They are involved in a delayed-type allergic reaction. Allergic reactions of delayed and immediate type

Anaphylactic shock

It is the most formidable allergic complication. Anaphylactic shock can be caused by almost all currently used drugs, sera and vaccines, pollen allergens during the period of incorrect provocative tests, foods, especially fish, milk, eggs and others, alcoholic beverages, bathing in cold water with cold allergies, wasp stings , bees, bumblebees, hornets. Anaphylactic shock refers to allergic complications that occur with circulating humoral antibodies, the main characteristic of which is their effect on the mechanism of biologically active substances of the antigen-antibody reaction in tissues and liquid tissue media, and as an intermediate link, the processes of excitation of the central nervous system. In the pathogenesis of anaphylactic shock (and other types of humoral, immediate type allergies), three stages are distinguished: immunological, pathochemical (biochemical) and pathophysiological. The initial stage of the immunological stage is sensitization, i.e. the process of hypersensitivity. Sensitization occurs within approximately 7-8 days (in the experiment), and in humans this period can last many months and years. The sensitization phase is characterized by the immunological restructuring of the body, the production of homocytotropic antibodies (or reagins). The interaction of an allergen with antibodies occurs in organs and cells where antibodies are fixed, i.e., in shock organs. These organs include skin, smooth muscles of internal organs, blood cells, nervous tissue, connective tissue. Especially important is the reaction in mast cells of the connective tissue, which are located close to small blood vessels under the mucous membranes, as well as on basophilic leukocytes. During the pathochemical stage, the allergen-antibody complex leads to suppression of the activity of inhibitors of tissue and serum enzymes, which causes intoxication and the release of some biologically active substances (histamine, serotonin, heparin, acetylcholine, etc.) and the formation of other biologically active substances (bradykinin, slow-acting substances of anaphylaxis responsible for bronchospasm, etc.). The pathophysiological stage gives a complex of pathophysiological disorders underlying the clinical picture. Characteristic are bronchospasm, spasms of smooth muscles of the intestine, bladder, uterus, impaired vascular permeability. In this phase, allergic inflammation also occurs, which develops on the skin, mucous membranes and internal organs. The pathomorphological basis of anaphylactic shock is plethora and swelling of the meninges and brain, lungs, hemorrhages in the pleura, endocardium, kidneys, adrenal glands, mucous membranes, stomach and intestines, emphysema. Drug anaphylactic shock, as a rule, develops in patients who have taken this medication repeatedly, and often with allergic complications, in people with drug sensitization that has developed as a result of professional contact (nurses, doctors, pharmacists, etc.), in patients with allergic diseases (hay fever, bronchial asthma, urticaria, neurodermatitis - atonic dermatitis, etc.).

The speed of the complication is from a few seconds or minutes to 2 hours. The symptoms of shock are diverse, their severity varies in different patients. The degree of severity is divided into four stages: mild, moderate, severe and extremely severe (fatal). Most patients complain of sudden weakness, shortness of breath, dry cough, dizziness, decreased vision, hearing loss, severe itching of the skin or a feeling of heat throughout the body, chills, abdominal pain, heart, nausea, vomiting, urge to stool and urination. Loss of consciousness may occur. Objectively, tachycardia, thready pulse, low or completely undetectable blood pressure, cold sweat, cyanosis or sharp reddening of the skin, muffled heart sounds, dilated pupils, convulsions, foam from the mouth, sometimes a sharp swelling of the tongue, swelling of the face (angioedema), larynx, involuntary defecation, urinary retention, widespread rash. The duration of the symptoms of anaphylactic shock depends on the degree of sensitization, the correctness and timeliness of treatment for concomitant diseases, etc. In some cases, the death of patients occurs within 5-30 minutes from asphyxia, in others - after 24-48 hours or several days from severe changes in the kidneys (due to glomerulonephritis), liver (hepatitis, liver necrosis), gastrointestinal tract (profuse gastrointestinal bleeding), heart (myocarditis) and other organs. After suffering anaphylactic shock, fever, lethargy, pain in the muscles, abdomen, lower back, vomiting, diarrhea, skin itching, urticaria or Quincke's edema, attacks of bronchial asthma, etc. are observed. Complications of anaphylactic shock, in addition to those mentioned above, include a heart attack, pneumonia, hemiparesis and hemiparalysis, exacerbation of chronic colitis with prolonged intestinal bleeding. Mortality in anaphylactic shock ranges from 10 to 30%. All patients who have suffered anaphylactic shock need dispensary observation of an allergist. The most important preventive measures are the targeted collection of an allergic history, as well as the elimination of unreasonable prescriptions of drugs, especially for patients suffering from one form or another of an allergic disease. The drug, to which there was an allergic reaction of any kind, should be completely excluded from contact with the patient in any pharmacological form.

Acute urticaria and angioedema (angioneurotic edema, giant urticaria)

This is a classic allergic skin disease, which is associated with a violation of the permeability of the vascular wall and the development of edema, often accompanied by damage to the cardiovascular system and other body systems. Etiological factors that can cause Quincke's edema are many drugs, foods, household, bacterial and fungal allergens, etc. According to the pathogenesis, Quincke's edema refers to an allergic disease that occurs with humoral, circulating antibodies. The main mediator of an allergic reaction is histamine. Mediators cause dilation of capillaries and increased permeability of blood vessels, leading to flushing, blistering, and edema. In the clinic of acute urticaria, complaints of excruciating local or widespread pruritus, chills, nausea, abdominal pain, and vomiting predominate.

With Quincke's edema, there is no skin itching, there is a feeling of tension in the skin, an increase in the size of the lips, eyelids, ears, tongue, scrotum, etc., with swelling of the larynx - difficulty swallowing, hoarseness of voice. Quincke's edema is considered as one of the forms of urticaria. Unlike urticaria, with angioedema, deeper sections of the skin and subcutaneous tissue are captured. Often these diseases are combined. Acute urticaria can occur with complications such as myocarditis, glomerulonephritis, and laryngeal edema, which can lead to severe asphyxia requiring urgent tracheotomy.

Serum sickness and serum-like reactions These are classical systemic allergic diseases that occur after the introduction of foreign therapeutic sera and many medicinal preparations. Diseases refer to allergic reactions that occur with humoral, circulating antibodies. In the clinical picture, an incubation period of 7 to 12 days is distinguished, which, depending on the degree of sensitization, can decrease to several hours or increase to 8 weeks or more. According to the degree of severity, mild, moderate and severe forms are distinguished. Patients complain of itching, chills, headache, sweating, abdominal pain, sometimes nausea, vomiting, joint pain. During the examination, rashes on the skin, Quincke's edema, fever from subfebrile numbers to 40 ° C, swollen lymph nodes, swelling of the joints, tachycardia, hypotension are determined. There may be swelling of the larynx with the threat of asphyxia. The duration of the course of the disease is from several days to 2-3 weeks, sometimes there is an anaphylactic form of serum sickness, which in its course resembles anaphylactic shock. Serum sickness can give complications: myocarditis, glomerulonephritis, hepatitis, polyneuritis, encephalitis. The prognosis in a significant number of cases is favorable, if there are no late severe complications from the internal organs indicated above.

Allergic reactions such as the Arthus-Sakharov phenomenon D Another name for these reactions is "gluteal reactions" because they occur at the injection site. The causes of these reactions are foreign sera, antibiotics, vitamins (for example, B1), aloe, insulin and many other drugs. The pathogenetic mechanism is that there is a local interaction of the antigen (or hapten) with antibodies in the wall of small vessels, the antibody approaches the vessel wall, but does not penetrate into the tissues. The antigen-antibody complex is formed in the subendothelial layer of the blood vessel wall, in which it irritates tissues, causing necrotic changes. Histamine does not participate in these reactions. In soft tissues, a granuloma is formed, which is complex in morphological structure. The following factors indicate increased sensitivity: the primary development of necrosis according to the type of Arthus phenomenon, the rapid formation of a capsule around the focus, pronounced vascular and cell proliferative reactions around the necrosis with the formation of granulomatous structures and giant forms of macrophages. A characteristic feature of the morphological granuloma is the development of tuberculoid structures, which are very similar to the picture of the tuberculous process. The term of the reaction is from 2-3 days to 1 month or more. Patients complain of severe pain at the injection site, local skin itching. Objectively marked hyperemia, compaction, painful when touched. If injections are not stopped in a timely manner, then the infiltrates increase in size, become sharply painful, and local necrosis may form. Granuloma in soft tissues has a tendency to aseptic abscess formation and fistula formation. The prognosis is favorable in most cases.

Bronchial asthma

Bronchial asthma is an allergic disease, in the clinical course of which the central place is occupied by expiratory type asthma attacks (expiration is difficult), caused by bronchospasm, hypersecretion and swelling of the bronchial mucosa. There are many reasons why asthma can develop. They can be allergens of infectious and non-infectious origin. Of the infectious allergens, Staphylococcus aureus, Staphylococcus aureus, Klebsiella, Escherichia coli and others, that is, opportunistic and saprophytic microorganisms, are in the first place. Non-infectious include household allergens (house dust and feathers, mites), book and library dust, pollen from trees, grasses, weeds, animal hair and dander, food for aquarium fish. Food allergens - fish, cereals, milk, eggs, honey and others - are important as the cause of bronchial asthma mainly in children, and in adults - with hay fever. Allergens can be pathogenic and non-pathogenic fungi, medicinal substances. Bronchial asthma is divided into atonic (non-infectious-allergic) and infectious-allergic. According to these two forms, the pathogenesis of the disease is also considered, while the pathogenesis of the attack and the pathogenesis of the disease are taken into account. The result of an allergic reaction occurring in the tissues of the bronchial tree is always an attack of bronchial asthma. In the atonic form, an attack is the result of an allergic reaction with circulating, humoral antibodies (reagins, which are mainly related to JgE), fixed on sensitized mast cells, a large number of which are located in the connective tissue of the bronchopulmonary apparatus.

In bronchial asthma, three stages are distinguished: immunological, pathochemical and pathophysiological. In the formation of an attack, the slow-acting substance anaphylaxin, histamine, acetylcholine and other biologically active substances, which are released during the formation of the antigen-antibody complex, take part. In the pathophysiological stage of the atonic form of bronchial asthma, a spasm of the smooth muscles of the bronchi and bronchioles develops, the permeability of blood vessels increases, there is an increase in mucus formation in the mucous glands, and excitation of nerve cells.

Allergic mechanisms are the main link in the pathogenesis of bronchial asthma, however, at some stage of the disease, second-order mechanisms are activated, in particular, neurogenic and endocrine ones. There is also a genetic predisposition to atonic diseases (about 50%). One of the constitutional genetic features is a decrease in ?-adrenergic receptor sensitivity, which causes an increase in the sensitivity of the smooth muscles of the bronchioles to the action of histamine, acetylcholine, and thereby leads to bronchospasm. In the infectious-allergic form of bronchial asthma, the pathogenesis is associated with an allergy of the cellular (delayed) type. In the mechanism of this type of allergy, the leading role is played by the processes of irritation of skin and connective tissue structures by allergens and the formation of various types of inflammation. The initial stage of a cell-type allergic reaction is the direct specific contact of sensitized lymphocytes with allergic agents on the surface of sensitized cells. In the histological picture, there are features of the proliferation of histiomonocytic elements that create structures of the tuberculoid type, massive perivascular infiltration by mononuclear cells such as medium and small lymphocytes. With the development of an allergic reaction of the cellular type, in addition to the factor of inhibition of macrophage migration, other humoral factors are released (lymph node permeability, lymphotoxin, chemotaxis, skin-reactive factor, etc.). In addition to macrophages and fibroblasts, the objects of influence of humoral factors, which are biochemical mediators of an allergic reaction of a cellular type, can be epithelial cells, endothelium of the walls of blood vessels, non-cellular elements (myelin), etc. An allergic reaction of a cellular type develops as a response to antigens of microorganisms, but can also occur in relation to purified proteins and simple chemicals in combination with autologous protein.

In the clinical picture of bronchial asthma, recurrent asthma attacks play a leading role. They usually start at night or early in the morning. A number of patients have some precursors: lethargy, itching in the nose, nasal congestion or sneezing, a feeling of tightness in the chest. An attack begins with a painful cough, usually dry (without sputum), then a typical expiratory-type shortness of breath appears (expiration is difficult). From the very beginning of the attack, breathing changes, becomes noisy and whistling, audible at a distance. The patient tries to maintain a state of rest, often takes a sitting position in bed or even on his knees, reflexively trying to increase lung capacity. The number of respiratory movements is reduced to 10 or less per minute. At the height of the attack, due to the great tension, the patient is covered with sweat. The pause between inhalation and exhalation disappears. The chest is in the position of a deep breath, breathing becomes possible mainly due to the participation of the intercostal muscles. There is tension in the abdominal muscles. During an attack, the skin of the face turns pale, cyanosis is often noted. When listening over the entire surface of the lungs, dry whistling rales are determined. The attack ends most often with a cough with the separation of light, viscous or thick and purulent sputum.

Asphyxiation attacks can be mild, moderate and severe, depending on their duration, the possibility of relief (cessation) with the help of drugs, the form of bronchial asthma, the duration of its course and the presence of concomitant diseases of the bronchopulmonary apparatus. There are cases when an attack of bronchial asthma cannot be stopped within 24 hours with conventional anti-asthma drugs. Then the so-called asthmatic state, or asthmatic status, develops. In the pathogenesis of the asthmatic condition in the atonic form of bronchial asthma, the main role is played by mucosal edema and spasm of the smooth muscles of the small bronchi. In the infectious form, mechanical obstruction of the bronchial lumen with thick viscous mucus is observed.

The clinical manifestation in an asthmatic condition is severe expiratory dyspnea with very rare shallow breathing. The skin becomes moist, cyanotic, with a grayish tint. The position of the patient is forced - sitting. Respiratory noises (wheezing with wheezing) weaken until they disappear completely (“silent lung”), creating a deceptive impression of well-being. In severe status asthmaticus, hypoxic coma develops, which can be of two types: quickly and slowly advancing. A rapidly flowing coma is characterized by an early loss of consciousness, the disappearance of reflexes, cyanosis, and frequent shallow breathing. Wheezing over the lungs ceases to be heard, heart sounds become loud, the pulse is frequent, blood pressure drops. With a slowly flowing coma, all signs are stretched in time. An asthmatic condition can be complicated by pneumothorax, atelectasis of the lung tissue due to blockage of the bronchi with viscous sputum. The prognosis for the atonic form is favorable. With an infectious form, it is much worse, in which case the disease often leads to disability. The causes of deaths are the abuse of certain drugs, drug allergy (anaphylactic shock), withdrawal syndrome in patients who have long received glucocorticoid hormones, strong sedatives.

Data from immunological studies in bronchial asthma. Allergic skin-sensitizing antibodies (or reagins) are various types of immunoglobulins that have the ability to specifically react with allergenic substances. They are the most important types of antibodies that are involved in the mechanisms of allergic reactions in humans. The differences between allergic antibodies and "normal" globulins are their immunological specificity and biological properties of various allergic reactions. Allergic antibodies are divided into damaging (aggressive) witness antibodies and blocking ones, which cause the transition of the state of allergy into immunity. The most reliable method for detecting reagins in the blood serum of patients with allergic diseases of the humoral type is the Prausnitz-Küstner method. In the atonic form of asthma, positive results were obtained with household, pollen, food, fungal and a number of other allergens, as well as in some cases with an infectious form with bacterial monovaccines. Reagins are immunologically heterogeneous, some of them are associated with JgA and JgJ, but the bulk are associated with the JgE type. With bronchial asthma and other allergic diseases in the blood serum, the content of JgE increases by 4–5 times. JgE is also found in very low concentrations in nasal mucus, bronchi, colostrum and urine. Complications of bronchial asthma are pulmonary emphysema, pneumosclerosis, chronic cor pulmonale, pulmonary heart failure.

Pollinosis (hay fever)

This is a classic disease that is caused by the pollen of wind-pollinated plants. It has a pronounced seasonality, i.e., it becomes aggravated during the flowering period of plants. Pollinoses are caused by pollen of trees and shrubs (such as birch, acacia, alder, hazel, maple, ash, poplar, etc.), meadow, cereal grasses (such as timothy, fescue, bluegrass, etc.), cultivated cereals (such like rye, corn, sunflower) and weeds (such as wormwood, quinoa, dandelion, etc.). Pathogenetically, hay fever is a typical allergic disease that occurs with circulating humoral antibodies. Reagins to pollen allergens are determined in blood serum, nasal mucosa, sputum, conjunctiva.

Clinical variants of pollinosis are rhinitis, conjunctivitis and asthmatic bronchitis or bronchial asthma. Other options are possible, for example, with neurodermatitis, urticaria. Patients in the period of exacerbation complain of painful and frequent bouts of sneezing with copious watery discharge from the nasal cavity, congestion and itching of the nose, itching of the eyelids, lacrimation, pain in the eyes, itching of the mucous membranes of the nasopharynx, larynx, widespread skin itching. Pollen asthma is characterized by attacks of expiratory dyspnea, which are combined with symptoms of rhinitis and conjunctivitis. Symptoms of the so-called pollen intoxication develop: headache, weakness, sweating, chills, low-grade fever. The eyes of the patients are swollen, inflamed, watery, the nose is swollen, the voice is nasal. Breathing through the nose is difficult. The course of the disease can be relatively mild with isolated rhinitis or conjunctivitis, moderate - with a combination of these diseases and a more pronounced picture of pollen intoxication, severe - with the addition of bronchial asthma, which can even be provoked by an asthmatic condition.

In patients suffering from hay fever, short exacerbations may occur outside the flowering period of plants after ingestion of food products that have common antigenic properties with tree pollen (nuts, birch, cherry, apple juice and other products). Also, mild exacerbations of hay fever in patients with chronic diseases of the gastrointestinal tract are caused by eating cereals in the form of bread, various cereals, and alcoholic beverages. Also, for patients suffering from hay fever, it is considered very dangerous to use decoctions of various herbs in the winter to treat colds. Phytotherapy in such patients can contribute to a severe exacerbation of hay fever and cause attacks of bronchial asthma.

A laboratory blood test reveals eosinophilia, lymphocytosis. In the blood serum, the content of histamine, serotonin, ?2- and ?-globulins is increased. In the sputum of patients with pollen bronchial asthma, an accumulation of eosinophils is found. In patients with pollen asthmatic bronchitis and bronchial asthma, bronchial hypersensitivity to acetylcholine and histamine was noted. With polynosis, complications are possible in the form of bacterial conjunctivitis, sinusitis, frontal sinusitis, ethmoiditis, asthmatic bronchitis and bronchial asthma. Patients with hay fever are potential asthmatics, but in general there are a sufficient number of cases of a long and rather favorable course of the disease, when the ability to work is disturbed only during the flowering period of plants, and in the rest of the year, good health is maintained. Patients with hay fever need long-term observation of an allergist.

Identification of an allergic reaction is not an easy, but necessary process for providing competent first aid to the patient and drawing up an effective plan for further treatment. In clinical situations, the same reaction in different patients may have its own characteristics, despite the same mechanism of occurrence.

Therefore, it is quite difficult to establish an exact framework for the classification of allergies, as a result, many diseases are intermediate between the above categories.

It should be noted that the time of manifestation of an allergic reaction is not an absolute criterion for determining a specific type of disease, because. depends on a number of factors (Arthus phenomenon): the amount of the allergen, the duration of its exposure.

Types of allergic reactions

Depending on the time of occurrence of allergic reactions after contact with the allergen, they differentiate:

• immediate type allergy (symptoms occur immediately after contact of the body with the allergen or within a short period of time);
• delayed-type allergy (clinical manifestations occur after 1-2 days).

To find out which category the reaction belongs to, it is worth paying attention to the nature of the process of disease development, pathogenetic features.

Diagnosing the main mechanism of allergy is a necessary condition for compiling a competent and effective treatment.

Allergy of the immediate type

An immediate type allergy (anaphylactic) occurs due to the reaction of antibodies of groups E (IgE) and G (IgG) with an antigen. The resulting complex is deposited on the mast cell membrane. This stimulates the body to increase the synthesis of free histamine. As a result of a violation of the regulatory process of the synthesis of immunoglobulins of group E, namely their excessive formation, there is an increased sensitivity of the body to the effects of stimuli (sensitization). The production of antibodies is directly dependent on the ratio of the amount of proteins that control the IgE response.

The causes of immediate hypersensitivity are often:

This type of allergy can occur due to the transfer of the patient's blood serum to a healthy person.

Typical examples of an immediate immune response are:

• anaphylactic shock;
• bronchial asthma of allergic type;
• inflammation of the nasal mucosa;
• rhinoconjunctivitis;
• allergic rash;
• skin inflammation;

The first thing to do to relieve symptoms is to identify and eliminate the allergen. Mild allergic reactions such as hives and rhinitis are treated with antihistamines.

In case of severe diseases, glucocorticoids are used. If an allergic reaction develops rapidly in a severe form, it is necessary to call an ambulance.

The state of anaphylactic shock requires urgent medical attention. It is eliminated by hormonal drugs such as adrenaline. During first aid, the patient should be laid on pillows to facilitate the breathing process.

The horizontal position also contributes to the normalization of blood circulation and pressure, while the upper body and head of the patient should not be raised. When breathing stops and consciousness is lost, resuscitation is necessary: ​​an indirect heart massage is performed, artificial respiration mouth to mouth.

If necessary, in a clinical setting, the patient's trachea is intubated to supply oxygen.

delayed allergy

Delayed-type allergy (late hypersensitization) occurs over a longer period of time (days or more) after the body has come into contact with the antigen. Antibodies do not take part in the reaction; instead, the antigen is attacked by specific clones - sensitized lymphocytes formed as a result of previous intakes of the antigen.

Response inflammatory processes are caused by active substances secreted by lymphocytes. As a result, the phagocytic reaction is activated, the process of chemotaxis of macrophages and monocytes, inhibition of the movement of macrophages occurs, the accumulation of leukocytes in the inflammatory zone increases, the consequences lead to inflammation with the formation of granulomas.

This painful condition is often caused by:

• bacteria;
• fungal spores;
• opportunistic and pathogenic microorganisms (staphylococci, streptococci, fungi, pathogens of tuberculosis, toxoplasmosis, brucellosis);
• some substances containing simple chemical compounds (chromium salts);
• vaccinations;
• chronic inflammation.

Such an allergy is not transferred to a healthy person by the patient's blood serum. But leukocytes, cells of lymphoid organs and exudate can carry the disease.

Typical diseases are:

Delayed-type allergies are treated with drugs intended for the relief of systemic connective tissue diseases and immunosuppressants (immune suppressive drugs). The pharmacological group of drugs includes drugs prescribed for rheumatoid arthritis, systemic lupus erythematosus, nonspecific ulcerative prick. They suppress hyperimmune processes in the body caused by impaired tissue immunity.

Conclusions: main differences between types of allergic reactions

So, the main differences between immediate and delayed type allergies are as follows:

• pathogenesis of the disease, namely the transience of the development of the disease;
• the presence or absence of circulating antibodies in the blood;
• groups of allergens, their nature of origin, causes of occurrence;
• emerging diseases;
• treatment of the disease, pharmacological groups of drugs indicated in the treatment of various types of allergies;
• the possibility of passive transmission of the disease.

Allergy (Greek “allos” - different, different, “ergon” - action) is a typical immunopathological process that occurs against the background of exposure to an allergen antigen on an organism with a qualitatively altered immunological reactivity and is accompanied by the development of hyperergic reactions and tissue damage.

There are allergic reactions of immediate and delayed type (respectively - humoral and cellular reactions). Allergic antibodies are responsible for the development of allergic reactions of the humoral type.

For the manifestation of the clinical picture of an allergic reaction, at least 2 contacts of the body with the antigen-allergen are necessary. The first dose of exposure to the allergen (small) is called sensitizing. The second dose of exposure - a large (permissive) is accompanied by the development of clinical manifestations of an allergic reaction. Allergic reactions of the immediate type may occur as early as a few seconds or minutes or 5 to 6 hours after repeated contact of the sensitized organism with the allergen.

In some cases, long-term persistence of the allergen in the body is possible and, in connection with this, it is practically impossible to draw a clear line between the impact of the first sensitizing and repeated resolving doses of the allergen.

Classification of allergic reactions of immediate type:

• 1) anaphylactic (atopic);
• 2) cytotoxic;
• 3) immunocomplex pathology.

Stages of allergic reactions:

I - immunological

II - pathochemical

III - pathophysiological.

Allergens that induce the development of allergic reactions of the humoral type

Allergen antigens are divided into bacterial and non-bacterial antigens.

Non-bacterial allergens include:

• 1) industrial;
• 2) household;
• 3) medicinal;
• 4) food;
• 5) vegetable;
• 6) animal origin.

Complete antigens (determinant groups + carrier protein) are isolated that can stimulate the production of antibodies and interact with them, as well as incomplete antigens, or haptens, consisting only of determinant groups and not inducing antibody production, but interacting with ready-made antibodies. There is a category of heterogeneous antigens that have a similar structure of determinant groups.

Allergens can be strong or weak. Strong allergens stimulate the production of a large number of immune or allergic antibodies. Soluble antigens, usually of a protein nature, act as strong allergens. An antigen of a protein nature is the stronger, the higher its molecular weight and the more rigid the structure of the molecule. Weak are corpuscular, insoluble antigens, bacterial cells, antigens of damaged cells of one's own body.

There are also thymus-dependent allergens and thymus-independent allergens. Thymus-dependent are antigens that induce an immune response only with the mandatory participation of 3 cells: a macrophage, a T-lymphocyte and a B-lymphocyte. Thymus-independent antigens can induce an immune response without the involvement of helper T-lymphocytes.

General patterns of development of the immunological phase of allergic reactions of immediate type

The immunological stage begins with the exposure to a sensitizing dose of the allergen and the latent period of sensitization, and also includes the interaction of the resolving dose of the allergen with allergic antibodies.

The essence of the latent period of sensitization lies, first of all, in the macrophage reaction, which begins with the recognition and absorption of the allergen by the macrophage (A-cell). In the process of phagocytosis, most of the allergen is destroyed under the influence of hydrolytic enzymes; the non-hydrolyzed part of the allergen (determinant groups) is exposed to the outer membrane of the A-cell in combination with Ia-proteins and macrophage mRNA. The resulting complex is called a superantigen and has immunogenicity and allergenicity (the ability to induce the development of immune and allergic reactions), many times higher than that of the original native allergen. In the latent period of sensitization, after the macrophage reaction, the process of specific and nonspecific cooperation of three types of immunocompetent cells occurs: A-cells, T-lymphocytes-helpers and antigen-reactive clones of B-lymphocytes. First, the allergen and Ia-proteins of the macrophage are recognized by specific receptors of T-lymphocyte-helpers, then the macrophage secretes interleukin-1, which stimulates the proliferation of T-helpers, which, in turn, secrete an immunogenesis inducer that stimulates the proliferation of antigen-sensitive clones of B-lymphocytes, their differentiation and transformation into plasma cells - producers of specific allergic antibodies.

The process of antibody formation is influenced by another type of immunocytes - T-suppressors, the action of which is opposite to the action of T-helpers: they inhibit the proliferation of B-lymphocytes and their transformation into plasma cells. Normally, the ratio of T-helpers to T-suppressors is 1.4 - 2.4.

Allergic antibodies are divided into:

• 1) antibodies-aggressors;
• 2) witness antibodies;
• 3) blocking antibodies.

Each type of allergic reactions (anaphylactic, cytolytic, immunocomplex pathology) is characterized by certain aggressor antibodies that differ in immunological, biochemical and physical properties.

When a permissive dose of the antigen penetrates (or in the case of the persistence of the antigen in the body), the active centers of antibodies interact with the determinant groups of antigens at the cellular level or in the systemic circulation.

The pathochemical stage consists in the formation and release into the environment in a highly active form of allergy mediators, which occurs during the interaction of the antigen with allergic antibodies at the cellular level or the fixation of immune complexes on target cells.

The pathophysiological stage is characterized by the development of the biological effects of immediate-type allergy mediators and the clinical manifestations of allergic reactions.

Anaphylactic (atonic) reactions

There are generalized (anaphylactic shock) and local anaphylactic reactions (atopic bronchial asthma, allergic rhinitis and conjunctivitis, urticaria, angioedema).

Allergens that most often induce the development of anaphylactic shock:

• 1) allergens of antitoxic serums, allogeneic preparations?-globulins and blood plasma proteins;
• 2) allergens of protein and polypeptide hormones (ACTH, insulin, etc.);
• 3) drugs (antibiotics, in particular penicillin, muscle relaxants, anesthetics, vitamins, etc.);
• 4) radiopaque substances;
• 5) insect allergens.

Local anaphylactic reactions can be caused by:

• 1) pollen allergens (polynoses), fungal spores;
• 2) allergens of domestic and industrial dust, epidermis and animal hair;
• 3) allergens of cosmetics and perfumes, etc.

Local anaphylactic reactions occur when an allergen enters the body in a natural way and develop in the places of the entrance gate and the fixation of allergens (mucous conjunctiva, nasal passages, gastrointestinal tract, skin, etc.).

Antibodies-aggressors in anaphylaxis are homocytotropic antibodies (reagins or atopenes) related to immunoglobulins of classes E and G4, capable of fixing on various cells. Reagins are fixed primarily on basophils and mast cells - cells with high affinity receptors, as well as on cells with low affinity receptors (macrophages, eosinophils, neutrophils, platelets).

With anaphylaxis, two waves of release of allergy mediators are distinguished:

• Wave 1 occurs approximately 15 minutes later, when mediators are released from cells with high affinity receptors;
• 2nd wave - after 5 - 6 hours, the sources of mediators in this case are carrier cells of low-affinity receptors.

Mediators of anaphylaxis and sources of their formation:

• 1) mast cells and basophils synthesize and secrete histamine, serotonin, eosinophilic and neutrophilic, chemotactic factors, heparin, arylsulfatase A, galactosidase, chymotrypsin, superoxide dismutase, leukotrienes, prostaglandins;
• 2) eosinophils are a source of arylsulfatase B, phospholipase D, histaminase, cationic proteins;
• 3) leukotrienes, histaminase, arylsulfatases, prostaglandins are released from neutrophils;
• 4) from platelets - serotonin;
• 5) basophils, lymphocytes, neutrophils, platelets and endothelial cells are sources of platelet-activating factor formation in case of activation of phospholipase A2.

The clinical symptoms of anaphylactic reactions are due to the biological action of allergy mediators.

Anaphylactic shock is characterized by the rapid development of general manifestations of pathology: a sharp drop in blood pressure up to a collaptoid state, disorders of the central nervous system, disorders of the blood coagulation system, spasm of the smooth muscles of the respiratory tract, gastrointestinal tract, increased vascular permeability, skin itching. A lethal outcome can occur within half an hour with symptoms of asphyxia, severe damage to the kidneys, liver, gastrointestinal tract, heart and other organs.

Local anaphylactic reactions are characterized by an increase in the permeability of the vascular wall and the development of edema, the appearance of skin itching, nausea, abdominal pain due to spasm of smooth muscle organs, sometimes vomiting, and chills.

Cytotoxic reactions

Varieties: blood transfusion shock, maternal and fetal Rh incompatibility, autoimmune anemia, thrombocytopenia and other autoimmune diseases, a component of transplant rejection.

The antigen in these reactions is a structural component of the membrane of the cells of one's own organism or an antigen of an exogenous nature (a bacterial cell, a medicinal substance, etc.), which is firmly fixed on the cells and changes the structure of the membrane.

Cytolysis of the target cell under the influence of a resolving dose of the antigen-allergen is provided in three ways:

• 1) due to complement activation - complement-mediated cytotoxicity;
• 2) due to the activation of phagocytosis of cells coated with antibodies - antibody-dependent phagocytosis;
• 3) through the activation of antibody-dependent cellular cytotoxicity - with the participation of K-cells (null, or neither T- nor B-lymphocytes).

The main mediators of complement-mediated cytotoxicity are activated complement fragments. Complement is a closely related system of serum enzyme proteins.

DELAYED TYPE HYPERSENSITIVITY REACTIONS

Delayed-type hypersensitivity (DTH) is one of the pathologies of cellular immunity carried out by immunocompetent T-lymphocytes against cell membrane antigens.

For the development of DTH reactions, prior sensitization is necessary, which occurs upon initial contact with the antigen. HRT develops in animals and humans 6-72 hours after penetration into the tissues of a resolving (repeated) dose of the allergen antigen.

Types of HRT reactions:

• 1) infectious allergy;
• 2) contact dermatitis;
• 3) graft rejection;
• 4) autoimmune diseases.

Antigens-allergens that induce the development of the HRT reaction:

The main participants in DTH reactions are T-lymphocytes (CD3). T-lymphocytes are formed from undifferentiated bone marrow stem cells that proliferate and differentiate in the thymus, acquiring the properties of antigen-reactive thymus-dependent lymphocytes (T-lymphocytes). These cells settle in the thymus-dependent zones of the lymph nodes, spleen, and are also present in the blood, providing cellular immunity reactions.

Subpopulations of T-lymphocytes

• 1) T-effectors (T-killers, cytotoxic lymphocytes) - destroy tumor cells, genetically alien transplant cells and mutated cells of their own body, performing the function of immunological surveillance;
• 2) T-producers of lymphokines - participate in the reactions of DTH, releasing DTH mediators (lymphokines);
• 3) T-modifiers (T-helpers (CD4), amplifiers) - contribute to the differentiation and proliferation of the corresponding clone of T-lymphocytes;
• 4) T-suppressors (CD8) - limit the strength of the immune response, blocking the reproduction and differentiation of T- and B-series cells;
• 5) Memory T-cells - T-lymphocytes that store and transmit information about the antigen.

General mechanisms for the development of a delayed-type hypersensitivity reaction

The allergen antigen, when it enters the body, is phagocytosed by a macrophage (A-cell), in the phagolysosome of which, under the influence of hydrolytic enzymes, a part of the allergen antigen is destroyed (about 80%). The unfragmented part of the antigen-allergen in complex with Ia-protein molecules is expressed on the A-cell membrane as a superantigen and presented to antigen-recognizing T-lymphocytes. Following the macrophage reaction, there is a process of cooperation between the A-cell and T-helper, the first stage of which is the recognition of a foreign antigen on the surface of the A-cell by antigen-specific receptors on the membrane of T-helpers, as well as the recognition of macrophage Ia proteins by specific T-helper receptors. Further, A-cells produce interleukin-1 (IL-1), which stimulates the proliferation of T-helpers (T-amplifiers). The latter secrete interleukin-2 (IL-2), which activates and maintains blast transformation, proliferation and differentiation of antigen-stimulated T-producers of lymphokines and T-killers in regional lymph nodes.

When T-producers-lymphokines interact with the antigen, more than 60 soluble mediators of DTH-lymphokines are secreted, which act on various cells in the focus of allergic inflammation.

Classification of lymphokines.

I. Factors affecting lymphocytes:

• 1) Lawrence transfer factor;
• 2) mitogenic (blastogenic) factor;
• 3) a factor that stimulates T- and B-lymphocytes.

II. Factors affecting macrophages:

• 1) migration-inhibiting factor (MIF);
• 2) macrophage activating factor;
• 3) a factor that enhances the proliferation of macrophages.

III. Cytotoxic factors:

• 1) lymphotoxin;
• 2) a factor that inhibits DNA synthesis;
• 3) a factor that inhibits hematopoietic stem cells.

IV. Chemotactic factors for:

• 1) macrophages, neutrophils;
• 2) lymphocytes;
• 3) eosinophils.

V. Antiviral and antimicrobial factors - α-interferon (immune interferon).

Along with lymphokines, other biologically active substances play a role in the development of allergic inflammation in HRT: leukotrienes, prostaglandins, lysosomal enzymes, and chalones.

If T-producers of lymphokines realize their effect remotely, then sensitized T-killers have a direct cytotoxic effect on target cells, which is carried out in three stages.

Stage I - target cell recognition. The T-killer is attached to the target cell through cellular receptors for a specific antigen and histocompatibility antigens (H-2D and H-2K proteins - products of the D and K genes of the MHC loci). In this case, there is a close membrane contact between the T-killer and the target cell, which leads to the activation of the metabolic system of the T-killer, which subsequently lyses the "target cell".

II stage - lethal strike. T-killer has a direct toxic effect on the target cell due to the activation of enzymes on the membrane of the effector cell.

Stage III - osmotic lysis of the target cell. This stage begins with a series of successive changes in the membrane permeability of the target cell and ends with a rupture of the cell membrane. Primary damage to the membrane leads to a rapid entry of sodium and water ions into the cell. The death of the target cell occurs as a result of osmotic lysis of the cell.

Phases of delayed-type allergic reactions:

I - immunological - includes the period of sensitization after the introduction of the first dose of the allergen antigen, the proliferation of the corresponding clones of T-lymphocyte-effectors, recognition and interaction with the membrane of the target cell;

II - pathochemical - phase of the release of DTH mediators (lymphokines);

III - pathophysiological - manifestation of the biological effects of DTH mediators and cytotoxic T-lymphocytes.

Separate forms of HRT

contact dermatitis

An allergy of this type often occurs to low molecular weight substances of organic and inorganic origin: various chemicals, paints, varnishes, cosmetics, antibiotics, pesticides, arsenic, cobalt, platinum compounds that affect the skin. Contact dermatitis can also be caused by substances of plant origin - cotton seeds, citrus fruits. Allergens, penetrating the skin, form stable covalent bonds with SH- and NH2-groups of skin proteins. These conjugates have sensitizing properties.

Sensitization usually results from prolonged exposure to an allergen. With contact dermatitis, pathological changes are observed in the surface layers of the skin. Infiltration with inflammatory cellular elements, degeneration and detachment of the epidermis, violation of the integrity of the basement membrane are noted.

infectious allergy

HRT develops in chronic bacterial infections caused by fungi and viruses (tuberculosis, brucellosis, tularemia, syphilis, bronchial asthma, streptococcal, staphylococcal and pneumococcal infections, aspergillosis, blastomycosis), as well as in diseases caused by protozoa (toxoplasmosis), with helminthic invasions.

Sensitization to microbial antigens usually develops with inflammation. The possibility of sensitization of the body by some representatives of the normal microflora (Neisseria, Escherichia coli) or pathogenic microbes when they are carriers is not excluded.

transplant rejection

During transplantation, the recipient's body recognizes foreign transplant antigens (histocompatibility antigens) and carries out immune responses leading to transplant rejection. Transplantation antigens are found in all nucleated cells, with the exception of adipose tissue cells.

Types of transplants

• 1. Syngeneic (isotransplant) - the donor and recipient are representatives of inbred lines that are antigenically identical (monozygous twins). The category of syngenes includes an autograft during tissue (skin) transplantation within the same organism. In this case, transplant rejection does not occur.
• 2. Allogeneic (homotransplant) - the donor and recipient are representatives of different genetic lines within the same species.
• 3. Xenogenic (heterograft) - the donor and recipient belong to different species.

Allogeneic and xenogenic transplants without the use of immunosuppressive therapy are rejected.

Dynamics of skin allograft rejection

In the first 2 days, the transplanted skin flap merges with the skin of the recipient. At this time, blood circulation is established between the tissues of the donor and the recipient, and the graft has the appearance of normal skin. On the 6th - 8th day, swelling, infiltration of the graft with lymphoid cells, local thrombosis and stasis appear. The graft becomes bluish and hard, degenerative changes occur in the epidermis and hair follicles. By the 10th - 12th day, the graft dies and does not regenerate even when transplanted to a donor. With repeated transplantation of a transplant from the same donor, pathological changes develop faster - rejection occurs on the 5th day or earlier.

Mechanisms of graft rejection

• 1. Cellular factors. The lymphocytes of the recipient sensitized by the donor's antigens migrate into the graft after graft vascularization, exerting a cytotoxic effect. As a result of exposure to T-killers and under the influence of lymphokines, the permeability of target cell membranes is disrupted, which leads to the release of lysosomal enzymes and cell damage. At later stages, macrophages also participate in the destruction of the graft, enhancing the cytopathogenic effect, causing the destruction of cells by the type of antibody-dependent cellular cytotoxicity due to the presence of cytophilic antibodies on their surface.
• 2. Humoral factors. With allotransplantation of the skin, bone marrow, and kidney, hemagglutinins, hemolysins, leukotokeins, and antibodies to leukocytes and platelets are often formed. During the antigen-antibody reaction, biologically active substances are formed that increase vascular permeability, which facilitates the migration of T-killers into the transplanted tissue. Lysis of endothelial cells in the transplant vessels leads to activation of blood coagulation processes.

Autoimmune diseases

Autoimmune diseases are divided into two groups.

The first group is represented by collagenoses - systemic diseases of the connective tissue, in which autoantibodies are found in the blood serum without strict organ specificity. So, in SLE and rheumatoid arthritis, autoantibodies to antigens of many tissues and cells are detected: the connective tissue of the kidneys, heart, and lungs.

The second group includes diseases in which organ-specific antibodies are detected in the blood (Hashimoto's thyroiditis, pernicious anemia, Addison's disease, autoimmune hemolytic anemia, etc.).

Several possible mechanisms have been identified in the development of autoimmune diseases.

• 1. The formation of autoantibodies against natural (primary) antigens - antigens of immunologically barrier tissues (nervous, lens, thyroid, testicles, sperm).
• 2. The formation of autoantibodies against acquired (secondary) antigens formed under the influence of damaging effects on organs and tissues of pathogenic factors of non-infectious (heat, cold, ionizing radiation) and infectious (microbial toxins, viruses, bacteria) nature.
• 3. Formation of autoantibodies against cross-reacting or heterogeneous antigens. The membranes of some varieties of streptococcus have antigenic similarity to cardiac tissue antigens and glomerular basement membrane antigens. In this regard, antibodies to these microorganisms in streptococcal infections react with tissue antigens of the heart and kidneys, leading to the development of an autoimmune lesion.
• 4. Autoimmune lesions may occur as a result of a breakdown in immunological tolerance to one's own unaltered tissues. Disruption of immunological tolerance can be caused by somatic mutations of lymphoid cells, which leads either to the appearance of mutant forbidden clones of T-helpers, which ensure the development of an immune response to their own unchanged antigens, or to a deficiency of T-suppressors and, accordingly, an increase in the aggressiveness of the B-system of lymphocytes against native ones. antigens.

The development of autoimmune diseases is due to the complex interaction of allergic reactions of the cellular and humoral types with the predominance of one or another reaction, depending on the nature of the autoimmune disease.

Principles of hyposensitization

In case of allergic reactions of the cellular type, as a rule, methods of non-specific hyposensitization are used, aimed at suppressing the afferent link, the central phase and the efferent link of delayed-type hypersensitivity.

The afferent link is provided by tissue macrophages - A-cells. Synthetic compounds suppress the afferent phase - cyclophosphamide, nitrogen mustard, gold preparations

To suppress the central phase of cell-type reactions (including the processes of cooperation of macrophages and various clones of lymphocytes, as well as the proliferation and differentiation of antigen-reactive lymphoid cells), various immunosuppressants are used - corticosteroids, antimetabolites, in particular, analogues of purines and pyrimidines (mercaptopurine, azathioprine), folic acid antagonists (ametopterin), cytotoxic substances (actinomycin C and D, colchicine, cyclophosphamide). allergic antigen medical electric shock

To suppress the efferent link of cell-type hypersensitivity reactions, including the damaging effect on target cells of T-killers, as well as delayed-type allergy mediators - lymphokines, anti-inflammatory drugs are used - salicylates, antibiotics with a cytostatic effect - actinomycin C and rubomycin, hormones and biologically active substances , in particular corticosteroids, prostaglandins, progesterone, antisera.

It should be noted that most of the immunosuppressive drugs used do not cause a selective inhibitory effect only on the afferent, central, or efferent phases of cell-type allergic reactions.

It should be noted that in the vast majority of cases, allergic reactions have a complex pathogenesis, including, along with the dominant mechanisms of delayed (cellular) hypersensitivity reactions, auxiliary mechanisms of humoral type allergies.

In this regard, to suppress the pathochemical and pathophysiological phases of allergic reactions, it is advisable to combine the principles of desensitization used in humoral and cellular types of allergies.

According to modern concepts, all allergic reactions, all manifestations of allergies depending on the rate of occurrence and intensity of manifestation of clinical signs after a repeated meeting of the allergen with the body, they are divided into two groups:

* Allergic reactions of immediate type;

* Allergic reactions of the delayed type.

Allergic reactions of immediate type (immediate type hypersensitivity, anaphylactic type reaction, chimergic type reaction, B - dependent reactions). These reactions are characterized by the fact that antibodies in most cases circulate in body fluids, and they develop within a few minutes after repeated exposure to the allergen.

Allergic reactions of the immediate type proceed with the participation of antibodies formed in response to the antigenic load in circulating humoral media. Re-entry of the antigen leads to its rapid interaction with circulating antibodies, the formation of antigen-antibody complexes. According to the nature of the interaction of antibodies and the allergen, there are three types of immediate hypersensitivity reactions: first type - r e a g i n o v y, including anaphylactic reactions. The reinjected antigen meets with an antibody (Ig E) fixed on tissue basophils. As a result of degranulation, histamine, heparin, hyaluronic acid, kallecrein, and other biologically active compounds are released and enter the bloodstream. Complement does not take part in reactions of this type. The general anaphylactic reaction is manifested by anaphylactic shock, local - by bronchial asthma, hay fever, urticaria, Quincke's edema.

Second type - cytotoxic, characterized by the fact that the antigen is sorbed on the surface of the cell or represents some of its structure, and the antibody circulates in the blood. The resulting antigen-antibody complex in the presence of complement has a direct cytotoxic effect. In addition, activated killer immunocytes and phagocytes are involved in cytolysis. Cytolysis occurs with the introduction of large doses of antireticular cytotoxic serum. Cytotoxic reactions can be obtained in relation to any tissues of the recipient animal if it is injected with the blood serum of a donor previously immunized against them.

The third type is reactions of the Artyus phenomenon type. It was described by the author in 1903 in rabbits previously sensitized with horse serum after subcutaneous injection of the same antigen. Acute necrotizing inflammation of the skin develops at the injection site. The main pathogenetic mechanism is the formation of an antigen + antibody complex (Ig G) with the complement of the system. The formed complex must be large, otherwise it does not precipitate. At the same time, platelet serotonin is of great importance, which increases the permeability of the vascular wall, promotes the microprecipitation of immune complexes, their deposition in the walls of blood vessels and other structures. At the same time, there is always a small amount (Ig E) in the blood, fixed on basophils and mast cells. Immune complexes attract neutrophils, phagocytize them, they secrete lysosomal enzymes, which, in turn, determine the chemotaxis of macrophages. Under the influence of hydrolytic enzymes released by phagocytic cells (pathochemical stage), damage (pathophysiological stage) of the vascular wall, loosening of the endothelium, thrombosis, hemorrhages, and sharp disturbances of microcirculation with necrotic foci begin. Inflammation develops.

In addition to the Arthus phenomenon, serum sickness can serve as a manifestation of allergic reactions of this type.

Serum sickness- a symptom complex that occurs after parenteral administration of sera into the body of animals and humans for prophylactic or therapeutic purposes (anti-rabies, anti-tetanus, anti-plague, etc.); immunoglobulins; transfused blood, plasma; hormones (ACTH, insulin, estrogen, etc.) some antibiotics, sulfonamides; with the bites of insects that release toxic compounds. The basis for the formation of serum sickness are immune complexes that arise in response to the primary, single entry of the antigen into the body.

The properties of the antigen and the characteristics of the reactivity of the organism affect the severity of the manifestation of serum sickness. When a foreign antigen enters the animal, three types of response are observed: 1) antibodies are not formed at all and the disease does not develop; 2) there is a pronounced formation of antibodies and immune complexes. Clinical signs appear quickly, as the antibody titer increases, they disappear; 3) weak antibody genesis, insufficient elimination of the antigen. Favorable conditions are created for the long-term persistence of immune complexes and their cytotoxic effect.

Symptoms are characterized by pronounced polymorphism. The prodromal period is characterized by hyperemia, increased skin sensitivity, enlarged lymph nodes, acute pulmonary emphysema, damage and swelling of the joints, swelling of the mucous membranes, albuminuria, leukopenia, thrombocytopenia, increased ESR, hypoglycemia. In more severe cases, acute glomerulonephritis, myocardial dysfunction, arrhythmia, vomiting, and diarrhea are observed. In most cases, after 1-3 weeks, the clinical signs disappear and recovery occurs.

Bronchial asthma - It is characterized by a sudden attack of suffocation with a sharp difficulty in the expiratory phase as a result of a diffuse patency disorder in the system of small bronchi. Manifested by bronchospasm, swelling of the mucous membrane of the bronchi, hypersecretion of the mucous glands. In the atopic form, the attack begins with a cough, then a picture of expiratory suffocation develops, a large number of dry whistling rales are heard in the lungs.

Pollinosis (hay fever, allergic rhinitis) - a recurrent disease associated with the inhalation and conjunctiva of plant pollen from the air during their flowering period. It is characterized by hereditary predisposition, seasonality (usually spring-summer, due to the flowering period of plants). It is manifested by rhinitis, conjunctivitis, irritation and itching of the eyelids, sometimes general weakness, fever. An increased amount of histamine, reagins (Ig E), eosinophilic granulocytes, globulin fraction of blood serum, an increase in transaminase activity are detected in the blood. Attacks of the disease disappear after contact with plant allergens is stopped after a few hours, sometimes after a few days. The rhino-conjunctival form of pollinosis can end with a visceral syndrome, in which a number of internal organs are affected (pneumonia, pleurisy, myocarditis, etc.).

Urticaria and angioedema- occur when exposed to plant, pollen, chemical, epidermal, serum, drug allergens, house dust, insect bites, etc. This disease usually begins suddenly, with the manifestation of very often unbearable itching. At the site of scratching, hyperemia instantly occurs, then there is a rash on the skin of itchy blisters, which are swelling of a limited area, mainly the papillary layer of the skin. There is an increase in body temperature, swelling of the joints. The illness lasts from several hours to several days.

One type of urticaria is Quincke's edema (giant urticaria, angioedema). With Quincke's edema, skin itching usually does not occur, since the process is localized in the subcutaneous layer, not spreading to the sensitive endings of the skin nerves. Sometimes urticaria and Quincke's edema proceed very rapidly, preceding the development of anaphylactic shock. In most cases, the acute phenomena of urticaria and Quincke's edema are completely cured. Chronic forms are difficult to treat, characterized by an undulating course with alternating periods of exacerbation and remission. The generalized form of urticaria is very difficult, in which edema captures the mucous membrane of the mouth, soft palate, tongue, and the tongue hardly fits in the oral cavity, and swallowing is very difficult. In the blood, an increase in the content of eosinophilic granulocytes, globulins and fibrinogen, a decrease in the level of albumins are found.

General pathogenesis of immediate allergic reactions .

Allergic reactions of immediate type, different in external manifestations, have common mechanisms of development. In the genesis of hypersensitivity, three stages are distinguished: immunological, biochemical (pathochemical) and pathophysiological. Immunological stage begins with the first contact of the allergen with the body. The hit of the antigen stimulates macrophages, they begin to release interleukins that activate T-lymphocytes. The latter, in turn, trigger the processes of synthesis and secretion in B-lymphocytes, which turn into plasma cells. Plasma cells during the development of an allergic reaction of the first type produce mainly Ig E, the second type - Ig G 1,2,3, Ig M, the third type - mainly Ig G, Ig M.

Immunoglobulins are fixed by cells on the surface of which there are corresponding receptors - on circulating basophils, mast cells of the connective tissue, platelets, smooth muscle cells, skin epithelium, etc. A period of sensitization sets in, sensitivity to repeated exposure to the same allergen increases. The maximum severity of sensitization occurs after 15-21 days, although the reaction may occur much earlier. In the case of reinjection of the antigen to a sensitized animal, the interaction of the allergen with antibodies will occur on the surface of basophils, platelets, mast and other cells. When an allergen binds to more than two adjacent immunoglobulin molecules, the membrane structure is disrupted, the cell is activated, and previously synthesized or newly formed allergy mediators begin to be released. Moreover, only about 30% of the biologically active substances contained there are released from the cells, since they are ejected only through the deformed section of the target cell membrane.

AT pathochemical stage changes occurring on the cell membrane in the immunological phase due to the formation of immune complexes trigger a cascade of reactions, the initial stage of which is, apparently, the activation of cellular esterases. As a result, a number of allergy mediators are released and re-synthesized. Mediators have vasoactive and contractile activity, chemotoxic properties, the ability to damage tissues and stimulate repair processes. The role of individual mediators in the overall reaction of the body to repeated exposure to the allergen is as follows.

Histamine - one of the most important mediators of allergy. Its release from mast cells and basophils is carried out by secretion, which is an energy-dependent process. The energy source is ATP, which breaks down under the influence of activated adenylate cyclase. Histamine dilates capillaries, increases vascular permeability by dilating terminal arterioles and constricting postcapillary venules. It inhibits the cytotoxic and helper activity of T-lymphocytes, their proliferation, differentiation of B-cells and the synthesis of antibodies by plasma cells; activates T-suppressors, has a chemokinetic and chemotactic effect on neutrophils and eosinophils, inhibits the secretion of lysosomal enzymes by neutrophils.

Serotonin - mediates smooth muscle contraction, increased permeability and vasospasm of the heart, brain, kidneys, and lungs. Released in animals from mast cells. Unlike histamine, it does not have an anti-inflammatory effect. Activates the suppressor population of T-lymphocytes of the thymus and spleen. Under its influence, T-suppressors of the spleen migrate to the bone marrow and lymph nodes. Along with the immunosuppressive effect, serotonin can have an immunostimulatory effect through the thymus. Enhances the sensitivity of mononuclear cells to various chemotaxis factors.

Bradykinin - the most active component of the kinin system. It changes the tone and permeability of blood vessels; lowers blood pressure, stimulates the secretion of mediators by leukocytes; to some extent affects the mobility of leukocytes; causes smooth muscle contraction. In asthmatic patients, bradykinin leads to bronchospasm. Many of the effects of bradykinin are due to a secondary increase in prostaglandin secretion.

Heparin - proteoglycan, which forms complexes with antithrombin, which prevent the coagulating effect of thrombin (blood clotting). It is released in allergic reactions from mast cells, where it is found in large quantities. In addition to anticoagulation, it has other functions: it participates in the reaction of cell proliferation, stimulates the migration of endothelial cells into the capillaries, inhibits the action of complement, activates pino- and phagocytosis.

Complement fragments - have anaphylactic (histamine-releasing) activity against mast cells, basophils, other leukocytes, increase the tone of smooth muscles. Under their influence, vascular permeability increases.

Slow-reacting substance of anaphylaxis (MRSA) - unlike histamine, causes a slow contraction of the smooth muscles of the trachea and ileum of a guinea pig, human and monkey bronchioles, increases the permeability of skin vessels, and has a more pronounced bronchospastic effect than histamine. The action of MRSA is not removed by antihistamines. It is secreted by basophils, peritoneal alveolar and blood monocytes, mast cells, various sensitized lung structures.

Protoglandins - prostaglandins E, F, D are synthesized in body tissues. Exogenous prostaglandins have the ability to stimulate or inhibit the inflammatory process, cause fever, dilate blood vessels, increase their permeability, and cause erythema. Prostaglandins F cause severe bronchospasm. Prostaglandins E have the opposite effect, having a high bronchodilating activity.

pathophysiological stage. It is a clinical manifestation of allergic reactions. Biologically active substances secreted by target cells have a synergistic effect on the structure and function of organs and tissues of the animal organism. The resulting vasomotor reactions are accompanied by blood flow disorders in the microcirculatory bed, and are reflected in the systemic circulation. Expansion of capillaries and an increase in the permeability of the histohematic barrier lead to the release of fluid beyond the walls of blood vessels, the development of serous inflammation. The defeat of the mucous membranes is accompanied by edema, hypersecretion of mucus. Many mediators of allergy stimulate the contractile function of the myofibrils of the walls of the bronchi, intestines, and other hollow organs. The results of spastic contractions of muscle elements can manifest themselves in asphyxia, disorders of the motor function of the gastrointestinal tract, such as vomiting, diarrhea, acute pain from excessive contractions of the stomach and intestines.

The nervous component of the genesis of an immediate type of allergy is due to the influence of kinins (bradykinin), histamine, serotonin on neurons and their sensitive formations. Disorders of nervous activity with allergies can be manifested by fainting, a feeling of pain, burning, unbearable itching. Immediate-type hypersensitivity reactions end with either recovery or death, which may be caused by asphyxia or acute hypotension.

Delayed allergic reactions (hypersensitivity of the delayed type, hypersensitivity of the delayed type, T - dependent reactions). This form of allergy is characterized by the fact that antibodies are fixed on the membrane of lymphocytes and are receptors for the latter. Clinically detected 24-48 hours after the contact of the sensitized organism with the allergen. This type of reaction proceeds with the predominant participation of sensitized lymphocytes, therefore it is considered as a pathology of cellular immunity. The slowdown in the reaction to the antigen is explained by the need for a longer time for the accumulation of lymphocytic cells (T- and B - lymphocytes of different populations, macrophages, basophils, mast cells) in the area of ​​​​action of a foreign substance compared with the humoral reaction antigen + antibody with immediate type hypersensitivity. Delayed-type reactions develop with infectious diseases, vaccinations, contact allergies, autoimmune diseases, with the introduction of various antigenic substances into animals, and the application of haptens. They are widely used in veterinary medicine for allergic diagnosis of latent forms of chronic infectious diseases such as tuberculosis, glanders, and some helminthic infestations (echinococcosis). Delayed-type reactions are tuberculin and maleic allergic reactions, rejection of transplanted tissue, autoallergic reactions, bacterial allergies.

General pathogenesis of delayed-type allergic reactions

Delayed hypersensitivity occurs in three stages:

AT pathochemical stage stimulated T - lymphocytes synthesize a large number of lymphokines - mediators of HRT. They, in turn, involve other types of cells, such as monocytes / macrophages, neutrophils, in response to a foreign antigen. The most important in the development of the pathochemical stage are the following mediators:

the migration-inhibiting factor is responsible for the presence of monocytes/macrophages in the inflammatory infiltrate; it is assigned the most important role in the formation of the phagocytic response;

factors affecting macrophage chemotaxis, their adhesion, resistance;

mediators that affect the activity of lymphocytes, such as a transfer factor that promotes the maturation of T-cells in the body of the recipient after the introduction of sensitized cells; a factor that causes blast transformation and proliferation; a suppression factor that inhibits the immune response to an antigen, etc.;

a chemotaxis factor for granulocytes that stimulates their emigration, and an inhibitory factor that acts in the opposite way;

interferon, which protects the cell from the introduction of viruses;

skin-reactive factor, under the influence of which the permeability of the skin vessels increases, swelling, redness, tissue thickening at the site of antigen reinjection appear.

The influence of allergy mediators is limited by opposing systems that protect target cells.

AT pathophysiological stage biologically active substances released by damaged or stimulated cells determine the further development of delayed-type allergic reactions.

Local tissue changes in delayed-type reactions can be detected as early as 2-3 hours after exposure to a resolving dose of antigen. They are manifested by the initial development of a granulocytic reaction to irritation, then lymphocytes, monocytes and macrophages migrate here, accumulating around the vessels. Along with migration, cell proliferation takes place in the focus of an allergic reaction. However, the most pronounced changes are observed after 24-48 hours. These changes are characterized by hyperergic inflammation with pronounced signs.

Delayed allergic reactions are induced mainly by thymus-dependent antigens - purified and unpurified proteins, microbial cell components and exotoxins, virus antigens, low molecular weight protein-conjugated haptens. The reaction to the antigen in this type of allergy can be formed in any organ, tissue. It is not associated with the participation of the complement system. The main role in pathogenesis belongs to T-lymphocytes. The genetic control of the reaction is carried out either at the level of individual subpopulations of T- and B-lymphocytes, or at the level of intercellular relationships.

malleic allergic reaction used to detect glanders in horses. The application of purified mallein obtained from pathogens to the mucous membrane of the eye of infected animals after 24 hours is accompanied by the development of acute hyperergic conjunctivitis. At the same time, an abundant outflow of grayish-purulent exudate from the corner of the eye, arterial hyperemia, and swelling of the eyelids are observed.

transplanted tissue rejection as a result of transplantation of foreign tissue, the recipient's lymphocytes become sensitized (become carriers of the transfer factor or cellular antibodies). These immune lymphocytes then migrate to the transplant, where they are destroyed and release the antibody, which causes the destruction of the transplanted tissue. The transplanted tissue or organ is rejected. Transplant rejection is the result of a delayed-type allergic reaction.

Autoallergic reactions - reactions resulting from damage to cells and tissues by autoallergens, i.e. allergens that originate in the body itself.

Bacterial allergy - appears with preventive vaccinations and with certain infectious diseases (with tuberculosis, brucellosis, coccal, viral and fungal infections). If the allergen is administered intradermally to a sensitized animal, or applied to scarified skin, then the response begins no earlier than 6 hours later. At the site of contact with the allergen, hyperemia, induration and sometimes skin necrosis occur. With the injection of small doses of the allergen, necrosis is absent. In clinical practice, delayed skin reactions Pirquet, Mantoux are used to determine the degree of sensitization of the body in a particular infection.

Second classification. Depending on the type of allergen All allergies are divided into:

Serum

infectious

1. Vegetable

   Animal origin

   drug allergy

   Idiosyncrasy

   household allergies

   Autoallergy

Serum allergy. This is such an allergy that occurs after the introduction of any therapeutic serum. An important condition for the development of this allergy is the presence of an allergic constitution. Perhaps this is due to the peculiarity of the autonomic nervous system, the activity of blood histaminase and other indicators that characterize the setting of the body to an allergic reaction.

This type of allergy is especially important in veterinary practice. Anti-erysipelas serum, with inept treatment causes the phenomenon of allergy, anti-tetanus serum can be an allergen, with repeated administration, anti-diphtheria serum can be an allergen.

The mechanism of development of serum sickness is that a foreign protein introduced into the body causes the formation of antibodies such as precipitins. Antibodies are partially fixed on the cells, some of them circulate in the blood. After about a week, the antibody titer reaches a level sufficient to react with a specific allergen for them - a foreign serum that is still preserved in the body. As a result of the combination of the allergen with the antibody, an immune complex arises, which settles on the endothelium of the capillaries of the skin, kidneys and other organs. This causes damage to the endothelium of the capillaries, an increase in permeability. Allergic edema, urticaria, inflammation of the lymph nodes, glomeruli of the kidneys and other disorders characteristic of this disease develop.

infectious allergy – such an allergy, when the allergen is any pathogen. This property may have a tubercle bacillus, pathogens of glanders, brucellosis, helminths.

Infectious allergy is used for diagnostic purposes. This means that microorganisms increase the body's sensitivity to preparations prepared from these microorganisms, extracts, extracts.

food allergy – various clinical manifestations of allergy associated with food intake. The etiological factor is food proteins, polysaccharides, low molecular weight substances acting as haptens (food allergens). The most common food allergies are to milk, eggs, fish, meat and products made from these products (cheeses, butter, creams), strawberries, strawberries, honey, nuts, citrus fruits. Allergenic properties are possessed by additives and impurities contained in food products, preservatives (benzoic and acetylsalicylic acids), food colorings, etc.

There are early and late reactions of food allergies. The early ones develop within one hour from the moment of ingestion, severe anaphylactic shock is possible, up to death, acute gastroenteritis, hemorrhagic diarrhea, vomiting, collapse, bronchospasm, swelling of the tongue and larynx. Late manifestations of allergy are associated with skin lesions, dermatitis, urticaria, angioedema. Symptoms of food allergies are observed in different parts of the gastrointestinal tract. Possible development of allergic stomatitis, gingivitis, damage to the esophagus with symptoms of edema, hyperemia, rashes on the mucous membrane, feeling of difficulty swallowing, burning and pain along the esophagus. The stomach is often affected. Such a lesion is clinically similar to acute gastritis: nausea, vomiting, pain in the epigastric region, tension in the abdominal wall, eosinophilia of gastric contents. With gastroscopy, swelling of the gastric mucosa is noted, hemorrhagic rashes are possible. With intestinal damage, there are cramping or persistent pain, bloating, tension in the abdominal wall, tachycardia, and a drop in blood pressure.

plant allergy – such an allergy, when the allergen is the pollen of a plant. Pollen of bluegrass meadow, cocksfoot, wormwood, timothy grass, meadow fescue, ragweed and other herbs. The pollen of various plants differs from each other in antigenic composition, but there are also common antigens. This causes the development of polyvalent sensitization caused by the pollen of many grasses, as well as the appearance of cross-reactions to various allergens in patients with hay fever.

The allergenic properties of pollen depend on the conditions in which it resides. Fresh pollen, i.e. when it is released into the air from the dust particles of the stamens of grasses and trees, it is very active. Getting into a humid environment, for example, on mucous membranes, the pollen grain swells, its shell bursts, and the internal contents - plasma, which has allergenic properties, is absorbed into the blood and lymph, sensitizing the body. It has been established that grass pollen has more pronounced allergenic properties than tree pollen. In addition to pollen, other parts of plants may have allergenic properties. The most studied of them are fruits (cotton).

Repeated exposure to plant pollen can cause suffocation, bronchial asthma, inflammation of the upper respiratory tract, etc.

Allergy of animal origin- cells of various tissues, components of various structures of a living organism have pronounced allergenic properties. The most significant are epidermal allergens, Hymenoptera poisons and mites. Epidermal allergens consist of integumentary tissues: dandruff, epidermis and hair of various animals and humans, particles of claws, beaks, nails, feathers, animal hooves, scales of fish and snakes. Frequent allergic reactions in the form of anaphylactic shock from insect bites. The presence of cross-allergic reactions caused by insect bites has been shown within the class or species. Insect venom is a product of special glands. It consists of substances with pronounced biological activity: biogenic amines (histamine, dopamine, acetylcholine, norepinephrine), proteins and peptides. Allergens of ticks (bed, barn, dermatophagous, etc.) are often the cause of bronchial asthma. When they enter with the inhaled air, the sensitivity of the body is perverted.

drug allergy - when the allergen is any medicinal substance. Allergic reactions caused by drugs presently present the most serious complications in drug therapy. The most common allergens are antibiotics, especially administered orally (penicillin, streptomycin, etc.). Most drugs are not full antigens, but have the properties of haptens. In the body, they form complexes with blood serum proteins (albumin, globulin) or tissues (procollagen, histone, etc.). This indicates the ability of almost every drug or chemical to cause allergic reactions. In some cases, haptens are not antibiotics or chemotherapy drugs, but the products of their metabolism. Thus, sulfanilamide preparations do not have allergenic properties, but acquire them after oxidation in the body. A characteristic feature of drug allergens is their pronounced ability to cause paraspecific or cross-reactions, which determines the polyvalence of drug allergy. Manifestations of drug allergies range from mild reactions in the form of skin rash and fever, to the development of anaphylactic shock.

Idiosyncrasy - (from Greek . idios - independent, syncrasis - mixing) is an innate hypersensitivity to food or drugs. When taking certain foods (strawberries, milk, chicken protein, etc.) or drugs (iodine, iodoform, bromine, quinine), certain individuals experience disorders. The pathogenesis of idiosyncrasy has not yet been established. Some researchers point out that in idiosyncrasy, unlike anaphylaxis, it is not possible to detect specific antibodies in the blood. It is assumed that food idiosyncrasy is associated with the presence of congenital or acquired increased permeability of the intestinal wall. As a result, protein and other allergens can be absorbed into the blood in an unsplit form and thereby sensitize the body to them. When the body encounters these allergens, an attack of idiosyncrasy occurs. In some people, characteristic allergic phenomena occur mainly from the skin and vascular system: hyperemia of the mucous membranes, edema, urticaria, fever, vomiting.

household allergies - in this case, the allergen can be mold, sometimes fish food - dried daphnia, plankton (lower crustaceans), house dust, household dust, mites. Household dust is the dust of residential premises, the composition of which varies in terms of the content of various fungi, bacteria and particles of organic and inorganic origin. Library dust in large quantities contains remnants of paper, cardboard, etc. According to most modern data, the allergen from house dust is a mucoprotein and a glycoprotein. Household allergens can sensitize the body.

Autoallergy- occurs when allergens are formed from their own tissues. With the normal function of the immune system, the body removes, neutralizes its own, degenerate cells, and if the body's immune system cannot cope, then the degenerate cells and tissues become allergens, i.e. autoallergens. In response to the action of autoallergens, autoantibodies (reagins) are formed. Autoantibodies combine with autoallergens (self-antigens) and form a complex that damages healthy tissue cells. The complex (antigen + antibody) is able to settle on the surface of muscles, other tissues (brain tissue), on the surface of the joints and cause allergic diseases.

According to the mechanism of autoallergy, diseases such as rheumatism, rheumatic heart disease, encephalitis, collagenoses occur (non-cellular parts of the connective tissue are damaged), kidneys are affected.

The third classification of allergies.

Depending on the sensitizing agent There are two types of allergies:

* Specific

* Non-specific

Allergy is called specific if the sensitivity of the organism is perverted only to the allergen with which the organism is sensitized, i.e. there is strict specificity here.

A representative of a specific allergy is anaphylaxis. Anaphylaxis consists of two words (ana - without, phylaxis - protection) and literally translated - defenselessness.

Anaphylaxis- this is an increased and qualitatively perverted response of the body to the allergen to which the body is sensitized.

The first introduction of an allergen into the body is called sensitizing administration, or otherwise sensitizing. The value of the sensitizing dose can be very small, sometimes it is possible to sensitize with such a dose as 0.0001 g of the allergen. The allergen must enter the body parenterally, i.e., bypassing the gastrointestinal tract.

The state of increased sensitivity of the body or the state of sensitization occurs after 8-21 days (this is the time required for the production of class E antibodies), depending on the type of animal or individual characteristics.

A sensitized organism looks no different from an unsensitized organism.

Re-introduction of an antigen is called the introduction of a resolving dose or reinjection.

The size of the resolving dose is 5-10 times higher than the sensitizing dose, and the resolving dose should also be administered parenterally.

The clinical picture that occurs after the introduction of a resolving dose (according to Bezredko) is called anaphylactic shock.

Anaphylactic shock is a severe clinical manifestation of allergy. Anaphylactic shock can develop at lightning speed, within a few minutes after the introduction of the allergen, less often after a few hours. Harbingers of shock can be a feeling of heat, redness of the skin, itching, fear, nausea. The development of shock is characterized by a rapidly growing collapse (pallor, cyanosis, tachycardia, thready pulse, cold sweat, a sharp decrease in blood pressure), suffocation, weakness, loss of consciousness, swelling of the mucous membranes, and convulsions. In severe cases, there is acute heart failure, pulmonary edema, acute kidney failure, allergic lesions of the intestines are possible, up to obstruction.

In severe cases, dystrophic and necrotic changes in the brain and internal organs, interstitial pneumonia, and glomerulonephritis may develop. At the height of shock in the blood, erythremia, leukocytosis, eosinophilia, an increase in ESR are noted; in the urine - proteinuria, hematuria, leukocyturia.

According to the rate of occurrence, anaphylactic shock can be (acute, subacute, chronic). Acute form - changes occur after a few minutes; subacute occurs after a few hours; chronic - changes occur after 2-3 days.

Different animal species do not show the same sensitivity to anaphylactic shock. The most sensitive to anaphylaxis are guinea pigs, and further on the degree of sensitivity, the animals are arranged in the following order - rabbits, sheep, goats, cattle, horses, dogs, pigs, birds, monkeys.

So, in guinea pigs there is anxiety, itching, scratching, sneezing, the pig rubs its muzzle with its paws, trembles, involuntary defecation is observed, takes a lateral position, breathing becomes difficult, intermittent, respiratory movements slow down, convulsions appear and may be fatal. This clinical picture is combined with a drop in blood pressure, a decrease in body temperature, acidosis, and an increase in the permeability of blood vessels. An autopsy of a guinea pig that died from anaphylactic shock reveals foci of emphysema and atelectasis in the lungs, multiple hemorrhages on the mucous membranes, and unclotting blood.

Rabbits - 1-2 minutes after the introduction of a resolving dose of serum, the animal begins to worry, shakes its head, lies on its stomach, shortness of breath appears. Then there is a relaxation of the sphincters and urine and feces are involuntarily separated, the rabbit falls, bends its head back, convulsions appear, then breathing stops, death occurs.

In sheep, anaphylactic shock is very acute. After the introduction of a permissive dose of serum, shortness of breath, increased salivation, lacrimation occur in a few minutes, pupils dilate. Swelling of the scar is observed, blood pressure decreases, involuntary separation of urine and feces appear. Then there are paresis, paralysis, convulsions, and often the death of the animal occurs.

In goats, cattle, and horses, the symptoms of anaphylactic shock are somewhat similar to those in the rabbit. However, they most clearly show signs of paresis, paralysis, and there is also a decrease in blood pressure.

Dogs. Essential in the dynamics of anaphylactic shock are disorders of the portal circulation and blood stasis in the liver and intestinal vessels. Therefore, anaphylactic shock in dogs proceeds according to the type of acute vascular insufficiency, at first there is excitement, shortness of breath, vomiting occurs, blood pressure drops sharply, involuntary separation of urine and feces, mostly red (an admixture of erythrocytes), appears. Then the animal falls into a stuporous state, while there is a bloody discharge from the rectum. Anaphylactic shock in dogs is rarely fatal.

In cats and fur-bearing animals (Arctic foxes, foxes, minks), a similar dynamics of shock is observed. However, Arctic foxes are more susceptible to anaphylaxis than dogs.

Monkey. Anaphylactic shock in monkeys is not always reproducible. In shock, monkeys experience difficulty in breathing, collapse. The number of platelets falls, blood clotting decreases.

In the occurrence of anaphylactic shock, the functional state of the nervous system matters. It is not possible to cause a picture of anaphylactic shock in anesthetized animals (narcotic blocking of the central nervous system turns off impulses going to the site of allergen introduction), during hibernation, in newborns, with sudden cooling, as well as in fish, amphibians and reptiles.

Antianaphylaxis- this is a state of the body that is observed after suffering anaphylactic shock (if the animal has not died). This condition is characterized by the fact that the body becomes insensitive to this antigen (allergen within 8-40 days). The state of anti-anaphylaxis occurs 10 or 20 minutes after anaphylactic shock.

The development of anaphylactic shock can be prevented by administering small doses of antigen to a sensitized animal 1-2 hours before the injection of the required volume of the drug. Small amounts of antigen bind antibodies, and the resolving dose is not accompanied by the development of immunological and other stages of immediate hypersensitivity.

Nonspecific Allergy- this is such a phenomenon when the body is sensitized to one allergen, and the sensitivity reaction to another allergen is perverted.

There are two types of nonspecific allergies (paraallergy and heteroallergy).

Paraallergy - they call such an allergy when the body is sensitized by one antigen, and sensitivity increases to another antigen, i.e. one allergen increases the sensitivity of the body to another allergen.

Heteroallergy is such a phenomenon when the body is sensitized by a factor of non-antigenic origin, and the sensitivity increases, perverts to any factor of antigenic origin, or vice versa. Factors of non-antigenic origin can be cold, exhaustion, overheating.

Cold can increase the body's sensitivity to foreign proteins, antigens. That is why in a state of cold, serum should not be administered; the flu virus shows its effect very quickly if the body is supercooled.

Fourth classification -according to the nature of the manifestation allergies are:

General- this is such an allergy, when, with the introduction of a resolving dose, the general condition of the body is disturbed, the functions of various organs and systems are disrupted. To obtain a general allergy, a single one-time sensitization is sufficient.

local allergy - this is such an allergy when, with the introduction of a resolving dose, changes occur at the injection site of the allergen, and at this site can develop:

hyperergic inflammation

ulceration

skin fold thickening

swelling

To obtain a local allergy, multiple sensitization is required with an interval of 4-6 days. If the same antigen is injected several times into the same place of the body with an interval of 4-6 days, then after the first injections, the antigen dissolves completely, and after the sixth, seventh injection, swelling, redness occurs at the injection site, and sometimes inflammatory reaction with extensive edema, extensive hemorrhage, i.e. local morphological changes are observed.

An allergy is an inadequate reaction of the immune system to substances that do not pose a threat to the body. In the modern world, the number of people suffering from various types of allergies is increasing daily. This is especially true for diseases of the immediate type.

In allergology, all allergic reactions are divided into two types - immediate and delayed type. The first is characterized by spontaneously rapid development. Already less than half an hour after the penetration of the allergen in the body, the circulation of antibodies occurs. The patient begins to react violently to the penetration of the provocateur into the oral cavity, respiratory tract or on the skin.

Depending on the age of the allergic person and the state of his health, before contact with the catalyst of the disease, he may manifest certain symptoms with different strengths. An immediate type allergy causes urticaria, atopic bronchial asthma, anaphylactic shock, serum sickness, hay fever, acute glomerulonephritis, Quincke's edema.

Diagnostics

Initially, the epithelium, cardiovascular, digestive and respiratory systems suffer from rapid allergies. The path of development of a reaction to an annoying stimulus is identified from the moment the antibody or immunoglobulin collides with the antigen.

The body's struggle with a foreign substance contributes to internal inflammation. In a situation of excessive activity of antigens, anaphylactic shock may occur.

An immediate allergic reaction occurs in three stages:

• contact of antigen and antibody;
• release of active toxic substances into the body;
• acute inflammation.

Acute urticaria and angioedema

Most often, with allergies, urticaria immediately occurs. It is characterized by abundant red rashes. Small spots affect the face, neck, limbs, sometimes other parts of the body. The patient complains of feeling chills, nausea, turning into vomiting.

Important! Quincke's edema concerns the deeper layers of the skin. Patients have swollen lips, eyelids, throat, hoarse voice. Sometimes there are problems with the heart and blood vessels. Urticaria in combination with Quincke's edema can cause complications in the form of severe asphyxia.

An anamnesis, a blood test for an increase in immunoglobulin E, provocative tests for physical effort, cold, vibration, etc. will help diagnose urticaria and Quincke's edema. In the clinic, a general examination of the stomach and intestines is carried out. In difficult cases, allergists prescribe immunological studies.

Treatment begins with the exclusion of provocateurs of the disease and the preparation of an individual nutrition plan. The purpose of specific drugs depends on the causes of the disease. In case of an emergency development of an allergy, the patient must be seated and an ambulance called, if this is a child, pick him up. To facilitate breathing, you need to remove the victim's tie and any other tight clothing. It is necessary to provide him with full-fledged breathing with a full chest.

If the allergy occurred from an insect bite, it is urgent to remove the sting from the patient's body. With the penetration of the allergen inside, you need to take sorbents - Smecta or activated carbon. It is impossible to wash the stomach. At home, you can apply a cold compress to the place of edema, give the person a plentiful drink - mineral water or a soda solution.

The doctor will prescribe the patient treatment with antihistamines - Suprastin, Tavegil. Against Quincke's edema, glucocorticosteroids - Dexamethasone or Prednisolone help. They are injected into a vein or under the skin, sometimes they are allowed to pour the ampoule under the tongue.

In some cases, an allergic person has to urgently raise the pressure. For this, an injection of adrenaline is used. It is important to know that untimely medical care can lead to asphyxia and clinical death. If the patient has stopped breathing, it is necessary to resume it artificially.

Bronchial asthma

The next common allergy development occurs due to infectious or non-infectious allergens. This is bronchial asthma.

Among the infectious catalysts of the disease, doctors designate Escherichia coli, microorganisms, golden and white types of staphylococcus aureus. It is noted that pathogens of non-infectious nature are much larger. These are dandruff, dust, drugs, pollen, feathers, wool.

In children, bronchial asthma can also be caused by food provocateurs of the disease. Most often, allergies develop after eating honey, cereals, milk, fish, seafood or eggs.

Allergists note that non-infectious asthma is much more mild. The main symptoms in this case are systematic attacks of nocturnal suffocation. Bronchial asthma is accompanied by sneezing, itching in the nose, tightness in the chest.

Important! To identify bronchial asthma, the patient should see a pulmonologist and an allergist-immunologist. Specialists conduct allergy tests of sensitivity to fungal, epidermal and domestic pathogens and prescribe treatment.

As a rule, the doctor prescribes allergen-specific immunotherapy. The patient is constantly injected with doses of the allergen solution, increasing them. Bronchodilators, aerosol inhalers, or nebulizer therapy can help relieve asthma attacks. Anti-inflammatory therapy includes corticosteroids. Bronchial patency is improved by expectorant syrups - Gerbion, Ambrobene, etc.

With allergic bronchial asthma, treatment with folk remedies should be approached with extreme caution. It would be better to do breathing exercises or sports, to establish a hypoallergenic diet.

Serum sickness

The key signs of this disease are joint and headaches, severe itching, increased sweating, nausea to vomiting. For more complex cases, skin rashes and swelling of the larynx are characteristic, the disease is accompanied by high fever, swollen lymph nodes.

Allergies can be caused by medical serums or drugs. Its diagnosis is related to identifying the specific substance that provoked the disease.

Treatment includes the abolition of those drugs that caused the development of a negative reaction, adherence to a hypoallergenic diet and a course of drugs. First, infusion therapy, a cleansing enema are carried out, enterosorbents and laxatives are prescribed.

After removing the allergens, it is necessary to take antihistamines. In difficult cases, the doctor prescribes glucocorticosteroids.

Anaphylactic shock

It is considered the most life-threatening manifestation of an allergy and can occur in a fairly short time - from a couple of moments to a couple of hours. At the same time, each patient notes shortness of breath and weakness, changes in body temperature, convulsions, nausea to vomiting, pain in the abdomen, rash, itching. There may be loss of consciousness, a decrease in blood pressure.

This allergic symptom sometimes flows into a heart attack, hemorrhages in the intestines and pneumonia. With a severe attack of the patient, it is necessary to immediately hospitalize and urgently start therapy. After that, the patient must constantly be under the control of allergists.

To eliminate anaphylactic shock, it is necessary to help isolate the allergen from the patient, lay him on a horizontal surface, raising his legs relative to his head. Then you can give one of the antihistamines that the doctor previously prescribed to the patient, and observe the pulse and pressure until the ambulance arrives.

conclusions

Knowing the symptoms and first aid rules for an immediate type of allergic reaction, it is not so difficult to maintain your own health and the health of loved ones. Remember that this type of allergy requires immediate attention.

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