Complications of allergic genesis in dermatocosmetology

Allergy is the body’s readiness for immune reactions, i.e. allergic reactivity. Allergic reactivity is such an increased sensitivity in which the development of a reaction to a specific antigen (a substance carrying genetically foreign information) causes tissue damage or disruption of their function. The concept of dysfunction needs to be introduced because in some allergic reactions, for example, mild anaphylactic or tuberculin shock, there are no macroscopically detectable damage.

The term “allergy” means altered sensitivity, namely increased sensitivity. But sensitivity and reaction are not the same thing. Therefore, it is inappropriate to use the term “allergy” to mean “allergic reaction.”

Increased sensitivity to antigen underlies all immunological reactions. Increased sensitivity is determined by the presence of high-avidity antibodies, clones of immunocompetent cells with highly specific receptors. But the presence of specific antibodies in the blood serum may not determine an allergy, but, on the contrary, resistance to its manifestations. Thus, allergic reactivity, or the state of allergy, is the property of the body, resulting from immunological restructuring, to give a reaction to a damaging antigen, which occurs with tissue damage or disruption of their functions. Reactions of this type are allergic reactions.

The process of formation of allergic reactivity should be called allergization . Allergization of the body is based on the process of developing hypersensitivity to the action of a specific antigen. The state of high allergic reactivity negatively affects the body's immunological defense. Allergic reactivity changes in accordance with phase patterns, and its absence or low level can correspond to both low and high immunity.

The main reasons for the rapid growth of allergic diseases can be considered the following ( Scheme 1 ).

1. A sharp increase in the number of allergens in the environment due to scientific and technological progress (chemicalization of production and everyday life, the medical process). Several tens of thousands of new chemical compounds are synthesized every year.
2. Agriculture, industry, environmental pollution - more people are exposed to allergens, and the pathogenic influence has become massive, frequent, long-lasting: the use of chemicals in construction and interior decoration.
3. Changes in the specific gravity of various routes of xenobiotics entering the body. Previously, allergens entered mainly through the gastrointestinal tract, but now more than half of the substances penetrate through the respiratory tract (lead, man-made gases, sulfur), and in the respiratory tract there are no such “filters” as in the liver. The main burden falls on macrophages and other immunocompetent cells, so the frequency of the allergenic population is growing, and new forms of allergic diseases are becoming more frequent.
4. Increased incidence of exposure to the body simultaneously of several substances, both allergenic and irritating. The basis of potentiation is a syndrome of decreased nonspecific resistance of the body as a result of changes in the immune status, metabolic processes, and neurohumoral regulation.
5. Among perinatal risk factors for allergic dermatoses, hereditary burden is 65-82.4%, and on the maternal side it is 3 times more common than on the paternal side. Early and late gestosis, consumption of obligate allergens during pregnancy, and early artificial feeding are of great importance [1, 2].

Scheme 1

As noted earlier, the basis of any allergy, no matter how it manifests itself, is changes in the immune status. Immunity can be defined as the body's ability to identify, neutralize and eliminate foreign structures in order to maintain its own integrity - homeostasis. This ability is provided by the immune system, which in the process of evolution arose from lymph cells and macrophages. They take part in the functioning of the immune system both on their own, providing cellular immunity, and together with the protein products of their own activity - antibodies, providing humoral immunity. The immune system functions as a single whole, and the division into two types is purely arbitrary.

The head of the EAACI (European Association of Allergy and Clinical Immunology) commission, Professor Paul Van Cauwenberghe (Belgium), believed that by 2015, half of the European population will suffer from some type of allergy. For infectious diseases, the epidemic threshold is considered to be 1% of cases. Thus, there is ample reason to believe that there is currently an epidemic of allergic diseases.

Once an antigen is recognized, the immune system must neutralize and remove it. This occurs with the help of special T cells that have a cytotoxic effect and their mediators - lymphokines, or with the help of B cells that produce antibodies. Nonspecific defense factors also take part in the neutralization and removal of antigenic factors from the body: phagocytosis, complement and factors of the properdin system.

The work of all of the listed components of the immune system forms an immunological network and is regulated in such a way that the immune reaction occurs at the right time, is aimed at a specific antigen, is adequate and is regulated in time. The absence of one of these qualities causes disturbances and serious diseases in the body that threaten its very existence [3].

Meanings of the terms "allergy"

This word comes from two Greek words: allos - “other”, “different” and ergon - “to do”, that is, literally “to do differently”.

Atopy is a hereditary predisposition to the development of immediate hypersensitivity reactions to common, common substances with a tendency to produce antibodies belonging to the class of immunoglobulins E (reagins) to extremely small amounts of allergens.

Systemic atopic diseases are characterized by the involvement of various organs and tissues in the pathological process. With atopy, the mucous membranes of various organs and systems of the body often change. Allergic reactions on the skin create a certain group of diseases called allergic dermatoses.

This is due to the fact that the largest number of mast cells (mast cells - cells that are the shock organ on which an immediate allergic reaction develops) is located in the skin. These include atopic dermatitis, urticaria, and Quincke's edema. Although the skin is not a lymphoid organ, it contains cells called mastocytes that participate in the immune response. Under physiological conditions, there is a constant influx of cells from the peripheral blood. It is believed that there is a special population of lymphocytes with an affinity specifically for the skin - mainly T lymphocytes - and that they recirculate between the skin and the blood. Antigenic irritation greatly enhances this effect, in which some lymphocytes are retained in the skin and are involved in the immune response [4].

Allergic reactions are associated, for the most part, with the use of either uncertified drugs or complex multicomponent formulations. But sensitization is also possible to the introduction of legitimate drugs that have been on the market for a long time. Allergic reactions can occur in the form of emergency conditions (immediate type) and delayed - in the form of allergic dermatitis (delayed type). Immediate allergic reactions include anaphylactic shock, bronchospasm, urticaria, and Quincke's edema . They occur within the first 48 hours, and sometimes during the procedure. Each of these reactions can threaten the patient's life.

Urticaria and Quincke's edema

Urticaria ( urticaria ) is a disease characterized by a rapid, more or less widespread rash of itchy blisters on the skin. A blister is swelling of a limited area of mainly the papillary layer of skin. One type of urticaria is Quincke's edema (giant urticaria, angioedema), in which the swelling extends to the dermis or subcutaneous layer. This form of urticaria was first described by N. Quincke in 1882 (Photo 1, 2)

Urticaria is a common disease - approximately every third person has suffered from urticaria at least once in their life. In the structure of diseases of allergic origin, urticaria ranks second after bronchial asthma, and in some countries, for example, in Japan, even first.

Urticaria and angioedema can occur at any age. The disease most often occurs in people between 21 and 60 years of age. Women are more often affected, which is associated with the characteristics of their neuroendocrine system. According to various authors, burdened allergic heredity is noted in 25-56% of cases. Urticaria is a heterogeneous disease characterized by the appearance of urticarial rashes on the skin.

Quincke's edema ( giant urticaria ) is a hereditary or acquired disease characterized by swelling of the skin and subcutaneous tissue. With Quincke's edema, swelling of the mucous membranes may develop. Both diseases occur at any age, but more often between 20 and 60 years. In almost half of the cases, urticaria is combined with Quincke's edema. Urticaria and angioedema can be caused by a number of factors.

Classification of urticaria

Urticaria occurs:

• allergic - food; for medicinal and chemical substances; household; epidermal; pollen; whey; insect; infectious);

• physical - mechanical; cold; thermal; radiation (light and x-ray); cholinergic;

• endogenous - enzymopathic (deficiency or insufficient activity of complement inhibitor C1; deficiency of digestive enzymes); dishormonal; idiopathic;

• pseudo-allergic - associated with a violation of the liberation of biologically active substances (histamine, serotonin, etc.), dose-dependent and occurring without the participation of the immune system.

Factors and diseases that cause the development of urticaria are given in Table 1 [5]. Each of the forms of urticaria indicated in the classification has its own mechanism of development. However, their common pathogenetic link is an increase in the permeability of the microvasculature and the development of acute edema in the surrounding area.

Table 1. Factors and diseases that cause the development of urticaria

The most dangerous consequences are considered to be due to Quincke's edema, which occurs on the membranes of the brain, joints, and internal organs.

Quincke's edema can develop either acutely or gradually. The formation of dense painless swelling of the subcutaneous fat is characteristic. Common localizations are places where loose subcutaneous tissue is located: face (especially lips), oral cavity (soft palate, tongue). The color of the rash is often unchanged, less often pink. Itching, unlike urticaria, is not typical. In a quarter of cases, the respiratory system (larynx, trachea, bronchi) is affected. In such cases, hoarseness and cough appear, and there is a high risk of asphyxia. Swelling of the walls of the esophagus, stomach, and intestines is possible.

Tissue swelling is associated with increased vascular permeability caused by the release of mediators (histamine, prostaglandins, leukotrienes, cytokines, etc.) from sensitized mast cells and basophils upon their contact with the allergen. Such an allergen can be food products (peanuts, chocolate, milk, exotic fruits, etc.), inhaled pollen or dust allergens, as well as medications. In addition, the cause of Quincke's edema can be exposure to various physical factors, such as cold, bright sunlight, etc., as well as food and medicinal allergens (sulfonamides, antibiotics, acetylsalicylic acid, bromides, etc.), cosmetics, odors, increased sensitivity to cold.

Particularly dangerous is Quincke's edema in the larynx, which occurs in approximately 25% of all cases. When laryngeal edema occurs, hoarseness of the voice and a “barking” cough are first noted, then difficulty breathing with shortness of breath of inspiratory, and then inspiratory-expiratory nature increases. Breathing becomes noisy and stridorous. The complexion acquires a cyanotic hue, then becomes sharply pale.

Clinical picture of Quincke's edema in the larynx: patients are restless and tossing about. When the edema spreads to the mucous membrane of the tracheobronchial tree, bronchial asthma syndrome with characteristic diffuse expiratory wheezing is added to the picture of acute laryngeal edema. In severe cases, in the absence of rational assistance, patients may die due to asphyxia. With mild to moderate severity, laryngeal edema lasts from an hour to a day. After the acute period subsides, hoarseness, sore throat, difficulty breathing remain for some time, dry and moist rales are heard on auscultation. Quincke's edema in the larynx requires immediate intensive care, including tracheostomy.

When edema is localized on the mucous membrane of the gastrointestinal tract, abdominal syndrome occurs. It usually begins with nausea, vomiting first food, then bile. Acute pain occurs, initially local, then spread throughout the abdomen, accompanied by flatulence and increased intestinal motility. During this period, a positive Shchetkin symptom may be observed. The attack ends with profuse diarrhea.

When processes are localized on the face, the serous meninges may be involved in the process with the appearance of meningeal symptoms, such as stiff neck, severe headache, vomiting, and sometimes convulsions. Rarely, Meniere's syndrome develops as a result of swelling of the labyrinthine systems. Clinically, it manifests itself as dizziness, nausea, and vomiting.

Treatment of urticaria and Quincke's edema

It is impossible to predict their development, even after collecting a detailed history. Therefore, every cosmetologist must be able to provide first aid to the patient in a timely manner. To do this, in the office where the manipulations are carried out (and not at the administrator or somewhere else!), there must be an emergency first aid kit. There are ready-made first aid kits on sale that contain adrenaline, Suprastin, Prednisolone, Dexamethasone, Salbutamol and other drugs.

The algorithm of actions for severe allergic reactions should be written down and included in the first aid kit, so that in an urgent situation the doctor does not get confused and lose valuable time.

It is necessary: stop the intake of the allergen, wash off the remaining drug from the surface of the skin; administer adrenaline, Suprastin, Prednisolone or other drugs, focusing on the developing clinical picture and treatment protocol for anaphylaxis . Do not throw away the ampoules - they should be presented to emergency personnel, who should be called to hospitalize a patient with a moderate or severe allergic reaction of an immediate type.

In the first aid kit, it is advisable to have a system for intravenous administration of solutions and a bottle of saline solution, since when shock develops, the pressure decreases sharply, and a timely placed dropper can provide the possibility of intravenous administration of drugs for more effective treatment. Accordingly, there should be everything necessary to carry out this manipulation: a tourniquet, an adhesive plaster, a drip system, etc.

Delayed allergic reactions, developing after 48-72 hours, are not so threatening, but cause a lot of trouble to patients: itching, redness, swelling, peeling. Their treatment follows the protocol for the treatment of allergic dermatitis.

For acute urticaria and Quincke's edema, the same treatment is carried out as for other acute allergic reactions, with an impact on different pathogenetic links of the process.

In acute urticaria and Quincke's edema, measures to quickly relieve symptoms come first. Mild reactions can only be treated with antihistamines. The rapid development of the action of modern antihistamines allows the use of second and third generation drugs that do not have a sedative effect: Aleron, Xizal, Zilola, Cetrilev, Fexofast, Erius, 1 tablet per day.

For speed of action, ampoule solutions of Tavegil and Suprastin can be administered. Cleansing enemas and the use of enterosorbents (activated carbon, Polyphepam, Algisorb, Enterosgel, Smecta) often have a positive effect. All patients with urticaria and angioedema should avoid taking aspirin and other non-steroidal anti-inflammatory drugs, as they cause exacerbation of existing urticaria in 50% of cases. You should also avoid taking angiotensin-converting enzyme inhibitors (Capoten, Enap, Prestarium, etc.), since there is a high probability of developing Quincke's edema. Non-specific triggers such as hot baths or alcohol intake should be avoided.

The causative factor and possible triggers, if they can be established, should be excluded. If the “culprit” food product is identified, it is excluded from the diet. But often with urticaria, pseudo-allergic reactions to natural food components and food additives occur. In such cases, a diet low in natural and artificial histamine liberators (substances that promote the release of histamine) is prescribed. If in acute urticaria the elimination of the causative factor leads to resolution of the symptoms within 24-48 hours, then in chronic urticaria it takes 2-3 weeks for the condition to improve.

Factors such as sun exposure for solar urticaria (it is important to use photoprotective creams with a high level of protection), carrying heavy objects for urticaria associated with exposure to physical factors, swimming in cold water for cold urticaria, etc. should also be avoided. Patients with hereditary angioedema Particular care should be taken when removing teeth, under anesthesia with intubation.

Anaphylactic shock

Anaphylactic shock is a state of sharply increased sensitivity of the body that develops with repeated administration of foreign proteins, serums, and medications. This is one of the most dangerous and complex complications of drug allergies, ending in death in approximately 10-20% of cases.

Clinical variants of anaphylactic shock with predominant lesions:

• skin with increasing skin itching, hyperemia, the appearance of widespread urticaria, Quincke's edema;
• nervous system (cerebral variant) with the development of severe headache, the appearance of nausea, hyperesthesia, paresthesia, convulsions with involuntary urination and defecation, loss of consciousness with clinical manifestations such as epilepsy;
• respiratory organs (asthmatic variant) with dominant suffocation and the development of asphyxia due to changes in the patency of the upper respiratory tract due to swelling of the larynx and impaired patency of the middle and small bronchi;
• heart (cardiogenic) with the development of a picture of acute myocarditis or myocardial infarction and other organs.

The severity of anaphylactic shock depends on the speed of development of vascular collapse and dysfunction of the brain.

• A mild degree of anaphylactic shock (the duration of development is from several minutes to 2 hours) is manifested by hyperemia of the skin, itching, sneezing, tickling, rhinorrhea, dizziness, headaches, hypotension, tachycardia, a feeling of heat, increasing weakness, and unpleasant sensations in various areas of the body.
• In anaphylactic shock of moderate severity, severe itching suddenly appears, followed immediately by difficulty breathing and a sharp decrease in blood pressure, which causes shock. The patient's pulse can barely be felt, profuse sweating, pallor, or, conversely, redness of the skin. A person experiences a sharp general weakness, feels incomprehensible anxiety, restlessness, fear, he experiences loss of consciousness , involuntary defecation and urination.
• Severe anaphylactic shock is characterized by vascular insufficiency in the form of collapse and the occurrence of coma with loss of consciousness, cardiac arrhythmia, and the appearance of convulsions.

In case of anaphylactic shock, urgent assistance is required, since minutes and even seconds of delay and confusion of the doctor can lead to the death of the patient.

Treatment of anaphylactic shock is based on:

• blocking the entry of the antigen drug into the bloodstream;
• neutralization of biologically active substances abundantly secreted and entering the bloodstream as a result of the antigen-antibody reaction;
• restoration of pituitary-adrenal insufficiency;
• bringing the patient out of collapse;
• relieving bronchospasm;
• elimination of asphyxia phenomena;
• reducing the permeability of the vascular wall;
• impact on psychomotor agitation;
• prevention of late complications from the cardiovascular system, kidneys, gastrointestinal tract, central nervous system.

Photo 1. Allergic urticaria

Photo 2. Allergic urticaria

Literature

1. Vetrov V.P., Onoprienko A.V., Arefieva I.S. Prognostic significance of perinatal risk factors and the implementation of hereditary predisposition to allergens // Kazan Medical Journal. - 1992. - No. 1. - P. 62.

2. Kobrinsky B. A. et al. The role of heredity in the formation of atopic diseases in children and preventive measures // Ros. Bulletin of Perinatology and Pediatrics. - 1995. - No. 1. - P. 17-20.

3. Khatskel S. B. Allergology in diagrams and tables: Reference Guide. - St. Petersburg - SpetsLit, 2000. - 715 p.

4. Vorontsov I.M., Matalygina O.A. Diseases associated with food sensitization in children. - L. - Medicine, 1986. - 272 p.

5. Berezhnaya N.M., Babina L.P., Petrovskaya I.A., Yalkut S.I. Allergology: A reference dictionary. - K.: Naukova Dumka. 1986.- 448 p.

Full version of the article in the magazine PRO Cosmetology by “Cosmetologist” No. 5, 2016