The main task of an allergy history is to find out the connection of the disease with hereditary predisposition and the effect of allergens external environment.

Initially, the nature of the complaints is clarified. They may reflect different localization of the allergic process (skin, respiratory tract, intestines). If there are several complaints, the connection between them is clarified. Next, find out the following.

Hereditary predisposition to allergies - the presence allergic diseases (bronchial asthma, urticaria, hay fever, Quincke's edema, dermatitis) in blood relatives.

Previously suffered allergic diseases by the patient (shock, rash and itching of the skin to food, medicines, serums, insect bites and others, what and when).

Influence environment:

climate, weather, physical factors(cooling, overheating, irradiation, etc.);

seasonality (winter, summer, autumn, spring - exact time);

places of exacerbation (attack) of the disease: at home, at work, on the street, in the forest, in the field;

time of exacerbation (attack) of the disease: during the day, at night, in the morning.

Influence of household factors:

• contact with animals, birds, fish food, carpets, bedding, upholstered furniture, books;

  the use of odorous cosmetics, detergents, and insect repellents.

Connection of exacerbations:

with other diseases;

with menstruation, pregnancy, postpartum period;

With bad habits(smoking, alcohol, coffee, drugs, etc.).

Relationship between diseases and intake:

certain foods;

medicines.

Improvement of the course of the disease with:

elimination of the allergen (vacation, business trip, visiting, at home, at work, etc.);

when taking antiallergic drugs.

4. Specific methods of allergy diagnostics

Allergy diagnostic methods make it possible to identify whether a patient is allergic to a particular allergen. A specific allergological examination is carried out only by an allergist during the period of remission of the disease.

Allergy examination includes 2 types of methods:

provocative tests on the patient;

laboratory methods.

Provocative tests on a patient involves introducing a minimum dose of an allergen into the patient’s body in order to provoke manifestations of an allergic reaction. Carrying out these tests is dangerous and can lead to the development of severe and sometimes fatal manifestations of allergies (shock, Quincke's edema, attack of bronchial asthma). Therefore, such studies are carried out by an allergist together with a paramedic. During the study, the patient's condition is constantly monitored (blood pressure, fever, auscultation of the heart and lungs, etc.).

According to the method of introducing the allergen, they are distinguished:

1) skin tests (cutaneous, scarification, prick test, intradermal): the result is considered positive if itching, hyperemia, edema, papules, necrosis appear at the injection site;

2) provocative tests on the mucous membranes (contact conjunctival, nasal, oral, sublingual, gastrointestinal, rectal): a positive result is recorded in the event of clinical conjunctivitis, rhinitis, stomatitis, enterocolitis (diarrhea, abdominal pain), etc.;

3) inhalation tests - involve inhalation administration of an allergen, are used to diagnose bronchial asthma, are positive when an attack of suffocation or its equivalent occurs.

When assessing test results, the occurrence of general manifestations of the disease – fever, generalized urticaria, shock, etc. – is also taken into account.

Laboratory tests are based on the determination of allergen-specific antibodies in the blood, hemagglutination reactions, basophil degranulation and mast cells, on antibody binding tests.

5. Urticaria: definition, basics of etiopathogenesis, clinical picture, diagnosis, emergency care.

Hives is a disease characterized by a more or less widespread rash of itchy blisters on the skin, which are swelling of a limited area, mainly the papillary layer, of the skin.

Etiopathogenesis. The etiological factor can be any allergen (see question 2). Pathogenetic mechanisms – allergic reactions of type I, less often type III. Clinical picture The disease is caused by an increase in vascular permeability with the subsequent development of skin edema and itching due to excessive (as a result of an allergic reaction) release of allergy mediators (histamine, bradykinin, leukotrienes, prostaglandins, etc.)

Clinic. The clinical picture of urticaria consists of the following manifestations.

for skin itching (local or generalized);

for localized or generalized itching skin rash with the size of skin elements from 1-2 to 10 mm with a pale center and hyperemic periphery, rarely with the formation of blisters;

to increase body temperature to 37-38 C (rarely).

History (see question 3).

Examination plays a big role in diagnosing the disease.

The onset of the disease is acute. A monomorphic rash appears on the skin. Its primary element is a blister. At the beginning it is a pink rash, the diameter of the elements is 1-10 mm. As the disease progresses (several hours), the blister in the center turns pale, the periphery remains hyperemic. The blister rises above the skin and itches. Less frequently detected are elements in the form of vesicles with serous contents (in the case of erythrocyte diapedesis - with hemorrhagic contents).

The skin elements are located separately or merge, forming bizarre structures with scalloped edges. Rashes on the mucous membranes of the mouth are less common.

Episode duration acute urticaria most often from several hours to 3-4 days.

Laboratory and allergological diagnostics– laboratory test data are nonspecific, indicating the presence of an allergic reaction and inflammation.

General blood test:

slight neutrophilic leukocytosis;

eosinophilia;

acceleration of ESR is rare.

Biochemical blood test:

increase in CRP levels;

increase in glycoproteins;

increase in seromucoid level;

increase in globulin fractions of protein;

increase in the concentration of class E immunoglobulins.

After the acute phase of the disease has stopped, an allergological examination is carried out to determine the “culprit” allergen.

Emergency care for urticaria- at acute attack measures should be aimed at eliminating the most painful symptom of the disease - skin itching. For these purposes, it is usually sufficient to use internally (less often by injection) antihistamines - diphenhydramine, diazolin, fenkarol, tagevil, suprastin, pipolfen and others, rubbing itchy areas of the skin with lemon juice, 50% ethyl alcohol or vodka, table vinegar (9% solution acetic acid), hot shower. The main thing in the treatment of urticaria is to eliminate contact with the allergen.

Allergy history is the first stage diagnosis, is collected in parallel with the general clinical history and analyzed together with it. The main objectives of the anamnesis are to establish an allergic disease in the child, its nosological form(taking into account the clinic) and presumably the nature of the causally significant allergen, as well as identifying all the circumstances (risk factors) that contribute to the development of an allergic disease, since their elimination has a positive effect on the prognosis of the disease.

For this purpose, when collecting anamnesis, along with the main complaints, attention is paid to studying the premorbid background. The presence of a hereditary constitutional predisposition to is revealed. The presence of allergic diseases in the family history indicates the atopic nature of the disease in the child, and previous exudative-catarrhal diathesis indicates altered allergic reactivity. It is clarified, especially in children of the first years of life, the nature of the course of the antenatal period in order to determine possible intrauterine sensitization, which develops as a result of poor nutrition of a pregnant woman, her intake of medicines, the presence of pregnancy toxicosis, professional and household contacts with chemicals and drugs. Our observations have shown that taking medications by a pregnant woman increases by 5 times the risk of developing an allergic disease in a child in the first year of life, and her poor nutrition causes the development of food allergies. The nature of the child’s nutrition in the first year of life and the diet of the nursing mother are also clarified, since the early development of food allergies is facilitated not only by the premature introduction of supplementary feeding, complementary foods, and juices into the child’s diet, especially in excess amounts, but also by the irrational nutrition of the nursing mother. Comparison of the timing of the onset of the disease with the introduction of certain food products into the diet of the child or mother allows us to presumably determine allergenic food products for him.

When assessing the premorbid background, previous diseases, the nature of the treatment, its effectiveness, the presence of reactions to medications and vaccines, etc. are taken into account. Presence of pathology gastrointestinal tract and liver predisposes to the development of food allergies, while frequent ARVI facilitates sensitization to inhalant allergens (household, epidermal, pollen), and the child’s existing foci chronic infection may determine the development bacterial allergy.

Finding out the child’s everyday life allows us to identify potential household and epidermal allergens.

Much attention is paid to the features of the occurrence and course of allergic diseases. The start date is being determined. In children this factor has important to determine causally significant allergens, since the development of one or another type of sensitization has age-related patterns, which are characterized by the development in the first years of life of food allergy with the subsequent layering on it after two to three years of household, epidermal, and after 5-7 years - pollen and bacterial (Potemkina A.M. 1980).

The nature of the course of the disease is determined - year-round or seasonal exacerbations. The first option is observed with constant contact with an allergen (house dust, food), the second - with temporary contacts: with pollen allergies - during the spring-summer flowering season of plants, with medicinal allergies - during the period of their use, with bacterial allergies - in cold spring and autumn. year. The connection between the exacerbation of the disease and specific allergens is being clarified: with house dust - exacerbation only at home, with epidermal allergens - after playing with animals, when visiting a circus, zoo; with pollen - the appearance of symptoms of the disease only in summer, worsening of the condition outside in sunny, windy weather; for food and medicinal purposes - after consumption certain products And medicinal substances. At the same time, it is important to establish whether an elimination effect is observed, that is, the disappearance of symptoms of the disease after separation from a given allergen, and if so, this further confirms the causal relationship of the exacerbation of the disease with it.

Allergic diseases are among the polygenic diseases - both hereditary and environmental factors play a role in their development. I.I. formulated this very clearly. Balabolkin (1998): “According to the relationship between the role of environmental and hereditary factors in pathogenesis, allergic diseases belong to the group of diseases etiological factor for which the environment is present, but at the same time the frequency of occurrence and severity of their course is significantly influenced by hereditary predisposition.”

In this regard, in case of allergic diseases, the standard medical history scheme is supplemented by the “Allergological history” section, which can be divided into two parts: 1) genealogical and family history and 2) anamnesis hypersensitivity To external influences(allergenic history).

Genealogical and family history. Here it is necessary to find out the presence of allergic diseases in the pedigree of the mother and father, as well as among the patient’s family members.

The following guidelines are important for clinicians: hereditary burden on the mother’s side in 20-70% of cases (depending on the diagnosis) is accompanied by allergic diseases; on the father's side - significantly less, only 12.5-44% (Balabolkin I.I., 1998). In families where both parents suffer from allergic diseases, the rates of allergic morbidity in children are 40-80%; only one of the parents - 20-40%; if brothers and sisters are sick - 20-35%.

And genetic research has provided the basis for a hereditary predisposition to allergic diseases (atopy). The existence of a genetic system of nonspecific regulation of IgE levels, carried out by genes of excessive immune response - Ih genes (immune hyperresponse), has been proven. These genes are associated with the major histocompatibility complex antigens A1, A3, B7, B8, Dw2, Dw3, and high level IgE is associated with haplotypes A3, B7, Dw2.

There is evidence of predisposition to specific allergic diseases, and this predisposition is supervised by different antigens of the HLA system, depending on nationality.

For example, a high predisposition to hay fever in Europeans is associated with the HLA-B12 antigen; in Kazakhs - with HLA-DR7; Azerbaijanis have HLA-B21. However, immunogenetic studies in allergic diseases cannot yet provide specific guidelines for clinicians and require further development.

Allergenic history. This is a very important section of diagnostics, since it allows you to obtain information about the most possible reason development of an allergic disease in a particular patient. At the same time, this is the most labor-intensive part of the anamnesis, since it is associated with a large number various environmental factors that can act as allergens. In this regard, it seems appropriate to provide a specific survey algorithm based on the classification of allergens.

Food allergens. Dependence on food allergens should be clarified especially carefully in case of allergic diseases of the skin and gastrointestinal tract.

It should also be remembered that food allergies are most common in children, especially those under 2 years of age.

“As with other types of allergies, the quality of the allergen is critical in food allergies, but in food allergens their quantity should not be underestimated. A prerequisite for the development of a reaction is exceeding the threshold dose of the allergen, which happens when there is a relative excess of the product in relation to the digestive capacity of the gastrointestinal tract. This is an important thesis, since it allows us to identify patients with various disorders digestion and correction of digestive disorders to be used in therapeutic and preventive programs for food allergies.

Almost any food product can be an allergen, but the most allergenic cow's milk, chicken eggs, seafood (cod, squid, etc.), chocolate, nuts, vegetables and fruits (tomatoes, celery, citrus fruits), seasonings and spices, yeast, flour. IN lately Allergens associated with additives and preservatives that increase the shelf life of foreign-made food products have become quite widespread. If these additives were used in domestic products, they also caused an allergic reaction in persons sensitive to them, and these people served as indicators of the presence of foreign impurities in domestic food. We gave this type of allergy the conventional name “patriotic allergy.”

Possible cross allergy within the same botanical family: citrus fruits (oranges, lemons, grapefruits); pumpkins (melons, cucumbers, zucchini, pumpkins); mustard (cabbage, mustard, cauliflower, Brussels sprouts); nightshades (tomatoes, potatoes); pink (strawberries, strawberries, raspberries); plums (plums, peaches, apricots, almonds), etc. You should also focus on meat products, especially on poultry meat. Although these products do not have great sensitizing activity, antibiotics are included in the diet of birds before slaughter, and they can cause allergic diseases associated not with food allergies, but with drug allergies. When it comes to flour, flour often becomes an allergen when inhaled rather than when ingested.

Important in collecting this history are indications of heat treatment, since heat treatment significantly reduces the allergenicity of food products.

House dust allergens. These allergens are most significant for allergic respiratory diseases, in particular bronchial asthma. The main allergens of house dust are chitinous cover and waste products of house mites Detmatophagoides pteronyssimus and Derm. Farinae. These mites are widespread in bedding, carpets, upholstered furniture, especially in older homes and old bedding. The second most important allergens of house dust are allergens of mold fungi (usually Aspergillus, Alternaria, PeniciUium, Candida). These allergens are most often associated with damp, unventilated areas and the warm season (April-November); they are also integral part library dust allergens. The third most important in this group are pet allergens, with cat allergens (dander, hair, saliva) having the greatest sensitizing ability. And finally, house dust includes insect allergens (chitin and cockroach excrement); Daphnia used as dry fish food; bird feather (pillows and feather beds, especially with goose feathers; parrots, canaries, etc.).

Plant allergens. They are primarily associated with hay fever, and the main place here belongs to pollen, and most often the etiological factor of hay fever is pollen from ragweed, wormwood, quinoa, hemp, timothy, rye, plantain, birch, alder, poplar, and hazel. Pollen from cereals, malvaceae, wormwood, ragweed, sunflower, pollen from birch, alder, hazel, poplar, and aspen has common antigenic properties (cross-allergy). These authors also note the antigenic relationship between pollen of birch, cereals and apples.

Insect allergens. The most dangerous poisons are insects (bees, wasps, hornets, red ants). However, allergic diseases are often associated with saliva, excrement and secretions of the protective glands of blood-sucking insects (mosquitoes, midges, horseflies, flies). More often, allergic diseases associated with these allergens occur in the form of skin manifestations, however (especially the poison of bees, wasps, hornets, ants) can also cause severe conditions(Quincke's edema, severe bronchospasm, etc.) up to anaphylactic shock and death.

Drug allergens. An anamnesis in this direction must be collected very carefully, since this is not only a diagnosis of an allergic disease, but, first of all, it is the prevention of a possible death due to the unexpected development of anaphylactic shock. There is no need to convince that this type of allergy history should become a mandatory tool for all clinicians, since cases of anaphylactic shock and deaths with the introduction of novocaine, radiopaque substances, etc.

Because medications tend to be relatively simple chemical compounds, they act as haptens, combining with body proteins to form a complete antigen. In this regard, the allergenicity of medicinal substances depends on a number of conditions: 1) the ability of the drug or its metabolites to conjugate with protein; 2) the formation of a strong bond (conjugate) with the protein, resulting in the formation of a complete antigen. Very rarely, an unchanged drug can form a strong bond with a protein; more often this is due to metabolites formed as a result of the biotransformation of the drug. It is this circumstance that determines the fairly frequent cross-sensitization of medicinal substances. L.V. Luss (1999) provides the following data: penicillin cross-reacts with all drugs penicillin series, cephalosporins, sultamicillin, sodium nucleinate, enzyme preparations, a number of food products (mushrooms, yeast and yeast-based products, kefir, kvass, champagne); sulfonamides cross-react with novocaine, ultracaine, anesthesin, antidiabetic agents (antidiabet, antibet, diabeton), triampur, para-aminobenzoic acid; analgin cross-reacts with salicylates and other non-steroidal anti-inflammatory drugs, food products, containing tartrazine, etc.

In this regard, another circumstance is important: the simultaneous administration of two or more drugs can mutually affect the metabolism of each of them, disrupting it. Impaired metabolism of drugs that do not have sensitizing properties can cause allergic reactions to them. L. Yeager (1990) makes the following observation: application antihistamines in some patients it caused an allergic reaction in the form of agranulocytosis. A careful analysis of these cases made it possible to establish that these patients were simultaneously taking medications that interfere with the metabolism of antihistamines. Thus, this is one of the compelling arguments against polypharmacy and a reason for clarifying the mutual influence on the metabolism of the drugs used in the allergy history. IN modern conditions To prevent allergic diseases, the doctor must know not only the names of drugs, indications and contraindications, but also know their pharmacodynamics and pharmacokinetics.

Quite often with the use medicines associated with the development of effects that A.D. Ado highlighted in separate group, which he called pseudoallergy or false allergy. As has already been shown, the fundamental difference between pseudoallergy and allergy is the absence of preliminary sensitization associated with reagin antibodies (IgE). The clinical effects of pseudoallergy are based on the interaction chemicals either directly with the membranes of mast cells and basophils, or with cell receptors for IgE, which ultimately leads to degranulation and release of biologically active substances, primarily histamine, with all the ensuing consequences.

It seems important to provide clinical guidelines to guide differential diagnosis drug allergies and pseudo-allergies. Pseudoallergy more often occurs in women after 40 years of age against the background of diseases that disrupt histamine metabolism or the sensitivity of receptors to biologically active substances (pathology of the liver and biliary tract, gastrointestinal tract, neuroendocrine system). The background for the development of pseudoallergy is also polypharmacy, oral use of drugs for ulcerative, erosive, hemorrhagic processes in the mucous membrane of the gastrointestinal tract; a dose of the drug that does not correspond to the age or weight of the patient, inadequate therapy for current illness, changes in the pH environment and temperature of solutions administered parenterally, simultaneous administration of incompatible drugs (LussL.V., 1999). Characteristic clinical signs pseudo-allergies are: development of the effect after the initial administration of the drug, dependence of severity clinical manifestations depending on the dose and route of administration, quite frequent absence of clinical manifestations when reintroduction the same drug, absence of eosinophilia.

At the end of the section medicinal allergens provides a list of medications that most often provoke the development of allergic diseases. IN this list, which was compiled on the basis of data given in the works of L.V. Luss (1999) and T.N. Grishina (1998), the principle from most to least was used: analgin, penicillin, sulfonamides, ampicillin, naproxen, brufen, ampiox, aminoglycosides, novocaine, acetylsalicylic acid, lidocaine, multivitamins, radiocontrast agents, tetracyclines.

Chemical allergens. The mechanism of sensitization by chemical allergens is similar to drugs. Most often, allergic diseases are caused by the following chemical compounds: salts of nickel, chromium, cobalt, manganese, beryllium; ethylenediamine, rubber production products, chemical fibers, photoreagents, pesticides; detergents, varnishes, paints, cosmetics.

Bacterial allergens. The question of bacterial allergens arises in the so-called infectious-allergic pathology of the mucous membranes of the respiratory and gastrointestinal tract and, above all, in infectious-allergic bronchial asthma. Traditionally, bacterial allergens are divided into pathogen allergens infectious diseases and allergens of opportunistic bacteria. At the same time, according to V.N. Fedoseeva (1999), “there is a certain convention in the concepts of pathogenic and non-pathogenic microbes. The concept of pathogenicity should include more wide range properties, including the allergenic activity of the strain.” This is a very principled and correct position, since diseases in which the allergic component plays a leading role in pathogenesis are well known: tuberculosis, brucellosis, erysipelas, etc. This approach allows us to give specific meaning to the concept of opportunistic microbes that are inhabitants of mucous membranes (streptococci, neisseria , staphylococci, E. coli, etc.).

These microbes, under certain conditions ( genetic predisposition, immune, endocrine, regulatory, metabolic disorders; impact unfavorable factors environment, etc.) can acquire allergenic properties and cause allergic diseases. In this regard, V.N. Fedoseeva (1999) emphasizes that “bacterial allergy plays vital role in the etiopathogenesis of not only particularly dangerous infections, but primarily in focal respiratory diseases, pathologies of the gastrointestinal tract, skin.”

Previously, bacterial allergy was associated with delayed-type hypersensitivity, since the high allergic activity of the nucleoprotein fractions of the microbial cell was established. However, back in the 40s. O. Swineford and J.J. Holman (1949) showed that polysaccharide fractions of microbes can cause typical IgE-dependent allergic reactions. Thus, bacterial allergies are characterized by a combination of delayed and immediate types, and this served as the basis for including bacterial allergic diseases in the complex of treatment specific immunotherapy(SIT). Currently, there are “neuserial” bronchial asthma, “staphylococcal” infectious allergic rhinitis etc. A practitioner should know that it is not enough to establish the infectious-allergic nature of a disease (for example, bronchial asthma); it is also necessary to decipher what type of opportunistic flora determines allergization. Only then, using this allergen vaccine as part of the SIT treatment, can a good therapeutic effect be obtained.

Currently, the significant role of dysbiosis in the formation of immunodeficiencies and immune failure has been established. From our point of view, dysbiosis of the mucous membranes is also one of the significant factors in the etioiatogenesis of allergic diseases. Clinicians should have in their hands not only a method for assessing intestinal dysbiosis, but also methods that allow them to assess the normality and dysbiosis of other mucous membranes, in particular the respiratory tract.

The most common etiopathogenetic factors of diseases of an infectious-allergic nature are: hemolytic and viridans streptococci, staphylococci, catarrhal micrococci, Escherichia coli, Pseudomonas aeruginosa, Proteus, and non-pathogenic Neisseria.

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