergy
  • 5.5.1. Histamine type of pseudoallergy
  • 5.5.2. Impaired activation of the complement system
  • 5.5.3. Disorders of arachidonic acid metabolism
  • Chapter 6. Pathological physiology of peripheral (organ) circulation and microcirculation
  • The state of blood flow in microvessels during arterial hyperemia, ischemia, capillary stasis and venous stagnation of blood,
  • Signs of peripheral circulatory disorder (V.V. Voronin, modification by G.I. Mchedlishvili)
  • 6.1. Arterial hyperemia
  • 6.3. Violation of the rheological properties of blood, causing stasis in microvessels
  • 6.4. Venous blood stasis
  • Prevalence of resorption by filtration of brain microvasculature
  • 6.6. Brain hemorrhage
  • 7.1. Microcirculation disturbance
  • 7.2. Inflammatory exudates
  • 7.3. Emigration of peripheral blood leukocytes
  • 7.4. Phagocytosis
  • 7.5. Specialized functions of neutrophils, monocytes
  • 7.6. Inflammatory mediators
  • 7.7. Outcomes of inflammation
  • 8.1. Etiology
  • 8.3. Function of organs and systems
  • 9.1. Protein metabolism disorder
  • 9.1.1. Impaired breakdown and absorption of proteins
  • 9.1.4. Pathology of interstitial protein metabolism (disorder of amino acid metabolism)
  • 9.1.5. Changing the rate of protein breakdown
  • 9.1.6. Pathology of the final stage of protein metabolism
  • 9.2. Lipid metabolism disorder
  • 9.2.1. Impaired transport of lipids and their transition to tissues
  • 9.2.2. The role of lipid metabolism disorders in the pathogenesis of atherosclerosis
  • 9.2.3. Fatty infiltration and fatty degeneration
  • 9.3. Carbohydrate metabolism disorder
  • 9.3.3. Dysregulation of carbohydrate metabolism
  • 9.4. Water imbalance
  • 9.4.1. Basics of water balance regulation
  • 9.4.2. Forms of water imbalance
  • 9.4.2.1. Increased extracellular fluid volume (hypervolemia)
  • 9.4.2.2. Decreased extracellular fluid volume (hypovolemia)
  • 9.5. Electrolyte imbalance
  • Human body
  • 9.5.1. Sodium imbalance
  • 9.5.2. Potassium imbalance
  • 9.5.3. Calcium imbalance
  • 9.5.4. Phosphate imbalance
  • 9.5.5. Magnesium imbalance
  • 9.6. Acid-base imbalance
  • 9.6.1. Basics of acid-base balance regulation
  • 0A* y k * 5 sz" 5 nesh Lshkzhy Anions KaikshyKat ions
  • 9.6.2. Key indicators kob
  • 9.6.3. Forms of acid-base imbalance
  • 9.6.3.1. Respiratory acidosis
  • 9.6.3.2. Metabolic acidosis
  • 9.6.3.3. Respiratory alkalosis
  • 9.6.3.4. Metabolic alkalosis
  • 9.6.3.5. Mixed acid-base imbalance
  • 10.2. Compensatory-adaptive reactions during hypoxia
  • 10.3. Metabolic disease
  • 10.4. Correction of hypoxia: is excess or deficiency of oxygen necessary?
  • 11.1. Mechanisms of cell division
  • 11"2. Pathophysiology of cell division
  • 11.2.1. Oncogene activation
  • 11.2.2. Inactivation of suppressor genes
  • 11.2.3. Apoptosis disorder
  • 11.2.4. Disruption of DNA repair mechanisms
  • 11.3. Tumor growth
  • 11.3.2. Etiology of tumors
  • 11.3.3. Properties of tumor cells in vitro
  • 11.3.4. Intercellular cooperation
  • 11.3.5. Properties of malignant tumors
  • 11.3.6. Relationship between tumor and body
  • 11.3.7. Mechanisms of tumor resistance to therapeutic effects
  • .Part three: dysfunction of organs and systems
  • Chapter 12. Pathological physiology of the nervous system
  • 12.1. General reactions of the nervous system to damage
  • 12.2. Dysfunction of the nervous system,
  • 12.3. Metabolic encephalopathies
  • 12.4. Brain damage
  • 12.5. Disorders of nervous system functions caused by myelin damage
  • 12.6. Disturbance of the nervous mechanisms controlling movements
  • 12.6.1. Movement disorders
  • 12.6.1.1. Motor unit diseases
  • 12.6.1.2. Movement disorders
  • 12.6.1.3. Movement disorders due to cerebellar damage
  • 12.6.1.4. Movement disorder
  • 13.1. Dysfunction of blood pressure regulation mechanisms
  • 13.2. Bladder function disorders
  • 13.5. Autonomic disorders,
  • 15.1. Violation of central regulatory mechanisms
  • 15.2. Pathological processes in the glands
  • 15.3. Peripheral (extraglandular) mechanisms of hormone disruption
  • 15.4. The role of autoallergic (autoimmune) mechanisms in the development of endocrine disorders
  • 1]DIOTYPICAL ahtuteaa
  • 16.1. Dysfunction of the pituitary gland
  • 16.1.1. Insufficiency of pituitary gland function
  • 16.1.2. Hyperfunction of the anterior pituitary gland
  • 16.2. Adrenal dysfunction
  • 16.2.1. Corticosteroid deficiency
  • 16.2.2. Hypercorticosteroidism
  • 16.2.3. Hyperfunction of the adrenal medulla
  • 16.3. Thyroid dysfunction
  • 16.3.1. Hyperthyroidism
  • 16.3.2. Hypothyroidism
  • 16.4. Dysfunction of the parathyroid glands
  • 16.5. Dysfunction of the gonads
  • 17.1. Brief information
  • 17.2. Atherosclerosis
  • 17.2.1. Origin theories
  • 17.2.2. Regression of atherosclerosis
  • 17.3. Coronary blood flow disturbance
  • 17.3.1. Myocardial ischemia
  • 17.3.2. Stunned and inactive myocardium
  • 17.4.Arterial hypertension
  • Hypertonic disease!
  • 17.4.1. Pathogenesis of hypertension
  • 17.4.2. Secondary arterial hypertension
  • 17.6. Mechanisms of heart failure development
  • 17.6.2. Diastolic form of heart failure
  • 17.7. Mechanisms of development of arrhythmias
  • 17.7.1. Impairment of impulse formation
  • 17,7,2, Reentry
  • 17.7.3. Conduction disturbance
  • External respiration
  • 18.1. Definition of “respiratory failure”
  • 18.2. Assessment of external respiration functions and respiratory insufficiency
  • 18.3. Pathophysiological variants of respiratory failure
  • 18.3.1. Centrogenic respiratory failure
  • 18.3.2. Neuromuscular respiratory failure
  • 18.3.3. "Framework" respiratory failure
  • 18.3.4. Mechanisms of respiratory failure in respiratory tract pathology
  • 18.3.5. Parenchymal respiratory failure
  • 18.4. Indicators of blood gas composition in respiratory failure
  • 18.4.1. Hypoxemic (type I) respiratory failure
  • 18.4.2. Hypercapnic-hypoxemic (ventilation) type of respiratory failure
  • 19.1. Basics of cell cycle regulation
  • 19.2. Pathology of red blood
  • 19.2.1. Anemia
  • 19.2.2. Erythrocytosis
  • 19.4. White blood pathology
  • 19.4.1. Leukocytopenia
  • 19.4.2. Leukocytosis
  • 19.5. Leukemia (hemoblastosis, leukemia)
  • 20.1. Blood clotting factors
  • VIll/vWf I
  • 20.2. Hemorrhagic syndromes
  • 20.4. Disseminated syndrome
  • 20.5. Methods for assessing hemocoagulation system disorders
  • 21.1. Lymph formation disorder
  • Chapter 1. General doctrine of illness 92
  • Chapter 6. Pathological physiology of peripheral (organ) circulation 705
  • Chapter 12. Pathological physiology 1247
  • 21.2. Insufficient lymph transport
  • 21.3. Lymphatic coagulation disorder
  • 21.4. The role of the lymphatic system in the development of edema
  • 21.5. Functions of the lymphatic system during the development of inflammation
  • 22.1. Esophageal dysfunction
  • 22.2. Stomach dysfunction
  • 22.2.1. Disturbances in the secretion of hydrochloric acid and pepsin
  • 22.2.2. Violation of the mucus-forming function of the stomach
  • 22.2.3. Pathophysiological mechanisms of peptic ulcer
  • 22.2.4. Impaired gastric motility
  • 22.3. Pathophysiological mechanisms of abdominal pain
  • 22.4. Violation of exocrine pancreatic function
  • 22.4.1. Pathophysiological mechanisms of development of acute pancreatitis
  • 22.4.2. Pathophysiological mechanisms of development of chronic pancreatitis
  • 22.5. Intestinal dysfunction
  • 22.5.1. Impaired digestion and absorption in the intestine
  • 22.5.2. Intestinal motility disorders
  • 23.1. Hepatocellular failure
  • 23.2. Pathophysiological mechanisms of portal hypertension syndrome
  • 23.3. Pathophysiological mechanisms of jaundice
  • 24.1. Glomerular filtration disorder
  • 24.2. Dysfunction of tubules
  • 24.3. Changes in urine composition
  • 24.4. Nephrotic syndrome
  • 24.5. Acute renal failure
  • 24.6. Chronic renal failure
  • 24.7. Urolithiasis disease
  • 5.4. Atopy. Atonic and pseudoatopic diseases

    5.4.1. Development mechanisms

    It has been established that people have diseases similar to anaphylactic reactions reproduced in experiments in animals. However, in a number of ways they differ from anaphylaxis, and to emphasize the difference between this group of diseases A.F. Coca and R.A. Cooke in 1923 designated them with the term “atopy” (from the Greek atopia - strangeness, unusualness).

    The group of classic atopic diseases includes year-round atopic rhinitis, hay fever (from the English pollen - pollen), atopic form of bronchial asthma and atopic dermatitis. Similar in mechanism of development to this group are certain acute allergic reactions to medications and foods.

    The signs characterizing atopy (Table 5.3) include natural occurrence, hereditary predisposition, the possibility of damage to any system of the body, in contrast to anaphylaxis, in which there is always a certain shock organ within one species of animal. In both types of reactions, tissue damage is caused by allergic mechanisms of the first type. However, recently it has become clear that atopy is different from anaphylaxis

    Another important sign is that nonspecific (nonimmune) mechanisms play a large role in its development. Thus, atopy is a broader phenomenon than anaphylaxis, so atopy cannot be reduced only to damage associated with the development of allergic mechanisms of the first type.

    Hereditary predisposition is the most important sign of atopy. Currently, the possibility of the participation of about 20 genes in its development is being discussed; for many genes, their localization and connection with one or another sign of atopy have been determined. They were found on chromosome 4, 5,6,7, 11, 13, 14. W. Cookson (1996) conditionally divided their inheriting classes:

      class - genes that generally predispose to the development of atopy (including

    reading IgE-mediated inflammation) and an increase in total IgE;

      class - genes influencing a specific IgE response;

      class - genes influencing bronchial hyperreactivity independently

    simo for atopy;

      class - genes that determine the development of inflammation, not associated with IgE-

    Thus, the basis for the development of atopy is the set of genes that is inherited. However, this hereditary predisposition does not create the atopic phenotype, but is only a contributing condition. The implementation of this predisposition into the clinical manifestations of atopy (atopic phenotype) occurs only when exposed to appropriate environmental factors. Such factors for each individual are “their own” allergens.

    Already It was mentioned that groups of mechanisms take part in the development of atopy: specific (immune) and nonspecific (non-immune). All changes in the body associated with the inclusion of these mechanisms are, to a greater or lesser extent, possible in all classical atopic diseases.

    Differences between anaphylaxis and atopy

    Peculiarity specific mechanism is expressed in the body’s increased ability to respond to allergens with the formation of IgE antibodies. The central link of this feature is the directionality

    differentiation of null T-helper cells (T x -0). Under normal conditions in response to an antigen, T x 0 differentiates mainly into T X 1, which secrete IL-2 (interleukin-2), γ-interferon (γ-IF) and a number of other mediators, which activates the development of the cellular mechanism of immunity (Scheme 5.1)

    T x 2 secretion of IL-4, IL-5, IL-10, IL-13

    Scheme 5.1. Pathways of TxO cell differentiation and the role of some interleukins. Ag - antigen; APC - Ag-presenting cell, IL - interleukin, T x - T-helper

    In people predisposed to the development of atonic reactions, there is a shift in T x 0 differentiation towards the preferential formation of T x 2 cells. The latter secrete mainly IL-4, IL-5, IL-3, IL-10 and a number of other mediators. These mediators, especially IL-4, switch the synthesis of antibodies in B lymphocytes from G-class to E-class. There is competition between T x 1- and T x 2-dependent responses. When the Tx2-dependent response predominates, the Tx1-dependent response is inhibited and vice versa. In this regard, in atopic diseases, inhibition of the cellular and, to a certain extent, humoral immunity is detected, which in advanced cases leads to the development of infectious processes in the form of pyoderma, chronic otitis, sinusitis, bronchitis, etc.

    In healthy people, the content of total IgE in blood plasma varies from 0 to 40-60 units/ml (1 International Unit = 2.4 ng). It is smallest at birth, then increases and stabilizes by 10-12 years of age. In atopic diseases, in 80-85% of cases, the concentration of total IgE increases to 100-120 units/ml or more and can reach several thousand units. It is called general because it contains both IgE antibodies to a specific allergen and IgE molecules that are nonspecific to a given allergen. Simultaneously with the increase in total IgE, as a rule, specific IgE also increases. However, in a number of cases of atopic diseases, together with an increase in the level of total IgE or without it, IgG4 was detected in the blood serum, which, like IgE, can be fixed by nabasophils and act as reagins.

    Formed under the influence of an allergen lgE -antibodies and molecules of nonspecific IgE are fixed to cells through Fc- receptors. There are two types of these receptors. The first type is classical high-affinity receptors (Fc e RI), which are found on mast cells and basophils. It is believed that on one basophil a fic can

    range from 30x10 3 to 400x10 3 IgE molecules. Most of them are nonspecific IgE molecules; the concentration of specific IgE is usually lower. The second type of receptors is low affinity (Fc e RII). They are found on macrophages, eosinophils and platelets and do not have cross-specificity with the first type of receptor. The affinity of these receptors, as well as the number of cells carrying them, can increase. This leads to the fact that the initial mechanism for the development of an immediate allergic reaction (early phase in the first 15-20 minutes) can continue in the form delayed phase (after 4-8 hours), characterized by the development of inflammation. In the development of the delayed phase, an important role is played by the accumulation of cells involved in inflammation at the site of the initial reaction. These are mainly eosinophils, but also neutrophils, macrophages and lymphocytes. Specific IgE is fixed on their surface through receptors of the second type. The corresponding allergen binds to it, as a result, these cells release a number of mediators with pro-inflammatory activity (cationic proteins, reactive oxygen species, etc.). The late phase of immediate-type allergic reactions in patients with bronchial asthma is manifested by increased sensitivity and reactivity of the bronchi to various nonspecific irritants ( cold air, sharp and strong odors etc.) and is accompanied by bronchial obstruction. In persons who have undergone anaphylactic shock, it may recur (several hours after the patient has been brought out of this state). U15-20% In patients with atopy, total IgE is within the normal range or its upper limit. In addition to atopic diseases, the level of IgE can increase in respiratory viral diseases, some primary immunodeficiencies, and liver diseases.

    The pathochemical stage of the type I reaction begins after the allergen binds to IgE antibodies, both circulating and fixed on cells (the allergen forms bridges between the IgE antibodies fixed on cells).

    Activation of mast and basophil cells leads to the release of various mediators, which is morphologically defined as their degranulation. The process of releasing mediators requires energy supply, so blocking energy production also blocks the release of mediators.

    From mast cells and basophilic leukocytes, various mediators have been isolated, and some of them are found in cells in finished form. Some of them are easily secreted from the existing “reserve” (histamine, serotonin, various eosinophilic chemotactic factors), others are more difficult to release from the cell, since they are part of the granule matrix (heparin, arylsulfatase A, galactosidase, chemotrypsin, superoxide dismutase, etc. ). A number of mediators are not pre-deposited. They are formed after cell stimulation (leukotrienes, platelet-activating factors, etc.). These mediators, designated as primary, act on blood vessels and target cells indirectly, including in the development allergic reaction eosinophils, platelets and other cells. As a result, eosinophilic and neutrophilic granulocytes migrate to the site of activation of mast cells, which in turn also begin to secrete mediators designated as secondary - phospholipase D, arylsulfatase B, histaminase (diamine oxidase), leukotrienes, etc.

    Accumulating mediators have a pathogenic effect on cells, which leads to the development of a pathophysiological stage.

    Nonspecific mechanisms:

      imbalance of the influences of the sympathetic and parasympathetic innervation of the body systems, less pronounced in rhinitis and most pronounced in atopic dermatitis.

    In all three classical atopic diseases, cholinergic reactivity is increased, which is manifested by a sharper constriction of the pupil when cholinomimetics are instilled into the eyes compared to that in healthy individuals. When asthma is combined with dermatitis, spontaneous sweating and sweating stimulated by cholinomimetics are increased. In atopic asthma, in addition, the cholinergic tone of the bronchi is increased, which is manifested either by an asthma attack or by an increase in the reactivity and sensitivity of the bronchi when conducting provocative tests with cholinomimetics.

    In atopy, p-2-adrenergic reactivity is reduced. A. Szentivahyi (1968) even put forward the P-adrenergic theory of atopic disorders in bronchial asthma and the development of atopy in general. Reduced P 2 -adrenoreactivity is manifested by a lower degree of glycogenolysis, lipolysis, increased pulse pressure and cAMP formation in leukocytes with the addition of adrenaline or isoproterinol compared with that in healthy individuals.

    At the same time, α-adrenoreactivity increases, which is not detected in rhinitis; it can be found in asthma and a particularly sharp increase in atopic dermatitis. The latter have pronounced vasoconstriction in the form of white dermographism, pale complexion and decreased temperature of the skin of the fingers;

    increased ability of mast cells and basophils to release mediators both spontaneously and in response to various non-immunological stimuli. It has been established that basophils from patients with atopic rhinitis and/or asthma, atopic dermatitis release histamine more easily than leukocytes from healthy people in response to various non-immunological (nonspecific) stimuli (methacholine, Con-A, calcium ionophores, polymyxin-B, etc.) . Moreover, in these patients, spontaneous release of histamine by basophils is possible. Mast cells from bronchoalveolar lavage in patients with atopic asthma have similar properties. This effect is associated with increased activity of cAMP phosphodiesterase in cells and a decrease in the concentration of the latter. Inhibition of phosphodiesterase in these cells led to an increase in cAMP levels and normalization of histamine release

    3) it is known that atopy is accompanied varying degrees eosinophilia and infiltration of the mucous membranes and secretions of the respiratory tract and gastrointestinal tract.

    Features of reactivity of people of three constitutional types

    At the same time, the fact that the genes responsible for the formation of the atopic genotype are located on different chromosomes leads to the independence and randomness of the transmission of a number of genes to the offspring and, consequently, to a different set of these genes in each individual. In this regard, some will have a more or less complete atopic genotype, others will have a set of genes encoding the development of predominantly specific or nonspecific mechanisms, and others will have only nonspecific mechanisms. Hence the possibility of various phenotypic manifestations of atopy: from its full picture to single signs of the atopic phenotype, and these signs can relate to both specific and nonspecific components of atopy. In this regard, in relation to atopy, all people can be divided into the following 3 constitutional types: atopic, pseudoatopic and non-atopic. The latter includes people who do not have genes encoding specific and nonspecific mechanisms in their genotype. Features of the reactivity of each of these types are presented in table. 5.4.

    Table 5.4


    Signs

    Constitution type

    atopic

    pseudoatopic

    non-atopic

    Mechanisms

    Specific and

    Only or

    development of atopy

    nonspecific

    mainly

    nonspecific

    Predominance

    T X 1-dependent

    Predominance

    T x 2-dependent

    Originally exists

    howling unspicy

    physical hyperreality

    tissue activity

    In persons with an atopic constitution, the intake of an allergen is accompanied by the development of typical atopic diseases (hay fever, year-round atopic rhinitis, atopic variant of bronchial asthma, etc.). Persons with a pseudoatopic constitution, having mainly nonspecific mechanisms from the atopic genotype, do not respond to allergens; causal factors they become irritants (irritating substances) and pseudoallergens (for example, non-steroidal

    anti-inflammatory drugs, physical activity, etc.). Manifestations of pseudoatopic diseases are similar to those of true atopic diseases, although they do not have IgE-mediated pathogenesis immune mechanisms, therefore, the total IgE in such individuals is normal and it is not possible to find an allergen.

    The object of atopic alteration can be any system of the body. The development of damage to one or another body system is determined not only by its general properties, or constitution, but also by the characteristics of the reactivity of one or another “shock” organ (body system). It is this, along with the nature of the allergen and the routes of its entry, that determines the localization of the process and the appearance of a specific atopic disease.

    The reactivity features of the “shock” organ are determined by many influences on its functioning. Of these, the greatest role is played by a shift in the balance of influences of the parasympathetic and sympathetic parts of the nervous system on a given organ. This usually manifests itself in one system of the body. Thus, white dermographism is detected only in atopic dermatitis, but, as a rule, it does not occur in atopic rhinitis or asthma. In asthma, cholinoreactivity is increased respiratory tract, but it does not appear in atopic dermatitis, which is accompanied by damage only to the skin.

    Skin atopy is a disease that means increased sensitivity of the skin to various external and internal factors. This disease is recurrent in nature and is a hereditary form of allergy caused by reagin antibodies. Among the titles of this disease you can find the following synonyms: syndrome atopic eczema, atopic eczema, constitutional eczema, atopic dermatitis syndrome, chronic allergic dermatitis.

    Atopic dermatitis

    This is a chronic allergic skin disease inflammatory in nature, the main clinical manifestations of which are itching and eczematous skin rashes. The disease has a seasonal dependence, for which exacerbations are natural in winter, and remissions (complete or partial) in summer. In most cases, if it is not cured in adolescence, then relapses of the disease are periodically observed in adulthood.

    Development mechanism

    Its origin depends on many factors, primarily on disorders associated with the immune system. In the blood of patients with atopy, the ratio of Th1 and Th2 lymphocytes can be changed, as a result of which the production of specific IgE antibodies (reagins) increases significantly. In dermatitis, an immune trigger is activated in which reagins interact with allergenic substances on the surface of mast cells. The latter contain biologically active substances that, under the influence of reagins, are released into the blood plasma. Thus entering the bloodstream, the active substances heparin and histamine thin the blood and make the walls of blood vessels more permeable. This provokes tissue swelling and the attraction of cells responsible for the mechanisms of the inflammatory response to this area of ​​the body.

    Chronic inflammation of the skin can be maintained by a fungal or bacterial infection (directly, or through an allergy to the components of fungal and bacterial cells).

    Prevalence and risk groups

    Atopy is called a “disease of civilization” because it occurs mostly in developed countries. This is due to the weakening immune system and failures in its work against the backdrop of environmental deterioration, stress, abundance of artificially synthesized food additives, aggressive detergents.

    It most often affects young children who have immune and digestive system not yet formed. Also, the risk of developing atopic eczema syndrome is higher in children whose immediate relatives have diseases of an allergic nature.

    The highest probability of the appearance of the first symptoms of the disease is observed in the first few days after birth, and accounts for 70-80% of all cases of atopy.

    Atopic triad and march

    The designation “atopic triad” has a conditional relationship between and atopy.

    Also, atopy may be the first disease in the so-called “allergic march” - the progression of diseases of allergic origin throughout a person’s life. Dermatitis provoked by food can accelerate the course of the “allergic march”.

    Causes of atopic eczema

    The relationship between food allergens (allergic triggers) and neurodermatitis has been scientifically proven. However, in addition to food allergens, microbial, inhaled and contact antigens, and medications may participate in the pathogenesis of the disease.

    Risk factors include endogenous (internal) and exogenous (external).

    Endogenous

    The main factor is heredity. Thus, in 80% of cases of the disease, patients had close relatives suffering from neurodermatitis, hay fever, food allergies, bronchial asthma, recurrent allergic reactions.

    In addition to the above factors associated with immunoglobulin E, the disease can be caused by non-immune factors. This may be pathological activity of mast cells, in which there is an increase in the production of pro-inflammatory substances. Such excessive synthesis provokes increased skin sensitivity, which becomes a factor embodying atopy. Also, the disease may depend on pathologies during the immune response or on severe stress, provoking spontaneous mutations.

    Exogenous

    At an early age, the dominant factor is the action of food allergens. In second place are psycho-emotional factors, which are caused by an excessive increase in workload, conflict situations in the social circle, and changes in weather conditions.

    Among the non-allergenic factors that aggravate the manifestations of the disease are:

    • overdrying the skin with soap, shower and bath products;
    • swimming in the sea or pool;
    • teething in children;
    • bad ecology;
    • fabric that irritates the skin (synthetic and woolen fabrics);
    • dry air;
    • high temperature, causing profuse sweating;
    • smoking.

    Symptoms

    The most characteristic symptoms of atopic dermatitis are itching of the skin and their specific changes (erythema, rashes, peeling, swelling). If a secondary infection is added to it, this may manifest itself as pustules.

    When diagnosing this disease, specialists use the following criteria:

    1. Localization of itchy spots (characteristic areas: neck, elbow, popliteal fossa, front of the ankle, face).
    2. The presence of heredity (allergic diseases in close relatives).
    3. Dry skin.
    4. Age at which symptoms first appeared (infancy is the most typical).

    Neurodermatitis has 2 stages: acute and chronic. The acute stage is characterized by redness of the skin (erythema), papular rash, swelling and peeling of the skin, skin erosion, and the presence of “crusts.”

    The chronic stage is characterized by thickening of the epidermis (due to high trauma to the skin), the appearance of cracks in hairless areas (feet and palms), pigmentation, and abundant traces of scratching.

    The chronic stage is also distinguished by the following characteristics:

    • shiny nails with smoothed edges;
    • the appearance of a bald area on the back of the head;
    • wrinkles on the lower eyelid (in children).

    Phases of the disease

    Every age period, in which the disease occurs, has its own clinical features. This depends on the difference in the reaction to the factor that provokes it, and, accordingly, the localization of the disease.

    Conventionally, atopic dermatitis is divided into 3 phases: infant, childhood and adult. Typically, the older the patient, the milder the symptoms. acute stage diseases.

    Infant phase

    This is the initial stage, the first signs of which can be observed in children under 2 years of age. Inflammatory skin changes are localized on the cheeks and forehead. As the disease develops, the process moves to the scalp area, the area behind the ears, the back of the neck, buttocks, and lower legs (from the outside).

    Inflamed areas are characterized by swelling and redness, weeping, and milky scabs (crusts) form. At subsequent stages, peeling and papular rashes appear.

    Child phase

    The next stage is typical for children aged 2 to 10 years. Pathological changes in the skin are localized in the folds of the skin, on the bend of the joints (wrist and ankle), on the neck from the back of the head, in the areas behind the ears. The skin is flaky, dry, uneven pigmentation. Cracks may appear, which increases the likelihood of a secondary infection.

    In more severe forms of the disease, the patient may develop an atopic face, which is characterized by pale grayish skin and excessive pigmentation of the area around the eyes. In this phase, especially upon contact with allergens, the “allergic march” often progresses - symptoms of Quincke’s edema, bronchial asthma or urticaria appear.

    Adult phase

    It occurs during adolescence and adulthood. Lesions of the dermis are localized over large areas and can cover the face, neck, top part body (including limbs). When the disease is severe, the entire body is affected. skin covering.

    There is a high probability of a secondary infection (fungal or viral), which entails an increase in body temperature and an increase in lymph nodes. Progression of other allergic diseases is observed.

    By the age of 30, the manifestations of atopy tend to decrease, but other diseases of allergic origin progress.

    Complications

    View Pathologies
    Allergic
    Non-allergic
    • gastrointestinal;
    • autoimmune;
    • oncological.
    Bacterial
    • , provoked by Staphylococcus aureus;
    Viral
    • rubella;
    • herpes virus.
    Fungal
    • dermatomycosis.
    Eye diseases
    • ectropion (inversion of the lower eyelid);
    • cataract;
    • corneal erosion.
    Pathologies of the lymphatic system dermatopathic lymphadenitis.

    Diagnostics

    First of all, if atopy is suspected, it is necessary to exclude symptomatically similar pathologies, so as not to waste time and not harm the body. Among these are:

    • limited neurodermatitis;
    • mycosis fungoides;
    • toxicoderma;
    • chronic eczema;
    • lichen planus.

    Laboratory diagnostics are required to identify the disease:

    • general urine analysis;
    • stool tests: bacteriaological, for dysbacteriosis, for helminths, coprogram (chemical, physical, microscopic characteristics);
    • blood tests: for antibodies, for sugar levels, biochemical;
    • allergy tests: skin application (applications with allergens), scarification (by damaging the upper layer of the skin with a scarifier), intradermal (subcutaneous injection of antigen) and provocative (by the action of allergens on the mucous membrane of the nose, eyes or mouth).

    An accurate diagnosis can be established only by taking into account the clinical picture and a well-collected history of the disease. Diagnosis and treatment are carried out by a dermatologist and allergist; it is possible to involve a gastroenterologist, otolaryngologist and endocrinologist.

    Treatment

    The treatment is complex and consists of diet, drug therapy and physiotherapeutic procedures.

    Diet for atopy

    Symptomatic pharmacotherapy

    To eliminate signs of the disease, use:

    • antihistamines – (from 2 years);
    • antibiotics that prevent the addition of a secondary infection - Bactroban (from 2 months);
    • anti-inflammatory drugs for external use – Afloderm cream (from 6 months);
    • vitamin B6, which helps restore skin;
    • , moisturizing the skin and restoring lipid metabolism, – Lipikar (from birth).

    Physiotherapy

    It is also possible to treat dermatitis using the following physiotherapeutic procedures:

    • phototherapy – ultra-violet rays suppress overly active cellular immunity in the affected area;
    • acupuncture – influence on certain points of the body;
    • Magnetic therapy improves the functioning of the autonomic nervous system and tissue nutrition;
    • extremely high-frequency therapy reduces the pathological activity of the immune system and affects metabolic processes;
    • Hyperbaric oxygen therapy improves blood circulation.

    Atopic skin care

    Dry problem skin First of all, cleansing is necessary. The patient is recommended to use purified water for washing. You should also not use hygiene products which dry out the skin. Atopic dermis needs softening and moisturizing. For this purpose, emonlents are used - fat-like substances that moisturize the skin, for example, Emolium, Locobase, Topicrem.

    It is important to remember that air humidity plays an important role in this matter. During the heating season, you should use a humidifier. In addition, you should always drink enough liquid.

    To minimize the manifestations of the disease, it is important:

    • avoid contact with the allergen;
    • regulate the temperature (the recommended room temperature should not exceed 23 degrees);
    • maintain the level of humidity in an apartment or house;
    • do not use aggressive detergents;
    • give preference to clothes made of cotton fabric;
    • avoid stressful situations;
    • do not use hard washcloths when bathing (only fabric ones are allowed);
    • do not scratch the affected areas;
    • avoid excessive sweating.

    Prognosis and prevention

    In a family in which the closest relatives of a small child have diseases of an allergic nature (that is, the baby is at risk of getting atopic dermatitis), parents should prevent the increased sensitivity of their child’s skin.

    When the first signs appear, all possible measures must be taken to minimize contact with antigens and relieve symptoms. At the very first stages of the disease, the child should receive correct diagnosis and a treatment regimen to avoid further development of atopy.

    Clinical recovery is considered to be the absence of symptoms for 3-7 years. Many patients recover during puberty, and almost 40% of patients get rid of the pathology upon reaching 30 years of age.

    With improper treatment and/or contact with an allergen, symptoms may intensify, and the “allergic march” progresses.