Allergic dermatitis is a disease of the epidermis that occurs due to an atypical reaction of the body to the influence of allergens and proceeds with an inflammatory process.

The disease is characterized by the appearance of rashes on the epidermis. Usually manifests itself in childhood and remains until the end of life. Only properly conducted therapy and adherence to certain nutritional rules will help to avoid relapse.

It is important to be able to distinguish between allergic and simple dermatitis. The cause of the first pathology are allergens. Simple dermatitis appears under the influence of high and low temperatures.

Both diseases are non-infectious in nature, so they are not transmitted from person to person. Allergic dermatitis, in turn, is of the following varieties:

• Contact. In this case, the pathology occurs due to the contact of the epidermis with the product - the causative agent of an atypical reaction of the body. In this case, rashes may appear not at the point of contact of the skin with the allergen, but in another area of ​​the skin. The causative agents of an atypical reaction are usually detergents and cleaning products, poisonous plants, low-quality cosmetics;
• Toxic-allergic. This pathology occurs due to the entry of allergens into the body through the epidermis, digestive organs, respiration, or as a result of injections. The causative agents of the disease are food, detergents and cleaning products, cosmetic and medical preparations, as well as ultraviolet radiation. A characteristic symptomatology is the occurrence of urticaria on the epidermis. In the absence of appropriate therapy, Quincke's edema may appear. This condition can cause death if timely medical care is not provided;
• Neurodermatitis. Another name is atopic dermatitis. This pathology is hereditary. The disease is chronic, so when a disease is detected, it is important to follow certain nutritional rules throughout life.

Regardless of the variety, allergic dermatitis appears on the hands, face or body. Usually there are rashes, accompanied by a rash. Allergic dermatitis on the face causes the most discomfort.

Here, rashes adversely affect the appearance, therefore, they cause aesthetic discomfort. Only the right therapy contributes to the convergence of formations, leaving no marks on the epidermis.

If acute allergic dermatitis is diagnosed, then urgent medical care is required. Lack of therapy can lead to or anaphylactic shock. These conditions can lead to death without prompt treatment.

Allergic dermatitis: symptoms and treatment in adults

Allergic dermatitis is a disease that occurs under the influence of allergens. . When they enter the body, antibodies begin to be produced. They try to destroy substances they perceive as hostile.

Antibodies provoke the synthesis of histamine, which is the cause of rashes on the epidermis. For this reason, it does not matter how many allergens have entered the body. The main thing is how much histamine is produced at the same time.

In adults, the symptoms of allergic dermatitis depend on the stages of development of the pathology, if the disease occurs in an acute form:

• erythematous stage. In this case, a spot of red hue appears on the epidermis, which rises above the epidermis;
• vesicular stage. Nodules form on the skin, which are also called bubbles. Such rashes can be small or large in size. The bubbles have a liquid center, so after the convergence of the formations on the epidermis, a crust or erosion remains;
• necrotic stage. This is where soft tissue destruction occurs. As a result, trophic ulcers appear on the epidermis.

Important! Formations in allergic dermatitis usually appear on the upper limbs, including the palms, and the rash also appears on the face and body. Therapy is carried out, regardless of the location of the formations.

Allergic dermatitis: causes

The cause of allergic dermatitis is the influence of pathogens on the body. Usually an atypical reaction appears on the following stimuli:

• Physical. These include low and high temperatures, ultraviolet radiation, pets, plants;
• Chemical. A common cause of allergies is the intake of certain medicinal products, the use of cosmetics and household chemicals, as well as perfumes;
• Vegetable. These are herbal products. A non-standard reaction of the body is provoked by folk remedies for oral and external use;
• Ecological. Allergies can occur in people living in regions with adverse environmental conditions. In this case, the ongoing therapy may not give the desired effect, so doctors often advise patients to change their region of residence;
• Food. In this case, the body reacts atypically to the use of certain foods. These include honey, chocolate, citrus fruits and other foods;
• Psychological. The occurrence of allergic dermatitis can provoke an unstable emotional background.

Allergic dermatitis also appears due to a genetic predisposition.

Is allergic dermatitis contagious or not? This is not an infectious pathology, therefore it is not transmitted by airborne droplets.

Symptoms of contact and toxic allergic dermatitis

Allergic contact dermatitis has the following symptoms:

• eczema on the hands, which is aggravated after contact with detergents and cleaners, and before this problem occurs, a spot appears on the epidermis that rises above the skin, which transforms into a rash with a liquid inside;
• white spots on the epidermis of the face;
• rashes of various types: small rash, vesicles, papules and others;
• redness of the skin;
• swelling of soft tissues;
• itching and burning on the affected areas of the epidermis.

Toxic allergic dermatitis also has additional symptoms:

• increase in body temperature;
• headaches;
• pain syndrome in the joints and muscles.

What dermatitis of the allergic nature of the contact variety looks like is shown in the photo below.

How to treat allergic dermatitis in adults

There are several ways to treat allergic dermatitis in adults. To get rid of the signs of pathology, complex therapy is prescribed. However, before starting treatment, the allergen should be identified and contact with the causative agent of the pathology should be limited.

Only this guarantees a positive effect from the therapy. For the treatment of allergic dermatitis on the face or body, oral medications and the use of products for external use are prescribed.

Systemic treatment

Systemic treatment of allergic dermatitis in adults is based on the use of antihistamine drugs. Most often, doctors prescribe Loratadin, Suprastin, Claritin, Zodak and other similar pharmaceutical preparations. Such products relieve signs of pathology. Means relieve itching, eliminate redness and swelling of soft tissues, and also contribute to the convergence of rashes.

How long such therapy lasts depends on the nature of the disease and the time of initiation of treatment. If you start taking drugs immediately after the onset of symptoms of the disease, then the therapy will quickly give a positive result.

Local treatment

Treatment of allergic dermatitis will not be effective without the use of topical agents. In this case, the following products are prescribed:

• Antihistamines. These funds quickly relieve itching in allergic dermatitis, relieve redness, swelling of soft tissues and rashes. The product is treated with the affected area of ​​the epidermis several times a day. Doctors recommend using drugs such as Claritin, Zodak and others;
• Glucocorticosteroid drugs. Such drugs are made on the basis of hormones. Products have a large number of contraindications and side effects. For this reason, hormonal ointments are prescribed only if antihistamines have proven to be ineffective. You can use glucocorticosteroid products only as directed by your doctor. The drugs relieve redness, itching, rashes, hives and other rashes. Experts recommend the use of hydrocortisone and prednisolone. The duration of therapy is determined by the doctor;
• Drugs containing antibiotics. This ointment is prescribed if an infection has joined the allergic dermatitis. Doctors recommend using Tetracycline, Geleomycin and Erythromycin ointment. Such funds should be used to prevent the occurrence and with the inflammatory process that has already appeared.

Treatment of dermatitis on the face and hands

When allergic dermatitis occurs on the face, it is important to prevent the infection from joining and start timely treatment in order to quickly get rid of the rashes, since the formations in this case bring not only physical, but also aesthetic discomfort.

For therapy, it is recommended to use topical agents. These include Flucinar and Lorinden. Such drugs relieve itching and rashes, and also prevent the occurrence of the inflammatory process. The funds are applied to the affected areas of the epidermis several times a day.

Allergic dermatitis on the hands can be treated with drugs such as Skincap, Panthenol or Bepanthen. These funds will not only help get rid of the uncomfortable sensations that accompany the disease, as well as rashes, redness and swelling, but also protect the skin from external negative influences. Panthenol is recommended if an allergic reaction occurs to elevated temperatures, such as hot water or ultraviolet radiation.

If symptoms of allergic dermatitis in adults appear, and the treatment does not give the desired effect, it is recommended to contact a professional with this problem. This may mean that the allergen was incorrectly identified or the prescribed drugs cannot cope with the symptoms of the pathology.

Treatment of dermatitis during pregnancy

If allergic dermatitis occurs in a woman during the period of bearing a baby, the question arises of how to treat the pathology. The fact is that during pregnancy, taking many medications is prohibited due to the negative impact on the baby.

Usually, during the period of bearing a baby, women are recommended to use traditional medicine, but only on the recommendation of a doctor, as well as Suprastin. Other drugs are prescribed only if the pathology causes more harm to the child than taking medications.

Diet for allergic dermatitis

If allergic dermatitis is diagnosed, then it is recommended to adhere to certain nutritional rules. It is important to exclude from the diet all foods that can provoke an atypical reaction of the body or aggravate the pathology. These include:

• citrus fruit;
• nuts;
• chocolate;
• vegetables, berries and fruits of red and yellow shades;
• sunflower oil and sunflower seeds;
• concentrated meat broths;
• fatty meat and fish;
• river bird; offal;
• seafood.

However, the diet of the patient should be varied. The menu is recommended to include:

• low-fat varieties of fish;
• dietary meat and poultry;
• fresh fruits, vegetables, berries, with the exception of prohibited ones;
• greens;
• porridge.

• Eat small meals 6 times a day. It is recommended to take 200 g of the product and 200 ml of liquid at a time;
• Observe the drinking regime. You should drink at least 1.5 liters of fluid per day. At the same time, you can use clean water without gas, compotes and fruit drinks, cooked and not prohibited berries and fruits. You can not drink sweet carbonated drinks, juices with preservatives, as well as alcoholic beverages;
• Cooking is recommended only for steaming, in the oven or by boiling. Do not fry or smoke food.

If you do not follow the rules of nutrition for atopic dermatitis, then the treatment does not give a positive result.

Allergic dermatitis: treatment with folk remedies in adults

How to cure allergic dermatitis with folk remedies will tell a specialist. The doctor may include the use of alternative medicine in complex therapy.

Ointment based on sea buckthorn oil

To prepare such a product, you will need:

• sea ​​buckthorn oil - 2 small spoons;
• baby cream - 2 large spoons.

Both products are combined and stirred. The resulting ointment is applied to problem areas of the epidermis. Manipulation is performed several times a day.

Decoction based on medicinal plants

To prepare the decoction you will need:

• chopped oak bark - 1 large spoon;
• calendula flowers - 1 large spoon;
• wild rosemary flowers - 1 large spoon;
• horsetail - 1 large spoon;
• Melissa - 1 large spoon;
• chopped burdock root - 1 large spoon;
• vegetable oil - 1 cup.

Any vegetable oil is suitable for this recipe, but experts recommend giving preference to olive oil. All plants are combined and 1 large spoon is separated from the total mass. The collection is added to the oil, and the product is boiled for a quarter of an hour.

Decoction based on wild rosemary

To prepare such a remedy, take:

• wild rosemary - 2 large spoons;
• water - 1 liter.

The plant is poured with boiling water and set to boil. The drug is boiled for 15 minutes, after which it is left to cool and infuse. The broth is filtered and added to the bath, which is recommended to take a quarter of an hour. The procedure is carried out 2 times in 7 days.

Infusion based on pansies

Required components:

• pansies - 2 large spoons;
• water - 1 liter.

The plant is poured with boiling water. After that, the product is left to infuse for 15 minutes. The infusion is filtered and added to the bath, which is recommended to take a quarter of an hour. The procedure is carried out 2 times a week.

In the video, experts talk about what allergic dermatitis is and how to deal with this pathology.

Photo of allergic dermatitis

It is impossible to diagnose the disease by external signs. This requires some research. However, you should know how allergic dermatitis looks visually and the photos below demonstrate this.

Outcome

Allergic dermatitis is a pathology that, if not properly treated, can provoke angioedema and anaphylactic shock. These conditions lead to the death of the patient if timely medical attention is not provided.

However, it is easiest to prevent their occurrence. For this reason, at the first sign of allergic dermatitis, it is recommended to visit a professional to identify the causative agent of the disease and get a treatment appointment.

Allergic itchy dermatosis always has a characteristic symptom - negative symptoms on the skin. The defeat of the epidermis of various kinds develops under the influence of a certain stimulus.

It is important to know the causes of negative skin reactions, types of allergic dermatoses, effective methods for eliminating itching, rashes. For adult patients and parents whose children suffer from skin lesions, the advice of an allergist will help prevent dangerous reactions.

Reasons for the development of the disease

The main factor causing skin symptoms, the appearance of rashes, hyperemia, swelling, itching, is a negative response of the body to the action of internal and external stimuli. With a high sensitivity of the body, a small amount of the allergen is sufficient for the development of a dangerous reaction.

Contact with a certain substance triggers an immune response:

• histamine is released in large quantities;
• increased permeability of the vascular wall;
• allergens penetrate tissues;
• the work of the digestive system is disrupted, antigens accumulate in the body;
• puffiness develops, signs of allergic dermatoses appear on the body.

Substances and factors that provoke the development of allergic dermatosis:

• pollen of ambrosia, alder, birch, quinoa, poplar fluff;
• house dust;
• wool, saliva, dry excrement of cats, dogs, feathers and fluff of parrots;
• genetic predisposition to allergies;
• poison of stinging insects;
• highly allergenic products;
• sudden hypothermia or overheating of the body;
• household chemicals, cosmetic preparations;
• substances that irritate the skin for a long period. Production factors: contact with lubricants, oils, varnishes, paints, gasoline, solvents.

Allergic pruritic dermatosis ICD code - 10 - L20 - L30 (section "Dermatitis and eczema").

First signs and symptoms

Negative signs on the skin appear in mild, moderate and severe forms. Each disease has a set of characteristic manifestations.

The main types of epidermal lesions in allergic dermatoses:

• itching of problem areas;
• small red rash;
• erosion, weeping, wounds, sores;
• flaky areas;
• pustules;
• red spots (large or small);
• plaques;
• erythema (pink spots, often with swelling);
• purple-colored blisters, size - from 5 mm to 12-15 cm. With increased swelling, the problem areas brighten, the edges of the formations remain red;
• foci of atrophy (dead tissue) with a severe form of the disease, lack of treatment or prolonged use of hormonal ointments.

Types of allergic dermatoses

Allergodermatosis, accompanied by itching and skin reactions:

• atopic. Small rash, redness appears on the cheeks, chin, forehead, elbows, inner surface of the legs. After the opening of the bubbles, erosion and weeping are formed. Gradually, the reaction subsides, zones with crusts and active peeling appear. The active phase of the disease is accompanied by severe itching, the skin cracks, the patient experiences discomfort. occurs more often than in adults, especially in babies under one year old;
• contact form. Skin reactions are noticeable in areas of contact with the allergen. Rashes, itching, redness, peeling - the result of the action of household chemicals, skin care formulations, harmful substances;
• toxic-allergic. A severe form of an immune reaction with active rashes all over the body, with a sharp increase in temperature, the development of allergic inflammation. Severe itching provokes irritation, the patient combs problem areas, there is a high probability of secondary infection;
• "pregnant herpes" Allergodermatosis is not accompanied by the penetration of the virus. Itching, small vesicles, inflammation are characteristic signs of an allergic reaction. The reason is the body's response to hormonal fluctuations. "Herpes of pregnancy" occurs suddenly, after a couple of weeks the symptoms disappear without consequences for the mother and fetus. To exclude dangerous diseases, a woman should visit a dermatologist and an allergist;
• erythema. The main symptom is the appearance of pink spots on the body. Education is noticeable one or more. Sometimes the spots rise above the skin, resemble large blisters, as with, but the shade is not purple, but pinkish.

Diagnostics

If you suspect the development of pruritic dermatosis, the patient should visit a dermatologist. The doctor will clarify the nature of the reaction, the frequency of occurrence of negative symptoms.

Prohibited names:

• fatty milk;
• cocoa beans in any form;
• seafood;
• fish caviar;
• peanuts, almonds, hazelnuts, walnuts;
• citrus;
• eggs, especially protein;
• fruits and vegetables, the pulp and peel of which has a bright color: red, orange;
• coffee;
• exotic fruits;
• spices, sauces;
• canned food;
• semi-finished products, sausages, boiled and smoked sausage;
• pickled vegetables, pickles;
• cheeses;
• ready-made mayonnaise;
• products with synthetic fillers: emulsifiers, flavors, dyes.

Medical therapy

Therapy of diseases accompanied by skin reactions includes a complex of drugs:

• for oral administration. Allergy pills suppress the release of histamine, reduce the strength of allergic inflammation, and prevent relapses in the chronic form of the disease. With a lightning reaction, classic compositions (1st generation) are used:,. In the chronic form of allergic dermatoses, drugs of new generations with a delicate effect are prescribed:, and others;
• non-hormonal local formulations to eliminate skin reactions. Effective gels, creams and with anti-inflammatory, antihistamine, wound healing action. The preparations dry the epidermis, reduce painful, reduce swelling of the epidermis, prevent secondary infection in severe forms of allergic dermatosis. Skin-Cap, Bepanten, Psilo-balm, Desitin, La Cree, Vundehil, Solcoseryl, Fenistil-gel, Gistan, Protopic, Epidel;
• hormonal ointments and. Glucocorticosteroids lower the local activity of the immune system, prevent the production of inflammatory mediators, and stop allergic inflammation. Potent agents are prescribed only for severe reactions for a short period (up to 10 days). For adults, drugs are suitable: Prednisolone, Hydrocortisone, Advantan, Elokom, Lokoid, Flukort, Sinaflan, Gistan N;
• tablets and solutions for injections that reduce the sensitization of the body. The compositions reduce the permeability of capillaries, prevent swelling, strengthen the immune system, and ensure the supply of useful trace elements. , sodium bromide, calcium gluconate, ascorbic acid;
• . Oral administration of tablets, hydrogel, suspensions with active adsorbing properties cleanses the body, prevents further penetration of antigens into tissues. Removal of irritant molecules reduces the strength of skin reactions, speeds up recovery. The best option is the use of sorbents with high absorbency. Modern means: Multisorb, Laktofiltrum, White coal, Smecta, Karbosorb, Enterumin;
• soothing ingredients. Itching is one of the unpleasant signs of allergic dermatoses. In the chronic course of the disease, the patient becomes irritable, suffers from insomnia. To normalize the state of the nervous system, non-addictive drugs are prescribed: Novopassit, Karvelis, valerian tablets, motherwort tincture, a decoction of mint, lemon balm, a soothing collection of medicinal herbs.

Folk remedies and recipes

To reduce the strength of negative symptoms in allergic dermatoses, remedies based on medicinal plants are suitable:

• Decoctions for oral administration. The compositions cleanse the body, show a weak anti-inflammatory effect. Components: sprigs of viburnum, elecampane and burdock root, mint, nettle,.
• Therapeutic baths. Herbs: string, sage, chamomile, mint, yarrow, calendula. Useful oak bark;
• Lotions with decoctions from medicinal plants listed in paragraph 2.
• . Dissolve a small amount of mountain resin in water, take daily for 10 days. For a year - 4 courses.
• . Washed, dried, peeled from films, grind the natural product from a raw egg to a powder state, mix with lemon juice. Take with a negative reaction to food,.

Allergic dermatoses in children

Causes: View a selection of effective treatments for hands and face.

For symptoms and treatment of toxic-allergic dermatitis in children, read the address.

There are also nuances:

• up to 6 or 12 years is prescribed in the form of syrup and drops;
• a decoction of a string can be drunk only from the age of three, before only baths and lotions are allowed;
• should include names that ensure the full growth and development of the child. Even from a limited list of products, parents can prepare healthy meals;
• it is important to minimize the influence of harmful factors, if it is impossible to fulfill this condition (the effect of cold, sun, strong wind), protect the baby's skin.

Prevention of negative reactions to an irritant includes several areas:

• limiting contact with substances / natural factors that cause damage to the epidermis against the background of an immune response;
• strengthening of protective forces, hardening;
• proper nutrition, a minimum of highly allergenic foods in the diet;
• treatment of chronic diseases;
• control of the state of the digestive tract, timely treatment of intestinal infections;
• limiting contact with irritants, using quality body care products, ditching powders in favor of gels.

Allergodermatosis in adults and children can be cured after timely diagnosis, the appointment of complex therapy. Skin reactions accompanied by itching require attention: advanced stages negatively affect the general condition of the body.

After watching the following video, you can find out more interesting details about the symptoms and treatment of itchy allergic dermatoses:

MINISTRY OF HEALTH OF THE REPUBLIC OF BELARUS

BELARUSIAN STATE MEDICAL UNIVERSITY

DEPARTMENT OF SKIN AND VENERAL DISEASES

DERMATOLOGY

Tutorial in two parts

2nd edition

NON-INFECTIOUS DERMATOLOGY

Edited by V. G. Pankratov

Approved by the Ministry of Education of the Republic of Belarus as a teaching aid for students of higher educational institutions

in medical specialties

Minsk BSMU 2009

UDC 616.5–002–001.1 (075.8) LBC 55.83 i 73

D 36

AND in t about r s: cand. honey. Sciences, Assoc. V. G. Pankratov (Ch. 1.1–1.3, 1.5, 2, 4, 5, 6.3, 9.1);

cand. honey. Sciences, Assoc. N. D. Khilkevich (Ch. 9.1, 9.2, 9.3, 10); dr med. sciences, prof. N. Z. Yagovdik (Ch. 1.3, 3, 6.1, 7, 8); dr med. Sciences, Assoc. O. V. Pankratov (Ch. 4, 9.3); cand. honey. Sciences, Assoc. I. N. Belugina (Ch. 6.1, 6.2); cand. honey. Sciences, Assoc. M. V. Kachuk (Ch. 1.2, 11); cand. honey. sciences, assistant. A. L. Barabanov (Ch. 1.4, 5)

Reviewers: head. cafe Dermatovenereology, Grodno State Medical University, Ph.D. honey. Sciences, Assoc. D. F. Khvorik; head Clinical Department of Occupational Pathology and Allergology, State Institution "Republican Scientific and Practical Center for Hygiene", Honored Scientist of the Republic of Belarus, Dr. med. sciences, prof. S. V. Fedorovich

Dermatology: textbook. manual in 2 hours. Part 2. Non-infectious dermatology /

D 36 V. G. Pankratov [and others]; ed. V. G. Pankratova. 2nd ed. - Minsk: BSMU, 2009. - 220 p.

ISBN 978-985-528-042-3.

The manual contains up-to-date information on the etiology, pathogenesis, clinic, treatment and prevention of the main nosological forms of skin diseases. The publication has been prepared in accordance with the standard program approved by the Ministry of Health of the Republic of Belarus. The first edition came out in 2008.

It is intended for students of medical, pediatric, military medical, preventive medical, dental faculties and the medical faculty of foreign students of medical educational institutions.

Chapter 1. Dermatitis and allergic dermatoses

1.1. D ERMATITIS

AT In a broad sense, the term "dermatitis" is used as a general name for all forms of inflammation of the skin as a result of exposure to exogenous irritant or sensitizing factors. External, or exogenous, stimuli can be mechanical, physical, chemical (including drugs) and biological (plant sap, jellyfish, some marine animals, fish, insects, etc.).

Dermatitis is divided into simple contact, allergic and toxic-allergic (toxidermia).

Simple contact dermatitis develop under the action of obligate and facultative irritants of a physical or chemical nature on areas of the skin. They can occur after a single exposure to obligate irritants such as concentrated solutions of acids, caustic alkalis, salts of heavy metals, blistering chemical warfare agents, as well as after repeated exposure to skin areas of facultative irritants that do not have sensitizing properties, but have a mild primary effect. irritating effect or inhibiting the secretion of sweat and sebaceous glands, which causes degreasing

and dry skin. Optional irritants include weakly concentrated solutions of acids, alkalis, salts of heavy metals, organic solvents (gasoline, kerosene, diesel fuel, acetone, white spirit, butanol, etc.), lubricating oils, cooling emulsions, fuel oil, tar, cyanide compounds, formalin, etc. They have a primary irritating effect. Some of them also have sensitizing properties (formalin, etc.). Facultative chemical irritants with prolonged repeated exposure can cause a number of forms of dermatitis: epidermitis, simple contact dermatitis, skin ulcerations or "burns", onychia and paronychia, oily folliculitis (horny and inflammatory acne, limited hyperkeratosis).

Repeated mechanical impacts can lead to the development of calluses. Among the physical factors leading to the development of simple dermatitis, high and low temperatures (burns and frostbite of I-III degrees), ultraviolet rays (solar dermatitis), and x-rays (radiation dermatitis) should be mentioned. Phytodermatitis is caused by biological factors, in particular, the juice of plants such as hogweed, primrose, etc.

In accordance with ICD-10, acute and chronic simple contact dermatitis are distinguished.

The clinical picture of simple contact dermatitis is characterized by the fact that the zone of skin irritation strictly corresponds to the zone of contact with the irritant, the severity of the lesion depends on the concentration, strength of the stimulus and exposure time. This contact is manifested by the development of severe erythema, edema, and often blisters with serous or serous-hemorrhagic contents.

The boundaries of the lesions are clear. In the lesions, necrosis may develop, for example, after exposure to very high temperatures. Subjectively, patients note a burning sensation, often soreness, less often itching in the lesions. Depending on the depth of the lesion, 4 stages of acute contact dermatitis are distinguished. When only the upper layers of the epidermis are affected, the first stage of dermatitis develops, which is manifested by erythema and moderate edema. If all layers of the epidermis are affected, then clinically, against the background of persistent erythema, blisters with serous or hemorrhagic contents appear - this is the second stage of dermatitis. If the lesion captures the epidermis and upper layers of the dermis (third stage), then such acute dermatitis already proceeds with the formation of a necrotic scab. Deep skin involvement, including the hypodermis, defines the clinic fourth stage acute contact dermatitis, with deep necrosis of damaged tissues.

Prolonged exposure of the skin to weak obligate irritants is accompanied by the development of erythema, infiltration, areas of lichenification, and pigmentation.

and peeling, which is regarded as chronic simple contact dermatitis.

AT In this chapter, we will not dwell on simple dermatitis caused by mechanical, thermal, chemical (chemical warfare agents, strong acids, alkalis, etc.), radiation factors or ionizing radiation, since most of them will be discussed

in section "Occupational skin diseases".

A few words about simulation dermatitis. This, as a rule, is the “needlework” of the patient himself in order to obtain contact dermatitis of varying severity (depending on the damaging agent chosen by him - exposure to acid, hot metal, burning cigarettes, prolonged friction of the skin area, etc.). The goals of such self-harm are very different: an attempt to achieve a commutation of the sentence for a crime committed, to receive a deferment from conscription into the army, to evade a business trip to hard work outside of one’s hometown, etc. In such cases, a forensic medical examination should be carried out, especially that, as a rule, the demonstrated clinical picture of the lesion does not correspond to the anamnesis data, and the lesions themselves are localized where the hands reach.

Diagnosis of simple dermatitis is based on the data of the anamnesis and the characteristic clinical picture, on the relatively rapid resolution of rashes after the elimination of contact with the etiological factor.

Allergic dermatitis occur by direct contact with the skin of substances that can provoke an allergic reaction of a delayed type. Allergens can be medicines, cosmetics and perfumes, paints, detergents, metals, insecticides, etc. Despite the fact that the allergen comes into contact with a limited area of ​​the skin, sensitization of the whole body occurs. Patients cannot always suspect the cause of their disease, especially since clinical manifestations occur several days after the onset of sensitization. Sensitized lymphocytes, Langerhans cells, mediators of immune inflammation, etc. are involved in the development of hypersensitivity in patients with allergic dermatitis.

In these patients, monovalent sensitization is initially formed, and later - polyvalent.

According to ICD-10, allergic contact dermatitis can also be acute and chronic. In acute allergic contact dermatitis, the skin turns red at the site of contact with the allergen, papules and microvesicles appear. Part of the microvesicles opens, forming small areas of weeping, which is short-term and unsharply expressed. The lesions do not have clear boundaries, the elements of the rash appear simultaneously. Gradually, all manifestations of dermatitis regress, but sensitization to this allergen persists for a very long time. This saves the ground for new relapses of the disease upon repeated contact with the allergen.

Chronic contact allergic dermatitis is manifested by moderate inflammation and hyperkeratosis in places of repeated contact with the allergen in low concentration. With multiple repeated exposures to allergens, dermatitis can transform into eczema with the development of polyvalent sensitization.

A kind of allergic dermatitis is photodermatitis. In this case, the pathogenesis is the same as with allergic contact dermatitis, but in addition to contact with the allergen, exposure to ultraviolet rays is necessary. Some drugs act as a sensitizer for photodermatitis (sulfonamides, griseofulvin, ichthyol, doxycycline, corticosteroids with prolonged external use, etc.), substances that make up cosmetics, perfumes and detergents, plant juice, etc. Open areas of the body are affected , on which persistent erythema, microvesicular rash, blisters, blisters appear. As a result of scratching, foci of lichenification may develop.

The diagnosis of allergic contact dermatitis is based on the history, characteristic clinical presentation, positive allergen skin tests or in vitro immunological tests.

Differential Diagnosis allergic dermatitis is carried out with simple dermatitis, toxidermia and eczema (Table 1).

Table 1

Differential diagnosis of simple contact, allergic contact dermatitis and toxidermia

Indicators	simple pin	Allergic	Toxidermia
	dermatitis	contact dermatitis
	Arises quickly	Occurs after exposure	Occurs after
diseases	when applied to the skin	on the skin of exo- and / or endo-	taking medication
	obligate exogenous	gene factor, often	or food products
	foot stimulus	known allergen	tov (mushrooms, strawberries,
			chocolate, etc.)
	Not necessary	The development of sensitization -	The development of the island
sensitization		required condition	casting reaction
			skin and mucous membranes
			polyvalent background
			sensitization

The end of the table. one

Indicators	simple pin	Allergic	Toxidermia
	dermatitis	contact dermatitis	In any area of
Localization	At the point of contact	On open and closed
	with an irritant	areas of the skin	la, more often fixed-
			affected area
Characteristic	More often monomorphic	Polymorphic	Polymorphic
			They take place along with
	May form	There is vesiculation
vesiculation		and weeping	with allergic
and weeping			rashes
Inflammatory	Acute or subacute	Acute or subacute with ten-	The reaction is sharp
	limited by place	tendency to spread	diffuse or local
	contact with irritants	to other areas	lysed
			Acute, when eliminated
Current and pro-	Acute, the process of	Acute or subacute
	resolved by eliminating	can transform	causal
	stimulus	in eczema, in the treatment and oral	forecast factors
		injury to endogenous factors	favorable
		ditch prognosis is favorable

Treatment. First of all, the factor that caused the disease should be eliminated. If the clinical picture of dermatitis is not pronounced, then, by eliminating contact with an irritant or allergen, one can limit oneself to external treatment with corticosteroid ointments, creams, and aerosols. In more severe cases, desensitizing and antihistamine drugs are prescribed in medium therapeutic doses (intravenous administration of a 30% solution of sodium thiosulfate, 10 ml daily, 5–10 injections per course, calcium gluconate, pipolfen, peritol, tavegil, claritin, zirtek, telfast, erius, etc.).

With dermatitis accompanied by the formation of blisters, the skin is washed with hydrogen peroxide or potassium permanganate solution, wiped with alcohol. The bubble covers should be cut with sterile scissors and smeared with aniline dyes. Antibacterial lotions are applied to the erosive surfaces, and after the weeping stops, water-zinc paste, Unna cream, corticosteroid external preparations (elokom, advantan, celestoderm, sinaflan, etc.).

1.2. T OXIDERMIA

Toxidermia is an acute toxic-allergic inflammation of the skin, which is the result of the action of chemicals that enter the body through the digestive and respiratory tract, parenterally or transcutaneously, and in the case of taking medications - with intravenous, intramuscular, subcutaneous, inhalation, vaginal, rectal, urethral, ​​transdural their administration and due to the absorption of drugs through the skin when applied externally. Thus, cases of toxidermia are described after rubbing a gray mercury ointment over large areas of the body in order to treat pubic pediculosis.

Toxidermia abroad is often referred to as toxic-allergic or drug exanthems.

The term toxidermia was proposed in 1905 by J. Jadassohn. Toxidermia can be caused by drugs, foods, industrial and household chemicals that have allergenic or toxic properties. Dermatologists most often deal with drug or food toxidermia.

The reason for the development of medicinal toxidermia are:

– antibiotics (in 32.4% of patients, according to Yu. F. Korolev): penicillin, erythromycin, tetracyclines;

– pyrozolone derivatives (butadione, analgin, amidopyrine) - in 12.7% of patients;

– sulfa drugs;

– sleeping pills (barbiturates, as well as corvalol, which includes luminal);

– tranquilizers, neuroleptics (reserpine, trioxazine, relanium, elenium);

– antimalarial drugs;

- vitamins (B 1, B12);

– halides (bromine- and iodine-containing mixtures);

– hormones, especially insulin, rarely prednisolone;

– anesthetics, antihistamines;

– medicinal plants (elecampane, celandine, snowdrops), bee products (propolis).

The development of medicinal toxidermia may be associated with the chemical structure of the drug, with its ability to bind to proteins, lipoproteins; be the result of improper drug administration.

The main ways in which pathological effects on the skin of drugs are carried out are:

– direct damaging effect of the drug (barbiturates cause toxic damage to the walls of blood vessels);

– cumulative action (accumulation of arsenic, bromine, iodine);

– intolerance to the drug due to a decrease in the threshold of sensitivity

to him;

– idiosyncrasy (genetic defect of some enzymatic systems); idiosyncrasy is one of the manifestations of atopy, while the body does not tolerate one or another medicinal substance or food product;

– allergic and autoimmune reactions;

– drug photosensitivity. It is based on the phototoxic, photodynamic and photoallergic properties of drugs (sulfonamides; some antibiotics, such as doxycycline; barbiturates, phenothiazines). Photosensitization occurs both with parenteral and external use of these drugs, and ultraviolet radiation acts as a resolving factor.

Food toxidermia accounts for about 12% of all toxidermia on average. The reason for their development is either the food product itself, or the substance formed during its long-term storage or cooking,

as well as preservatives, dyes or medicinal substances contained in it. A case of drug toxidermia is described after eating the meat of a pig, which was treated with penicillin 3 days before.

Among the dermatoses caused by the action of metals on the skin or mucous membranes, one should mention the toxidermia caused by metal dentures and structures used in traumatology and orthopedics for metal osteosynthesis. In these cases, allergens are chromium, nickel, molybdenum, which, undergoing partial diffusion in the body,

in the form of ions and corrosion products are washed out of the prostheses and enter

in blood. Even seminal fluid in some cases can act as an etiological factor for toxidermia, which was confirmed by a positive result of skin tests.

Speaking about the pathogenesis of toxidermia, it should be emphasized once again that the main mechanism of their development is an allergic, less often a toxic reaction, as well as the possibility of their combination in various proportions. E. V. Sokolovsky (2006) notes that "allergic damage to the skin is carried out through the mechanisms of B- and T-cell immunity through various types of allergic reactions: anaphylactic, IgE-mediated, immunocomplex, delayed-type hypersensitivity." Toxic mechanisms of toxidermia occur during the accumulation of drugs, overdose, due to the interaction of various drugs during polypharmacy.

AT drug allergy is based on the reaction antigen - an antibody in which the antigen is a drug substance. A number of drugs used by us have a protein or polypeptide basis (vaccines, therapeutic sera, gamma globulin, insulin, ACTH) and, from the point of view of classical immunology, are full-fledged antigens. They are able to induce the formation of antibodies without any additional transformation.

Along with them, in practice, we often encounter chemicals or drugs that are incomplete antigens (haptens), which only after the formation of a conjugate (compound with skin, blood or tissue proteins in the human body) acquire the properties of a full-fledged antigen.

The possibility of sensitization depends on the amount and frequency of antigen entry into the body, its antigenic activity, which is associated with the structure of the substance (for example, the presence of a benzoic ring or a chlorine atom facilitates the binding of such substances to body proteins). Contribute to sensitization also hereditary predisposition to allergic reactions, the presence of allergic diseases, such as atopic dermatitis or bronchial asthma.

Drug allergy occurs when a minimal amount of the drug enters the body, the sensitization period lasts 5-7 days. The structure of a number of medicinal substances contains common antigenic determinants that can cause the development of cross-allergic reactions. If

at the patient has common determinants among drugs and microorganisms, then toxidermia may develop, for example, with the first administration of penicillin

in a patient with mycosis of the feet (common determinant groups of an antibiotic and a pathogenic fungus). It is also known that a concomitant staphylococcal infection can be a provoking factor for toxidermia.

Studies by Belarusian dermatologists Yu. F. Korolyov and L. F. Piltienko (1978) showed that hypersensitivity to antibiotics, sulfanilamide drugs, pyrazolone derivatives and some other drugs persists for up to 10–12 years or more, often has a group and cross character.

Clinic. The manifestations of toxidermia are very diverse, and the same substance can cause different manifestations in the same person at different times, and the same clinical picture may be the result of the action of different chemicals.

Txidermia usually occurs acutely or after a few hours, or 2-3 days after exposure to the etiological factor, although the latent period can be extended up to 10-20 days. The rash may be patchy, papular, nodular, vesicular, bullous, pustular, papular-pustular, urticarial. The nature of the location of the eruptive elements, as a rule, is disseminated, symmetrical; rashes can be both on the skin and on the mucous membranes. The general condition is often disturbed.

Toxidermia is more often manifested by a monomorphic rash, although a polymorphic rash is often observed - macular-vesicular, maculopapular, etc. The St. Petersburg school of dermatologists divides all toxidermia into generalized, localized and toxic-allergic syndromes (Quincke's edema, Lyell's syndrome, multiform exudative erythema ).

Toxidermia can manifest itself:

1. Urticaria - urticarial toxidermia is very common, according to foreign authors. In Russia and in our country, this clinical form is considered as acute urticaria and is usually not included in the group of toxicoderma.

2. Spotted toxidermia. There are hyperemic, hemorrhagic and age spots. Hyperemic patches, such as day 9 erythema, are a complication of arsenic treatment. A morbilliform and scarlet-like roseolous and hemorrhagic rash may be observed in drug addicts. Toxidermia, manifested by a rash of age spots, can be caused by arsenic, bismuth, mercury, gold, silver, quinine, quinine, aspirin, antipyrine, penicillin, metacycline, methotrexate, contraceptives, oil and coal hydrocarbons.

3. Papular toxidermia, according to the type of lichenoid rashes resembling lichen planus, which may be the result of the use of quinine, chingamine, arsenic, streptomycin, tetracycline, iodine, bismuth, mercury, gold, antimony, antidiabetic sulfo drugs.

4. Knotty toxidermia, for example, acute erythema nodosum, the etiological factors of which can be sulfonamides, methotrexate, cyclophosphamide, griseofulvin, iodine, bromine, arsenic preparations, vaccines. Painful acute inflammatory nodes develop, slightly rising above the level of the skin, having a vague outline.

5. Vesicular toxidermia in which the rash consists of disseminated vesicles and microvesicles, may be limited only to damage to the palms and soles (like dyshidrosis), but sometimes vesicular erythroderma develops (as a result of the action of arsenic, bismuth, antibiotics, barbiturates, bromine, quinine), manifested by universal edematous erythema , vesiculation, copious weeping, swelling of the face and extremities, large-lamellar peeling.

6. Pustular toxidermia, which are usually associated with the action of halogen drugs - iodine, bromine, chlorine, fluorine, which are actively excreted from the body with sebum, while the rash consists of pustules or acne;

Vitamins B6, B12, isoniazid, phenobarbiturates, lithium, azathioprine can be the cause of the development of acne toxidermia.

7. Bullous toxidermia.They are very versatile:

– pemphigoid toxidermia (disseminated blisters surrounded by a hyperemic border);

– fixed toxidermia (bubbles on a limited area of ​​the skin);

– erythema multiforme exudative or erythroderma.

Bullous toxidermia occurs after taking certain antibiotics, sulfonamides, bromine, iodine, mercury, barbiturates.

8. Fixed drug-induced erythema. With it, one or more rounded bright red, large spots (2–5 cm in diameter), in the center of which bubbles may appear. The spots gradually acquire a bluish tint, rashes after the disappearance of inflammation leave persistent pigmentation of a peculiarslate browncolors. With each repeated intake of the appropriate medication, the process recurs in the same places, increasing pigmentation and the process gradually spreads to other areas of the skin. The favorite localization of fixed toxidermia is the limbs, genitals and oral mucosa. The cause of the development of fixed toxidermia is pyrazolone drugs (antipyrine, analgin, amidopyrine), sulfonamides, barbiturates, salicylates, antibiotics, quinine, iodine, arsenic, bismuth, antihistamines.

In addition, widespread toxidermia can occur as lichen planus, allergic vasculitis, lupus erythematosus.

One of the most severe forms of toxidermia is Lyell's syndrome - acute toxic epidermal necrolysis. This is a severe immunoallergic

medical, drug-induced disease. In more than 80% of cases, the disease is caused by drugs: antibiotics, sulfanilamide drugs, barbiturates (luminal, medinal), pyrazolone derivatives (butadione, amidopyrine), aspirin, pyrogenal, gamma globulin, tetanus toxoid. The development of the disease is facilitated by a hereditary predisposition to allergies, due to a genetic defect in the detoxification system of drug metabolites. As a result, drug metabolites can bind the epidermal protein and trigger an immunoallergic reaction. Lyell's syndrome is often associated with an

tigens HLA-A2, A29, B12, Dr7. The pathogenetic basis of the syndrome is delayed-type hypersensitivity, a hyperergic reaction of the Shvartsman-Sanarelli type, accompanied by the development of endogenous intoxication syndrome. At the same time, in patients with a decrease in the function of the detoxifying systems of the body, there is a pronounced violation of protein metabolism, an imbalance develops in the protease-proteolysis inhibitors system, accumulation of medium molecular weight, uremic and other proteins in the fluid media of the body and a violation of the water-salt balance. There is infiltration of the epidermis with activated T-lymphocytes and macrophages. These cells and the keratinocytes involved release pro-inflammatory cytokines that cause cell death, fever, and malaise. The growth of all these processes can lead to death, which is observed in 25-70% of cases.

Clinical picture. The disease is characterized by an acute onset several hours or 2-3 days after taking the drug. The patient develops weakness, fever up to 39–41 ºС, prostration, profuse disseminated rash on the skin of the face, trunk, extremities in the form of rich red edematous spots of a confluent nature or in the form of multiform exudative erythema. Within a few hours, in the foci of inflammation of the skin, detachment of the epidermis begins and the formation of multiple blisters with a thin, flabby tire, which is easily torn, exposing extensive painful erosions that bleed easily. The process captures huge areas and resembles a second-degree burn. If you hold a finger pressed against the inflamed skin, then the epidermis shifts sliding, wrinkling under the finger (symptom of "wet linen"). There may be a "symptom of gloves" and "symptom of socks", when the exfoliated epidermis retains the shape of the hand or foot. Nikolsky's symptom is sharply positive. In Lyell's syndrome, detachment of the epidermis occurs on an area of ​​30% of the body surface or more, and in Stevens-Johnson syndrome - on an area of ​​no more than 10% of the body surface. Lips, mucous membranes of the oral cavity are involved in the process, and mucous membranes of the pharynx, larynx, trachea, digestive tract, bladder, and urethra may also be involved. In severe cases, loss of eyebrows, hair on the head, separation of the nail plates, erosive blepharoconjunctivitis are observed. The general condition of the patients is severe and extremely severe: high body temperature, headache, prostration, drowsiness, excruciating thirst, impaired renal function, up to acute tubular necrosis. Medium molecular weight oligopeptides accumulate in the blood and the leukocyte index of intoxication increases.

There are three types of course of Lyell's syndrome: a) hyperacute course with a fatal outcome; b) acute with the addition of a toxic-infectious process and a possible lethal outcome; c) a favorable course with a decrease in hyperemia and swelling of the skin and the beginning of erosion epithelialization by the 6-10th day from the start of the patient's treatment.

Diagnosis of toxidermia. It is based on an allergic history, the clinical picture of the disease, allergological tests and immunological tests. The disappearance of the skin can serve as confirmation of the diagnosis.

rashes after cessation of the allergen and recurrence of rashes after repeated exposure to the same substance.

To confirm the etiological role of a suspected chemical, various diagnostic tests are used, including skin tests (drip, compress or scarification). More convincing results are given by provocative tests (if toxidermia occurred after oral administration of the drug, then the provocative test should be carried out by oral administration of a single minimum therapeutic dose of the suspected drug). The sample is considered positive if it provoked a recurrence of toxidermia. But provocative tests can be carried out only after the resolution of the rash. In addition to provocative, immunological tests are also used: leukocyte agglomeration reactions, leukocytolysis, inhibition of leukocyte migration, tests of basophil degranulation and lymphocyte blast transformation, monocytic test, hemolytic tests, etc.

Diagnostic criteria for drug toxidermia are the following signs:

– the appearance of clinical manifestations after taking the medicine;

– burdened by allergies personal or family history;

– good tolerability of the drug in the past;

– the presence of a latent period of sensitization;

– positive allergic tests: application, drip, scarification, intradermal, sublingual, intranasal, oral;

– positive immunological tests: passive hemagglutination test, lymphocyte agglomeration test, direct and indirect test of basophil or mast cell degranulation, neutrophil damage indicator, leukocyte migration inhibition test, etc.

differential diagnosis. Differential diagnosis of various clinical forms of toxicoderma is based on the differential diagnosis of primary elements. So, roseolous toxicoderma has to be differentiated from roseolous syphilides, pink lichen, spotted psoriasis, and cat scratch disease.

1. Provide for the termination of the etiological factor.

2. Sparing diet, plentiful drink.

3. Extracorporeal hemosorption in Lyell's syndrome (it is better to start

in the first 2 days - at least 3 sessions).

4. 2-3 sessions of plasmapheresis in Lyell's syndrome, which provides both detoxification (removal of endogenous toxins, allergens, immune complexes, sensitized lymphocytes) and acceleration of the normalization of the immune status.

5. Painkillers (morphine, omnopon, etc.).

6. Intravenous administration of detoxifying solutions for at least 1.5-2 liters per day with Lyell's syndrome under the control of kidney and heart function.

7. Enterosorbents (polyphepan, belosorb, polysorb).

8. Diuretics and laxatives in order to quickly remove an allergen or toxic substance from the body.

9. Calcium antiallergic drugs, sodium thiosulfate.

10. Antihistamines: diphenhydramine, fencarol, diazolin, tavegil, loratadine, kestin, zirtek, telfast, desloratadine and others (in medium therapeutic doses).

11. Proteolysis inhibitors (kontrykal, etc.) - 10 000–100,000 IU per day.

12. Askorutin.

13. In severe cases - glucocorticoids, start from the calculation 2–3 mg/kg of body weight, followed by dose reduction after stabilization of the process.

14. Potassium supplements for hypokalemia or lasix for hyperkalemia.

15. With penicillin toxicoderma - penicillinase.

16. With toxic reactions - 5% solution of unitiol in the form of intramuscular injections of 5–10 ml daily.

17. In order to prevent septic complications, patients with Lyell's syndrome are prescribed parenterally with broad-spectrum antibiotics, which were rarely used before in this area.

Outwardly: aerosols with corticosteroids, bactericidal and epithelial agents, aqueous solutions of aniline dyes, ointments and creams: elokom, diprogent, solcoseryl, celestoderm V, locoid, advantan, flucinar, fluorocort, etc.

Prevention. A rational scheme-plan for the treatment of a patient, taking into account the allergic anamnesis, the exclusion of polypharmacy and long-term prescription of drugs; while it is necessary to take into account the functional state of the liver, gastrointestinal tract, kidneys involved in biotransformation and excretion of drugs.

1.3. MNOFORMAL EXUDATIVE ERYTHEMA

(Erythema exudativum mutriforme)

Erythema multiforme exudative - acute infectious disease

onno-allergic or toxic-allergic nature, characterized by lesions of the skin, mucous membranes and manifested by spotty, papular

and vesiculobullous rash. The disease is characterized by a cyclical course

and tendency to relapse, mainly in spring and autumn. Dermatosis is more common in young and middle-aged people. Men get sick more often.

Etiology and pathogenesis. Depending on the etiology, two forms of exudative erythema are distinguished: infectious-allergic and toxic-allergic. In most patients, the infectious-allergic form predominates (up to 85–90%) and is classified by some authors as idiopathic. Less commonly, toxic-allergic forms (symptomatic) of the disease are diagnosed. Currently, erythema is considered as a polyetiological disease, which is based on allergic reactions in response to the action of infectious and non-infectious factors.

To infectious factors include viral (usually herpetic), bacterial (streptococcus, staphylococcus, tuberculosis, diphtheria, brucellosis, etc.), mycotic (histoplasmosis, candidiasis) and protozoal (malaria, trichomoniasis) infections.

To non-infectious factors include medicines (tetracyclines, sulfonamides, barbiturates, pyrazolone derivatives, vaccines, therapeutic sera, toxoids); chemicals used in everyday life and at work; malignant neoplasms.

Relapses of the disease provoke hypothermia, hyperinsolation, and sometimes nutritional factors.

Clinic. According to the severity of the course of the disease, mild (small, Hebra type), moderate (vesicular-bullous), severe (Stevens-Johnson syndrome) and extremely severe (Lyell's syndrome) forms are distinguished.

Erythema multiforme exudative is manifested by the appearance of spotty, papular, vesicular and bullous rashes on the skin of the extensor surface of the extremities, palms, soles, knee and elbow joints, face, genital organs, on the red border of the lips, mucous membranes of the mouth, nose, eyes, genitals.

The disease begins acutely. There is a headache, malaise, pain in the throat, muscles, joints. After 1-2 days, against this background, rashes appear on the skin and mucous membranes for several days. With a mild form, inflammatory edematous, sharply limited spots appear on the back of the hands and feet, the extensor surface of the forearms and legs, against which, in some cases, flat papules ranging in size from 1–2 cm or more are formed. The central part of the element acquires a bluish tint and sinks, while the peripheral part remains pink (bird's eye, cockade, target for shooting). In the future, blisters with serous or serous-hemorrhagic contents may appear on the surface of the rash. The opening of the latter leads to the formation of erosions and crusts. Rashes appear paroxysmal with an interval of several days. Patients experience itching and burning. One of the mechanisms for the appearance of itching is the predominance of the tone of the sympathetic division of the autonomic nervous system and developing hypoxia in the lesions, which leads to an increase in lipid peroxidation, the accumulation of its products, which provoke skin itching. Active manifestations are recorded within 8–14 days, sometimes leaving behind pigmentation.

In the moderate form, in addition to the skin, the red border of the lips, the mucous membranes of the mouth, pharynx, genitals, and the conjunctiva of the eyes are involved in the pathological process. The mucous membrane of the mouth is affected in about a third of patients. Isolated lesions of the oral mucosa are observed only in 5% of patients. When involved in the pathological process of the oral mucosa, rashes are more often localized on the lips, on the eve of the mouth, cheeks and palate. Suddenly diffuse or limited edematous erythema appears. After 1–2 days, blisters form against the background of erythema. They exist for 2-3 days, open up and in their place very painful erosions form. The latter, merging, form extensive erosive

ny areas. Erosions can be covered with a yellowish-gray coating, which, when removed, easily causes parenchymal bleeding.

At some patients experience extensive lesions of the oral mucosa,

at others - the process is limited to single painless erythematous and erythematous bullous eruptions. On the lips on the surface of erosions, bloody crusts of different thickness are formed, which greatly complicate the opening of the mouth. In case of accession of a secondary infection, the crusts acquire a dirty gray color.

A common form of damage to the oral mucosa is accompanied by severe soreness, salivation, difficulty in eating and difficulty in speech.

After 10–15 days, skin rashes begin to resolve and disappear by 15–25 days. On the oral mucosa, the resolution of rashes occurs within 4-6 weeks. In place of erythematous-papular elements, when they resolve, hyperpigmentation remains.

The toxic-allergic form of exudative erythema multiforme is not characterized by seasonality of relapses, it is not always preceded by general symptoms

and often the process is fixed in nature with frequent localization on the oral mucosa.

A severe form of erythema multiforme exudative (Stevens-Johnson syndrome, described in 1922) begins acutely with fever (39-40.5 ºС), headache, musculoskeletal pain, soreness of the oral mucosa

and pharynx, may be accompanied by the development of pneumonia, nephritis, diarrhea, otitis media, etc. Skin, mucous membranes of the oral cavity, genitals, anus, eyes are affected. Extensive blisters appear on the lips, mucous membrane of the mouth (cheeks, tongue), followed by the formation of painful erosions, which are covered with massive hemorrhagic crusts, which makes it difficult to eat. Eye damage is characteristic in the form of severe catarrhal or purulent conjunctivitis, against which vesicles may appear.

Often develop corneal ulceration, uveitis, panophthalmitis, leading to loss of vision. Damage to the mucous membranes of the genitals in men leads to impaired urination with possible involvement in the process of the bladder.

Skin lesions in the form of maculopapular rashes or blisters, less often - pustules, multiple and extensive, often with the development of paronychia, occur against a background of a serious general condition. Without treatment, mortality in Stevens-Johnson syndrome reaches 5-15%.

Extremely severe form (Lyell's syndrome) - see Ch. "Toxidermy". Histopathology. In the initial stage of the disease, edema develops in the upper

part of the dermis, there is an expansion of blood vessels with lymphohistiocytic infiltration around the vessels and in the area of ​​the basement membrane. Later - extravasation of erythrocytes. Characteristic changes include vacuolar degeneration in the deep layers of the epidermis and necrosis of epidermal cells. Acantholysis is absent. Pathological structure of mucosal lesions

membranes is similar to changes in the skin, but with a greater severity of degenerative processes in the epithelium.

Diagnosis. It is based on an acute onset, polymorphism of eruptive elements, the symmetry of their localization, and a tendency to form rings. Differential diagnosis should be carried out with other forms of drug toxidermia, pink lichen, pemphigus, pemphigoid, Dühring's dermatosis.

Treatment. The nature of the therapy depends on the severity of the disease. In a mild form, antihistamines are prescribed (suprastin, fenkarol, tavegil, amertil, claritin, erius, etc.), hyposensitizing (calcium, sodium thiosulfate) agents, ascorutin, heavy drinking, enterosorbents (activated charcoal, polyphepan, belosorb, etc.)

In the moderate form of exudative erythema multiforme, in addition to the above therapy, prednisolone is prescribed at a daily dose of 30–60 mg or another corticosteroid at an equivalent dose for 4–6 days, followed by a gradual decrease in the dose of the drug over 2–4 weeks. In addition, ethacridine 0.05 g three times a day for 10–15 days is recommended. Detoxification therapy is shown (saline solutions, microdesis, polyglucin, reopoliglyukin, etc., heavy drinking, diuretics). If the exacerbation of the disease is associated with a herpes infection, acyclovir preparations are prescribed, if with a bacterial one - antibiotics.

Patients with Stevens-Johnson syndrome are recommended: drinking plenty of fluids, diuretics, a sparing diet, antihistamines and hyposensitizing drugs, ascorutin, intravenous drip neorondex, microdez, polyglucin, reopoliglyukin, saline solutions of 200–400 ml, daily or every other day, total 3 -5 infusions, daily dose of prednisolone (0.8–1.2 mg/kg) 50–90 mg or equivalent dose of another corticosteroid for 10–15 days until a pronounced therapeutic effect is achieved, followed by a gradual decrease in the drug until it is completely discontinued.

External therapy is carried out taking into account the nature of the skin lesion. Lotions are recommended for erosive-weeping areas (2% solution of boric acid, furacilin solution 1:5000, etc.), treatment with anti-inflammatory aerosols (levomekol), fucarcin.

Spotty-papular manifestations of the disease on the skin can be lubricated with calendula ointment, dermoref, 5–10% dermatol ointment, creams and ointments containing glucocorticoids. In case of damage to the oral mucosa, it is recommended to rinse with a solution of potassium permanganate 1: 8000, a 2% solution of boric acid, a 2–3% solution of tannin, a decoction of chamomile, a diluted tincture of propolis, calendula, lubrication of the affected mucosa with sea buckthorn oil, rose hips, an oil solution vitamin A, dental paste "Solko". For the treatment of lesions on the lips, drugs recommended for the treatment of the oral mucosa can be used.

When secondary purulent complications appear, broad-spectrum antibiotics are prescribed.

Prevention. In cases of an infectious-allergic nature of the disease: sanitation of foci of infection and other concomitant pathologies, an increase in nonspecific resistance (multivitamins, biostimulants, autohemotherapy, ultraviolet irradiation, hardening). In the toxic-allergic form of exudative erythema multiforme, it is necessary to identify the allergen that causes the disease, explain to the patient the danger of repeated use of the medication, indicating it on the patient's identification bracelet.

1.4. ECZEMA

Eczema is a chronic relapsing skin disease characterized by evolutionary polymorphism of morphological elements, weeping and itching.

Eczema is a widespread dermatosis, accounting for up to 40% of all skin diseases according to some sources. In recent years, the number of people suffering from this disease has increased significantly due to an increase in the number of various environmental, domestic and industrial negative factors affecting the human body. Eczema occurs in all age groups, but affects mainly people of the most able-bodied age, has a tendency to chronic relapsing course and is a common cause of temporary disability. Men are more often affected. The disease can affect any area of ​​the skin, up to the development of erythroderma. The predominant involvement of certain areas of the skin in the eczematous process depends on the form of the disease. The frequent development of foci of eczema against the background of wounds, trophic ulcers, vascular pathology is a contraindication to surgical treatment, which leads to untimely provision of specialized care, the development of complications and disability.

The name of this disease comes from the Greek "eczeo" - to boil, and is explained by the characteristic rapid appearance and opening of bubbles with the formation of weeping erosions. The term "eczema" has been in use since the 2nd century BC. BC e. to refer to any acute dermatoses, until in the first half of the 19th century eczema was identified by R. Willan (1808) as a separate nosological form.

Etiology and pathogenesis. Despite a significant number of studies, the pathogenesis of this dermatosis has not been studied enough, many issues are debatable, and the data of different authors are often contradictory. At various stages of the development of the doctrine of eczema, special importance in the etiology and pathogenesis of the disease was given to the central and peripheral nervous system (neurogenic theory), the role of the endocrine glands, microbial contamination of the skin, the allergic state of the body (allergic theory), and hereditary factors. Currently, most authors consider eczema to be a polyetiological disease with a complex pathogenesis, developing as a result of the complex effect of genetic predisposition, as well as neuroallergic, endocrine, metabolic and exogenous diseases.

ny factors. These elements of pathogenesis are to varying degrees characteristic of individual forms of the eczematous process, but there is no information about the leading significance of any of them. The longer and more severe the disease is, the greater the number of organs and systems involved in the pathological process.

In the pathogenesis of eczema, the following are important: a genetic predisposition that determines the dysfunction of the immune system, disturbances in the activity of the central and peripheral nervous system, endocrine regulation, as well as prolonged exposure to resolving exogenous and endogenous factors that cause sensitization of the body. Developing immunodeficiency in cellular, humoral and phagocytic links is expressed in their qualitative and quantitative insufficiency, imbalance of regulatory subpopulations, which determines the weakness of the immune response. The failure of protective mechanisms contributes to the formation of chronic infectious foci, intestinal dysbacteriosis, and the occurrence of relapses of the disease. There is a change in the composition of the microflora of the skin, both in the lesions and apparently healthy, with a predominance of Staphylococcus aureus and gram-negative microorganisms; this significantly increases the density of microbial contamination. Exposure to exogenous xenobiotics (chemical and biological), endogenous allergens (microbial antigens from foci of chronic infection, endotoxins) against the background of an inadequately weak response of the immune system leads to their persistence, sensitization of the body to both them and to the protein components of one's own skin, causes pathological immune responses . Allergic activity at the onset of the disease is sometimes monovalent - hypersensitivity to one causative factor develops, with the further course of dermatosis and "re-irritation" of the immune system, the sick organism qualitatively and quantitatively begins to respond to many irritants and allergens, which indicates the development of polyvalent sensitization characteristic of eczema. At the same time, an extensive allergic inflammation of the skin develops according to a mixed type (combining delayed, immediate types of hypersensitivity, as well as cytotoxic and immunocomplex mechanisms). The consequence is a pathological intensification of peroxidation processes with the destruction of biological membranes, an increase in the activity of lysosomal enzymes in the blood and an imbalance in the protease–proteolysis inhibitors system, and destruction of one's own tissues. In addition, patients have changes in the functions of internal organs (hepatobiliary system, gastrointestinal tract, kidneys), metabolism (carbohydrate, protein, fat), metabolic disorders of electrolytes, amino acids, biogenic amines, a number of glycolytic enzymes. In parallel, a violation of the regulation of vascular tone develops in combination with an increase in the coagulation activity of the blood, which leads to changes in hemorheological parameters, while microcirculation suffers, edema and hypoxia of the affected tissues occur. All of these factors lead to a shift in metabolism towards catabolic reactions. In the liquid media of the body in unusually high concentrations, a large number of intermediate and final metabolic products, biologically active substances,

compounds formed as a result of tissue destruction and enhanced proteolysis of plasma proteins, products of incomplete digestion of food absorbed from the gastrointestinal tract due to an increase in the permeability of the intestinal mucosa, microbial toxins, lipid and protein hydroperoxides, etc., which leads to the development of endogenous intoxication,

in in turn, aggravating all the pathogenetic links of the eczematous process.

Eczema classification. Generally accepted unified classification of eczema

in does not currently exist. In practice, however, the clinical classification of M. M. Zheltakov (1964) is most often used, according to which four main types of eczema are distinguished: true (which also includes pruriginous, dyshidrotic, tylotic, intertriginous), microbial (including paratraumatic, nummular, varicose and mycotic), seborrheic and professional. Children's eczema, which develops in infancy against the background of exudative-catarrhal diathesis and is the initial clinical manifestation of atopy, is considered separately. In addition, along the course, each of the eczemas is divided into acute, subacute and chronic (LN Mashkilleyson, 1965).

According to the International Classification of Diseases X revision (ICD-X),

in which is based on pathological changes, the terms "eczema" and "dermatitis" are used interchangeably synonyms. In this case, true eczema corresponds to endogenous (allergic) - L20.8, dyshidrotic - dyshidrosis L30.1, tylotic - hypertrophic eczema L28.0, intertriginous is designated L30.4. AT ICD-X does not distinguish microbial eczema separately, while the paratraumatic form corresponds to infectious dermatitis or pustular eczema (L30.3), nummular is designated by the code L30.0, mycotic is closest to candida and dermatophytosis skin autosensitization (L30.2), varicose or hypostatic eczema (I83.1-I83.2) is considered in the section "Vascular diseases" as a complication of varicose veins. Seborrheic eczema and seborrheic dermatitis in ICD-X are the same disease with the code L21.9, the same applies to occupational eczema and dermatitis (L25.9). Children's eczema is coded L20.8, children's intertriginous or seborrheic - L21.1, herpetiform - B00.0. In addition, eczema of the external ear (H60.5) is considered separately in the ICD-X, which is classified as a disease of the ENT organs.

Clinical picture of eczema. The onset of eczema varies. Sometimes its manifestations are preceded by infectious diseases, neuropsychic stress, damage to the skin, contact with irritating and sensitizing substances, and medication. Often the patient cannot associate the occurrence of eczema with any causes.

Acute eczema develops suddenly, begins with prodromal phenomena (weakness, chills, headache, etc.) or occurs without them. The skin of the sick

in this stage is characterized by increased sensitivity to various factors, responding to a wide variety of stimuli with an increase in the inflammatory reaction, subjective sensations and the appearance of fresh rashes. Character-

ny intensity of inflammatory phenomena and a rapid change in the stages of the eczematous process. The disease usually begins with the appearance of bright erythema.

and sharp puffiness(edematous-erythematous stage), against which small papules appear (papular stage), and after them or simultaneously - papulovesicles and vesicles (vesicular stage). Perhaps the accession of a secondary infection and the formation of not vesicles, but pustules. Cavitary elements quickly open up and turn into weeping erosions of various sizes, the most typical for eczema are “serous wells” - point erosions that separate transparent exudate with small droplets (weeping stage). As a rule, in acute eczema, there is abundant weeping and pronounced subjective sensations in the form of itching, burning and pain, a feeling of tightness of the skin. Itching results in multiple excoriations, neurotic disorders, sleep disturbances up to insomnia. Vesicles, pustules and discharge of erosion can shrink with the formation of serous or purulent crusts and microcrusts (crust stage), which are rejected with the transition to the peeling stage

and the formation of secondary dyschromia, without leaving behind scars and atrophy. The evolution of morphological elements in eczema is clearly presented

in the form of the "Kreibich triangle" (Fig. 1).

Rice. one . Kreibich triangle

Clinical manifestations of eczema are characterized by clear polymorphism (usually evolutionary) and variegation of rashes, when edema, erythema, nodules, vesicles, weeping erosions, crusts and peeling are simultaneously present in one lesion. This is due to the fact that the eczematous process in its course can stop at a certain stage and undergo regression, or new rashes appear at any time, not always consistently going through all stages of development.

The disease may initially acquire a subacute or chronic course, or a gradual transition of acute eczema to chronic is possible, through subacute stage. The subacute course of dermatosis is manifested by a weeping or dry process with an increase in infiltration of the affected areas of the skin and an increase in the skin pattern according to the type of lichenification. On the surface of moderately infiltrated, slightly hyperemic foci, there is a small amount of small erosions, crusts and microcrusts, the process is accompanied by peeling, which can suddenly turn into weeping.

If the hallmarks of acute eczema are inflammatory edema, the formation of erosions and exudation, then in the chronic clinic, pronounced infiltration predominates - an inflammatory thickening of the skin. In addition, signs of chronic eczema are moderate congestive hyperemia, lichenification, peeling and severe itching. Edema, erosion

and there is no weeping, polymorphism is not expressed, there is no rapid change in the stages of the process. With a long course of eczema, hyperkeratotic layers with cracks sometimes appear on the palms and soles, and the nails are deformed. Chronic eczema usually takes a cyclic course, lasting for years.

and decades. At the same time, periods of remission, when the patient's skin becomes clear, or improvements can be replaced by exacerbations at unequal intervals. Subacute or chronic eczema under certain conditions

in any moment can become aggravated, acquiring an acute clinical picture. In this case, against the background of thickening of the skin and its peeling, edema, bright hyperemia, vesicles and weeping appear, itching increases and new rashes appear on healthy skin.

The staging of the course described above is characteristic to varying degrees for all forms of eczema, but there are also specific features for each.

True eczema is most fully characterized by the mentioned signs. Clinical symptoms of true eczema are manifested by pronounced polymorphism (true and false) and variegation of rashes, a clear change in the stages of the eczematous process. Rashes are symmetrical, more often localized on the skin of the upper extremities, less often - on the face, lower extremities and torso. The shape of the lesions is usually irregular, their borders are not sharp, they smoothly pass into unchanged skin. The eczematous process can occupy a limited area, the formation of small foci with diffuse lesions of individual anatomical regions (limbs, torso), their continuous lesion, disseminated involvement of almost the entire skin, the development of eczematous erythroderma is possible. Characteristic is the alternation of the affected areas of the skin with the unaffected ones, the grouping in the immediate vicinity of large rashes of small foci according to the type of "archipelago of islands". Patients are concerned about itching of varying intensity. Dry patches may occur

and peeling of the skin, cracks in the stratum corneum. With a long chronic course of eczema, calloused hyperkeratotic formations with cracks sometimes appear on the palms and soles. Often, the course of eczema is complicated by the addition of a pyogenic infection: pustules and purulent crusts appear.

To special varieties of true eczema include pruriginous, dyshidrotic, tylotic, intertriginous, peculiar clinical

manifestations of which are associated with the predominant localization of the process, as well as the possible cause that caused the disease.

Pruriginous eczema is characteristic of childhood, manifested by rashes of small (with millet grain) nodules with a bubble at the top, which form on a compacted base, do not open and do not form erosions. Lesions are located on the skin of the face, around large joints, in the inguinal region, on the extensor surfaces of the limbs. Ill-

vanie proceeds chronically, often recurs. Characterized by paroxysmal itching, severe neurotic reactions, accompanied by sleep disturbance. Due to scratching, the nodules are covered with hemorrhagic microcrusts. With a long course, infiltration of the foci occurs, the skin in the affected areas coarsens, lichenizes, acquires a grayish tint, becomes dry and rough. Remission of the disease is observed in summer, and relapse - in winter. It occupies an intermediate position between true eczema and pruritus.

Dyshidrotic the form may be an independent disease or part of the lesions in other varieties of eczema. The pathological process is localized on the palms, soles and lateral surfaces of the fingers, characterized by the formation against the background of edema and hyperemia of small (pinhead-sized) blisters that are dense to the touch. Less common are large bubbles, the size of a pea. The elements of the rash tend to merge, multi-chamber vesicles appear, lesions of various sizes and shapes are formed. Located in the epidermis, the bubbles shine through the thick stratum corneum, resembling grains of cooked rice. Patients are often disturbed by severe itching. It is possible to attach a secondary infection with the formation of pustules. Bubbles and pustules can open, turning into scalloped erosions with a border of exfoliated epidermis along the periphery, or dry out, forming flat yellowish crusts. It is characterized by a long course and resistance to treatment.

Tylotic eczema (hyperkeratotic, horny) can also develop on the palms and soles. This form of the disease proceeds with the greatest infiltration and the appearance of powerful hyperkeratotic layers. It is characterized by deep painful cracks and itching, bubbles may not form. The clinical picture is very similar to mycosis and psoriasis. Sometimes tylotic eczema develops in women during menopause.

For intertriginous eczema is characterized by localization in the folds of the skin (armpits, groin, under the mammary glands, between the fingers, etc.) The lesions have clear boundaries, bright red with a purple tint, a shiny, moist surface without scales and crusts. Characterized by profuse weeping, the formation of deep painful cracks. Itching is moderate. The process can suddenly spread beyond the folds with the development of the clinical picture of acute generalized eczema.

Microbial eczema. The microbial form of eczema is a kind of allergic reaction, a consequence of monovalent sensitization to microorganisms, pathogenic fungi or their metabolic products in the foci of acute or chronic infection of the skin, ENT organs, dental area, internal organs (pyoderma, infected wounds, pharyngitis and tonsillitis, pyelonephritis, cholecystitis, etc.). These reasons determine the presence, along with the main features of the eczematous process, some features of the clinical picture of microbial eczema.

Most often found paratraumatic(near-annual) form of the disease, which begins as an asymmetric process on the skin of the legs, the back of the hands, the scalp - around the wound surface, the focus of pyoderma

mii, fistulous tract, bedsores, trophic ulcers, burns, etc. Initially, small bubbles appear in the area of ​​​​the infectious focus, then one or more typical lesions form with clear boundaries, scalloped outlines and a "collar" of the exfoliating stratum corneum of the epidermis along the periphery, characterized by a tendency to slow peripheral growth. The focus of microbial eczema is a moderately itchy area of ​​acute inflammatory erythema with exudative papules, microvesicles, pustules, weeping erosions, massive accumulations of loose greenish-yellow serous-purulent and bloody crusts on the surface. After removing the latter, a weeping surface of a red or stagnant red color is exposed, which bleeds easily. Sometimes there is also a point weeping characteristic of eczema (“serous wells”). On the periphery of the main focus, screenings are often formed in the form of papulo-pustules, pustules and conflicts due to secondary infection with discharge containing pyococci. The main signs of microbial eczema are characteristic of all its forms, but each has distinctive features.

With nummular (coin-shaped) eczema, which is usually associated with foci of infection on the skin (without the formation of a wound defect) or in internal organs, multiple or single, slightly elevated above the skin level, sharply limited edematous infiltrated plaques of a more or less rounded shape, regular outlines, appear, with a diameter of 1–5 cm or more. Foci are usually localized on the extremities, less often on the trunk and face. Their surface is characterized by the appearance of erythema, exudative papules and pronounced drip weeping, serous-purulent crusts and scales. The disease also tends to disseminate the process, is prone to relapse and is resistant to therapy. In subacute and chronic course, when peeling is expressed, nummular eczema in the clinic resembles psoriasis.

emergence varicose eczema promotes varicose symptom complex with impaired hemodynamics and microcirculation in the lower extremities. Lesions are localized on the shins and feet in the area of ​​varicose veins, around the circumference of varicose ulcers, against the background of hemosiderin deposits and areas of skin sclerosis. The development of the disease is favored by injuries, increased sensitivity of the skin to drugs used to treat varicose ulcers, and maceration of the skin when bandages are applied. Polymorphism of elements, sharp, clear boundaries of foci, moderate itching are characteristic, which makes varicose eczema clinically similar to nummular and paratraumatic.

If the rashes characteristic of microbial eczema are the result of sensitization to pathogenic fungi, the patient is diagnosed mycotic eczema. Lesions characteristic of other forms of microbial eczema and the dyshidrotic form of the disease develop against the background of mycosis and onychomycosis of the hands, feet or smooth skin, localized mainly in the limbs, with frequent lesions of the hands and feet.

Often the disease combines signs of several forms and develops as a result of a complex of causes (for example, against the background of infection

varicose ulcer in a patient with mycosis and onychomycosis of the feet). With the further development of any form of microbial eczema, the process becomes disseminated due to secondary allergic rashes and acquires a symmetrical character. If the infectious focus persists, microbial eczema is characterized by a torpid course with the gradual development of polyvalent sensitization of the body and the transition of the disease to the true form with the formation of a large number of rapidly opening microvesicles and point erosions with drip weeping. Periodic exacerbations of the disease lead to increased itching. When the focus of chronic infection is eliminated, the eczematous process subsides.

seborrheic eczema develops in persons with seborrheic status and is localized in places richest in sebaceous glands: on the skin of the scalp, face, chest, in the interscapular region, behind the ear folds. Lesions in the form of rounded yellowish-pink erythematous spots with clear boundaries and even contours, covered with greasy yellowish-gray scales and loose crusts. Characterized by dry skin, moderate infiltration, vesiculation and weeping are present only in rare cases - with irritation, irrational treatment, secondary infection. Abundant layered yellowish crusts form on the scalp

and scales, the hair on the affected areas is shiny, sometimes stuck together with the formation of a tangle. In the folds of the skin, edema, hyperemia is often observed

and thickening of the skin, cracks, weeping may appear. Patients complain of intense itching, which may precede clinical manifestations. Rashes can exist for a long time without changing

and without causing subjective sensations. Perhaps the accession of a secondary infection, rapid dissemination of the process.

Occupational eczema, which is discussed in more detail in the section "Occupational skin diseases", initially develops as a result of monovalent sensitization to any irritant that a person comes into contact with in the course of performing professional duties. The diagnosis is established only when the professional nature of the disease is confirmed and the corresponding industrial allergen is found. Dermatosis begins with manifestations of contact allergic dermatitis in the area of ​​exposure to a professional factor, at this stage the rashes are limited. To cure, it is enough to eliminate the corresponding irritant and prevent repeated contact with it. In the case of prolonged exposure to profallergen, an immune imbalance occurs with the development of polyvalent sensitization. At the same time, the clinical picture of the disease is similar to that of true or, in the case of infection, microbial eczema, with a chronic relapsing course and less pronounced polymorphism of the rash.

Children's eczema. It has been established that eczema in children most often develops against the background of exudative diathesis associated with a congenital anomaly of the constitution, characterized by a hereditary predisposition to allergic diseases, which is inherited in an autosomal dominant manner and is associated with anomalies.

HLA histocompatibility tigens. The process is etiologically associated with atopy, a genetically determined increased IgE-dependent reaction associated with a deficiency of cellular immunity, mainly suppressor T-lymphocytes. A variety of environmental factors, both in the process of intrauterine and extrauterine development of the child, have a great influence. Significant importance is attached to intrauterine fetal sensitization not only to various food products, but also to certain medicines and cosmetics used by the mother during pregnancy. Many mothers have an unfavorable course of pregnancy, complication of infectious diseases, nervous experiences and stress, poor nutrition during pregnancy. In the postnatal period for an infant, allergens that come with food are of the greatest importance. The protein in the mother's diet can pass into breast milk and sensitize the naturally fed baby. Early introduction of complementary foods or complementary foods, which include potential allergens, is a resolving factor and is accompanied by the manifestation of clinical signs of dermatosis. In most sick children, it is possible to establish certain disorders in the nature of nutrition (artificial feeding from the first days or in the first months). With a sufficiently long course of the disease, children develop polyvalent sensitization and autoallergy. An important role in the development of childhood eczema is played by a violation of the function of the digestive organs in children, helminthic invasions.

Children with eczema make up 30–70% of all children with dermatoses. Eczema in children is manifested by clinical signs of a true, seborrheic or microbial form of the disease, which can be combined in various combinations in different parts of the skin. For the clinical picture of true childhood eczema, the onset of the disease is most typical in the 3rd month of life; in some children, eczema may occur as early as 2-3 weeks after birth. Initially, the rash is localized on the face, with the exception, as a rule, of the nasolabial triangle. First of all, there is redness and swelling of the skin of the face, an abundant amount of microvesicles, weeping in the form of “wells”, followed by the formation of yellow-brown crusts and peeling, there may be papules, i.e. there is a polymorphism of rashes. Subsequently, the scalp, auricles and neck may be affected, a symmetrical arrangement of foci is characteristic. In some children, the process becomes more widespread - eczematous lesions appear on the trunk, arms, legs; in some cases, the first rashes may appear on the limbs. As a rule, after some "lull" comes a relapse of the disease. In some children, at the onset of the disease or periodically during exacerbations of the skin process, symptoms from the gastrointestinal tract appear in the form of vomiting, abdominal pain due to colon spasm and diarrhea. There are indications of the possibility of severe itching in the area of ​​the oral mucosa and anus.

Clinical manifestations of the seborrheic form of childhood eczema develop on the 2–3rd week of life in hypotrophic children on the skin of the scalp.

you, forehead, cheeks, chin, on the ears, behind the ear and neck folds in the form of foci of dim hyperemia, unexpressed infiltration, on the surface of which excoriations and grayish-yellow crusts are observed. Microvesiculation and weeping are not typical, with localization in the folds, as a rule, cracks and maceration of the epidermis are formed. In the future, the entire skin may be involved.

Clinical manifestations of microbial (paratraumatic, nummular) eczema in children correspond to those in adults

In most patients, the disease is accompanied by a persistent relapsing course, intense itching, insomnia, anxiety, increased nervous excitability, inadequate strong reactions to the slightest irritation, and other disorders of the nervous system. It is known that children with eczema are very sensitive to cold, which often exacerbates the course of the process in spring and autumn-winter.

Children's eczema usually disappears by the end of the 2-3rd year of life, but then often such patients experience diffuse atopic neurodermatitis, that is, eczema transforms into neurodermatitis. According to the results of a study by various authors, childhood eczema and atopic neurodermatitis are two stages of the same pathological process.

Kaposi's eczema herpetiformis (pustulosis varioliformis) was first described in 1887 by the Hungarian dermatologist Kaposi as a severe complication of eczema or neurodermatitis, predominantly in young children. It has been proven that the main cause of the disease is the infection of a child with eczema or neurodermatitis with the herpes simplex virus, which usually occurs between the ages of 6 months and 2 years, when antibodies to this virus transmitted in utero from the mother disappear. Therefore, prevention of contact of such patients with persons suffering from herpes simplex is of great importance.

The disease develops acutely, with a sudden rise in temperature to 39–40 ºС, a sharp deterioration in the general condition and the development of symptoms of intoxication. Often the onset of eczema herpetiformis is accompanied by increased swelling and weeping in the area of ​​primary eczematous lesions. Typical rashes appear on the skin in the form of grouped vesicles and pustules, ranging in size from a pinhead to a pea with a characteristic umbilical depression in the center, mainly localized on the face, scalp, neck, less often on the limbs and torso. In the process of evolution of vesicles and pustules, most patients develop rounded hemorrhagic crusts, which are considered pathognomonic for Kaposi's herpetiform eczema; when such crusts are removed, bleeding of the affected skin easily occurs and, as a result of the formation of deep bleeding cracks and erosions, the face acquires a “mask-like” appearance. Along with changes in the skin, children may develop aphthous stomatitis, conjunctivitis, keratitis, lesions of the genital mucosa, and regional lymph nodes increase. Maybe

herpetic lesions of internal organs and the central nervous system. A secondary infection often accompanies with the development of pyoderma, purulent otitis media, bronchitis and pneumonia, sepsis, patients have an increased ESR and a decrease in the number of eosinophils in the blood. With the development of Kaposi's eczema in patients, as a rule, itching disappears, and the manifestations of eczema seem to fade away, however, with an improvement in the general condition, normalization of temperature and resolution of herpetiform rashes, itching intensifies, and the manifestations of eczema become more intense than before the onset of complications. In place of the former vesicular-pustular elements, small scars may remain. Mortality in this disease is, according to different authors, from 1 to 20%. Kaposi's eczema herpetiformis can also occur in adults, complicating the course of chronic skin diseases - atopic dermatitis, ichthyosis, eczema, pemphigus vulgaris.

Histopathology. For the acute period of eczema, foci of spongiosis in the germ layer of the epidermis are most characteristic. Spongiosis is an edema of a predominantly spinous layer, with stretching and rupture of intercellular bridges, the formation directly under the stratum corneum of small, often multi-chamber cavities filled with serous fluid, which, when merged, form vesicles. In the stratum corneum, parakeratosis is determined. In the dermis, edema of the papillary layer develops, swelling of collagen fibers, dilation of the vessels of the papillary and subpapillary networks and the formation of a lymphocytic-histiocytic infiltrate around them, which in microbial eczema contains polymorphonuclear leukocytes.

Chronic eczema is characterized by acanthosis, parakeratosis, a more pronounced cellular infiltrate of the dermis.

With seborrheic eczema, moderate thickening of the epidermis, parakeratosis, significant acanthosis, absence of a granular layer, mild vacuolar degeneration are noted, while spongiosis is not pronounced. In the dermis, a slight perivascular infiltrate of lymphocytes and neutrophils is formed.

Diagnosis and differential diagnosis. The diagnosis of eczema is made on the basis of a characteristic clinical picture.

Differential diagnosis is carried out depending on the form of eczema. So, true eczema must be distinguished from atopic neurodermatitis, Dühring's dermatosis, psoriasis, toxidermia, pemphigus, mycosis of the hands and feet, and pruritus. For example, atopic neurodermatitis may have a great clinical similarity with subacute and chronic eczema, when lichenification is present among the manifestations, especially in the case of a secondary infection or the development of its eczematoid form. However, in the case of neurodermatitis, a long (from early childhood) course of the disease is characteristic, which develops against the background of diathesis or transforms from childhood eczema. The exacerbation is associated with non-compliance with the diet, often there is a burdened hereditary history. Eczema, unlike neurodermatitis, is characterized by punctate weeping that occurs spontaneously, without scratching. Dermographism in atopic neurodermatitis is usually white, in eczema it is pink. With neurodermatitis, there is always a pronounced lichenification of foci,

typical localization - face, back of the neck, flexion surface of the wrist, elbow, knee joints.

Microbial eczema is distinguished from allergic contact dermatitis, pyoderma, psoriasis, limited neurodermatitis, erysipelas, mycosis of smooth skin, vasculitis, scabies; seborrheic eczema - from psoriasis, seborrheic dermatitis, mycosis of smooth skin, the initial stage of skin lymphoma. So, with nummular eczema of subacute and chronic course, when the foci are infiltrated, clearly delimited from the surrounding healthy skin, their surface is flaky, then it is necessary to carefully differentiate with nummular or plaque psoriasis. Coin-shaped eczema is characterized by the presence of microerosions and microcrusts on the surface of the foci, drip weeping is present during examination or there are indications of it in the anamnesis. As a rule, the disease develops against the background of purulent inflammation on the skin or in the internal organs. With psoriasis, there is a seasonality of the course, the scalp, extensor surfaces of the limbs, the sacrum, and the trunk are affected; for eczema there is no attachment to any localization. Scales from the surface of psoriatic plaques are easily removed, scraping the surface of the papules leads to the appearance of the psoriatic triad, the appearance of new rashes at the sites of mechanical irritation is characteristic. In addition, the ingress of water on the foci of eczema provokes an exacerbation of the disease, patients with psoriasis normally tolerate this irritant. Children's eczema is differentiated from allergic contact dermatitis, enteropathic acrodermatitis, impetigo, mycosis of smooth skin; eczema herpetiformis - from primary herpes, chickenpox, erythema multiforme exudative, pyoderma. It is especially difficult to conduct differential diagnosis in subacute and chronic dermatosis.

Treatment . Due to the polyetiology and complex pathogenesis of eczema, treatment should be complex, it should be carried out differentially, depending on the form and stage of the disease, the clinical course of the skin process, the age of patients and their tolerance to drugs. It is necessary to take into account the pathology of internal organs, endocrine and nervous systems, metabolic disorders identified in patients. It is undesirable to simultaneously prescribe a large number of drugs, since there is a high probability of developing polyvalent drug sensitization, which can aggravate the course of the disease.

A significant role in the treatment of eczema is played by a hypoallergenic diet (normal content of proteins and fats, restriction of salt, easily digestible carbohydrates, spicy foods, smoked and fried foods, chocolate, eggs, nuts, most fruits, etc.), exclusion of alcohol and smoking. Exposure to suspected allergens should be eliminated. An important point in the treatment of microbial eczema is the sanitation of foci of chronic infection on the skin and in internal organs, with professional treatment - the elimination of the causative factor, a change of job. It is necessary to prevent physical and chemical irritation of the foci, especially in the acute stage, including with water when washing.

To stop allergic reactions and reduce sensitization, the appointment of non-specific hyposensitizers is indicated: calcium preparations (10% calcium chloride solution intravenously, 10% calcium gluconate solution intramuscularly), 30% sodium thiosulfate solution. You can prescribe antihistamines - diphenhydramine, suprastin, tavegil, diazolin, loratadine (claritin), desloratadine (erius), phencarol, telfast, inhibitors of mast cell degranulation (ketotifen). The use of systemic corticosteroid hormones (prednisolone, dexamethasone, betamethasone, etc.) for eczema is undesirable due to their immunosuppressive effect, but it is possible in severe, generalized forms, in the acute stage with the ineffectiveness of other methods of treatment.

With a long course of eczema, in the subacute and chronic stages, an individualized appointment of immunomodulators is possible, taking into account the parameters of the immunogram.

In order to correct endogenous intoxication, detoxifying blood substitutes (rheopolyglucin, microdez, neorondex, etc.), as well as enterosorbents (activated carbon, belosorb, etc.), complexing drugs (unithiol) are used.

To improve microcirculation in old foci of eczema, the use of vasodilators (xanthinol nicotinate, teonikol, cinnarizine) and antiplatelet agents (pentoxifylline) is recommended.

The use of antioxidant complexes (aevit, antioxycaps), vitamins A, E, C, P, group B is shown.

To normalize the functions of the central and autonomic nervous system, sedatives are prescribed (sodium bromide solution, preparations of valerian, motherwort, Markov's mixture, novo-passitis, etc.). With more severe disorders of the neuropsychic status, manifested by agitation, insomnia, emotional stress and irritability, it is possible to use tranquilizers and neuroleptics (diazepam, relanium, alprazolam, etc.) after consulting a neurologist or psychotherapist.

When eczema is combined with impaired function of the digestive organs, preparations containing pancreatic enzymes (pancreatin, festal, panzinorm, creon), lacto- and bifidobacteria (bifilife, bifikol, lactobacterin, bifidumbacterin), hepatoprotectors (Essentiale) are shown.

AT in the case of secondary infection and microbial eczema, antibacterial and antifungal drugs from different groups are used, taking into account the sensitivity of the flora. With microbial eczema, in addition, directed sanitation of the primary focus of chronic infection is necessary.

AT acute stage of eczema, with severe weeping and edematous syndrome, diuretics are used (furosemide, lasix, hypothiazide).

For the treatment of eczema, methods of physiotherapy are widely used, mainly for subacute and chronic course: transcutaneous laser, ultraviolet irradiation, acupuncture, inductothermy and UHF of the adrenal glands

and sympathetic nodes, baths with peat oxidate, electrophoresis and phonophoresis of drugs, etc.

The most important role in the treatment of eczema is played by local treatment, the choice of which is determined by the stage and clinical form of the process. In the acute stage, with abundant oozing, it is recommended to use cooling lotions with anti-inflammatory, antibacterial, astringent solutions (2% boric acid solution, 0.25% silver nitrate, 1% resorcinol solution, 2% tannin, 3 % sodium tetraborate, etc.) until weeping disappears. Perhaps the use of aerosols with corticosteroids. Whole bubbles are opened and solutions of aniline dyes (brilliant green, methylene blue, fucorcin) are applied to the eroded surfaces. In the subacute and chronic stages, ointments containing corticosteroids (sinaflan, celestoderm, fluorocort, advantan, locoid, elocom, etc.) are applied to dry surfaces around erosions or after wetting has stopped. In the case of a secondary infection and with microbial eczema, the use of ointments with steroid hormones and ointments with antibiotics (gentamicin, erythromycin, tetracycline, etc.) is combined, or compound ointments are used that contain anti-inflammatory and antimicrobial agents (triderm, celestoderm with garamycin, cortomycetin , oxycort, gioksizon, lorinden C, etc.). With a decrease in the phenomena of acute inflammation, when

in the clinical picture is dominated by infiltration, ointments with keratoplastic agents are prescribed(5-20% naftalan, 1-2% tar, 2-5% salicylic acid, 2-5% ichthyol), or containing a steroid in combination with keratoplasty (diprosalik, betasalik, lorinden A, etc.).

AT In the treatment of childhood eczema, great importance is attached to the normalization of care and regimen, the elimination of factors that increase the excitability of the nervous system, the fight against secondary pyococcal infection, the sanitation of foci of focal infection, the treatment of concomitant diseases, and diet therapy. In breastfed infants, an appropriate correction of the child's feeding regimen and mother's nutrition should be carried out, from the food of which products that are potential allergens are excluded. Breastfeeding a child with eczema is the most appropriate. For the treatment of childhood eczema, the same groups of drugs are used as in adults, but all drugs are prescribed

in age dosages and taking into account contraindications for use in young children. In particular, the use of antihistamines in infants can lead to the development of dry mouth, constipation, tachycardia, convulsions, nervous excitement and vomiting. In this case, preference should be given to calcium preparations. In external treatment in young children, it is undesirable to use lotions.(due to the danger of hypothermia), as well as ointments containing ichthyol and tar, alcohol solutions of drugs should be replaced with water. Also, the external use of antibiotics is not recommended due to the high risk of allergization to them and fluorinated steroids, especially with a large affected area, due to the high resorptive properties of children's skin and the possibility of developing systemic side effects.

Treatment of Kaposi's herpetiform eczema is desirable to be carried out in boxed wards, together with an infectious disease specialist, ENT doctor, neurologist, ophthalmologist, depending on the degree of involvement of internal organs. The main and most effective treatment for this condition is considered to be acyclovir, administered intravenously or orally. Also, special influence should be given to detoxification measures and the prevention of dehydration, antibiotic therapy must be prescribed to prevent the development of a secondary infection. All other principles of treatment are the same as those for other forms of eczema.

The prognosis for eczema is usually good, but 50–70% of patients develop a recurrence of the disease within a year.

Prevention of the disease consists in the timely and rational treatment of allergic dermatitis, foci of pyoderma and focal infection in the upper respiratory tract and internal organs, fungal infections and onychomycosis, varicose veins and trophic ulcers, as well as diseases of the gastrointestinal tract. Patients with eczema are advised to follow a hypoallergenic diet to prevent recurrence. Smoking, drinking alcohol, salty and spicy foods, canned food is prohibited, contact with industrial and household allergens should be avoided, it is not recommended to wear underwear made of synthetics and wool.

To prevent the professional form of eczema, it is necessary to improve the technical and sanitary and hygienic working conditions, to provide workers with personal protective equipment. To prevent recurrence of occupational eczema, rational employment is necessary, excluding contact with industrial allergens.

Prevention of childhood eczema includes a rational diet for pregnant and lactating mothers, timely and gradual transition of the child from natural to artificial feeding, deworming, sanitation of foci of chronic infection; to prevent the occurrence of eczema herpetiformis, contact of a child with childhood eczema with patients with chickenpox is excluded.

KNOWLEDGE TESTS

1. Which of the following is not characteristic of simple contact dermatitis?

a) localization at the site of contact with the obligate stimulus; b) hyperemia; c) the presence of blisters;

d) clear boundaries of rashes; e) the presence of bubbles.

2. Toxidermia is characterized by:

a) violation of the general condition; b) active inflammatory reaction of the skin; c) a large area of ​​damage;

d) rapid resolution after cessation of contact with the allergen; e) all of the above.

3. What form of eczema is not true?
a) nummular;	b) dyshidrotic;	c) intertriginous;
d) tylotic;	e) pruriginous.
4. All of the following apply to microbial eczema except:
a) dyshidrotic;	b) nummular;	c) varicose;
d) paratraumatic;	e) mycotic.

5. In Lyell's syndrome, the following are indicated: a) detoxifying agents;

b) corticosteroid hormones in high doses; c) analgesics; d) rehydration therapy;

e) all of the above.

6. For eczema are not typical:

7. What is common for microbial and true eczema? a) the clarity of the boundaries of the foci; b) symmetry of rashes;

c) punctate weeping in the foci; d) the presence of sensitization to infectious agents;

e) development against the background of skin lesions.

8. Where can seborrheic eczema be localized?

e) interscapular region.

9. What is the main difference between occupational eczema? a) low intensity of itching; b) absence or lack of expression of weeping;

c) localization in areas rich in sebaceous glands; d) localization around skin lesions obtained at work;

e) the presence of sensitization to the production factor.

10. What mechanism underlies the formation of blisters in eczema?

12. What drugs are not used in the treatment of eczema? a) antihistamines; b) sedatives;

c) vasodilating; d) non-steroidal anti-inflammatory; d) vitamins.

Sample answers: 1 - c, 2 - e, 3 - a, 4 - a, 5 - e, 6 - d, 7 - c, 8 - b, 9 - e, 10 - d, 11 - c, 12 - d.

1.5. ATOPIC DERMATITIS

Atopic dermatitis (syn.: endogenous eczema, constitutional eczema, diffuse neurodermatitis) is a hereditary multifactorial allergic disease of the body with a predominant skin lesion, with an abnormal orientation of the immune response to environmental allergens, manifested by an erythematous-papular itchy rash with skin lichenification phenomena, polyvalent hypersensitivity and eosinophilia in peripheral blood. Patients have a genetic predisposition to allergic reactions.

In the CIS countries, from 5 to 20% of children suffer from atopic dermatitis. Etiology and pathogenesis. There are currently 3 main

concepts of the development of atopic dermatitis: constitutional predisposition, immunopathology and psychosomatic disorders. The greatest importance is attached to the immunological concept of the pathogenesis of atopic dermatitis. It is based on the concept of atopy as a genetically determined allergy. Atopy, that is, the tendency to hyperproduce IgE in response to contact with environmental allergens, is the most important identifiable risk factor for the development of atopic dermatitis. Thus, the IgE-dependent mechanism plays a decisive role in the pathogenesis of atopic dermatitis. In 85% of patients with atopic dermatitis, the level of IgE in the blood serum is elevated and there are positive skin tests of the immediate type with various food and aeroallergens. In young children, the leading role belongs to food allergens, of particular importance is sensitization to cow's milk. Quite often the first clinical manifestations of the disease are initiated by antibiotics. With age, the number of provoking allergens expands: pollen, household, bacterial, and mycotic allergens are added to food allergens.

The process of sensitization to a certain allergen begins from the moment it enters the body through the enteral, less often through the aerogenic route. In the mucous membrane, this allergen interacts with auxiliary antigen-presenting cells (macrophages, dendritic cells), and the latter, through their cytokines, accelerate the differentiation and activation of type 2 T-helpers (Th2 lymphocytes), the activation of which leads to hyperproduction of interleukins-4, 5, 13. In turn, interleukin 4 switches B-lymphocytes to the synthesis of IgE antibodies. There is evidence of a genetically determined tendency to develop sensitization to certain types of allergens. On the sensi

The bilization of the body is indicated by the presence of allergen-specific IgE antibodies. The activity of the course of atopic dermatitis is due to the high content of total IgE and allergen-specific IgE. Fixation of specific IgE antibodies on target cells (basophils, mast cells) of the shock organ (skin) determines the completion of the sensitization process. The interaction of IgE on target cells changes the properties of cytoplasmic membranes and leads to the release of histamine, prostaglandins, leukotrienes, which directly implement the development of an allergic reaction. The inferiority of the immune response contributes to increased susceptibility to various skin infections. There is evidence that in 80% of patients with atopic dermatitis

at the age of 4–14 years, polyvalent sensitization is detected, often a combination of sensitivity to food allergens, drugs and house dust micromites.

Exacerbation of atopic dermatitis can be caused not only by allergens, but also by nonspecific triggers (irritants). We are talking about synthetic and woolen clothing, chemical compounds present in topical medicines and cosmetic preparations; preservatives and dyes contained in food products; detergents remaining on the laundry after washing.

Attention should be paid to the features of the psycho-emotional status of patients with atopic dermatitis. These patients show changes

in psycho-emotional sphere and behavioral features: emotional lability, resentment, isolation, irritability, features of depression and anxiety, sometimes aggressiveness. Social maladjustment in one's society is noted, symptoms of autonomic dysfunction are often revealed. Almost half of patients with atopic dermatitis, which began in early childhood, develop bronchial asthma and/or allergic rhinitis with age, i.e. atopic dermatitis can be considered, with a certain assumption, as a kind of systemic disease.

For atopic dermatitis, a clear clinical picture is not typical, usually they only talk about the most characteristic manifestations of the disease. Currently, the diagnosis of AD is based on the main and additional criteria, fixed by the decisions of the I International Symposium on Allergic Dermatitis in 1980. 5 main and 20 additional criteria are defined.

Main criteria:

1. Itching - more intense in the evening and at night.

2. Typical skin changes (in children - damage to the face, trunk and extensor surface of the limbs; in adults - foci of lichenification on the flexion surfaces of the limbs).

3. Family or individual history of atopy: bronchial asthma, urticaria, allergic rhinoconjunctivitis, allergic dermatitis, eczema.

4. The onset of the disease in childhood (usually infancy).

5. Chronic relapsing course with exacerbations in spring and autumn non-winter season, which manifests itself no earlier than from 3–4 years of age.

Additional Criteria: xeroderma, ichthyosis, palmar hyperlinearity, follicular keratosis, elevated serum IgE levels, tendency to pustular skin diseases, nonspecific dermatitis of the hands and feet, dermatitis of the nipples, cheilitis, keratoconus, dryness and small cracks in the red border of the lips, seizures in the corners of the mouth , darkening of the skin of the eyelids, anterior subcapsular cataract, recurrent conjunctivitis, Denny-Morgan infraorbital fold, pallor and redness of the skin of the face, white pityriasis, itching with sweat, perifollicular seals, food hypersensitivity, white dermographism.

The diagnosis is considered reliable in the presence of 3 main and several additional criteria.

Clinic. Atopic dermatitis begins in the first year of life, most often against the background of an eczematous process, and can continue into old age. Usually with age, its activity gradually decreases. It is customary to distinguish several phases of the development of the disease: infant (up to 3 years), children (from 3 to 16 years), adult. In children under 3 years of age, atopic dermatitis is represented by edematous, red, scaly, often weeping foci with predominant localization on the face. Sick children are disturbed by severe itching. When the face, trunk, limbs are affected, the process actually corresponds to constitutional eczema. By the end of the infantile stage, the skin in the lesions coarsens due to constant scratching, areas of lichenification appear. In the second age period, edematous papules, scratching, especially on the flexion surfaces of the limbs, on the neck, foci of lichenification in the elbows and popliteal cavities predominate, pigmentation of the eyelids, a double fold on the lower eyelid, dryness and small cracks in the red border of the lips appear with age. In adults, the clinical picture of atopic dermatitis is characterized by the predominance of infiltration with skin lichenification against the background of non-inflammatory erythema. The main complaint is persistent skin itching. Often there are foci of continuous papular infiltration with multiple excoriations. Characterized by dry skin, persistent white dermographism. In this case, skin lesions can be localized, widespread and universal (like erythroderma). Among the clinical forms of atopic dermatitis, erythematous-squamous, prurigo-like, vesiculocrustous, lichenoid with a large number of lichenoid papules are distinguished. In adults, the course of atopic dermatitis is long, the process is often complicated by impetiginization, eczematization.

A number of patients have hypotension, weakness, hyperpigmentation, hypoglycemia, decreased diuresis, fatigue, weight loss, i.e., signs of hypocorticism. In summer, most patients note a significant improvement in the skin process, especially after staying in the southern resorts. With age, patients with atopic dermatitis may develop early cataracts (Andogsky's syndrome).

Histopathology. On the part of the epidermis: hyperkeratosis, parakeratosis, acanthosis, moderate spongiosis. In the dermis, dilated capillaries, lymphocytic infiltrates around the vessels of the papillary layer are found.

Treatment of patients with atopic dermatitis is always complex, taking into account the age of the patient, the phase of the disease and the degree of activity of the pathological process. It is important to maintain a healthy lifestyle, that is, a rational mode of work activity, sleep, rest, food intake, a hypoallergenic diet, the most severe during exacerbations, proper skin care (detergents with an acidic pH level, fattening and moisturizing creams and emulsions). It is important to identify and exclude alimentary, psychogenic, infectious, meteorological and other irritating factors. If a child has an allergy to cow's milk, then dairy products in any form (milk, cottage cheese, cheese, milk yogurts) are excluded from the diet, sour cream and whole butter should be limited, and beef, veal, beef liver. The meat of young animals is more allergenic than old ones. An approximate composition of a hypoallergenic diet for children suffering from atopic dermatitis is given in Table. 2 (quoted in V.F. Zhernosek, 2000).

With exacerbations of the disease, it is necessary to take measures to eliminate allergens and immune complexes from the body and reduce the body's response to histamine. For this purpose, antihistamines are prescribed, better than the second and third generation (fencarol, claritin, kestin, zyrtec, telfast, erius), detoxifying agents (5% unithiol solution 5 ml intramuscularly, 30% sodium thiosulfate solution 10 ml each intravenously), infusion therapy (microdesis, neorondex, reopoliglyukin intravenously drip). From H2 - blockers, you can use duovel 0.04 g or histodil 0.2 g at night every day for 1 month. Valerian, motherwort, peony preparations, as well as pyrroxan 0.015 g 1-2 times a day for 10 days have a positive effect. Enterosorbents are recommended: activated carbon at the rate of 0.5 g per 1 kg of body weight per day in 4–5 doses, enterodesis 0.5–1.0 g/kg per day

in 3 appointments during 2-3 days, then the dose is reduced by 2 times and the drug continues for at least 2 weeks. With an eczema-like form, hydroxyzine (atarax) 0.025 g 1–2 tablets per day or cinnarizine 0.025 g each (2 tablets 3 times a day for 5–7 days, and then 1 tablet 3 times a day for another 1– 2 weeks). In severe cases, plasmapheresis is used. With the appointment of cyclosporine A (sandimmun), the manifestations of the disease are relatively quickly resolved, but the effect is unstable. If there are changes

in immunogram, immunocorrective therapy is carried out (polyoxidonium 6 mg intramuscularly 2-3 times a week, 5-6 injections in total; immunofan solution, taktivin, thymalin in usual dosages). With sharp exacerbations with a generalization of the process, corticosteroids 15–30 mg per day are indicated for

2-3 weeks or diprospan 1 ml intramuscularly 1 time in 10 days, only 2-3 injections.

table 2

Approximate composition of a hypoallergenic diet for children with atopic dermatitis

Products and dishes	Allowed	Forbidden
	White, gray, black, lean cookies,	Sweets, cakes
	savory apple pie
	Salad of fresh cabbage, fresh cucumbers, vine	tomatoes, caviar,
	rheta (with tolerance to carrots and beets)	herring, canned
	Butter (in limited quantities),
	vegetable oil, lard
Dairy products	Milk (boil for at least 15 minutes), dry
(when tolerated)	milk, kefir, acidophilus, cottage cheese, cottage cheese
	casserole, sour cream (limited)
meat products and	Lean pork, turkey, rabbit meat	chicken meat, fish,
dishes from them	(boiled, meatballs, beef stroganoff, meatballs)	beef, veal
	Hard boiled, no more than 2 times a week
	(when tolerated)
Cereals and dishes from	Pasta, cereals: buckwheat, oatmeal,
	barley, rice (no more than 1 time per day)
	Vegetables, cereals	meat broths,
		mushroom soups
Vegetables, fruits, ze-	Cabbage, potatoes, carrots and beets (when re-	Green pea,
laziness and dishes from them	portability in limited quantities), apples	mushrooms, citrus fruits,
	fresh and baked, cranberries, blueberries, gooseberries,	strawberry, melon, grain
	blackcurrant (with limited tolerance)	nata, pear, nuts
	exact amount)
Drinks and sweets	Dried or fresh fruit compote	chocolate, coffee,
		cocoa, honey, sweets

In violation of the function of the gastrointestinal tract and the development of dysbacteriosis, eubiotics, lactobacterin, colibacterin, bifidumbacterin, hepatoprotectors, enzymes are indicated. An antioxidant complex of vitamins is also used.

For external therapy, creams and pastes containing anti-inflammatory and antipruritic drugs, skin-cap cream are used. Creams and ointments with naftalan, tar, sulfur, the 3rd fraction of ASD are well tolerated and give a satisfactory therapeutic effect. Of the topical steroids, non-fluorinated drugs are the safest: elokom, advantan, lokoid. A promising drug is the calcineurin inhibitor pimecrolimus (elidel), which has a selective effect on T-lymphocytes and mast cells and does not cause skin atrophy. It can be used on the skin of the face and neck from early childhood.

From physiotherapeutic procedures, ultraviolet radiation, inductothermy, electrosleep, endonasal electrophoresis of diphenhydramine are used; in severe cases, PUVA therapy is indicated. From water procedures, you can prescribe baths with sea salt, with a decoction of medicinal herbs (St. John's wort, sage, valerian).

LECTURE №5.

ALLERGODERMATOSIS.

Allergodermatosis is a group of skin diseases associated with changes in reactivity and sensitization of the body. This concept includes:

1. Dermatitis.
2. Dermatoses.
3. Neurodermatitis.

According to WHO, about 20% of the population suffers from allergic diseases. Currently, there is an increase in allergic morbidity among the child population compared with the incidence of adults. According to forecasts, by 2008-2010 the incidence of allergic diseases will take the 2nd place after the incidence of mental disorders. In recent years, there has been a steady increase in allergic dermatoses, which is associated with social and biological factors:

Ø Increasing pollution of the environment (atmospheric air, water bodies, soil).

Ø Changes in the nutrition of the population (the development of allergic dermatoses is influenced by an unbalanced diet: excessive consumption of fats and carbohydrates - load on the functional systems of the body - metabolic disorders). Proper and nutritious nutrition is one of the measures to prevent allergic dermatitis.

Ø Chemicalization of everyday life (increase in the use of detergents, cleaners).

Ø Reduced health indicators of women of childbearing age, artificial feeding (breastfeeding protects the child from infection in infancy and during the 1st 2 years of life). WHO data support the role of breastfeeding in stopping or significantly reducing diseases such as neonatal sepsis, measles, diarrhea, pneumonia, and meningitis.

Ø Unreasonable widespread use of various drugs (self-medication).

Ø Growing social burden - stress, a decrease in the standard of living, which is generally reflected in the suppression of the immune system and the development of secondary immunodeficiencies.

For the development of allergic skin diseases, the action of external (contact - through the epidermis) or internal (hematogenous) stimuli is necessary.

Depending on the ability to cause allergic dermatosis, irritants are divided into:

1. obligate (mandatory) - those factors that, when exposed to the skin in all cases, cause an inflammatory reaction - unconditional reactions;
2. chemical (acids, alkalis);
3. physical (exposure to high and low temperatures);
4. mechanical (friction);
5. biological (sap and pollen of plants);

The action of these factors is associated with their sharp effect on the skin exceeding the limit of its resistance. As a result, the inflammatory process develops.

1. optional (conditional) - cause a disease in the presence of a predisposition on the part of the body (allergens).

ü Complete allergens.

ü Incomplete allergens (hoptens).

Classification of allergic dermatoses (clinical).

Dermatitis: simple (contact); contact-allergic; allergic - toxicoderma (sometimes toxicoderma is isolated separately).

eczema: true; microbial; seborrheic.

Neurodermatosis(itchy skin diseases): skin itching (as an independent disease); neurodermatitis; diffuse; limited; atopic; hives; prurigo (prurigo).

DERMATITIS.

Dermatitis is an inflammatory skin lesion caused by various factors. Allocate dermatitis:

Ø Simple (contact) - caused by obligate reactions.

Ø Allergic - caused by allergens.

contact dermatitis occurs when the skin is exposed to a strong irritant (chemical, physical and biological factors) exceeding the resistance limit of the skin. It develops in any person, regardless of the sensitization of the body. For example, frostbite, skin hyperemia from UV exposure.

Distinctive features of contact dermatitis.

It is characterized by severe redness, swelling, intense itching, and in more severe cases, the appearance of vesicles and blisters. Simple dermatitis is characterized by a number of features that distinguish them from allergic:

1. The degree of severity depends on the strength of the stimulus and the time of its exposure.

2. The stimulus has the same effect on different people.

3. Rapid recovery of the original state of the skin after elimination of the irritant (with the exception of ulcerative necrotic lesions).

4. The area of ​​the lesion strictly corresponds to the area of ​​action of the stimulus.

5. There are no papular elements of the rash.

Allergic dermatitis- inflammation of the skin of an allergic nature. It occurs as a result of increased skin sensitivity to a particular allergen. The process does not develop in all people, but only in the sensitized population. Allergic dermatitis does not occur immediately, but after a certain period of time necessary for the formation of an immune response.

Etiology.

Allergens, more often chemical and biological haptens, play an important role in the occurrence of allergic dermatitis.

Types of allergens:

1. Chemical: nickel salts, chromium compounds (earrings, bracelets), bromine, resins, dyes, pharmacological agents (antibiotics, sulfonamides, B vitamins, novocaine), perfumes (deodorants, lotions, creams).
2. Biological: pollen and juice of some plants (primrose, geranium, buttercup, chrysanthemum, hogweed, etc.), insects, caterpillars, etc.

Pathogenesis.

Allergic dermatitis is a typical manifestation of an allergic reaction of a delayed and immediate type. The process of sensitization begins with the allergen (haptens) hitting the skin surface. After passing through the stratum corneum and zona pellucida, the haptens reach the cells of the prickly layer, where they combine with tissue proteins. Here he acquires an immunogenic conjugate, i.e. The hapten is converted into a complete antigen (allergen). The immunogenic conjugate is taken up and processed by epidermal Langerhans cells (dermal macrophages). They absorb the antigen on their surface and deliver it through the lymphatic system to the lymph node.

Subsequently, the immunogenic conjugate is transferred to free specific T-lymphocytes, which, already as sensitized lymphocytes with the corresponding receptors, create generalized sensitization. After repeated contact of the sensitized organism with the allergen, an allergic reaction of the body develops, as a result of which cells are irritated, mainly mast and basal cells, and histamine-like substances (histamine, heparin, serotonin, bradykinin) are released, causing vasodilation.

Features of the clinical picture.

1. polymorphism of rashes (less typical than for eczema) - both primary and secondary morphological elements are noted;
2. the allergen acts by contact, therefore, after a while they appear;
3. bright erythema, as a sign of inflammation;
4. edema;
5. papular rashes, vesicles;
6. at the opening of the bubbles - areas of weeping. Moknute is short-term and unsharply expressed. In the future, serous crusts are formed;
7. the spread of rashes beyond the boundaries of irritants;
8. tendency to dissemination to other areas of the skin;
9. subjectively, the patient is disturbed by a burning sensation, itching.

Allergic contact dermatitis is the mildest form of an erythematous reaction. After elimination of the allergen, recovery occurs. The process is resolved by the formation of light pigmentation, which then disappears.

Toxicoderma- an allergic disease of the body that develops on the systemic exposure to allergens, and manifests itself in a predominant lesion of the skin and mucous membranes (internal organs may be affected). It arises as a result of the endogenous action of various chemicals, medicinal substances, industrial and household factors, food products.

.

1. per os;
2. per rectum (enema);
3. conjunctival cavity (eye drops, ointments);
4. vagina;
5. upper respiratory tract;
6. directly into the bloodstream (intravenous, intramuscular administration of drugs);

Often, sensitization develops on the parenteral administration of drugs (antibiotics, B vitamins, analgesics, sulfonamides, less often under the influence of food), while both the skin and internal organs are sensitized. Manifested by the phenomena of general malaise (weakness, headache, fever), changes in the blood formula, an increase in the number of lymphocytes, the appearance of young cells, an increase in ESR and other changes.

Clinical features of toxicoderma:

1. infrequently, an allergen can be established from the clinical picture. The same allergen can cause different clinical manifestations. For example, penicillin may develop urticaria, erythematous spots, anaphylactic shock; on sulfonamides - mild skin lesions or Lyell's syndrome.
2. the presence of erythematous inflammatory foci with a bluish-violet tint, of various shapes and sizes.
3. the appearance of blisters, vesicles, vesicles and blisters with transparent contents, upon opening of which erosions are formed, covered with crusts. After the disappearance of the rashes, pigmented spots may remain.
4. possible localization of lesions on the mucous membrane, sometimes only on the mucous membrane.
5. development of intoxication syndrome (weakness, malaise, fever, headache).
6. some medications cause a chronic clinical picture.
7. for iodide or bromide toxicoderma, the development of acne is characteristic.

Clinical forms of toxicoderma:

Common - damage to the entire skin.

Fixed erythema - the development of the process on the same area of ​​​​the skin.

Often, toxicoderma develops on sulfanilamide drugs, antibiotics, B vitamins. A thorough collection of an allergological history is necessary. When reacting to sulfonamides, drugs containing a benzoic ring in their structure should not be prescribed.

Sulfonamides - fixed erythema in the same place. Rounded, bright pink spots with a bluish tinge appear on the skin. After their disappearance, pigmentation remains.

Severe forms of toxicoderma - Lyell's syndrome (toxic epidermal necrosis - TEN). Extensive red lesions suddenly appear on the skin and mucous membranes, against the background of which flaccid blisters form. When the blisters open, continuous erosive weeping surfaces are formed. There is a septic increase in temperature up to 39-40 0 in such patients, a violation of the activity of the heart, an increase in ESR up to 40-60-88 mm / h. In advanced cases, patients die.

The cessation of the action of the allergen leads to recovery. Upon re-encounter with the allergen, the process can be localized in the same place or in another part of the skin.

Eczema is a chronic relapsing disease with acute inflammatory symptoms caused by serous inflammation of the epidermis and dermis.

Ways of penetration of allergens into the body:

1. through the gastrointestinal tract;
2. through the upper respiratory tract;
3. through the urinary tract.

Occurs in individuals sensitized to this allergen. In the occurrence of eczema, a pathogenetic factor plays a role - changes in the central nervous system, internal organs (achilia, pancreatitis), endocrine system and metabolism. If at the initial stages the disease was caused by 1-2 allergens, then over time polyvalent sensitization may occur.

Endogenous factors:

1. neurogenic dysfunction;
2. endocrine dysfunction;
3. gastrointestinal dysfunction;
4. metabolic disease;
5. allergic hyperreactivity;
6. immune deficiency.

Eczema classification.

True (idiopathic):

1. dyshidrotic (characterized by the appearance of small vesicles on the skin of the hands, which open, an infection joins and secondary infection develops).
2. pruriginous (itching).
3. telotic (increased hyperkeratosis).
4. cracked???

Microbial (infectious):

1. numular;
2. paratraumatic;
3. mycotic;
4. intertriginous (localized in natural folds);
5. varicose (with varicose veins and trophic ulcers);
6. sycosiform (localized on the face);
7. eczema of the nipples and areola in women (differentiate with Paget's disease).

Seborrheic.

Professional.

Hypertrophic Kaposi's eczema.

True eczema.

Favorite localization: face, extensor surfaces of limbs, torso. The process is symmetrical. The foci do not have clear boundaries, but gradually move to the surrounding tissues. Pronounced polymorphism of rashes (both primary and secondary morphological elements). With an exacerbation of the process, weeping is observed, resembling dew, due to the release of water droplets from microerosions, resembling "serous wells". The course is undulating: periods of remission are replaced by relapses. Severe paroxysmal itching of varying intensity. In a chronic process: congestive erythema, infiltration, lichenification.

microbial eczema.

It develops with sensitization to the waste products of microorganisms, fungi, protozoa, helminths (not the worms themselves, but their decay products). Protein particles of microbes appear on the skin, which penetrate into the Malpighian layer and cause the formation of allergens. The process of sensitization takes place against the background of specific and nonspecific immunodeficiencies and leads to the formation of immediate and delayed sensitivity. It is characterized by confinement to foci of chronic infection (varicose veins, trophic ulcers). The process is asymmetric. The foci have clear boundaries, often with a collar of exfoliating epidermis along the periphery. Favorite localization: shins, skin folds, navel area. Often there are pustules and purulent crusts around the focus, in contrast to true eczema. Polymorphism is less pronounced. Itching is moderately intense, lichenization does not develop, weeping is pronounced - continuous, rough. There is no pronounced infiltration in the foci.

seborrheic eczema.

An allergic disease associated with a violation of the secretion of sebum. The process extends to the scalp, face, ears, interscapular region, upper back, chest area. Sensitization to microorganisms, fungi is noted. It is characterized by inflammation, which, as it were, “drains” from the scalp to the neck, often skin folds are involved in the process - behind the ear, axillary. On seborrheic areas, seborrheic inflammatory spots of pink color with a yellow tint appear. Greasy scales are visible on the spots (if smeared on paper, a greasy spot remains). Seborrheic spots seem to "flow" down. There is no polymorphism. There may be intense itching. Tendency to flow. The appearance of bubbles and weeping is atypical.

Prevention of allergic dermatitis .

1. diet and sparing regimen;
2. sanitation of foci of chronic infection and prevention of colds;
3. periodic examination for helminthiases (giardiasis, opisthorchiasis, amebiosis, etc.);
4. wearing cotton underwear;
5. maintaining a healthy lifestyle.

Allergodermatosis is a heterogeneous group of skin diseases, the leading role in the development of which is given to an allergic reaction of an immediate or delayed type.

This group includesallergic dermatitis, toxidermia, eczema, atopic dermatitis, urticaria .

Dermatitis

Dermatitis is a contact acute inflammatory skin lesion that occurs as a result of direct exposure to obligate or facultative irritating factors of a chemical, physical or biological nature. There are simple and allergic dermatitis.

Dermatitis simple arise in response to the impact of an obligate stimulus (mandatory for all people) - chemical (concentrated acids, alkalis), physical (high and low temperatures, radiation, mechanical effects, current, etc.) and biological nature. An inflammatory reaction occurs at the site of exposure, strictly corresponding to the boundaries of the stimulus. The degree of severity of inflammatory phenomena in this case depends on the strength of the stimulus, the time of exposure and, to some extent, on the properties of the skin of one or another localization. There are 3 stages of simple dermatitis: erythematous, whiziculo-bullous and necrotic. More often, simple dermatitis is manifested in everyday life by burns, frostbite, skin abrasions when wearing ill-fitting shoes. With prolonged exposure to a low-strength irritant, congestive erythema, infiltration, and skin desquamation may occur.

Simple dermatitis develops without an incubation period and usually proceeds without disturbing the general condition of the body. The exception is burns and frostbite of a large area and depth.

In the treatment of simple dermatitis, local remedies are most often used. It is important to eliminate the irritant. In case of chemical burns from concentrated acids and alkalis, the emergency remedy is to flush them with plenty of water. With severe erythema with edema, lotions (2% solution of boric acid, lead water, etc.) and corticosteroid ointments (sinalar, fluorocort, flucinar, etc.) are indicated; liquids (methylene blue, gentian violet, etc.) and the application of epithelializing and disinfecting ointments (2–5% dermatol, celestoderm with garamycin, etc.). Treatment of patients with necrotic skin changes is carried out in a hospital.

Allergic dermatitis occurs in response to the contact effect on the skin of an optional irritant to which the body is sensitized and in relation to which the irritant is an allergen (monovalent sensitization).

Etiology and pathogenesis. At the heart of allergic dermatitis is an allergic reaction of a delayed type. Most often, chemicals (washing powders, insecticides, chromium, nickel), drugs and cosmetics (synthomycin emulsion and other antibiotic ointments, hair dyes, etc.) act as an allergen. Allergens are often haptens, forming a complete antigen when combined with skin proteins. Epidermal macrophages play an important role in the formation of contact hypersensitivity. Already in the first hours after the application of the allergen, their number in the skin increases. In this case, the allergen is associated with macrophages. Macrophages present the allergen to T-lymphocytes, in response to this, T-lymphocytes proliferate with the formation of a population of cells specific for this antigen. Upon repeated contact with the allergen, circulating sensitized lymphocytes rush to the site of exposure to the allergen. Lymphokines secreted by lymphocytes attract macrophages, lymphocytes, polymorphonuclear leukocytes to the focus. These cells also secrete mediators, causing an inflammatory response in the skin. Thus, skin changes in allergic dermatitis appear when the allergen is repeatedly applied under conditions of sensitization of the body.

The clinical picture of allergic dermatitis is similar to the acute stage of eczema: against the background of erythema with fuzzy boundaries and edema, many microvesicles form, leaving weeping microerosions, scales, and crusts upon opening. At the same time, although the main changes in the skin are concentrated at the sites of exposure to the allergen, the pathological process will go beyond its impact, and due to the general allergic reaction of the body, allergic rashes such as seropapules, vesicles, and erythema areas can also be observed at a considerable distance from the site of exposure. For example, in allergic dermatitis that has developed on mascara, bright erythema with edema and vesiculation can capture the skin of the face, neck and upper chest. The process is usually accompanied by severe itching.

The diagnosis of allergic dermatitis is based on the history and clinical picture. Often, to confirm the diagnosis, allergic skin tests with a suspected allergen (compress, drip, scarification) are resorted to, which are mandatory for identifying an industrial allergen in the development of occupational allergic dermatitis. Samples are placed after the elimination of clinical changes in the skin. The differential diagnosis is carried out with eczema, which is characterized by polyvalent (rather than monovalent) sensitization and a chronic relapsing course, with toxidermia, in which the allergen is reduced inside the body.

Treatment of allergic dermatitis includes, in addition to eliminating the irritant, hyposensitizing and external therapy, as in eczema. Assign 10% calcium chloride 5.0–10.0 ml intravenously, 30% sodium thiosulfate 10 ml intravenously, 25% magnesium sulfate 5.0–10.0 ml intramuscularly, antihistamines (suprastin, fenkarol, tavegil, etc.), local lotions of 2% solution of boric acid, etc., corticosteroid ointments (lorinden C, advantan, celestoderm, etc.).