What are atopic diseases and atopic skin? Atopic diseases

Type I hypersensitivity reactions include atonic and many allergic disorders. The terms atopy and allergy are often used interchangeably, but in reality they are different concepts. Atopy is an excessive IgE-mediated immune response; all atonic disorders are classified as type I hypersensitivity reactions. An allergy is any, regardless of mechanism, excessive immune response to an external antigen. Thus, the basis of any atopy is an allergic reaction, but many allergic reactions (for example, hypersensitivity pneumonitis) are not atopic disorders. Allergic diseases are the most common diseases in humans.

Atopy most often affects nasal cavity, eyes, skin and lungs. These disorders include atopic dermatitis, contact dermatitis, urticaria and angioedema(which may primarily manifest as skin lesions or symptoms of a systemic disease), latex allergy, allergic lung diseases (eg, asthma, allergic bronchopulmonary aspergillosis, hypersensitivity pneumonitis), and allergic reactions to stinging insects.

Causes of atopic conditions

The development of allergies is caused by a complex of genetic factors, environmental factors and local factors. The role of genetic factors is the presence of a hereditary predisposition to diseases associated with atopy and specific HLA loci, and polymorphism of genes responsible for high affinity, the tnf chain of the IgE receptor, IL-4nCD14.

Environmental factors interact with genetic ones at the level of maintaining the Th2 immune response, which activate eosinophils and IgE production and are proallergic. Normally, the initial encounter with bacterial and viral infections and endotoxins (lipopolysaccharides) in early childhood shifts the response from natural Th2 to TM, which suppress Th2 and induce tolerance to foreign antigens; this mechanism can be mediated by Toll-like receptor-4 and is realized through the development of a population of regulatory T lymphocytes (CD4+, CD25+), which suppress the Th2 response. Currently, in developed countries, there is a tendency to form small families with a small number of children, a cleaner home environment, early use of vaccination and antibiotic therapy, which deprives children of such exposure to antigens and suppresses Th2 suppression; such behavioral changes may explain wide use some allergic conditions. Other factors contributing to the spread of allergic conditions include chronic contact with the allergen and sensitization, diet, and physical activity.

Local factors include adhesion molecules of the epithelium of the bronchi, skin, and gastrointestinal tract, which direct Th2 to target tissues.

Thus, the allergen induces IgE-mediated and Th2 cell immune responses. Allergens are almost always low molecular weight proteins, many of which can be found among air particles. Allergens, including house dust, house dust mite excrement, waste products of domestic animals, pollen (trees, grasses, weeds) and mold, are often responsible for the development of acute and chronic allergic reactions.

Pathological physiology of atopic and allergic conditions

After the allergen combines with IgE, histamine is released from the intracellular granules of mast cells; these cells are found everywhere in the body, but their greatest concentration is observed in the skin, lungs, and gastrointestinal mucosa; histamine enhances the activation of immune cells and is the primary mediator of the clinical manifestations of atopy. Violation of tissue integrity and various chemical agents (eg, irritants, opioids, surfactants) can cause the release of histamine directly, without the participation of IgE.

Histamine causes local vasodilation (erythema), which increases capillary permeability and causes edema (blisters), surrounding arteriolar vasodilation is mediated by a neuronal reflex mechanism (hyperemia) and stimulation of sensory endings (itching). Histamine causes contraction of smooth myocytes of the airways (bronchoconstriction) and the gastrointestinal tract (increased gastrointestinal motility), increases the secretion of the salivary and bronchial glands. When histamine is released systematically, it becomes an effective arteriolar dilator and can cause widespread peripheral blood stasis and hypotension; cerebral vasodilation may be a factor in the development of headaches of vascular origin. Histamine increases capillary permeability; the resulting loss of plasma and plasma proteins from the vascular bed can cause circulatory shock. This causes a compensatory increase in the level of catecholamines, the source of which are chromaffin cells.

Symptoms of atopic and allergic conditions

Most general symptoms include rhinorrhea, sneezing, nasal congestion (damage to the upper respiratory tract), shortness of breath and dyspnea (damage to the lower respiratory tract) and itching (eyes, skin). Symptoms include swelling of the turbinates, pain in the accessory sinuses during palpation, shortness of breath, conjunctival hyperemia and swelling, and lichenification of the skin. Stridor, shortness of breath, and sometimes hypotension are life-threatening signs of anaphylaxis. In some children, chronic allergic lesions are indicated by a narrow and highly arched palate, a narrow chin, an elongated upper jaw with a deep bite (allergic face).

Diagnosis of atopic and allergic conditions

A thorough history is usually more reliable way than conducting tests and screening. The history includes information about the frequency and duration of attacks, changes occurring over time, precipitating factors if known, relationship with seasons or a specific situation (for example, predictable onset of attacks during the flowering season; after contact with animals, hay, dust; during exercise times; in certain locations), family history of similar symptoms or atopic disorders; response to the treatment used. The age at onset of the disease may be important in diagnosing asthma, since childhood asthma is atonic in nature, but asthma that begins after 30 years of age is not.

Non-specific tests

Certain tests can confirm or refute the allergic nature of the symptoms.

You can examine conjunctival, nasal secretion or saliva for the content of leukocytes; detection of any number of eosinophils suggests Th2-mediated allergic inflammation.

Specific tests

Skin testing uses a standardized concentration of antigen injected directly into the skin; special tests are performed when a careful history and general examination do not reveal the cause of the symptoms. Skin tests are more informative in diagnosing rhinosinusitis and conjunctivitis than in diagnosing allergic asthma or food allergies; The negative response for food allergies is very high. The most commonly used antigens are pollen (trees, grass, weeds), mold, house dust mite, animal waste products and serum, stinging insect venom, food products, p-lactam antibiotics. The choice of the administered antigen is based on medical history and geographic location. Two technologies can be used: subcutaneous injection (injection) and intradermal. The first method allows you to identify large quantity allergens. The intradermal test is more sensitive but less specific; it can be used in assessing sensitivity to an allergen when the results of a subcutaneous test are negative or equivocal.

In a subcutaneous test, a drop of antigen extract is applied to the skin, then the skin is stretched, pricked, or punctured through the drop of extract using the tip of a 27-gauge needle at a 20° angle or using an approved device. With the intradermal technique, the extract is injected intradermally with a 0.5- or 1-mm syringe using a 27-gauge needle with a short bevel until a 1- or 2-mm blister is formed (usually about 0.02 ml). Both subcutaneous and intradermal tests should include another solution as a negative control and histamine (10 mg/ml for the subcutaneous test, 0.01 ml in a 1:1000 solution for the intradermal test) as a positive control. For patients with a rare generalized reaction (less than once a year) to the test antigen, the test begins with the standard reagent diluted 100 times, then 10 times, and finally the standard concentration. The test is considered positive when a blister and hyperemia appear, and the diameter of the blister is 3-5 mm larger than in the negative control after 15-20 minutes. A false positive response occurs with dermographism (blisters and hyperemia are provoked by stroking or scarifying the skin). A false negative response occurs when the allergen extract is improperly stored or expired or when taking certain (for example, antihistamines) drugs that suppress reactivity.

Radioallergosorbent diagnostics (RASD, RAST - radioallergosorbent testing) determines the presence of allergen-specific serum IgE and is performed when skin tests are contraindicated, for example, with generalized dermatitis, dermographism, a history of anaphylactic reaction to an allergen, or the need to take antihistamines. The known allergen in the form of an insoluble polymer-allergen conjugate is mixed with serum and detected using 125 1-labeled anti-1gE antibodies. Any allergen-specific serum IgE binds to the conjugate and is determined by measuring the amount of 125 1-labeled antibodies.

Provocative tests involve direct contact of mucous membranes with the allergen and are used in patients who need to document a reaction (for example, establishing occupational hazard or disability) and sometimes to diagnose food allergies. Ophthalmic examination has no advantage over skin tests and is rarely performed. Nasal or bronchial administration of a provoking agent is also a possible test, but the bronchial challenge test is used only if clinical significance positive skin test is not clear or no antigen extracts are available (eg, occupational asthma).

Treatment of atopic and allergic conditions

Environmental control

Removing or preventing contact with the allergen is the basis of allergy treatment.

Therefore, preference should be given to pillows with synthetic fibers and dense covering on mattresses; it is necessary to wash bed linen frequently in hot water; exclude soft upholstery, soft toys, carpets, and contact with pets; fight cockroaches; It is also recommended to use desiccant absorbers in restrooms, basements and other poorly ventilated, damp areas. Other measures may include vacuuming and filtering living areas using high-efficiency particulate air (HEPA), eliminating food allergens, limiting pets to certain rooms, and frequently damp-cleaning furniture and carpets. Additional non-allergenic triggers of allergic reactions should be excluded or strictly controlled ( cigarette smoke, strong odors, irritating smoke, air pollution, low temperatures, high humidity).

Antihistamines

Antihistamines do not affect the production or metabolism of histamine, but block its receptors. H2 blockers are the main element in the treatment of allergic diseases. H2 blockers are used primarily to suppress gastric acid secretion and have limited value in the treatment of allergies; they may be used for certain atopic disorders, especially chronic urticaria.

Oral H2 blockers provide symptomatic treatment of various atopic and allergic disorders (seasonal hay fever, allergic rhinitis, conjunctivitis, urticaria, other dermatoses, minor reactions due to transfusion of incompatible blood and administration of radiocontrast agents); they are less effective for allergic bronchoconstriction and vasodilation. The onset of action is usually observed after 15-30 minutes, the peak reaches after 1 hour, the duration of action is usually 3-6 hours.

Among oral H2-blockers, drugs with or without sedation are distinguished (preference should be given to drugs with less sedation). Sedating antihistamines are widely available without a prescription. All of these drugs have significant sedative and anticholinergic effects; but they also have certain limitations when prescribed to elderly patients, patients with glaucoma, incipient prostate hyperplasia, constipation, and dementia. Non-sedating (non-anticholinergic) antihistamines are preferred unless sedation is necessary (eg, nighttime treatment for an allergic condition or short-term treatment insomnia in adults or nausea in younger patients). Anticholinergic effects may also partially justify the use of sedating antihistamines for symptomatic treatment rhinorrhea with acute respiratory infections.

Antihistamine solutions can be used intranasally (azelastine for the treatment of rhinitis) or in the form of drops for instillation into the eyes (azelastine, emedastine, ketotifen, levocabastine, olopatadine for the treatment of conjunctivitis). Diphenhydramine is also available for local application, but it is not recommended for use; its effectiveness has not been proven, it can cause drug allergies in young children who are simultaneously using oral H2 blockers; Anticholinergic toxicity may develop.

Mast cell stabilizers

Examples of this group of drugs are cromolyn and nedocromil. These drugs block the release of mediators from mast cells; they are used when other drugs (antihistamines, local glucocorticoids) are ineffective or have low tolerance. Ophthalmic forms are also used (eg, lodoxamide, olopatadine, pemirolast).

Anti-inflammatory drugs.

NSAIDs are ineffective. Glucocorticoids can be given intranasally or orally. Oral glucocorticoid drugs are used for systemic severe but self-limited allergic disorders (eg, seasonal asthma flare-ups, severe widespread contact dermatitis) and for the treatment of conditions refractory to current therapy.

Antileukotriene drugs are used to treat mild forms of persistent bronchial asthma and seasonal allergic rhinitis.

Anti-1gE antibodies (omalizumab) are used to treat moderate severity or persistent or severe bronchial asthma refractory to standard therapy; this drug can be used in the treatment of refractory allergic rhinitis.

Immunotherapy

Contact with the allergen in gradually increasing doses (hypo- or desensitization) by injection or large doses sublingually can induce tolerance and is used if contact with the allergen cannot be prevented and drug therapy does not give desired results. The mechanism is unknown, but may be related to the induction of IgG, which competes with IgE for the allergen and blocks IgE from binding to their receptors on mast cells; and may be associated with the induction of interferon γ, IL-12 and cytokines secreted by TM lymphocytes or the induction of regulatory T lymphocytes.

To achieve the full effect, injections must be carried out monthly. Typically start with a dose of 0.1 to 1.0 biologically active units (BAU) depending on initial sensitivity and then increase weekly or biweekly as needed. th 2 times for each injection until the maximum tolerant concentration is reached. Patients should be observed for 30 minutes with each dose increase due to the risk of anaphylaxis after injection. Maximum dose should be administered every 4-6 weeks year-round; this treatment is better than pre-season or seasonal treatment even with seasonal allergies. In this treatment, allergens are used, contact with which usually cannot be excluded: pollen, house dust mites, mold, venom of stinging insects. Insect venom is standardized by weight, with the usual starting dose being 0.01 mcg and the usual maintenance dose being 100 to 200 mcg. Desensitization to pet products is commonly used for patients who cannot avoid exposure to the allergen (veterinarians, laboratory workers), but there is insufficient data on the benefits of such treatment. Food desensitization is not indicated.

Inhaled nasal glucocorticoids and mast cell membrane stabilizers

A drug	Dosage per injection	Initial dose	Number of doses in a can (per nostril)
Inhaled nasal glucocorticoids
Beclomethasone dipropionate		> 12 years: 1 spray 2 to 4 times a day. 6-12 years: 1 spray 2 times a day
Budesonide		6 years: 2 sprays 2 or 4 times a day
Flunisolide		6-14 years: 1 spray in each nostril 3 times a day or 2 sprays in each nostril 2 or 3 times a day
Fluticasone		4-12 years: 1 spray in each nostril once a day. > 12 years: 2 sprays in each nostril once a day
Triamcinolone acetonide		> 6 years: 2 sprays 1 time per day
Systemic glucocorticoids
Dexamethasone		6-12 years: 1-2 injections 2 times a day. > 12 years: 2 sprays 2 or 4 times a day
Mast cell stabilizers
Cromolyn		6 years: 1 spray 3 or 4 times daily
Nedocromil		6 years: 1 spray in each nostril 2 times a day

Desensitization to penicillin and foreign (xenogeneic) serum can be performed.

Side effects are usually associated with overdose, sometimes with negligent administration of the drug intramuscularly or intravenously, and are manifested by a variety of symptoms from mild cough or sneezing to the point of generalized hives, severe asthma, anaphylactic shock and sometimes death. They can be prevented by a very slight increase in dose, repeating or reducing the dose if the local reaction to the previous injection was excessive (2.5 cm in diameter), reducing the dose when using fresh extracts. It is recommended to reduce the dose of pollen preparations during the flowering period.

Allergy is a disease known to mankind for a long time, which is becoming more and more common. Most allergic diseases belong to atopic pathologies.

Terminologically, atopy has existed since 1923. The clear difference is its hereditary nature.

General characteristics and reactions of the disease

Atopy is common name allergic diseases, a significant role in the development of which is played by a genetic predisposition to sensitization. Sensitization is increased sensitivity to irritants (allergens). That is, if one of the parents suffers from this disease, then the child will also suffer with a probability of 50%. If both parents suffer from this disease, then the probability of passing it on to the child increases to 75%.

Atopy is usually accompanied by a number of immune disorders:

1. Increased ability of the immune system to produce specific immunoglobulin in response even to weak antigens, to which healthy people there is no such reaction. A healthy body either completely ignores weak antigens or forms antibodies of a different class of immune globulins. In atopy, in the blood there is increased content specific and general immunoglobulin.
2. Impaired functioning of lymphocytes, expressed in a decrease in the number of T cells and an inadequate response to antigens, expressed in a skin allergic reaction.
3. Slowing down the movement of monocytes and neutrophils, which leads to a decrease in the ability of cells to digest and capture solid particles and disrupts the connections between lymphocytes and monocytes.

In addition to these immune disorders, a number of pathogenic nonspecific reactions are also monitored:

1. Violated equilibrium nervous system , which is responsible for providing organs with nerve cells.
2. Increasing ability of cells to stimulate nerve responses both for no reason at all, and for reasons not related to immunity.
3. The number of leukocytes increases, saturating the mucous membranes of organs, secretions of the respiratory system and intestines.

The external manifestations of atopic diseases in humans are similar to how allergies manifest themselves. The most characteristic atopic disease that manifests itself externally is atopic dermatitis. First external manifestation is itching. The rashes are localized in certain places - in the armpits, groin, neck, face and scalp area where hair grows. If a child suffers from atopy, dermatitis will manifest itself in the form of redness, peeling and itching of the skin immediately after taking a bath.

Causes and risk factors

All the reasons why atopy can develop can be divided into 3 groups. Among them:

1. Reasons related to genetics. According to statistics, if at least one relative in a family suffered from this disease, future offspring have a 50% chance of getting it.
2. Environmental reasons. Can complement genetic predisposition environment. The manifestation and development of atopy is influenced by contact with allergens, physical activity, various diets and a high degree of sensitization. In addition, in view of the trends in the small number of children in the family, the child receives the first vaccines and vaccinations early and may simply not have time to develop the antigens necessary to fight the disease.
3. The reasons are local. Depending on the physiological characteristics body, one or another person can tolerate the disease easier or more difficult.

As for the factors, they include various external stimuli. It could be tobacco smoke, synthetic fibers, mineral oils, mold, pets, etc. In addition, risk factors include increased sweating and taking showers or baths too often without emollients. Both can cause an exacerbation of the disease.

Symptoms of atopic reactions

Dermatologists have identified 3 stages of atopy development. These include:

1. Elementary. Develops in early childhood. Symptoms include a rash on the skin, swelling and a red coloration of the skin. If adequate therapy is used, the symptoms can be relieved quite easily.
2. Expressed. There are acute and chronic forms. Symptoms are pronounced - severe itching, swelling, blisters and crusts appear on the skin, the skin becomes scaly.
3. Remission. There are almost no symptoms. It can last up to several years.

The mechanism of atopic type reactions is quite simple:

1. Something enters the human body substance, provocative . This could be a piece of food, air, or tactile contact with an allergen.
2. By virtue of hereditary pathologies the intestines are unable to eliminate this substance on its own. Remaining in the body, it is perceived as foreign and accelerates the response of the immune system.
3. Eventually, immunoglobulin is released into the blood, which provokes an atopic reaction.

How and with what to treat pathology

When starting treatment for atopy, you need to understand what you need to achieve. There are several approaches to treatment:

1. Elimination therapy, aimed at stopping all contacts of the patient with substances that cause an allergic reaction. In addition, this therapy includes treatment with anti-allergy medications.
2. Basic type therapy, aimed at suppressing inflammation of the skin and inside the skin.
3. Treatment directed for restoration and adjustment of work immunity.
4. Treatment of diseases that accompany atopy and complicate it.

Atopic dermatitis (atopy) can only be treated under the strict supervision of a specialist who selects medications and monitors how they affect the patient.

As mentioned above, the reaction is provoked by histamine, so antihistamine therapy is also necessary.

Antihistamine therapy

To block the harmful effects of histamine on the patient, he is prescribed special medications that he takes orally. As a result, it is possible to slow down the process of inflammation of the skin. The process of taking medications can last quite a long time (from 14 days to several months), and medications can be combined. There are 3 generations of drugs. The 1st generation has the mildest effects and the body easily gets used to it, while the 2nd and 3rd are already more serious drugs, but they have more side effects, although at the same time they last longer. These generations include the following drugs:

• 1st generation. This includes drugs containing chlorphenamine, clemastine, promethazine, dimethindene, mebhydrolin;
• 2nd generation. It includes drugs containing azelastine, acrivastine, ebasin, cetrizine, loratadine;
• 3rd generation. It includes drugs containing sehifenadine, hifenadine, desloratadine, levocetrizine.

Used in the treatment of atopy antihistamines as injection solutions or tablets.

In addition to internal medications, external medications are also used, namely:

• nourishing, softening and medicinal ointments based on fats;
• well-absorbing water-based creams;
• high molecular weight and low molecular weight gel mixtures;
• anti-exudative paste mixtures;
• disinfectant compresses;
• solutions from vegetable oil and water or water and alcohol for disinfection.

Lotions made of lead and silver, as well as decoctions of medicinal herbs, are good against inflammation and itching. Birch buds, oak bark, pear leaves, chamomile and fireweed inflorescences help heal the skin and relieve inflammation.

If there is thickening of the skin, then creams and ointments containing Naftalan oil, sulfur, children, ichthyol. On initial stage Treatments use weaker ointments and creams, gradually moving to stronger ones.

To further prevent relapses in the future, patients with atopy are prescribed a diet.

Diet for atopic diseases

Often, an aggravation is caused by poor nutrition. It is possible to determine which product caused this only through laboratory testing. Based on the results of the examination, an individual diet is prescribed, excluding foods that can have a harmful effect on the body.

The most common cause of allergies is fish products, fried foods, meat-based broths, sweets, citruses, spices, mushrooms, etc. At first you will have to go on a very strict diet, but later you can slowly return harmful foods to your diet.

But the basis of the diet should remain unchanged - fruit porridge, fruits, yoghurts, cereals, steamed meat and dairy products. The composition of the diet can be selected for special cases when, in addition to allergies, there are other diseases.

What to do if complications arise?

Often the disease in question occurs simultaneously with one or more other diseases. Usually, allergies are further complicated by diseases of the digestive tract (stomach and intestines). Therefore, if complications make themselves felt, first of all, you should take care to normalize the digestive processes occurring in the body. With normal digestion, the disease can be cured faster.

To regulate the digestive organs, take the following medications:

1. Enterosorbents. They remove metabolic products and cleanse microflora. However, there is a danger that along with metabolic products they will also remove vitamins, which is not very good. Therefore, in parallel with the use of energy sorbents, it is recommended to replenish the supply of vitamins in the body from the outside. Enterosorbents are prescribed in a course and are needed to prepare the body for intestinal treatment. The most famous and frequently used enterosorbent are activated carbon tablets and attapulgite- and diosmectite-containing preparations.
2. Drugs that bring the intestinal microflora in order. These are drugs based on prebiotics (Lakitol, Lysozyme, Inulin), probiotics (Linex, Probifor), synbiotics (Normoflorin, Maltodophilus), enzymes (Pancreatin), hepatoprotectors (Beatin, Phospholipid) and bacteriophages (staphylococcal, coliproteal, Pseudomonas).

Complications can be caused not only by the disease, but also by a general deterioration of the immune system. The patient has severe vitamin deficiency. In this case, you need to think about how to provide the patient with the vitamins and minerals he needs. If the body is completely depleted, vitamins may be required in very large quantities.

Vitamins normalize metabolism, accelerate the regeneration process in the body, reduce toxicoderma and restore the natural moisture of the skin.

Historical sketch . Allergic diseases, which today are classified as a complex of atopic reactions of the body, were widely known already in ancient times under the name “idiosyncrasy”. Isolated anecdotal reports, sometimes indicating a specific allergen, appeared several centuries ago, but systematic research began only at the end of the 19th century. The first detailed publications by Dunbar, Blackley, Noon, devoted to the study of hay fever. Despite the purely empirical approach, some of the developed methods still form the basis of diagnosis and therapy (skin tests, desensitization). At the turn of the 19th and 20th centuries, Pirquet coined the term "allergy". During this period, Richet and Porticr conducted famous experiments that made it possible to formulate the concept of anaphylaxis. As a result, it was found that humoral factors (antibodies) are responsible for these phenomena. This made it possible to interpret classic allergic diseases such as asthma, allergic rhinitis and some forms of dermatoses. According to the view that immune responses serve the real reason allergic manifestations, two hypotheses have become widely known. Unitary anaphylaxis was considered as an experimental analogue known diseases, and the antigen-antibody reaction as a general pathogenetic mechanism. The dualist concept assumed that there were fundamental differences between experimental models and clinical forms allergies. Followers of this theory referred to the fact that, unlike experimental anaphylaxis clinical manifestations are observed only in some patients, and their serum injected into animals (passive transfer of antibodies) does not cause characteristic immune reactions in them. Coca proposed the term "hypersensitivity" as a general concept that included two different phenomena: anaphylaxis (an acquired, non-inherited form of hypersensitivity characterized by the presence specific antibodies in tissues) and allergies ( congenital form hypersensitivity observed only in humans and not dependent on antibodies).

The first refutation of the dualistic concept was made by Prausnitz and Kustner, who proved that allergies, in particular to fish products, are caused by humoral factors. Taking this fact into account, Coca identified atonic diseases in special group(a topos is a perverted reaction of the body). From this point of view, they are characterized by antibodies with special physical and chemical properties, which, when administered to other lindens (but not experimental animals), cause a test reaction (allergic rash). These antibodies were designated "reagins". In addition, there was a need to distinguish infectious allergies, serum sickness and contact dermatitis from the group of atopic diseases. Finally, a peculiar form was represented by familial (not caused by reagins) food allergy, although for inexplicable reasons the generally accepted intradermal test and the Prausnitz-Küstner reaction were often negative.

An accurate classification of atopic conditions became possible only after the study of Ishizaka and Johansson, who, based on immunological properties, identified the long-known reagin as immunoglobulin E (IgE).

Currently, the term “atopic diseases” refers to a group of allergic diseases that are characterized by the production of IgE reagin. When examining families of people suffering from atopic diseases, an increased incidence of allergies was repeatedly revealed. As a result of numerous studies, it was found that sensitization is not a congenital, but an acquired condition and the body’s predisposition to it can be inherited. Recently, it has been proven that similar diseases occur in animals, for example, hay fever in horses and dogs, accompanied by conjunctivitis, bronchospasms and dermatitis. Pathogenetic mechanism corresponds to type I according to the Coombs and Cell classification. However, there are still a number of questions that need to be answered:

Based on what reasons does sensitization develop due to the production of reagins, if IgE is also produced in the body of a healthy person;

Why does sensitization develop to a certain allergen;

What mediators, in addition to histamine, are important for the development of atopic conditions?

Clinical manifestations. Atopic diseases characterized not only by symptoms, but also by a certain pathogenesis. As a result of sensitization, pathological signs can be detected in virtually every organ, however practical significance have only certain symptoms. Firstly, these are those local disorders that are associated with the “entry gate” of the allergen, and secondly, these are manifestations of a generalized antigen-antibody reaction (urticaria, Quincke's edema, anaphylactic shock). All these conditions can be caused by the action of immune mechanisms, as well as by non-immunological causes. Let's consider the main clinical manifestations of atopic diseases.

1. Bronchial asthma. Atopic forms primarily include exogenous allergic asthma. The importance of IgE antibodies directed against bacterial antigens is still under debate.

2. Allergic runny nose. Classic sign serves as hay fever. With gynerplastic sinusitis and nasal polyps, atopic reactions may be one of the causes of the development of the disease.

3. Allergic diseases gastrointestinal tract. In this case, a particular problem is differential diagnosis: similar symptoms appear as a result of metabolic disorders caused by enzyme deficiency (milk allergy - lactase deficiency).

4. Atopic dermatitis. Analysis of genetic and immunological data (IgE level) leaves no doubt that this disease belongs to atopic forms.

5. Allergic rash and Quincke's edema. Acute forms of urticaria can be caused by allergies; chronic forms, as a rule, are not associated with it. Similar patterns are characteristic of Quincke's edema.

6. Anaphylaxis and serum sickness. Anaphylactic reaction observed in clinical settings, has its own characteristics. Although patients exhibit increased production of reagins, there is every reason to believe that disturbances may also cause other reactions of the immune system. A similar situation was noted in serum sickness, in the pathogenesis of which reagins, along with immune complexes, take part.

7. Migraine, epilepsy. A critical analysis of the data obtained refutes the previous assumption about the association of these diseases with atopic forms.

8. Drug allergies. Reactions after taking medications are often classified as atopic forms, without taking into account the action of a number of immune mechanisms. Basically medications capable of causing all types of allergic reactions that can occur in combination.

Atopic diseases refer to allergic skin diseases. Today this disease has reached high level distribution and is approaching the leading lists. The term appeared in the last century and refers to hereditary factor in the development of skin allergies. But atopic disease and allergies are two different things.

Why does atopy appear?

Atopy is an allergic skin disease. The patient has hypersensitivity, aggravated by a congenital predisposition. The HLA gene, which is capable of awakening it, is directly involved in the development of this disease. This pathology tends to develop in the presence of the following factors: genetics and allergenic pathogens in the external environment (food, household, industrial).

In this case, it is not a disease that arises, but a platform for its implementation. That is, under certain conditions, its awakening is easy to provoke. Even mild stress or frequent excitability can have an impact here.

The absence of atopy in parents is 20% of the risk of its occurrence in children; if one of them has an allergy, the risk increases to 50%. The atopic condition is an exclusively special case.

Symptoms

The symptoms of atopy are similar to ordinary allergies.

• dyspnea;
• nasal congestion, itchy nose;
• sneezing;
• dermatitis.

Stages of disease development

IN initial stage symptoms appear in childhood and manifest themselves in small amounts skin rash, redness and swelling.

On early stage Atopy is easy to treat.

The deep stage occurs in acute and chronic forms and is more pronounced. This is itching and swelling, the skin becomes covered with blisters, scales or crusts. During remission, symptoms are almost invisible. The remission itself can last for years.

Atopic skin

Or common in newborns up to 3 months. Mainly develops on the face (cheeks, chin). As the child grows up, the lesion covers areas of the neck, hands and skin under the knees. The disease is aggravated by attacks, but after each attack there is a remission. Attacks begin, for example, with red spots that itch very much. The skin becomes dry and may develop blisters or discharge.

The reason for the appearance of atopic skin is its increased dryness. The skin is naturally dry and weakened the immune system people suffering from this disease react instantly. External allergens can penetrate deep into the layers of the epidermis. The skin becomes very irritated, which leads to atopic eczema. Inflammation may be affected passive smoking, dirt and other external irritants.

Skin atopy is a skin allergy. Infants are susceptible to atopic skin disease. children, teenagers and adults.

The nature of childhood atopic dermatitis

Clinical manifestations are varied and depend on age.

Decisive factors can intensify the course of the disease:

• frequent washing;
• infections;
• dry air;
• food allergens;
• change in external temperature;
• contact with cosmetics and detergents.

Common Complications

The most common complications are:

1. Skin atrophy. Scratching the skin has a detrimental effect on its protective barrier. This promotes the proliferation of microbes, which gives rise to fungal flora.
2. . Ulcers form on the skin; over time, they dry out and are replaced by crusts. Various parts of the body are susceptible to purulent rashes. A person’s temperature rises and their general health deteriorates.
3. Viral infection. Stricken skin covering covered with liquid filled. The causative agent of this infection is herpes. It appears directly in the area of ​​inflammation, but can affect the genitals or mucous membranes (throat, mouth, eyes).
4. Fungus. The lesion also covers skin folds.

Treatment

The nature of atopic skin is not fully understood, but medicine is able to control the process of skin inflammation. Emollients for dry skin are the main helpers for the patient. Doctors carry out thorough infection prevention. All other actions towards the patient are aimed at soothing the skin.

The issue of treatment remains a pressing issue. Atopy - genetic disease, and therefore is chronic. Of course, steps are being taken in medicine, various drugs are prescribed, but the main thing is that treatment must be comprehensive. The following means are used:

1. Boosting the functioning of the immune system.
2. Antibiotics and antihistamines.
3. Rectal suppositories.
4. Corticosteroid injections.
5. Creams, nasal sprays.
6. Following a hypoallergenic diet.
7. Infusions of soothing herbs.

Diet and regimen for atopic dermatitis

Only a doctor can prescribe the right diet. It is not possible to identify the allergen and eliminate it on your own. After the doctor prescribes treatment, you should strictly follow the diet.

In everyday life it is important to avoid irritating factors:

• increased physical activity leads to sweating, which is not desirable for the skin;
• control over the effects of humidity (optimal humidity up to 40%);
• You can’t dry things in the room, wear clothes made of rough fabric, when washing bed linen do not use conditioner, rinse all laundry thoroughly;
• remove dust and do wet cleaning in a timely manner;
• It will be useful to install an extractor hood in the kitchen and an air purifier in the bedroom;
• during water procedures give preference regular soap no pungent odor. After showering, use skin moisturizers;
• Tanning and prolonged exposure to the sun are contraindicated.

Prevention

Preventive actions against atopy will only be effective if they are carried out in a timely manner. You need to start acting during the development of the child in the womb. Maternal toxicosis and intake play a role here. pharmacological agents and food allergens. Taking into account all these points, preventive therapy should be started.

In the first year of a baby’s life, it is important to avoid taking unnecessary medications and follow a diet. The next stage of prevention includes identifying and correcting the child’s chronic diseases and eliminating provoking factors. The local doctor will also play a coordinating role. The child must be under the supervision of a doctor. The prospect for solving the problem will be timely and high-quality diagnosis, therapy, strict adherence to preventive rules and adherence to a diet.

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 allergies is a hypersensitivity reaction to immunological mechanisms. Increased sensitivity consists in 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.

In children with atopic dermatitis, there is high probability the occurrence of allergic asthma and allergic rhinitis in the 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. Probably for characteristic symptoms More than one gene is responsible for 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, however, as a rule, it intensifies in the evening and at night, which can cause sleep disturbances, and in extreme cases may 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 infants;
• atopic dermatitis in children;
• atopy in adolescents and adults.

At atopic dermatitis Infants typically:

• the occurrence of exudative changes, localized mainly on the skin of the face, which then dry out, forming crusts;
• this often leads to bacterial infection, which is associated with scratching 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, house dust mites, and animal dander 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 infections skin.

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 based on skin atopy chronic 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 - increased level may indicate an allergy.

When setting correct diagnosis Skin tests are also used. 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 care mainly for skin we're talking about about 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. It is also important to avoid foods that cause new skin changes or strengthen existing ones.