Representing one of the most insidious types of skin lesions, toxicerma is considered the most difficult type of skin disease to treat, resulting from damage to the upper layer of the epidermis by a certain allergen. In this case, the method of exposure to a substance that causes a pathological reaction is not a direct effect on the skin, as in the case of other types of skin lesions, but the penetration of the allergen through the bloodstream. Penetration from the inside causes many difficulties in diagnosing pathology and in determining the most effective method of drug treatment.

Toxidermia is accompanied by numerous skin lesions, and the degree of manifestation of the disease depends on the body’s susceptibility to a particular substance and the area of ​​influence of the allergen. In this article we will look at photos of patients with medicinal and other types of toxicoderma, and study the symptoms and treatment of such a disease.

Features of the disease

A feature of toxicerma can be considered symptoms, which can vary significantly among different people when exposed to the same allergen. This is the particular insidiousness of this condition and causes difficulties in making the correct diagnosis.

The ICD-10 code is L27 Toxicodermia.

Also, when toxidermia occurs, there is a sharp damage to the skin, the rate of manifestation of the pathology depends on the degree of decrease in the patient’s body’s immunity (the disease almost always manifests itself when the protective function of the patient’s body declines), susceptibility to the allergen and the presence of concurrent ongoing diseases.

• The occurrence of this pathology can occur in all age categories, however, toxicerma is most often observed between the ages of 45-48 years.
• Doctors have also recorded cases of manifestations of toxicerma in younger children. The frequency of detection of the disease in women and men is approximately the same.

Toxidermy on the face (photo)

Classification of the disease

Today, doctors distinguish 4 main types of this skin lesion, which differ in the cause and type of allergen that penetrated the bloodstream and became the cause of the disease.

The classification is carried out as follows:

1. Medication a type of toxicerma is characterized by the effect on the patient’s body of certain medications, which became the cause of the disease. These can be either potent drugs or vitamin complexes: antibacterial drugs, B vitamins.
2. Nutritional the form usually appears when eating a certain food product that contains disease-provoking substances such as flavorings and dyes, as well as preservatives.
3. Professional toxicerma, accompanied by the entry of an allergen into the bloodstream of harmful chemicals, usually associated with the professional activities of the patient. It could be benzene, ammonia vapor.
4. Autotoxic form of the disease is characterized by poisoning of the patient’s body with products resulting from a current chronic disease, for example, damage to the liver or kidneys.

Thanks to the above classification, it becomes possible to classify the disease as a specific type, which makes it possible to determine the type of allergen and eliminate it from contact with the patient as quickly as possible. This allows you to prevent the development of more advanced stages of the disease, which are more difficult to treat.

This video will tell you what toxicerma is:

Causes of toxicoderma

Toxidermia has various causes. They are reflected when classifying the disease, and they can be divided as follows:

• infectious lesions of the body that sharply reduce the efficiency of the immune system;
• the use of certain medications that contain an allergen;
• penetration of the allergen into the bloodstream of chemical substances when working with them or with food (these include preservatives, flavorings);
• lesions of the body of a malignant nature, which include AIDS.

Also, the reasons for the development of toxicoderma include a combination of the listed reasons or a combination of them.

Symptoms

• The manifestation of this disease should include the appearance of altered areas of the skin with pronounced sensitivity, while the surface of such areas may be smooth, ulcerated, uneven, and may develop on it.
• The affected areas can be of different sizes, their localization is different: most often such manifestations of toxicerma are located in the area of ​​skin folds, in the knee and elbow bends, and on the lower back.
• Also, manifestations of the disease include the appearance of pustules, lumps on the skin, the mucous membranes also suffer: the genital area and anus become very sensitive and painful.

In advanced stages of the pathological process, the lesion is likely to penetrate into internal organs, which requires immediate hospitalization of the patient and active treatment to prevent the possibility of negative consequences of the disease.

Fixed toxicoderma in children (photo)

Diagnostics

To identify this pathology, diagnostic measures are carried out such as scraping damaged skin, performing general and urinalysis, as well as if damage to internal organs is suspected - ultrasound and examinations.

We will find out further whether toxicerma in children and adults can be treated with traditional and folk remedies.

Treatment

The treatment method for toxicoderma, like any other type of allergic reaction, is determined by the attending dermatologist after diagnosing the patient’s condition. His age, degree of weakening of the body and susceptibility to the treatment are also taken into account.

Treatment can be divided into therapeutic and medicinal.

In a therapeutic way

At the onset of symptoms accompanying the course of toxicoderma, the root cause of this condition should be eliminated - the allergen that entered the bloodstream upon contact with it. For this purpose, cleansing enemas and cleaning of affected surfaces with disinfectants and drying agents are used.

When weeping areas appear in the affected area, the use of talkers and ointments with drying properties is prescribed; for serious and deep skin lesions, hormonal ointments are used to restore the structure of the skin and eliminate the manifestations of the lesion. However, their use should be limited to 5-7 days of use.

By medication

In case of serious damage and when the pathological process spreads to the internal organs, the patient is prescribed hospitalization with mandatory bed rest. To relieve itching and burning of the skin, the victim is prescribed droppers with antihistamines to reduce the symptoms of the disease.

Blood and plasma purification is also used, which allows you to quickly remove the allergen from the body.

Operation

When treating toxicerma, surgery is usually not required.

Disease prevention

• As a preventive measure, it may be recommended to exclude from the menu food products that may contain preservatives, flavorings, chemical compounds, and when contacting household chemicals, avoid inhalation and contact with the skin.
• It would also be correct to give up bad habits such as,.
• Regular preventive examination by a doctor in order to identify chronic diseases will maintain immunity at the required level and will eliminate the possibility of any diseases associated with allergic manifestations.

Manifestation of toxicoderma

Complications

With insufficient treatment, toxicermia can have complications such as damage to internal organs with deterioration in their functioning, a decrease in the patient’s general immunity and an increase in his susceptibility to other diseases.

Forecast

• Detection of toxidermia at an early stage makes it possible to quickly eliminate the symptoms characteristic of the disease and avoid possible complications. The prognosis in this case will be positive: the 5-year survival rate ranges from 92 to 98%.
• When starting treatment at later stages, the prognosis is slightly different: 82-91%.
• In the absence of treatment and assistance to the patient when he develops toxicoderma, the probability of death is high: 97%.

Causes

Toxidermia can develop due to exposure to certain medications, foods, and chemicals that have toxic or allergenic properties. The main mechanism for the development of toxidermia is an allergic reaction of the body. Much less common is a toxic reaction that can develop, most often, to mercury preparations, poor quality food products and arsenic preparations.

In some cases, toxicerma occurs as exudative erythema multiforme, erythroderma. It is also possible for the disease to manifest itself in the form of lichen planus, erythema nodosum, allergic vasculitis, stomatitis and keratoderma. The most severe form of toxicerma is considered to be toxic epidermal necrolysis.

Irritants that lead to the development of toxicoderma usually enter the body through the digestive system or through the respiratory tract. In addition, irritants can enter the body through intramuscular, intravenous, or subcutaneous injection.

After the irritant penetrates the skin cells, it connects with certain structures, which leads to a pathological process starting in the skin tissues. After some time, toxic compounds enter the blood, which causes the formation of new fresh sources of damage on the surface of the skin. The pathological process is complicated by the fact that during its course the natural protective functions of the body are significantly reduced.

The disease often develops against the background of certain chronic diseases. In this case, taking certain medications is considered a provoking factor.

As for drug toxicity, it usually does not have any symptoms characteristic of the use of a specific substance. However, some medications can cause distinctive symptoms of the disease, which immediately makes it possible to determine the specific irritant that led to the development of toxicoderma. In particular, the drugs cause an acne-like rash, and sulfonamides contribute to the appearance of lesions of a reddish-brown or lilac hue. Toxidermy, in which age spots appear, can develop due to the use of quinine and phenolphthalein.

Symptoms

The symptoms of toxicdermia depend on the characteristics of the patient’s body and on the factor that provoked the development of the disease. In particular, with toxicerma, lichenoid rashes, urticarial rashes, eczematous rashes, as well as scarlet fever-like, rubella-like or measles-like rashes can form. The rash is often accompanied by fever and itching. In the case of drug toxicoderma, edematous spots may appear, in the center of which there is a bubble. The bubble usually forms on the skin of the genital organs and oral mucosa. If contact with causative factors occurs, rashes can form again both in new places and in places where rashes have already occurred. With such rashes, the patient may notice a burning sensation, but the patient’s general condition, as a rule, does not suffer.

Rashes with toxicoderma usually occur acutely. They can appear either a few hours or a few days after exposure to the causative factor. The latent period of the disease can be up to 20 days. The general clinical picture of the disease is most often characterized by a widespread, symmetrically located rash. The rash is most often disseminated and monomorphic, and can also be combined with damage to the mucous membranes of certain internal organs. The rash can form on the mucous membranes of the liver, kidneys and heart. Such eruptions usually consist of macular, nodular, papular, bullous, vesicular, papulopustular or pustular pruritic elements.

Damage to intercellular structures and cells that occur as a result of the toxic effects of allergic reactions or medications imparts to them an autoantigenic property, which ultimately leads to the formation of autoantibodies. Under certain conditions, “autoantigen-autoantibody-immune complexes” complexes lead to increased damage to tissues, organs, cells and blood vessels.

Autoallergic reactions play an important role in the causes of the development of drug reactions such as vasculitis. In addition, they are an important provoking factor in the occurrence of eczema-like lesions and systemic lupus erythematosus. In some forms of toxicoderma, it is necessary to take into account the damaging effect of the microbial factor.

Iodine and bromine preparations affect the skin in such a way that they change the chemical composition of sebum. This leads to the activation of staphylococcal infection. This infection is considered one of the main causes of the development of such forms of toxicerma as iododerma and bromoderma.

Kinds

There are fixed and widespread toxicoderma. Fixed toxicoderma usually manifests itself locally, mainly on cut areas of the skin or on the mucous membranes. This type of toxicoderma is usually milder than the common form of toxicermy. Widespread toxicdermia is considered a dangerous disease in which the rashes that appear on the mucous membranes and skin are mixed with lesions of other systems and organs of the patient’s body.

Toxiderma can manifest itself in the form of urticaria, which is considered a fairly common reaction to taking certain medications. In this case, rashes usually occur already in the first days of taking the drug. Urticaria rashes look like blisters, the appearance of which causes severe itching.

The size of urticarial lesions can range from the size of a lentil to the size of the palm of your hand. The shape of the rash can be either round or take on bizarre shapes. The rashes have clear boundaries of the elements. The consistency is densely elastic. The color of the rash can vary from bright red to pearly white. This type of rash is usually profuse. In this case, the entire surface of the limbs, face or torso is covered.

Severe cases of the disease are characterized by swelling of the mucous membranes of the larynx and mouth. Edema can develop into Quincke's edema. When generalizing the skin process, malaise, general weakness, headaches, joint pain, muscle pain may appear, and a rise in body temperature to 38-38.5 ° C is possible. In this case, a blood test shows an increase in the number of eosinophils.

Toxidermia, which occurs when taking bromide and iodide drugs, is considered to be rare forms of toxidermia. These forms of the disease are respectively called bromoderma and iododerma. These types of diseases are quite difficult to diagnose. With bromoderma, rashes of various types appear: urticarial, vesicular, erythematous, papulopustular, acne-like and warty rashes.

The most common characteristic of bromoderma is bromide acne, which usually appears as follicular pustules. Their size ranges from the size of a pinhead to the size of a lentil. They appear as pinkish-purple nodules that primarily occur on the back, limbs, and facial skin. After the pustules heal, superficial scars of a brownish-purple color may remain on the skin.

As for iododerma, this form of the disease most often manifests itself in a tuberous and bullous form. The tuberose form is usually complicated by various vegetations. And rashes with bullous iododerma appear in the form of tense blisters with a diameter of 1-5 centimeters. These blisters are usually filled with hemorrhagic contents. After the opening of these bubbles, significant vegetation is observed on the exposed bottom. Rashes with tuberoenic iododerma, as a rule, begin with small nodules, which over time turn into a tumor-like formation and pustule. In this case, the peripheral edge of the lesion is slightly elevated and consists of small vesicles containing serous-purulent contents.

Diagnostics

The primary diagnosis of toxidermia consists of examining the patient and collecting information. To clarify the stimulus, provocative tests are used. Provocative tests must be performed with extreme caution. Such tests can be prescribed after the rash resolves. Provocative tests are contraindicated for persons who have suffered severe toxicosis. In order to clarify the allergen, in some cases immunological tests of the patient’s blood are performed. Such methods in particular include the blastotransformation reaction of lymphocytes.

In addition, skin tests and a variety of laboratory tests, which include a general urine test and a complete blood count, are used to diagnose the disease.

Treatment

Treatment of this disease should be carried out under the supervision of the attending physician. The main thing in this case is the detection and elimination of the irritant that caused the occurrence of toxidermite. To stop exposure to the irritant, stop taking medications and release you from work that is associated with hazards at work. The patient's contact with household chemicals is also excluded.

Antihistamines are usually prescribed to treat the disease. Such drugs in particular include such drugs as suprastin, diphenhydramine and tavegil. In severe cases, intramuscular injections are prescribed. In the case of toxic epidermal necrolysis and Stevens-Johnson syndrome, intensive care is required in a special hospital. In the treatment of common toxicoderma, calcium preparations are used. In addition, such patients are prescribed corticosteroid ointments.

During the treatment of toxicerma, the following are also prescribed: a gentle diet, enterosorbents, laxatives and diuretics. The latter are necessary to remove an allergen or toxic substance from the body. Drinking plenty of fluids is also important. The patient is given injections of solutions of calcium gluconate, sodium chloride or thiosulfate. Typically, the administration of these drugs alternates every other day. In addition, antihistamines, ascorbic acid and vitamin P preparations are prescribed.

If the general manifestations of the disease are accompanied by an increase in body temperature, then such patients need treatment in a therapeutic or dermatological hospital. In addition, glucocorticoids are prescribed, which are taken orally or administered intravenously with rheopolyglucin or hemodez.

For external treatment of the skin, anti-inflammatory, antipruritic, corticosteroid ointments, as well as special aerosols are prescribed. Wet dressings or lotions with disinfectant solutions are applied to wet areas of inflammation.

Adherence to the correct regimen plays an important role in the treatment of toxicoderma. At first, you must strictly adhere to a hypoallergenic diet. This diet excludes the consumption of salty, spicy, sweet, smoked, fried, chocolate, coffee, cocoa, foods with simple protein, honey and nuts. In addition, most berries and fruits are excluded. During treatment, it is necessary to monitor your stool. You should refrain from water treatments. At least until the rashes regress.

If the disease is not accompanied by severe damage to internal organs, the prognosis is usually favorable.

Prevention

Prevention of toxicoderma involves avoiding any contact with food products and chemicals to which the human body has increased individual sensitivity.

If a person needs treatment with drugs that have pronounced allergic properties, then such patients are prescribed antihistamines, as well as calcium pantothenate. In particular, some antibiotics, analgesics, sulfonamides and barbiturates can cause allergies.

Description:

By toxicoderma we mean non-infectious toxic-allergic damage to the skin and mucous membranes, manifested by an acute inflammatory process. Most often, the pathology is of medicinal origin, i.e. develops against the background of the toxic effects of medications. Moreover, medications can enter absolutely any way - the respiratory tract, gastrointestinal tract, contact exposure, various types of injections. In other words, this is a complicated allergic reaction.

Causes:

At its core, this disease is a kind of response of the body’s cells to something poisonous (toxin) or individually intolerable (allergen) entering it in any possible way. The main difference from contact dermatitis is the effect of these substances not directly on the skin or mucous membranes, but from the inside, reaching these areas through blood vessels.

The toxin/allergen enters the body, penetrates the skin cells, reacts with certain cellular structures, as a result of which an inflammatory process develops and inflammatory substances are released into the blood. After some time, these substances spread through the blood throughout the body and form new sources of inflammation. In addition to local irritation, a decrease in the general protective functions of the body may be observed.

This disease can exist in four forms:

Medication– the most common toxicoderma in adults, developing after taking absolutely any medications (vitamins, antibiotics, vaccinations, sulfonamides, etc.).

Professional– develops when a person inhales or accidentally ingests toxic chemicals associated with his professional activities (ammonia, chlorine or benzene derivatives, etc.).

Alimentary form– this is a common toxicoderma in children, because this is the result of exposure of the body to various synthetic dyes from food, preservatives, flavorings, etc. It is children's bodies that are most sensitive to these substances. But it occurs in adults too.

Autotoxic toxicoderma manifests itself in cases when the body poisons itself with its own toxins, which are formed against the background of impaired functioning of individual organs or systems (pathologies of the kidneys or liver, gastrointestinal tract, decaying oncological processes in the body, etc.).

Symptoms:

The main symptoms of the disease are considered to be skin rashes that affect the general condition of the body due to local irritation (for example, itching). According to the severity of symptoms, the disease has a mild, moderate and severe course.

Toxidermia can be called one of the most insidious forms of allergic dermatitis. Although the allergen affects human skin, it does not come into contact with it. A substance that causes hypersensitivity of the body chooses a different, more complex path.

In this article we will introduce you to toxicermy better by talking about the following:

Causes of toxicoderma

Toxidermia is a rapidly developing allergic reaction that occurs when the body has acquired hypersensitivity to any substance or is a congenital intolerance to a certain product, medication, etc. But unlike contact dermatitis, which develops when the skin comes into contact with an allergen, with toxidermia the allergen acts from the inside, penetrating into the skin through blood vessels.

There are 4 types of this disease, differing in the route of penetration of the allergen into the body.

• Drug toxicity is the most common form. An allergic reaction develops after ingestion of any medications (antibiotics, vaccines, B vitamins, sulfonamides, barbiturates, etc.).
• Alimentary toxicoderma develops after consuming any food product or a substance that is part of this product (dyes, flavors, preservatives, etc.).
• Professional toxicoderma is the result of harmful chemicals (benzene and its derivatives, ammonia, chlorine, etc.) entering the bloodstream through the respiratory tract or digestive system.
• Autotoxic toxidermia develops against the background of chronic or acute diseases, as a result of which toxins and allergens are formed in the body (diseases of the gastrointestinal tract, kidneys, endocrine system, malignant processes).

Symptoms of toxicoderma

Symptoms of toxidermia are another manifestation of the insidiousness of this disease. Ten patients suffering from toxicoderma to the same substance may have completely different symptoms.

The most characteristic symptoms of toxicerma are the following:

• skin rashes of various types - in the form of nodes, blisters, ulcers, etc.;
• lesions of the mucous membranes of the oral cavity and lips in the form of blisters, ulcers, hematomas. In some cases, the mucous membrane of the genitals and anal rectum may be affected;
• a feeling of burning, itching, tightness at the site of skin and mucous membranes;
• general feeling of malaise, weakness, increased body temperature;
• irritability, sleep disturbances, loss of appetite, developing against the background of skin symptoms.

Some manifestations of toxicoderma

In severe cases, toxicerma can cause damage to internal organs - a condition requiring immediate hospitalization and appropriate treatment.

Diagnosis of toxicoderma

Due to the variety of symptoms and the unstable clinical picture of this disease, the primary diagnosis of toxicerma is aimed at excluding rubella, scarlet fever, measles, lupus erythematosus, secondary syphilis and other diseases that have similar signs and symptoms. For this, the following diagnostic procedures are prescribed:

• clinical, biochemical analysis of blood and urine;
• blood test for HIV and syphilis;
• bacterial culture of scrapings taken from the lesion;
• Ultrasound, CT, MRI for signs of damage to internal organs.

When the initial diagnosis has been carried out and the doctor has ruled out infectious diseases, laboratory tests for allergens are carried out. In the case of toxicderma, skin and provocative tests are not prescribed, as they can cause a severe allergic reaction and aggravate the course of the disease.

Treatment

To treat toxicoderma, as well as any other type of allergic reaction, the most important thing is to stop contact with the allergen.

The next stage of treatment for toxicoderma is removing toxins from the body, eliminating intoxication, normalizing immune reactions and relieving symptoms. For this, depending on the nature and severity of toxicoderma, the following procedures and means can be used:

• for autotoxic or alimentary toxidermia, cleansing enemas, diuretics, and enterosorbents are prescribed;
• for any type of toxicoderma (excluding reactions caused by taking sulfonamides), drugs that reduce the sensitivity of the immune system (sodium thiosulfate, calcium chloride) and antihistamines (Suprastin, Claritin, Tavegil, etc.) are prescribed intravenously;
• Locally, on the affected areas, astringents, anti-inflammatory, antipruritic ointments and gels, and zinc oxide mash are used. For weeping lesions, before applying the medicinal ointment, the weeping area is treated with a solution of brilliant green.
• for severe skin lesions, hormonal ointments are used (hydrocortisone, prednisolone, etc.);
• in case of damage to internal organs by toxicerma, the patient is subject to hospitalization, where he is prescribed treatment appropriate to his condition and the severity of the disease. Additionally, blood purification is carried out using the method of hemosorption, plasmapheresis, plasma filtration, etc. in order to remove the allergen from the bloodstream or reduce its concentration to the possible minimum;
• in some cases, antibacterial drugs may be prescribed as a preventive measure.

The symptoms of a person with toxicoderma can fluctuate over a short period of time from minor to severe. Therefore, diagnosis, treatment and monitoring of the patient’s condition should be carried out only by a qualified specialist.

Prevention measures

The most important preventive measure that will reduce the frequency of exacerbations and, accordingly, prevent a possible deterioration in health, is identifying the allergen.

At the first signs of an allergy of any form (skin, respiratory, gastrointestinal), you must contact an allergist who will prescribe laboratory tests for allergens.

Having identified the substance that causes hypersensitivity of the immune system, you can exclude contact with it or, if this is not possible, take appropriate precautions if forced contact with the allergen. If it is quite easy to exclude a food or drug allergen, then the professional environment often requires the following measures:

• wear a respirator and safety glasses when working with chemicals that evaporate into the air and can get on the mucous membranes of the eyes, nose, mouth (paint and varnish compounds, acetone, benzene, chlorine, etc.);
• Wear protective, tightly buttoned clothing (ideally one specifically designed for working in hazardous conditions);
• observe the rules of personal hygiene (wash your hands thoroughly, take a shower, change clothes after finishing work).

To prevent toxicoderma of autotoxic origin, be attentive to any signs of trouble in your body. Consult a doctor in a timely manner, even if you have minor ailments, undergo regular preventive examinations and visit the dentist.

Toxidermia (syn.: toxicoderma, toxidermia) is an acutely developing inflammatory disseminated lesion of the skin and mucous membranes that occurs as a result of exposure to an allergen introduced into the body. The term is conditional, because Both toxic and allergic components may be predominant. Toxic manifestations are usually associated with a severe course of the pathological process, however, in rare cases, intoxication may be due to the action of the administered substance.

In the literature, the terms “allergic oxidermia” and “toxicoallergic exanthema”, “toxicoallergic dermatitis” are also found.

The term “toxicidermy” was proposed by I. Jadasson; in 1905 he proposed his own classification of toxicodermas:

1. drug toxicoderma;
2. toxicoderma associated with intoxication, incl. contact dermatoses (dermatitis), from chemical warfare agents, of professional origin, from insect bites, poisonous animals, contact with poisonous plants, cosmetics, clothing fabrics, etc.;
3. nutritional;
4. autotoxic.

Subsequently, autotoxic and contact dermatoses were removed from this Jadassohn classification, and the concept of “toxicoderma” itself began to be more often used to refer specifically to drug or nutritional allergic reactions.

Fixed toxicoderma

Sometimes a patient develops a drug allergic reaction with a stereotypical lesion in the same place every time after taking this drug. Sometimes such a lesion appears on the skin of the vulva. Most often, fixed toxicoderma develops as a reaction to tetracycline and phenolphthalein, contained in some laxatives. The diagnosis can be established only by carefully collecting anamnesis. The reaction disappears after stopping the drug.

Aspects of the pathogenesis of toxicerma. Types of allergic reactions according to Jelu-Coombs

Risk factors for the development of toxicoderma: hereditary predisposition, diseases of the gastrointestinal tract, liver. Currently, the presence of atopic dermatitis and/or bronchial asthma in a patient is not regarded as a risk factor for toxicoderma, however, the concept of “hereditary predisposition” includes the presence of atopic and allergic diseases in blood relatives; the latter is taken into account as a risk factor when collecting anamnesis from a particular patient.

Most often, drug-induced toxicerma occurs from the use of the following medications (in descending order of frequency):

• high risk: carbamazepine, gold preparations; Baralgin, Sedalgin, Askofen); antipyretics, antibiotics and other antibacterial agents (penicillins more often, chloramphenicol - average risk, tetracyclines less often), vitamins (usually group “B”);
• medium risk: contraceptives, sulfanyl urea preparations; benzodiazepines, phenothiazines, chloramphenicol, preparations of copper, arsenic (Osarsol), silver;
• low risk: therapeutic (cardiological) drugs, metal dentures containing chromium, cobalt, nickel, molybdenum.

Drug reactions (DRs) are harmful unintended consequences of taking medications at recommended doses for humans. Skin reactions are the most common type of LR. Among hospitalized patients, the frequency of skin reactions from the total number of drug reactions is 1-3%, for a specific drug up to 10%.

Risk factors for LR: immunogenicity of the drug - the ability to act as a hapten, prohapten or covalently bind to receptors.

Intermittent therapy causes greater sensitization than continuous therapy, and the parenteral route causes greater sensitization than oral therapy.

Property of the body as a risk factor YES: HIV infection, Epstein-Barr virus infection, female gender, age, ethnicity, other genetic factors.

Atopy is not a risk factor for J1P!!

LR type A predictable, depending on the dose and pharmacological properties of the drug.

LR type B- allergic, unpredictable, independent of dose, determined by the properties of the body.

In rare cases, it is possible to develop toxidermia from drugs whose main purpose is to treat allergic conditions: antihistamines, blood substitutes and even corticosteroids: over 30 years of practice, we once observed a case of allergic dermatitis to prednisolone: ​​the rashes were relieved by dexamethasone.

The pathogenesis of toxidermia involves immune reactions of immediate and delayed hypersensitivity. The first type of reactions develops over several hours or days and is caused by changes in humoral immunity, in the ratio of IgE and IgA. The second type is caused by cellular mechanisms, predominantly of the T-cell level.

There are 4 types of immunological hypersensitivity reactions:

• chimeric, immediate type, GNT:

Type 1 - anaphylactic: target organ - mast cells and basophils.

Development ways:

1. reagin - develops with the participation of IgE (atopic diseases, urticaria, acute angioedema);
2. anaphylactic, with the participation of IgG4 - shock.

The specific IgE antigen on the surface of mast cells and basophils causes their degranulation with the release of histamine, prostaglandins, and leukotrienes. Mediators cause rapid vasodilation with increased permeability of the vascular wall (erythema, edema - urticaria). Contraction of smooth muscles with bronchospasm, cramping abdominal pain (and diarrhea), goose bumps. With excessive release of mediators, a systemic anaphylactic reaction develops.

Type 2 - cytotoxic: target organ - erythrocytes, epithelium. Characteristic of lupus erythematosus, allergic vasculitis, hemolytic anemia, myasthenia gravis; develops with the participation of IgG. Binding of IgG antibodies to antigenic structures on the surface of different types of cells. In this type of reaction, the drug itself acts as an antigen.

Type 3 - immunocomplex: target organ - platelets, erythrocytes, vascular endothelium, leukocytes. Develops with the participation of the CEC (IgG, IgM). Circulating immune complexes (CIC) with low-affinity IgG antibodies attach to the vascular endothelium, fix complement → attraction and activation of neutrophils → endothelial damage, extravasation of erythrocytes, allergic vasculitis (such as purpura), etc.

• kythergic, delayed type, HRT:

Type 4 - cellular: target organ - cells of various organs; This type includes photoallergic and allergic contact dermatitis, fixed erythema, erythema nodosum; develops with the participation of sensitized lymphocytes.

Criteria for diagnosing cutaneous LRs

1. Other possible causes of the rash, including viral exanthema/enanthema, have been excluded.
2. There must be a temporal relationship between the medication and the onset of the rash.
3. After stopping the medication, improvement occurs.
4. Subsequent intake of the drug leads to reactivation of the process.
5. It is advisable to have data on the association of a given drug with a given type of reaction.

After the first contact with an immunogen, at least 7 days are required for the formation of immunological memory. Subsequent administration of the drug triggers effector mechanisms. The effector chain involves immunoglobulins of various classes, T-lymphocytes (helper, cytotoxic), and the complement system.

Toxidermy and allergic contact dermatitis

In addition to the allergic and secondary toxic components, a third component, a photoallergic component, may be involved in the pathogenesis of toxic-allergic dermatosis, which, naturally, is reflected in the clinical picture of a particular dermatosis. For example, this is the pathogenesis of toxic melasma.

Time frames and mechanisms for the development of LR

After the first contact with an immunogen, at least 7 days are required for the formation of immunological memory. Subsequent administration of the drug triggers effector mechanisms.

The effector chain involves immunoglobulins of various classes, T-lymphocytes (helper, cytotoxic), and the complement system.

To date, it is not known what factors determine the type of immune response to drugs. But each type of reaction has its own clinical characteristics.

Drugs most commonly associated with drug exanthema

• Allopurinol
• Amphotericin B
• Barbiturates
• Benzodiazepines
• Captopril
• Carbamazepine
• Gold preparations
• Lithium
• Penicillins and cephalosporins
• Phenothiazines
• Phenytoin
• Quinidine
• Sulfonamides
• Thiazide diuretics.

When the body re-enters even an inferior allergen (hapten), it combines in the internal environment with already prepared ones.

In the pathogenesis of toxidermia, enzymatic rather than immune mechanisms may also play a role, which, for example, underlie the development of idiosyncrasy - congenital intolerance to a particular drug or product.

Idiosyncrasy. Enzymepathies

Enzymopathies that can manifest as skin rashes:

• lactase deficiency: when drinking whole milk, flatulence and diarrhea occur. During the day, a healthy person produces up to 1 liter of gases in the intestines.
• sucrase deficiency: diarrhea, excess sugar in stool, stool pH shifted to the acidic side.
• gluten enteropathy - celiac disease: manifested by intolerance to all grains (wheat, rice, etc.), developmental delays, anemia, diarrhea, dermatitis herpetiformis are noted.

Genetic factors in the pathogenesis of toxicerma

Today, it is believed that about 10% of the human population is genetically predisposed to allergic reactions. These are individuals who are directly predisposed to the appearance of pathological changes in the body as a result of the “antigen-antibody” reaction. For example, screening for the presence of the HLAB5701 allele in HIV-infected Caucasians before prescribing Abacavir can prevent severe LR. In general, white Europeans are thought to be more susceptible to allergic reactions than other nations.

At the same time, there are known examples of toxic-allergic manifestations that occur against the background of enzymopathies. Thus, it is believed that gluten deficiency today underlies the occurrence of Dühring's dermatitis herpetiformis.

In the USA and Canada, it is recommended to screen for HLAB1502 in risk groups in people of the Mongoloid race before prescribing carbamazepine (Finlepsin). The presence of the HLAB5801 allele is associated with a high risk of hypersensitivity to allopurinol.

It is known that 100% of American blacks (African Americans) suffer from lactase deficiency.

Thus, the group of congenital enzymopathies may include both individuals with pathological reactions caused by immune mechanisms (true allergies) and individuals who develop pseudo-allergic reactions against the background of enzymopathy.

Symptoms and signs of toxicerma

According to the severity of toxicoderma, they are divided into mild, moderate and severe.

The first degree (mild) is characterized by spotty, papular, urticarial rashes and itching of varying intensity. After the allergen stops entering the body, recovery occurs within a few days.

The second degree (moderate) is accompanied by the appearance of erythema and cavitary inflammatory elements - vesicles or blisters.

The third degree (severe) is characterized by a pronounced tendency to necrotic changes in tissue, angioedema with impaired respiratory function, generalization of rashes, erythroderma (affecting more than 90% of the skin surface), symptoms of intoxication of the nervous system (weakness, weakness, irritability), nausea, vomiting, temperature rise over 38 °C, systemic damage to the liver, kidneys, gastrointestinal tract such as acute vasculitis, eosinophilia over 25%, ESR over 30 mm/hour.

Since in most cases the “culprits” of toxic-allergic reactions are drugs, when we talk about various rashes during such reactions and give their characteristics, we will more often mention rashes of medicinal origin, although we must always remember that very often the substances are far from medicinal Applications may cause toxic-allergic lesions.

Clinical classification of LR

1. Exanthema.
2. Hives.
3. Fixed erythema.
4. Severe drug reactions.

Drug exanthemas account for 51% of all LRs. Primary elements: erythematous spots, papules, prone to fusion.

Itching: vesicular rashes accompanied by spongiosis in the epidermis are considered the most itchy.

Dynamics of the rash: begins on the torso, spreads quickly, symmetrical.

The rash develops 1-2 weeks from the moment of “first acquaintance” with the drug.

Histology. In the subepidermal parts of the dermis (border zone) there is an inflammatory lymphocytic infiltrate with vacuolar degeneration and dyskeratosis of individual keratinocytes of the basal layer. In the papillary dermis there is edema and interstitial eosinophils.

Urticaria ranks second in frequency. Clinically, urticarial rashes do not have specific features. Urticaria last no more than 24 hours.

Drugs that cause urticaria: ACE inhibitors, aminoglycosides, azoles antifungals, cephalosporins, hydrolasine, narcotics, penicillins, phenythine, quinidine, sulfonamides, salicylates, tetracyclines, protamine.

Skin symptoms toxicoderma is nonspecific, the rash can be represented by all types of primary elements, with their true polymorphism: erythematous, roseolous, exudative-papular, vesicular, bullous, urticarial, hemorrhagic, such as angioedema, reminiscent of exfoliative dermatitis. The formation of erythroderma is possible. The general condition may be disturbed: severe weakness, malaise, lethargy, chills, fever up to 38-39°C. In approximately half of cases of toxidermia, the rash is monomorphic, and enanthems are not uncommon.

Fixed erythema (sulfanilamide)- one of the types of spotted toxicoderma: dark brown spots up to 3-5 cm in size, uniform in color, non-inflammatory in nature, with clear boundaries, in quantities from 1-2 to several dozen.

A form of nutritional toxicoderma is desquamative erythroderma of newborns Leiner-Moussou. The disease is associated with autointoxication that occurs in the first 2-7 weeks of life against the background of malnutrition, pancreatic dysfunction (impaired secretion of lipase and amylase), malabsorption syndrome against the background of villous atrophy and fibrosis of the submucosal layer of the small intestine, hypovitaminosis A, B, C, E, folic acid. Antibodies against components of mother's milk are detected in children. The skin lesion is symmetrical, represented by erythematous or erythematous-squamous rashes, mainly in the area of ​​​​the folds of the body, quickly leading to the state of erythroderma; The face and mucous membranes, as a rule, are not affected; a mask-like appearance of the face is possible. Loose stools and frequent regurgitation are possible. Hypochromic anemia in the blood; total protein is reduced to 40 g/l. The temperature is subfebrile, with complications it rises to 38-40°C. Complications: purulent conjunctivitis, blepharitis, otitis, pneumonia, pyelonephritis, abscesses, phlegmon. The prognosis depends on the timeliness of diagnosis and hospitalization.

Differential diagnosis: Ritter exfoliative dermatitis, seborrheic eczema, lamellar ichthyosis. Treatment: vitamins, gammaglobulin, transfusion of fresh plasma, antibiotics for complications, baths with manganese, oak bark, bran (decoction of wheat bran at the rate of 0.5-2.0 kg per 4.0 liters of water, pour into a baby bath, temperature 37 -38°С); ointments with antibiotics and antiseptics.

As a form of toxicerma, such as limited erythema, it can be considered peripheral erythema of the extremities resulting from chemotherapy. It occurs after completing the next course of chemotherapy or closer to its end, in a word, when the course dose of the drug becomes sufficient; that is, the direct toxic effect of a medicinal substance or a complex of substances is obvious. More often, erythema develops after the use of doxorubicin, fluorouracil, and cytosine arabinoside. The timing of the onset of erythema varies widely, from 1 day to 10 months. A peculiar prodrome is a burning sensation on the palms and soles, and then, after 5-7 days, a symmetrical edematous erythema with clear boundaries appears, more pronounced on the hands. The next stage of the process is the formation of blisters (usually after cytosine) at the site of erythema. Over time, the process undergoes regression: the skin in areas of erythema turns pale, the covers of the blisters undergo desquamation, and erosions become epithelialized. Treatment: elevated position of the limbs, cold lotions and cool baths help to reduce the intensity of blood circulation and, accordingly, reduce the reaction. The results of the use of systemic corticosteroids for the treatment of this erythema are contradictory.

Papular toxicoderma: rashes are often disseminated, acutely inflammatory in nature, hemispherical papules, ranging in size from miliary to lenticular; are found in intoxication with chingamine, quinine, phenothiazines, arsenic, PAS, streptomycin, tetracycline, vitamin B, iodine, mercury, bismuth, gold, antimony, and antidiabetic sulfonylurea drugs. The rash may resemble lichen planus and merge into plaques and rings.

Gold preparations are often the cause of lichenoid tissue reaction. About 25% of all cases of rashes caused by gold preparations are of the lichen planus type and are usually accompanied by itching. Erythematous rashes take on the appearance of pityriasis rosea. The duration of the existence of rashes directly correlates with their prevalence, and the nature of the morphological elements does not affect the duration of the process in this case. The average duration of existence of rashes is up to 2.5 months. Treatment: GCS, both topical and systemic, helps relieve rashes; the latter are prescribed for severe cases of the process.

Vesicular toxicoderma: the rash consists of disseminated vesicles and microvesicles; localizations in the area of ​​the palms and soles are manifested by dyshidrosis. When erythroderma develops: universal edematous erythema, vesiculation, profuse weeping, swelling of the face and limbs, large-plate peeling, intertriginous crusts. It is vesicular toxidermia that is often accompanied by intense, painful itching.

Pustular toxicoderma: most often caused by halogens, which are released from the body, including with sebum; therefore, the rashes are most abundant in seborrheic areas. The rash consists of pustules and acne (acute inflammatory hemispherical papules with a pustule in the center). In addition to halogens, vitamins B6, B12, isoniazid, lithium, phenobarbital, and azathioprine can be the cause of toxidermia.

Bullous toxicoderma. There are pemphigoid and fixed varieties. Bullous toxidermia often occurs after taking antibiotics, sulfonamides, barbiturates, bromine, iodine.

With iodine toxicoderma, the blisters are located mainly in the folds of the skin and on the neck, large, with rapid eccentric growth, with a tendency to suppuration; after their opening, vegetative erosions are found, reminiscent of vegetative pemphigus. Often mucous membranes are affected.

With mercury toxicoderma, erythroderma develops quite quickly with large-plate peeling and large blisters in the folds of the skin.

Acute generalized exanthematous pustulosis- a variant of toxicerma, usually developing after taking medications, often antibacterial (penicillin), 5-10 days after taking the drug. Resolved independently 14 days after discontinuation of penicillin. The rashes are widespread, localized throughout the body, and tend to cluster. The photographs often resemble chickenpox. The eruptive element is a miliary superficial pustule. The temperature is febrile, there is leukocytosis in the blood.

There is also a description in the literature medicinal pemphigus- bullous dermatosis that occurs in response to taking a drug whose active substance contains a “-SH” group in its molecule. Most often it is D-penicillamine (dimethylcysteine). The development of medicinal pemphigus can also be provoked by captopril, enalapril, piroxicam, pyritinol, gold preparations, penicillin, ampicillin, amoxicillin, rifampicin, phenylbutazone, dipyrone, phenobarbital, and other drugs containing thiol groups in their molecule. These chemical groups can cause thiol acantholysis: being a chemical and pharmacological competitor of cysteine, the thiol group competes with this amino acid for a place in the keratin protein molecule.

Two variants of medicinal pemphigus are described:

• the first variant develops in the absence of antibodies to the structures of the desmosomes of the spinous layer, and the main etiological factor in it is the medication itself;
• the second option develops against the background of an immunological and genetic predisposition and is, in fact, a manifestation of true acantholytic pemphigus.

In the first option, drug withdrawal leads, if not to complete resolution of the process, then at least to a significant improvement. The second option is difficult from the very beginning, and its treatment requires tactics completely similar to those for vulgar idiopathic pemphigus.

The clinical manifestations of both variants of medicinal pemphigus are also somewhat different:

• the first option - occurs more often in the form of leaf-shaped or erythematous pemphigus, the appearance of blisters is preceded by erythematous spots or seropapules resembling prurigo;
• the second option - usually proceeds like pemphigus vulgaris, coinciding with it in clinical picture, course and prognosis.

Diagnosis of medicinal pemphigus involves a particularly careful collection of anamnesis to establish a cause-and-effect relationship with the use of any medication. A biopsy can help establish the variant of the process, since the pathomorphological findings completely coincide with the nature of the clinical picture: with thiol intoxication and the development of pemphigus foliaceus, acantholysis is observed almost at the border of the styloid and granular layers of the epidermis; during a course similar to pemphigus vulgaris, acantholysis forms cavities above the basal layer. Specific pathomorphological symptoms that allow one to suspect a medicinal origin of the pathological process are the following: spongiosis of the epidermis with eosinophilia, necrosis of keratinocytes, multi-level separation of the spinous layer.

Differentiate medicinal pemphigus follows with nosologies: seborrheic eczema - when it occurs like seborrheic pemphigus; Stevens-Johnson syndrome - with a course of the type of pemphigus vulgaris (a careful history taking, histological examination, immunofluorescent study may help); lupus erythematosus - with a process similar to erythematous pemphigus (Senir-Usher syndrome).

To denote severe hypersensitivity reactions with a predominance of damage to internal organs, the term “drug rash with eosinophilia and systemic symptoms” is sometimes used in the English literature. The severity of the syndrome is often associated with the development of hepatic-renal failure, which cannot be eliminated by any treatment. High doses of GCS, prescribed for vital indications, quickly relieve skin symptoms, but dose reduction is often delayed or carried out very slowly. This is due both to the period of elimination of the substance from the body and to the time of circulation of antibodies and immune complexes in the bloodstream: an attempt to reduce the dose of GCS without taking these periods into account leads to a recurrence of the process. At the same time, long-term use of high doses of GCS against the background of predominant organ pathology, as is the case with DRESS syndrome, can itself also lead to decompensation of vital functions.

Heavy LR It is customary to divide into 3 groups, of which the first is the most numerous:

1. Exudative erythema multiforme is widespread.
2. Stevens-Johnson syndrome.
3. Lyell's syndrome.

Differential diagnosis of toxicerma

Roseola toxicoderma should be differentiated from atypical roseola syphilides, pityriasis rosea, guttate psoriasis, parapsoriasis.

Papular toxicoderma should be distinguished from lichen planus, acute lenticular psoriasis, psoriasiform syphilide, discoid lupus erythematosus.

Differential diagnosis of toxicoderma and infectious erythema (IE)

Characteristic clinical differences between infections and allergies

• Prodromal period: disturbance of general condition, low-grade fever, arthralgia, myalgia, dyspepsia (nausea, diarrhea) - observed more often with infections.
• Isolated rashes on the hands and feet during infections almost never occur (exceptions are “socks and gloves after scarlet fever, viral pemphigus of the mucous membranes and feet).
• Lesions of the mucous membranes: conjunctivitis with toxidermia is not frequent, petechiae occur only in severe allergosis, in allergic vasculitis.
• The monomorphism of the rash is more characteristic of infections.
• No scratching for infections, polishing of nails.
• With allergic eczesanthemas, there is often a staged pattern of rashes, but there is no favorite localization.
• There is no weeping due to infections.
• Roseolas with vitropresia turn pale with an infectious rash.
• In infections, the enanthema resolves by the time the exanthema appears.

Infectious mononucleosis- caused by DNA human herpes virus type IV, transmitted by airborne droplets; incubation period 4-20 days, severe or moderate course: sharp enlargement of cervical and submandibular lymph nodes, tonsils (tonsillitis from the first days), hepatospleno-megaly, temperature up to 38-40°C, pronounced leukocytosis with a mononuclear reaction up to 15-65% ; polymorphic, often maculopapular, with a hemorrhagic component, a rash that appears on the 3-5th day of illness, lasts for 1-3 days and then disappears without a trace; occurs in 25% of patients. Lethal outcomes are rare, and are almost always associated with rupture of the spleen, or (rarely) with hemorrhagic meningoencephalitis.

Penicillin drugs should not be prescribed for infectious mononucleosis, as they provoke petechial rashes!

Erythema infectiosum- a disease caused by parvovirus B 19; the incubation period is 4-18 days, the prodrome can last up to 2 days; eruptive and regressive phases are distinguished: the eruptive phase is characterized by roseolous-papular rashes, quickly merging into large plaques, often on the cheeks in the form of a “butterfly” (symptom of “slapped cheeks”), and on the body and limbs in the form of “lace” (“fishing net” "); this phase lasts 4 days. This is followed by a regression phase, which is characterized by almost complete resolution of the rash.

Sudden exanthema. Children aged 0.5-2 years are most often affected, adults and adolescents rarely. The causative agent is herpesvirus types 6 and 7 (they are less virulent than HSV-1,2). Happens once in a lifetime, less often than twice. The incubation period is 5-15 days.

Clinic. A rash on the body is observed in 100% of cases, on the face it is smaller and paler, represented by roseola up to 2-5 mm in size, which can slightly elevate (rise); lasts 3-7 days. Differential diagnosis. Unlike measles, the rash is not bright, there are no papules, spots (monomorphic), disappears without a trace, there are no changes in the pharynx; there is no intoxication, even against the background of elevated temperature. Leukopenia is observed in some cases, lymphocytosis in others.

Scarlet fever- acute streptococcal disease. A characteristic rash appears on the second day; these are spotty, pinpoint rashes that thicken in folds (Pastia's symptom).

Measles- acute viral disease, with fever, intoxication, enanthema, maculopapular exanthema. Enanthema is the earliest sign; by this time there is already a runny nose, barking cough, and conjunctivitis. Other maculopapular elements are located on the mucous membrane of the cheeks, whitish, surrounded by a reddish border - Velsky-Filatov-Koplik spots. With the appearance of exanthema, rashes on the mucous membranes (enanthema) resolve at the end of the 4th day of the disease, and the temperature rises again. In the classic version, the appearance of the rash is characterized by stages: the first day - the face, neck, the second day - the torso, arms, thighs, the third day - the legs and feet, and the face begins to turn pale. The primary element is a milliary papule (2 mm), surrounded by an irregularly shaped spot, prone to fusion. Sometimes petechiae are found against the background of maculopapular elements.

Gianoti-Crosti acrodermatitis infantile eruptive- caused by hepatitis B viruses, infectious mononucleosis, Coxsackie A-16, cytomegalovirus; in children under 10 years of age, more often in boys, an acute onset with low-grade fever, dyspepsia, asthenia, sudden erythematous-papular rashes on the limbs and face, with a bluish tint, sometimes with hemorrhages, mild itching, sometimes with polyadenopathy and hepatosplenomegaly; on diascopy, ocher coloration; the disease lasts 25-60 days, spontaneously regresses without treatment, and there are no relapses.

Usually, the differential diagnosis of severe and severe forms of toxicerma does not cause difficulties. Stevens-Johnson syndrome should be differentiated from aphthous stomatitis in Behçet's syndrome and pemphigus vulgaris.

Epidemic exfoliative dermatitis (Sayville syndrome)- presumably of a viral nature, occurs in the form of epidemic outbreaks, more often in nursing homes. There is an exudative form, reminiscent of eczema, and a dry form, imitating pityriasis rosea: the rash is bright red, maculopapular, round in shape, peels off, merges into plaques and rings, sometimes with blisters. At the same time, baldness and polyadenopathy occur with a predominant enlargement of the submandibular lymph nodes. The duration of the disease is 4-6 weeks, relapses are possible. We observed several times the simultaneous appearance of pityriasis rosea rashes in several patients who were in the same room in a boarding house for the disabled; Moreover, in not a single case did the eczema-like symptoms described above, characteristic of epidemic Sayville syndrome, occur.

Behçet's disease (Touraine's major aphthosis, mucocutaneous-uveal syndrome)- a disease of unknown etiology, characterized by a combination of a triad of symptoms: aphthous rashes on the oral mucosa and genitals, ulcerative lesions of the eyes (up to 80% of patients), papulovesiculopustular rashes and lesions such as erythema nodosum on the skin (70%), arthralgia and arthritis (50%), neurological (encephalopathy, up to 14%), cardiac (myocarditis, up to 40%), pulmonary, gastrointestinal symptoms (up to 21%).

Paraneoplastic reactions are a different type of rash with which toxicdermia must be differentiated.

Sweet's syndrome- presumably autoimmune etiology; is represented by abundant rashes of papules and plaques ranging in size from 0.5 to 12 cm, red in color, with a more intense bluish color in the center. Sometimes small blisters and sterile pustules are found; with peripheral growth and fusion, even larger plaques with floors and cyclic edges are formed. In the malignant variant, the rashes become bullous, hemorrhagic, necrotic, and spread over the entire surface of the skin. Fever up to 39°C, headache, arthralgia; in the blood there is neutrophilia up to 70-90%, IgA, IgM, and CEC are increased. The prognosis is generally favorable, the rash resolves after 1-3 months, relapses occur in 30% of patients. Rapid regression of the rash is observed with oral intake of potassium iodide up to 200 mg/day; good results from the use of aspirin, non-steroidal antiphlogistics, less encouraging - from corticosteroids, antimalarial drugs, cyclosporine A.

chills- typical for infants and young children, it is facilitated by the lability of vascular tone and imperfect innervation. Often in asthenic or, conversely, obese children; localized on the nose, ears, cheeks, fingertips. Skin with a liquid-red tint, with pasty compaction and erythematous spots and nodules, without the depression in the center characteristic of MEE. Possible itching, which intensifies during the transition to heat.

Ritter von Rittershain exfoliative dermatitis- the most severe form of staphyloderma of newborns, caused by Staphylococcus aureus, which is cultured from the blood in 1/3 of cases. There is a relationship between age and severity of the disease. The disease begins with hyperemia, then blisters appear on various parts of the skin, on the 8-12th day erythroderma forms, and the overall picture resembles a 2nd degree burn. The condition is severe, temperature up to 41 °C, often accompanied by pyelonephritis, pneumonia, phlegmon and abscesses, otitis, etc. Before the introduction of antibiotics into practice, the mortality rate was up to 70%. Sometimes an abortive course of the syndrome is observed; some authors considered exfoliative dermatitis as an infectious-allergic variant of Lyell's syndrome.

Nikolsky's symptom is positive in almost all bullous toxidermia, and in severe forms it is sharply positive. At the same time, acantholysis is not typical for bullous toxidermia; acantholytic cells are found only in Ritter's disease.

Toxic shock- sudden increase in body temperature, hypotension, redness of the skin and mucous membranes, multiple organ failure; etiology: damage to Staphylococcus aureus toxins; often occurs in women aged 23-27 years, but can also occur with burns, injuries, wounds, nasal tamponade, postpartum infections, barrier methods of contraception, certain diseases (paratraumatic eczema with varicose symptom complex, diabetes mellitus; influenza, in children - chicken pox).

The incubation period is 4-5 days.

Clinic: muscle pain, headache, disorientation, confusion, convulsions, profuse diarrhea, shortness of breath. Throughout the body - a pinpoint spotty rash, expressed near the source of infection, rarely - petechiae, blisters, later - large-plate peeling on the palms and soles; on the mucous membranes - injection of the conjunctiva, hyperemia of the mucous membranes of the mouth, tongue, pharynx, vagina.

Differential diagnosis of toxic shock: scarlet fever, scalded skin syndrome, other infectious agents (meningococci, pneumococci, adenoviruses, toxoplasma); non-communicable diseases.

Treatment of toxicoderma

Stop the action of the etiological factor. This task is not always easy to accomplish. Since the beginning of the 21st century, modern medicine has been faced with the problem of long-acting medications that are eliminated from the body sometimes after several weeks. A classic example of a long-acting drug is the antibiotic Bicilin-5, used to treat various infections, including syphilis), in injections of 1.5 million units, once every 1-2 weeks, which are in the arsenal of means to combat infections since the 1980s. Nowadays, the number of such funds has increased many times. These are Retarpen (Extencillin), and Itraconazole (staying in the body for up to 9 months), and aromatic retinoids (used to treat acne, psoriasis, ichthyosis and having a half-life of up to 100 days). Simply stopping the drug is not always enough to ensure its rapid elimination in the body.

Thus, we observed a case of the development of drug toxicoderma in a man after 5 hot naphthalan baths, used to treat arthrosis and arthritis. The effect of naphthalan on joints resembles the effect of NSAIDs, and it is removed from the body after 5 general baths over two weeks. The patient's itchy, widespread, erythematous, macular rash persisted for two weeks, despite intravenous infusions of blood substitutes and treatment with prednisolone.

A gentle diet, sometimes No. 1. The classic recommendation is a low-calorie, hypoallergenic diet, excluding the consumption, first of all, of spicy foods and sweets containing flavor enhancers, all kinds of extractives, and essences. A hypoallergenic diet is used to help the body remove the allergen that has entered it relatively painlessly. After all, most of the listed food products are themselves gnetamine liberators, promoting the release of not only histamine, but also other pro-inflammatory substances that can contribute to the torpid course of the allergic process.

Mechanical sparing of the gastrointestinal mucosa also plays a significant role, especially with erosive and bullous lesions. Rough food and acidic foods that can cause pain when chewing and swallowing (for example, with erythema multiforme exudative) are excluded. In some cases, with toxicoderma of moderate severity, when patients continue treatment on an outpatient basis, the doctor has to give detailed recommendations on almost every food product: how chicken should be boiled, whether buckwheat should be cooked, oatmeal, whether potatoes should be eaten. These issues are resolved individually at an outpatient appointment, often taking into account the psychological characteristics of the patient. For severe Stevens-Johnson and Lyell syndromes, even tube feeding is used in intensive care units (preferably in a burn hospital).

Drink plenty of fluids- is a classic means of detoxification at the first stage of treatment, used in patients with mild to moderate severity of the toxic-allergic process. For the purpose of detoxification, you should not use teas, compotes, jelly, which themselves contain extractive substances with the properties of histamine liberators. The best means of enteral detoxification, in our opinion, is hypomineralized water, with a total mineralization of no more than 3 g/l.

Enterosorbents

These drugs should be taken according to certain rules, since as a result of enterosorption, not only toxins are removed from the intestinal lumen, but also vitamins and various medications that the patient takes both for the present disease and for the concomitant one. The bioavailability of antibiotics, antihistamines, antimycotics, tranquilizers, etc. sharply decreases. The main principle of prescribing enterosorbents is to maintain a period of time sufficient for the passage through the intestines of the enterosorbent to be substantially completed, and as a result, the bioavailability of another drug will not be reduced.

Polyphepan and its tablet preparations Filtrum and Lactofiltrum are prescribed according to the same rules.

Activated carbon can be taken once a day, in the evening, 1.5 hours after meals and taking any medications. More than 8 tablets are not prescribed. The tablets taken should be crushed into powder, which will significantly increase the sorption capacity of the drug.

Unfortunately, the severity of the sorption capacity of each sorbent directly correlates with the ability to cause constipation. Below we have presented a scale of enterosorbents in descending order of their sorption capacity, from the strongest to the least strong (from left to right).

The scale shows that activated carbon, as the most powerful sorbent, is equally capable of causing constipation. Patients suffering from severe constipation should not be prescribed enterosorbents, since we may get the opposite effect of detoxification, i.e. increased toxic effect. Patients who only have a tendency to constipation should be prescribed the least strong sorbents, for example, Enterosgel, but according to the same principles.

Antihistamines

Drugs in this group are among the most frequently prescribed, both for toxicerma and other allergic dermatoses. They are especially indicated for toxidermia, accompanied by severe itching and vesicular rashes.

In the treatment program for toxicoderma, you can introduce either one antihistamine drug, for example, Suprastin, or combine the first generation drug with one of the blockers of mast cell degranulation (ketotifen, cetirizine). In the latter case, the regimen for using two drugs will be as follows: twice a day, after breakfast and after lunch, the patient takes ketotifen, and at night an intramuscular injection of Tavegil is given, 2 ml; The duration of taking ketotifen should be about 1 month, and Tavegil - 5-7 days. This scheme allows you to simultaneously influence the acute process and ensure the prevention of relapses.

Diuretics and laxatives

Currently, diuretics (diuretics) are rarely included in complex treatment programs for allergic diseases. Sodium thiosulfate has a diuretic effect; intravenous solutions enhance fluid excretion. The technique of forced diuresis, so popular among doctors in the 1980s and 90s, is now almost never used for toxidermia. Indications for the use of diuretics are edema, which complicates the course of the main process. In these cases, thioside saluretics are usually used.

Furosemide(derivative of sulamoyl-anthranilic acid) - for toxicoderma, it is usually used in small doses, 20 mg each.

Diakarb(carbonic anhydrase inhibitor) is used in the same way as furosemide.

You need to remember a few simple rules for the use of diuretics in case of toxidermia: 1) diuretics are only an integral part of a complex therapeutic effect, and after achieving a stable effect they should be discontinued; 2) all of the diuretic drugs listed above are capable of greatly lowering blood pressure (and they are often used in therapeutic practice to relieve hypertensive crises); 3) chemical diuretics themselves can cause intoxication; 4) high doses of diuretics should be avoided - this can lead to significant fluid loss and an increase in the concentration of the toxic substance; 5) the drugs listed above should not be combined even with medium doses of glucocorticosteroids due to increased potassium excretion by both drugs.

If treatment with diuretics is necessary while taking prednisolone, it is preferable to use veroshpiron (spironolactone), a potassium-sparing diuretic, a competitive aldosterone antagonist. During treatment with veroshpiron, there is no need to prescribe potassium supplements to patients to avoid hyperkalemia.

Unlike diuretics, laxatives have become used much more often for toxicoderma. They are often combined with enterosorbents. As a rule, elderly patients need to be prescribed laxatives.

Currently, we rarely use chemical laxatives (Regulax, Guttalax). Preference is given to a laxative diet and senna preparations (Senade). In some cases, with a clear tendency to constipation, castor oil can also be used: it is currently available for oral administration in capsules of 1.0 g.

A well-known desensitizing agent such as sodium thiosulfate, used orally in powders, also has a laxative and diuretic effect.

Hemodez, rheopolyglucin, Reamberin

These drugs are intravenous detoxification therapy.

Hemodez is a derivative of polyvinylpyrrolidone. The mechanism of its action is due to the ability to bind toxins circulating in the blood and accelerate their elimination from the body. The drug increases renal blood flow and increases diuresis.

Reopoliglucin is a drug from the group of low molecular weight dextran derivatives. It helps move fluid (and toxins) from tissues into the bloodstream. In pediatric practice, doses of 5-20 ml/kg are used for detoxification; the dose is administered intravenously over 1.5 hours.

It should be noted, however, that allergic reactions are also possible to the plasma replacement solutions themselves.

Calcium preparations and sodium thiosulfate

One of the most common and often used in everyday practice is a 10% calcium gluconate solution. The drug has a desensitizing effect and slightly increases the tone of the sympathetic nervous system. The drug contains 9% calcium. It is prescribed intramuscularly or intravenously. In pediatric practice, calcium gluconate is used much less frequently than in adults due to the increased risk in children of developing infiltrates and even necrosis. Calcium gluconate should be administered intravenously slowly, 10 ml over 2-3 minutes, due to possible autonomic reactions, which, of course, are less pronounced than those of calcium chloride, but can still occur (dizziness, slow pulse, feeling of heat, nausea). Since the complex action of calcium gluconate shows an increase in sympathetic tone, the drug is especially good for the treatment of erythematous-urticarial dermatoses, and is less suitable for the treatment of atopic dermatitis, in which the sympathetic tone is already increased (white dermatographism).

Sodium thiosulfate for intravenous administration it is used in the form of a 30% solution. The drug has a desensitizing, antitoxic, anti-inflammatory effect. In case of toxicerma, this action is nonspecific, the mechanism of which is associated with an increase in toxins. However, the drug can also be used as an antidote. It can also be administered intravenously in 200 ml of saline solution at a rate of 60 drops per minute. However, it must be remembered that all sulfur compounds have their own toxicity and are not always predictable in a particular patient. Therefore, we recommend starting the first 2 infusions with a dose of 5 ml for an adult, and then, if well tolerated, administering the drug in 10 ml doses.

Ascorbic acid, ascorutin and other vitamins

Ascorbic acid preparations can be used in the complex treatment of toxidermia; they have the property of stabilizing the vascular wall, reducing its permeability, and stimulating the adrenal cortex. As an additional means of recovery, they can be prescribed during the period of reducing the dose of GCS, when the daily dose of prednisolone is half the starting dose.

It is the combination of ascorbic acid with rutin that provides a positive effect on the vascular wall.

For diabetes mellitus, a tendency to thrombosis, and arterial hypertension, ascorbic acid preparations are contraindicated.

A drug that significantly improves the tolerability of corticosteroids is vitamin E (α-tocopherol). It also reduces the permeability of the vascular wall and has antioxidant properties. The usual dose of α-tocopherol for short-term treatment with corticosteroids is 100-400 mg per day. In order to ensure better tolerability of GCS, pure α-tocopherol should be prescribed, avoiding combination with vitamin A (Aevit). Large doses of α-tocopherol are prescribed with caution for ischemic heart disease and a tendency to thrombosis.

Glucocorticosteroids (GCS)

The purpose of prescribing GCS is to relieve inflammation as quickly as possible. The main indication for their use is the severe course of the toxic-allergic process.

Prednisolone in tablets of 5 mg and dexamethosone in tablets of 0.5 mg are the main drugs for the treatment of toxicoderma according to classical regimens. Typically, to relieve the inflammatory process, these corticosteroids are prescribed in a starting dose of 6 tablets per day. A noticeable clinical effect is achieved on the 3-4th day of administration, the patient is kept on the starting dose for another 4-6 days to consolidate the effect, after which they begin to gradually reduce the dose of the corticosteroid by 1 tablet per week until complete withdrawal. Sometimes, with a favorable course of a moderate-severe process, you can reduce the dose of GCS by 1 tablet per week, so that after 3 weeks of treatment the patient will receive 3 tablets of corticosteroids per day. Starting from three tablets per day, withdrawal in all cases should be carried out by 1/2 tablet per week.

However, the clinical effect of tableted GCS usually develops gradually, as already noted, over 3-4 days, while our main goal is to achieve the effect as quickly as possible, within a few hours. The pharmacokinetics of injectable GCS meets these requirements.

Today we have at our disposal the following groups of injectable corticosteroids, according to their speed of action:

• fast-acting and “short-lived” (Dexamethasone solution at a concentration of 4 mg/ml, Prednisolone solution available at concentrations of 25 and 30 mg/ml);
• GCS only for intramuscular administration of medium duration of action - crystalloids (Diprospan, Flosteron);
• Long-acting GCS (Kenalog-40).

GCS for intramuscular administration only - crystalloids. These drugs are a water-insoluble emulsion and cannot be administered intravenously. The pharmacokinetics of the drug Diprospan is determined by the fact that it contains two salts of betamethasone: betamethasone sodium phosphate (2 mg) acts quickly, like dexamethasone, and is eliminated from the body within one day, and the effect of betamethasone dipropionate (5 mg) develops slowly, it is eliminated from the body completely within 10 days. The total strength of this drug can be characterized as follows: after administration of 1 ml of Diprospan the next day, the effect corresponds to approximately 7.5 tablets of prednisolone, and by the end of the 7th day it falls and begins to correspond to approximately 2.5 tablets of prednisolone. When detoxification agents (Reamberin) are used simultaneously with Diprospan, the kinetics of the drug is faster, and its effect decreases not by the 7th, but by the fifth day after the intramuscular injection.

The drug Kenalog-40 is a long-acting corticosteroid. It is used not so much in dermatology as in rheumatological practice. The drug is a 4% aqueous suspension of triamcinolone. In dermatology, Kenalog-40 can be used for steroid-sensitive dermatoses, when the treatment regimen does not plan for a long-term dose adjustment of the corticosteroid, or a single injection is sufficient to stop the pathological process.

For the treatment of toxidermia in the acute period, it is preferable to prescribe GCS drugs that have a rapid therapeutic effect, and “short-lived” prednisolone and dexamethasone in solutions have this property. Their action begins 10 minutes after administration, which is second only to adrenaline in terms of the speed of development of the effect. As a rule, these corticosteroids are used for drug reactions accompanied by an urticarial component and the threat of laryngeal edema. In some cases, starting with intramuscular administration of dexamethasone, you can later transfer the patient to tablets, or to intramuscular administration of medium-acting corticosteroids - Diprospan, Flosterone.

Treatment with GCS drugs of intermediate duration of action should be treated as treatment with tablets. In some patients, already after the sixth to eighth injection of crystalloids, performed once every 5-7 days, signs of Itsenko-Cushing syndrome develop.

Systemic corticosteroids have long been considered the drugs of choice. At the beginning of the 21st century, works appeared about their poor effectiveness and even an increase in mortality. Currently the data is contradictory.

The effectiveness of cyclophosphamide at a dose of 300 mg per day for 3 days has been shown.

Cyclosporine A is currently considered the drug of choice. Blocks CD8+ T lymphocytes and further initiation of apoptosis.

Intravenous immunoglobulin J. Data are conflicting.

Plasmapheresis. Hemosorption

For toxicoderma caused by the ingestion of poisons, it is prescribed Unithiol, No. 2EDTA, for nephropathy (mercury) - hemodialysis. In some cases, a drug is prescribed that specifically interacts with a specific toxin. Above we have already discussed this almost specific effect of sodium thiosulfate, which can be used for intoxication with heavy metals, arsenic, etc. The old method of treating toxicerma caused by sulfamide drugs has not yet lost its significance.

For allergic reactions to penicillin, the enzyme penicillinase was sometimes used: the drug was administered intramuscularly at 800,000 units, once every 2 days, the effect developed within 30 minutes and lasted 2-6 days. However, we must remember that the enzyme itself is a protein molecule that can also cause sensitization. Considering the presence in the modern arsenal of means that make it possible to control the activity of the process, primarily corticosteroids, during the time required for the breakdown and elimination of penicillin, enzyme preparations are now rarely used.

Bradykinin- it is advisable to use its inhibitors, one of which is ε-aminocaproic acid.

Previously prescribed for MEE Hexamethylenetetramine (Urotropin), 40% solution, 10 ml, intravenously, daily, under the control of a general urine test. At present, this technique has only historical significance. Refusal to use it is associated with the rapid development of symptoms of irritation of the renal parenchyma, after 3-4 injections: in a general urine analysis, a large amount of epithelium, altered red blood cells, and sometimes leukocytosis appear.

After the completion of the active process, when there are no fresh rashes, there is confidence in the durability of the effect obtained, you can prescribe histaglobulin - a remedy that has been undeservedly forgotten since the beginning of the 21st century. Meanwhile, this drug allows you to increase the histaminopexic function of blood plasma. You just need to decide in which processes the use of histaglobulin is justified. It certainly should not be prescribed for toxicoderma caused by heavy metals, consumption of poor-quality products, alcohol, etc. We have listed dermatoses in the development of which the leading role belongs either to the molecule of the drug itself, large enough to become an antigen itself (vaccine), or such a molecule is able to combine with a blood protein and from a hapten become a full-fledged allergen. There is no point in prescribing histaglobulin if the leading role in the development mechanism of a particular dermatosis belongs to the toxic effect of the substance, as, for example, with mercury intoxication.

The issue of using immunomodulatory drugs for the treatment of toxidermia has so far been decided unambiguously: immunomodulators are usually prescribed at the final stage of treatment - after the acute process has stopped, the appearance of new rashes has stopped, and sometimes after all rashes have resolved. It is clear that the purpose of prescribing immunomodulators in this case will not be to stop the acute process, but to correct immune disorders that may have led to the occurrence of an episode of toxicoderma. Such immunological correction will be carried out by a specialist immunologist if there are appropriate indications!

External treatment It is used quite often for toxicerma. The main indications for the use of external agents are itching (one of the most common indications), vesicular and pustular rashes. Shaked mixtures, corticosteroid ointments, creams and aerosols have an antipruritic effect. Weeping is an acute process in which the main task of external treatment is to relieve this condition as quickly as possible, since the weeping surface is fertile ground for the development of a secondary infection. Therefore, antibacterial lotions and combined aerosols (corticosteroid + antibiotic) are used on areas of weeping. Often a combination of corticosteroid ointment or cream with an antibacterial lotion is used: for example, Powercourt cream is applied to the weeping area, and then a lotion with a 0.05% solution of chlorhexidine digluconate is applied to the cream. This technique allows you to cope with weeping during the day. Even more preferable in such cases is the use of aerosols (Oxycort aerosol, Polcortolone aerosol) that eliminate weeping within 2-3 hours.

After the elimination of the most acute, and sometimes acute, process, it is recommended, as gently and gradually as possible, to “get away” from external use of the corticosteroid. This task is fully met by the ancient method of using a corticosteroid drug in the form of dilution. However, modern corticosteroid creams are not designed to be mixed with any indifferent cream, or, even worse, with internal lard, as doctors did in the mid-20th century. But we cannot agree with those “innovators” who completely deny the possibility of mixing corticosteroids. In our practice, we recommend a differentiated approach to this problem.

For example, old ointments Flucinar, Sinaflan can be mixed (only carefully!) with baby cream, ointments Radevit, Actovegin, Solcoseryl, 10% methyluracil. In practice we use only one ratio, 1:1. Ointment preparations of GCS began to be used in the 1970s, containing salicylic acid (Lorinden A, Diprosalik, Belosalik), can also be stirred if we rely on the action of salicylic acid not as an exfoliating component, but as a substance that promotes deeper penetration of GCS into the skin . Lorinden A ointment, for example, contains salicylic acid in a 3% concentration. After a 1:1 dilution with Actovegin ointment, the concentration of this acid will become 1.5%, and the concentration of the corticosteroid will also decrease.

A particularly good “preparation” is obtained by mixing 1:1 Fluorocort ointment with Actovegin ointment. We used this combination in patients with particularly dry but inflamed skin.

So, you can mix the so-called “old” ointments, the production of which began in the 70s of the 20th century, with any indifferent creams and ointments. You can even stir Celestoderm ointment.

What ointments and creams should not be stirred? Firstly, all modern creams. They cannot be stirred because their composition is “self-sufficient”, verified and balanced, and the introduction of a “third-party” component upsets this balance and leads to unnecessary contamination, including bacterial contamination. Moreover, please note that, for example, Celestoderm cream cannot be stirred, but Celestoderm ointment can be stirred!

Secondly, you cannot stir ointments and creams containing antibacterial substances (antibiotics), antifungal components, and, of course, combined ointments and creams, the composition of which is also balanced and which includes antibacterial and antifungal components. Why can't you stir them? Because by stirring these ointments, we obtain reduced concentrations of the antibiotic, on which the local flora is “raised,” and we very quickly get bacteria resistant to this antibiotic, fungi resistant to this antimycotic. That is, stirring such ointments is simply unacceptable!

For pustulization in the acute period, it is recommended to use shaken suspensions (“chatterboxes”) containing 5-10% derma-tol, bismuth subnitrate. Often we simply use a water-zinc suspension, without active additives. Below are approximate recipes for such “talkers”.

Since the beginning of the 21st century, the issue of stirring creams and ointments in order to adapt them for individual use has faded into the background due to the emergence of many indifferent substances, mainly in the form of creams, the characteristics and properties of which make it possible to avoid stirring them. Instead, a technique is emerging for the layer-by-layer application of corticosteroid ointments and creams and so-called emollients - relatively indifferent creams and ointments. There are even recommendations according to which corticosteroid ointments and creams should not be used at all without simultaneously “connecting” an emollient. The combination of topical corticosteroids and emollient in a certain order and time is considered useful.

Each time we should clearly understand the task that faces us: if a quick effect on the inflammatory process is necessary, then it is preferable to use a strong GCS cream, and then an emollient; if we are counting on long-term use of tGCs for a chronic inflammatory process, then we need to protect the skin as much as possible from possible side effects from the use of tGCS, and then it is preferable to first apply an obesity emollient, and then, again after 15 minutes, tGCS ointment. Intervals of 15 minutes were chosen empirically; they correspond to the pharmacokinetics of creams and ointments, and are the most compliant: it is convenient for the patient to maintain these intervals.

Prevention of toxicoderma

A thorough collection of allergy history is the first line of preliminary prevention. In the process of collecting such an anamnesis, it is possible to identify both the general predisposition of the patient’s body to allergic reactions, and the presence of a history of reactions that have already occurred. The patient can report a history of an allergic reaction, and in approximately 20% of cases can name a specific chemical agent.

Avoiding contact with already identified allergens, prescribing antihistamines and calcium preparations before prescribing antibiotics, sulfonamides, analgesics, etc. to the patient, especially when these drugs are prescribed for the first time, and the body’s reaction to their administration is unpredictable - all this significantly reduces the risk of toxicity. - allergic reactions.

The prognosis for toxicoderma is generally favorable.

You can predict a possible reaction to the introduction of an antigen (hapten) based on the results of in vitro tests:

• determination of antibodies by RPHA and ELISA,
• indicator of neutrophil damage,
• reaction of inhibition of macrophage migration,
• blast transformation reaction of lymphocytes,
• reaction of specific agglomeration of leukocytes,
• Shelley's basophil degranulation reaction.

Most of these reactions are based on the interaction of sensitized blood cells with specific allergens. Essentially, by performing these studies in vitro, we create a model of the immunological reaction that occurs in the body as a result of the introduction of an allergen and the occurrence of specific sensitization. In vitro tests allow you to perform the necessary research without putting the patient at risk; this risk is always present when performing in vivo skin tests. A classic example of the riskiness of skin tests is the Jadassohn iodine test for Dühring's dermatitis herpetiformis: the application of an iodine solution causes an exacerbation of the process so sharp that it requires additional therapeutic measures.

The main paradigm of any allergic process is the formation of the “antigen-antibody” complex. The second most important paradigm for such processes is the imbalance of individual parts of the immune system:

1. most often there is a decrease in the number of T-lymphocytes due to an absolute decrease in the number of T-suppressor and T-killer cells;
2. With almost the same frequency, a relative decrease in the number of T-lymphocytes is observed due to an increase in the B-cell link (although this phenomenon is more characteristic of autoimmune than allergic processes);
3. change in the ratio of helper and suppressor subpopulations. It is more typical for immunodeficiency conditions, but can also be observed in allergic conditions;
4. disimmunoglobulinemia - observed in almost all diseases whose pathogenesis involves the pathology of the immune system: with allergies, the content of Ig G and Ig E usually increases, the amount of secretory IgA decreases;
5. An increased number of circulating immune complexes in general is not typical for an acute allergic disease, since such a process, not being autoimmune, after elimination of the allergen and in the absence of additional antigenic stimulation, should tend to fade.

Skin tests (application or compress, drip, scarification, intradermal) have not lost their importance.

Sometimes, in terms of predicting the body’s possible response to the intended use of a drug, it can be valuable to determine IgE, both general and specific, the determination of which was carried out previously. Some patients carry the results of such studies with them.

A very simple and at the same time informative method for tentatively predicting whether a patient has drug intolerance was proposed by domestic scientists. First, the osmotic stability of the patient's erythrocytes is determined, after which the erythrocytes are kept in another sample together with the drug under study, and their osmotic stability is again determined. A decrease in osmotic resistance by more than 10% allows us to confidently predict the presence of drug intolerance.

In case of toxicoderma caused by any substances in industrial conditions (occupational toxicoderma), patients after recovery are advised to rationally find employment with the exception of further contacts with the occupational allergen. Establishing a connection between a disease, including toxicerma, and professional activity has not only a medical, but also a legal aspect. Any case of toxicoderma with suspected occupational nature of the disease is subject to investigation.