Antipyretics for children are prescribed by a pediatrician. But there are emergency situations with fever when the child needs to be given medicine immediately. Then the parents take responsibility and use antipyretic drugs. What is allowed to be given to infants? How can you lower the temperature in older children? What medications are the safest?
Atopic dermatitis is a hereditary condition chronic illness the whole body with a predominant skin lesion, which is characterized by polyvalent hypersensitivity and eosinophilia in the peripheral blood.
Etiology and pathogenesis. Atopic dermatitis is a multifactorial disease. Inherited predisposition to atopic diseases is realized under the influence of provoking factors environment. An inadequate immune response contributes to increased susceptibility to various skin infections.
An important role in the pathogenesis of atopic dermatitis is played by the inferiority of the skin barrier associated with impaired ceramide synthesis.
The characteristics of the psycho-emotional status of patients are essential.
Clinic. Age periodization. Atopic dermatitis usually manifests itself quite early - in the first year of life, although its manifestation is possible at a later date. There are three types of atopic dermatitis:
1) recovery up to 2 years (most common);
2) pronounced manifestation up to 2 years with subsequent remissions;
3) continuous flow.
Atopic dermatitis occurs with chronic recurrence. Clinical manifestations of the disease change with the age of patients. Long-term remissions are possible during the course of the disease. There is an infant stage of the disease, which is characterized by an acute and subacute inflammatory nature of the lesions with a tendency to exudative changes and a certain localization - on the face, and with widespread lesions - on the extensor surfaces of the limbs, less often on the skin of the body. In the vast majority of cases, there is a clear connection with nutritional stimuli. Initial changes usually appear on the cheeks, less often on the outer surfaces of the legs and other areas.
The primary ones are erythematoedematous and erythematosquamous lesions. In more acute cases, papulovesicles, cracks, weeping, and crusts develop. Characterized by severe skin itching.
By the end of the first – beginning of the second year of life, exudative phenomena usually decrease. Infiltration and peeling of lesions increase. Lichenoid papules and mild lichenification appear. In the future, complete involution of the rash or a gradual change in morphology and localization is possible with the development of the clinical picture characteristic of the second age period.
The second age period (childhood stage) covers the age from 3 years to puberty. It is characterized by a chronically relapsing course, often depending on the season of the year (exacerbation of the disease in spring and autumn). Exudative phenomena decrease, pruriginous papules, excoriations predominate, and a tendency to lichenification, which increases with age.
By the end of the second period, the formation of changes typical for atopic dermatitis on the face is possible.
The third age period (adult stage) is characterized by a lesser tendency to acute inflammatory reactions and a less noticeable reaction to allergic irritants.
ANNOTATION
An informational and methodological letter was prepared as part of the implementation of the Moscow Regional Program of State Guarantees for Providing Citizens Russian Federation free medical care.
The letter provides information about the etiology, pathogenesis, clinical picture, diagnostic criteria, therapeutic and preventive measures, dispensary registration for atopic dermatitis.
The information letter is intended for dermatovenerologists, pediatricians, clinical residents and interns.
Compiled by:
Vazhbin L.B. – Chief Physician of the GUZMO “Moscow Regional Clinical Dermatovenerological Dispensary”;
Shuvalova T.M. – Candidate of Medical Sciences, Head of the Organizational and Methodological Department of the Moscow Regional Clinical Dermatovenerological Dispensary, Chief Children's Dermatovenerologist of the Moscow Region;
Maksimova I.V. – Head of the advisory and outpatient department of the Moscow Regional Clinical Dermatovenerological Dispensary;
Lezvinskaya E.M. – Doctor of Medical Sciences, doctor of the State Healthcare Institution “Moscow Regional Clinical Dermatovenerological Dispensary”;
Klochkova T.A. – Candidate of Medical Sciences, doctor of the State Healthcare Institution “Moscow Regional Clinical Dermatovenerological Dispensary”;
Kalenichenko N.A. – doctor of the GUZMO “Moscow Regional Clinical Dermatovenerological Dispensary”;
Nefedova E.D. – doctor of the State Medical Institution “Moscow Regional Clinical Dermatovenerological Dispensary”.
Reviewer – Doctor of Medical Sciences, Professor, Suvorova K.N.
Introduction
Atopic dermatitis (AD)– an urgent problem in pediatric dermatovenerology, since its debut in most cases occurs in early childhood (in 60–70% of children in the first year of life). AD accounts for 20-30% of all allergic diseases in childhood.
Despite the large number of designations for AD, such as “endogenous eczema”, “infantile eczema”, “atopic neurodermatitis”, “Broca’s diffuse neurodermatitis”, “Besnier’s prurigo”, all of them are currently outdated and inherently reflect the stages of development a single pathological process.
AD is a chronic allergic disease that develops in individuals with a genetic predisposition to atopy, which has a relapsing course with age-related evolutionary features clinical manifestations and hypersensitivity to specific (allergenic) and nonspecific irritants.
The most characteristic distinguishing feature of AD is itching and age-related changes in the topography and clinical morphology of skin lesions, which are not characteristic of other multifactorial dermatoses.
Skin diseases that are clinically similar to AD, but do not have an atopic basis for pathogenesis, are not AD. The main purpose of compiling these guidelines is to reduce diagnostic errors among practicing dermatologists and increase the level of treatment and preventive care for patients with AD.
Severe forms of AD sharply reduce the quality of life of the patient and his entire family and contribute to the formation of psychosomatic disorders. 40–50% of children suffering from AD subsequently develop hay fever and/or allergic rhinitis, bronchial asthma.
The risk group includes:
- Children whose parents have a family history of allergic diseases (eczema, bronchial asthma, allergic rhinitis, etc.), mainly through the mother (identification of a burdened family history reaches 80%);
- Children born weighing more than 4 kilograms;
- Children born weighing less than 3 kilograms are low birth weight babies;
- Children born by caesarean section;
- In addition, the risk group includes children born to mothers who had chronic foci of infection during pregnancy, including helminthic infestations and giardiasis, endocrinopathies, suffered from vegetative-vascular dystonia, severe toxicosis, anemia, and suffered acute infectious diseases, were exposed to stress, took various medications for diseases, ate poorly, had bad habits and occupational hazards.
Etiology
The onset of the disease, as well as its course and severity, is determined by the interaction of predisposing genes and trigger factors. Trigger factors can be very diverse: physical and mental stress; emotional trauma; inhalation of poisonous gases, chemicals and taking medications; pregnancy and childbirth; moving to a permanent place of residence in an environmentally unfavorable area, etc. (see table 1). Susceptibility to trigger factors depends on the patient’s age, his endogenous constitutional characteristics, such as morphofunctional characteristics gastrointestinal tract, endocrine, nervous, immune systems.
In infancy and early childhood among the trigger factors, food allergens, poor feeding and nutrition, infectious agents, preventive vaccinations predominate, and their effect becomes more pronounced if the child has immunodeficiency conditions, chronic foci of infection, food allergies, immaturity of enzyme systems, liver diseases, vitamin metabolism disorders. Often the manifestation of skin manifestations occurs after an unreasonably early transfer of children infancy for artificial feeding
In the future, the importance of inhalation allergens increases: household, epidermal, pollen. Among household allergens, house dust is the most important. If you are allergic to plant pollen during the flowering period, it is necessary to seal the windows, limit walks in windy and sunny weather, and use hygiene products containing plant components with caution.
It is necessary to explain to the parents of sick children and the patients themselves that woolen or synthetic clothing and detergents can also provoke an exacerbation. In addition, it is necessary to keep in mind nonspecific, non-allergenic exacerbation factors, which include stress, extreme values of air temperature and humidity, intense exercise stress, infectious diseases.
In adults, the development of exacerbations of the disease is facilitated by contact allergens, medications taken for concomitant somatic pathologies, and poor nutrition.
Table 1
Trigger factors for blood pressure
| Food allergens | Products with high allergenic activity: cow's milk proteins, cereals, eggs, fish, soy, cocoa, chocolate, caviar and seafood, mushrooms, carrots and tomatoes. Products with average allergenic activity include: peaches, apricots, cranberries, bananas, green peppers, potatoes, peas, rice, corn, buckwheat. Green and yellow apples, pears, white currants and cherries, gooseberries, zucchini, squash, and fermented milk products have weak allergenic activity. |
| Inhalant allergens | Household and library dust, pillow feathers, pollen from flowering plants, mold, dander, pet epidermis, tobacco smoke. The main source of allergens in house dust is the mite Dermatophagoides pteronyssimus, with mite feces being the main allergenic agent. |
| Contact irritants and allergens | Soaps, solvents, wool clothing, mechanical irritants, detergents, preservatives, fragrances |
| Infectious agents | Staphylococcus aureus, Helicobacter pylori, Trichophyton rubrum and Malassezia furfur (Pityrosporum ovale or Pityrosporum orbiculare), Candida fungi, Herpes simplex virus, cytomegalovirus, worms and Giardia |
| Reception medicines | Antibiotics, sulfonamides, vitamins, non-steroidal anti-inflammatory drugs |
| Psycho-emotional factors | Fear, overexertion, overexcitement |
| Endocrine factors | Exacerbation of the disease during pregnancy, in infants, exacerbation of blood pressure during menstruation in a nursing mother. |
| Increased physical activity | Increased sweating, contributing to secondary skin infection |
| Poor nutrition | Early artificial feeding, late breastfeeding, poor diet, excessive consumption of foods rich in histamine liberators |
| Preventive vaccinations | They can provoke both the onset of the disease and the exacerbation of the process (especially DPT) |
| Climate impacts | Frequent exacerbations in spring and autumn |
Sensitivity to several allergens is often recorded, which is often associated with the development of allergic cross-reactions due to the presence of common antigenic determinants. They note simultaneous intolerance to fresh cow's milk, eggs, meat broths, citrus fruits, chocolate.
There is also structural homology between tree pollen allergens, and it is much less pronounced than the existing affinity of grass pollen allergens. Therefore, patients who are hypersensitive to birch pollen simultaneously react to hazel and alder pollen. Antigenic determinants of pollen and other classes of allergens (for example, when eating leaves and fruits of the same plants) may have similar allergenic properties (Table 2).
table 2
Possible options for intolerance to related plant allergens, foods and herbal remedies for allergies to pollen
| Environmental factor (Pollen) | Possible cross-reactions | ||
| Pollen, leaves and plant stems | Plant foods | Medicinal plants (herbal medicines) | |
| Birch | Hazel, alder, apple tree | Apples, cherries, nuts (hazelnuts), peaches, plums, carrots, celery, potatoes, tomatoes, cucumbers, onions, kiwi | Birch leaf (buds), alder cones |
| Cereals | Food grains (oats, wheat, barley, etc.), sorrel | ||
| Sagebrush | Dahlia, chamomile, dandelion, sunflower | Citrus fruits, sunflower seeds (oil, halva), chicory, honey | Wormwood, chamomile, calendula, coltsfoot, elecampane, string |
| Quinoa Ambrosia | Sunflower, dandelion | Beets, spinach, melon, bananas, sunflower seeds | |
Pathogenesis of atopic dermatitis
The development of AD is based on a genetically programmed feature of the body’s immune response to allergens, resulting in immunopathological reactions. The most significant in the pathogenesis of AD is the delayed-type hypersensitivity reaction (DTH), in which the leading role is played by sensitized lymphocytes and their interaction with allergens. The end result of this reaction is the production of HRT mediators and the development of chronic immune inflammation. Morphologically, this is manifested by a lymphohistiocytic reaction around the vessels of the dermis. At the same time, in cases of active production of IgE class antibodies, hypersensitivity reactions are often involved in the pathogenesis of AD immediate type(HNT), with the reaction of mast cells and basophils. with their subsequent degranulation and release of HNT mediators into the blood, the main of which are histamine, a slow-reacting substance of anaphylaxis. Clinically, this is manifested by erythematous-urticarial rashes. Treatment should be determined taking into account the prevalence of the type of immunopathological reactions (immediate or delayed type).
The basis of pathogenesis is immunopathological processes. The most typical disorders of the immune status are:
- Changes in the phagocytic system: disturbances in the phase of absorption of antigenic material by phagocytic cells and completed phagocytosis are more often observed;
- Decrease in the content of T-lymphocytes, increase in B-lymphocytes, imbalance of immunoregular T-lymphocytes: increase in T-helper cells and suppression of T-suppressors;
- The predominance of the Th-2 subpopulation leads to increased production of cytokines with pro-inflammatory and pro-allergenic effects (interleukin -3, interleukin - 4, interleukin - 5);
- Disimmunoglobulinemia - often increased levels of IgE, IgG;
- Increased content of circulating immune complexes;
- Impaired function of local immunity of the gastrointestinal tract, decreased synthesis of secretory immunoglobulin A, which deprives the intestines of the necessary protective secretion and creates a background for the damaging effects of microbial and antigenic factors on it;
- Failure of local immune protective functions of the skin and local skin immunity.
Along with disturbances in the immune status of patients, other factors also participate in the formation of the pathogenesis of AD:
- imbalance of intracellular regulatory mechanisms (cAMP/cGMP ratio);
- violation of membrane reception (mast cells of patients with atopic diseases contain 10 times more receptors for IgE than cells of healthy people);
- activation of non-immune mechanisms for the release of mediators of allergic inflammation;
- disturbance of neurovegetative function and peripheral blood circulation (spasm of peripheral vessels);
- psychophysiological and psychosomatic abnormalities;
- imbalance of the sympathetic and parasympathetic systems (blockade of β-adrenergic receptors and predominance of α-receptors);
- genetic disruption of the barrier function of the skin leads to the penetration of allergens from the environment into the skin, which causes immunological reactions and inflammation, as well as colonization of pyococci and fungi;
- endocrine dysfunctions (hypercortisolism, hypoandrogenism, hypoestrogenism, hyperthyroidism);
- dysfunction of the gastrointestinal tract (food fermentopathy, intestinal dysbiosis, gastritis, dysfunction of the hepatobiliary system);
- the presence of chronic foci of infection (usually ENT organs and gastrointestinal tract);
- helminthic and protozoal infestations;
- diseases of the spine;
- dysmetabolic nephropathies;
- violation of the metabolism of fatty acids in formed elements, blood plasma, adipose tissue.
Clinical picture
The manifestation of AD occurs in infancy, occurs with remissions of varying durations, can last until puberty, and sometimes does not go away until the end of life. Relapses usually occur seasonally (autumn, winter, sometimes spring), improvement or disappearance of manifestations is usually observed in the summer.
In severe cases, blood pressure develops torpidly, without remissions, with the development of atopic erythroderma.
AD is characterized by clinical polymorphism of rashes. True polymorphism of rashes is a common feature of all clinical forms of AD; they create a complex clinical syndrome with combined features of eczematous and lichenoid lesions, accompanied by itching.
Each age period has its own clinical and morphological features, which is manifested in the age-related evolution of the elements of the rash. In this regard, five clinical and morphological forms are distinguished (exudative, erythematous-squamous, erythematous-squamous with lichenification, lichenoid, pruriginous) and three stages of disease development - infant, child and adolescent-adult (Table 3).
Table 3
Age stages of development and clinical and morphological forms of atopic dermatitis
Based on the severity of AD, mild, moderate and severe forms of the disease are distinguished. During the course, acute, subacute periods and remission are distinguished (Table 4).
Table 4
Working classification of atopic dermatitis
Diagnosis examples:
Atopic dermatitis, exudative form, infant stage, stage II. severity, period of exacerbation.
Atopic dermatitis, erythematous-squamous form, childhood stage, stage I. severity, subacute period.
Atopic dermatitis, lichenoid form, teenage stage, stage III. severity, period of exacerbation
Appendix 2.
| Atoderm mousse, soap (BIODERMA) (from the neonatal period) |
| Cu-Zn+ gel, Cu-Zn+ dermatological soap (URIAGE) (from the neonatal period) |
| Xemoz syndet, soft cleansing cream-gel without soap (URIAGE) (from the neonatal period) |
| Trixera+ cleansing softening gel (AVENE) (from the neonatal period) |
| Trixera+ cleansing softening bath (AVENE) (from the neonatal period) |
| Exomega cleansing shower oil (A-DERMA) (from the neonatal period) |
| Cleansing softening gel (AVENE) (from the neonatal period) |
| Shampoo for removing milk crusts in infants (A-DERMA) |
| Friederm pH-Balance shampoo (MSD) |
| Dermalibur antibacterial cleansing gel for irritated skin at risk of infection (A-DERMA) (from the neonatal period) |
| Lipikar Syndet gel (LA ROCHE POSAY) (from 1 year) |
| Skin cap shampoo (CHEMINOVA INTERNACIONAL S.A.) (from 1 year) |
Appendix 3.
Non-steroidal drugs used for the treatment and care of the skin of patients with AD.
| Drug name | Age from which use is permitted | Indications |
| Atoderm R.O. zinc cream (BIODERMA) | From the neonatal period | In the acute period, it can be used during the period of weeping |
| Atoderm RR anti-relapse balm (BIODERMA) | From the neonatal period | When acute symptoms subside, before remission occurs |
| Atoderm cream (BIODERMA) | From the neonatal period | During remission |
| Spray with smectite Cu-Zn+ (URIAGE) | From the neonatal period | In the acute period when weeping |
| Cu-Zn+ cream (URIAGE) | From the neonatal period | |
| Xemosis cream-emollient, Xemosis cerate (URIAGE) | From the neonatal period | During remission |
| Locobase Ripea (ASTELLAS) | From the neonatal period | |
| Locobase Lipocrem (ASTELLAS) | From the neonatal period | During the acute period (in the absence of weeping) and during remission |
| Dermalibur cream (A-DERMA) | From the neonatal period | In the acute period, possibly due to wetting |
| Sitelium lotion (A-DERMA) | From the neonatal period | During the wet period |
| Trixera+ cream and balm (AVENE) | From the neonatal period | |
| DARDIA cream, milk, balm (INTENDIS) | From the newborn period cream, from 1 year balm and milk. | During remission |
| Locobase RIPEA (ASTELLAS) | From the neonatal period | In the acute period in the absence of weeping, as well as during remission |
| Lipikar balm (La Roche Posay) | From 1st year | In the acute period in the absence of weeping, as well as during remission. |
6. Atopic dermatitis. Etiology, pathogenesis, clinic
Atopic dermatitis is a hereditarily determined chronic disease of the entire body with a predominant lesion of the skin, which is characterized by polyvalent hypersensitivity and eosinophilia in the peripheral blood.
Etiology and pathogenesis. Atopic dermatitis is a multifactorial disease. Inherited predisposition to atopic diseases is realized under the influence of provoking environmental factors. An inadequate immune response contributes to increased susceptibility to various skin infections.
An important role in the pathogenesis of atopic dermatitis is played by the inferiority of the skin barrier associated with impaired ceramide synthesis.
The characteristics of the psycho-emotional status of patients are essential.
Clinic. Age periodization. Atopic dermatitis usually manifests itself quite early - in the first year of life, although its manifestation is possible at a later date. There are three types of atopic dermatitis:
1) recovery up to 2 years (most common);
2) pronounced manifestation up to 2 years with subsequent remissions;
3) continuous flow.
Atopic dermatitis occurs with chronic recurrence. Clinical manifestations of the disease change with the age of patients. Long-term remissions are possible during the course of the disease. There is an infant stage of the disease, which is characterized by an acute and subacute inflammatory nature of the lesions with a tendency to exudative changes and a certain localization - on the face, and with widespread lesions - on the extensor surfaces of the limbs, less often on the skin of the body. In the vast majority of cases, there is a clear connection with nutritional stimuli. Initial changes usually appear on the cheeks, less often on the outer surfaces of the legs and other areas.
The primary ones are erythematoedematous and erythematosquamous lesions. In more acute cases, papulovesicles, cracks, weeping, and crusts develop. Characterized by severe skin itching.
By the end of the first – beginning of the second year of life, exudative phenomena usually decrease. Infiltration and peeling of lesions increase. Lichenoid papules and mild lichenification appear. In the future, complete involution of the rash or a gradual change in morphology and localization is possible with the development of the clinical picture characteristic of the second age period.
The second age period (childhood stage) covers the age from 3 years to puberty. It is characterized by a chronically relapsing course, often depending on the season of the year (exacerbation of the disease in spring and autumn). Exudative phenomena decrease, pruriginous papules, excoriations predominate, and a tendency to lichenification, which increases with age.
By the end of the second period, the formation of changes typical for atopic dermatitis on the face is possible.
The third age period (adult stage) is characterized by a lesser tendency to acute inflammatory reactions and a less noticeable reaction to allergic irritants.
From the book ENT diseases by M. V. Drozdov From the book Urology by O. V. Osipova From the book Urology by O. V. Osipova From the book Dermatovenerology author E. V. Sitkalieva author From the book Internal Diseases author Alla Konstantinovna Myshkina From the book Internal Diseases author Alla Konstantinovna Myshkina From the book Internal Diseases author Alla Konstantinovna Myshkina From the book Internal Diseases author Alla Konstantinovna Myshkina author N.V. Gavrilova From book Infectious diseases: lecture notes author N.V. Gavrilova From the book Infectious Diseases: Lecture Notes author N.V. Gavrilova From the book Infectious Diseases: Lecture Notes author N.V. Gavrilova From the book Infectious Diseases: Lecture Notes author N.V. Gavrilova From the book Infectious Diseases: Lecture Notes author N.V. Gavrilova From the book Infectious Diseases: Lecture Notes author N.V. GavrilovaAtopic dermatitis, bronchial asthma Etiology Pathogenesis Clinical picture Laboratory and instrumental diagnostics Treatment Care Prevention
Atopic dermatitis
Atopic dermatitis - chronic allergic inflammatory disease skin, characterized age characteristics clinical manifestations and relapsing course.
The term " atopic dermatitis"has many synonyms (childhood eczema, allergic eczema, atopic neurodermatitis, etc.).
Atopic dermatitis is one of the most common allergic diseases. Its prevalence among children has increased significantly in recent decades and ranges from 6% to 15%. At the same time, there is a clear tendency towards an increase in the proportion of patients with severe forms of the disease and a continuously relapsing course.
Atopic dermatitis is a significant risk factor for the development of bronchial asthma, since the emerging sensitization is accompanied not only by skin inflammation, but also by a general immune response involving various parts of the respiratory tract.
Etiology. The disease in most cases develops in individuals with a hereditary predisposition. It has been established that if both parents suffer from allergies, then atopic dermatitis occurs in 82% of children, if only one parent has an allergic pathology - in 56%. Atopic dermatitis is often combined with allergic diseases such as bronchial asthma, allergic rhinitis, allergic conjunctivitis, and food allergies.
In the etiology of the disease, food allergens, microscopic house dust mites, spores of some fungi, and epidermal allergens of domestic animals play an important role. The main food allergen is cow's milk.
In some patients, the causative allergens are pollen from trees, cereal plants, and various herbs. The etiological role of bacterial allergens (Escherichia coli, pyogenic and Staphylococcus aureus) has been proven. Drugs, especially antibiotics (penicillins) and sulfonamides, also have a sensitizing effect. Most children with atopic dermatitis have a polyvalent allergy.
Pathogenesis. There are two forms of atopic dermatitis: immune and non-immune. In the immune form, there is an inherited ability to produce when encountering allergens. high level antibodies classified as IgE, resulting in allergic inflammation. Currently, genes that control IgE production have been identified.
Most children with the non-immune form of atopic dermatitis have adrenal dysfunction: insufficient secretion of glucocorticoids and overproduction of mineralocorticoids.
Clinical picture. Depending on age, the infant stage of atopic dermatitis is distinguished (from 1 month to 2 years); children (from 2 to 13 years old) and teenagers (over 13 years old).
The disease can occur in several clinical forms: exudative (eczematous), erythematosquamous, erythematosquamous with lichenification (mixed) and lichenoid.
Based on the prevalence of the process on the skin, limited atopic dermatitis is distinguished ( pathological process localized mainly on the face and symmetrically on the hands, the area of skin damage is no more than 5-10%), widespread (the process involves the elbow and popliteal folds, the back of the hands and wrist joints, the anterior surface of the neck, the affected area is 10-50%) and diffuse (extensive lesions of the skin of the face, trunk and limbs with an area of more than 50%).
Usually the disease begins in the 2nd month of a child’s life after he is transferred to artificial feeding. During the infant stage, hyperemia and skin infiltration, multiple rashes in the form of papules and microvesicles with serous contents appear on the face in the area of the cheeks, forehead and chin. The vesicles quickly open with the release of serous exudate, resulting in abundant oozing (exudative form). The process can spread to the skin of the trunk and limbs and is accompanied by severe itching.
In 30% of patients, the infant stage of atopic dermatitis occurs in the form of erythematosquamous form. It is accompanied by hyperemia, infiltration and peeling of the skin, the appearance of erythematous spots and papules. The rash first appears on the cheeks, forehead, and scalp. There is no exudation.
At the childhood stage, exudative lesions characteristic of infantile atopic dermatitis are less pronounced. The skin is significantly hypersmeared, dry, its folds are thickened, and hyperkeratosis is noted. The skin has foci of lichenification (emphasized skin pattern) and lichenoid papules. They are most often located in the elbow, popliteal and wrist folds, the dorsum of the neck, hands and feet (erythematosquamous form with lichenification).
Subsequently, the number of lichenoid papules increases, and multiple scratches and cracks appear on the skin (lichenoid form).
The patient's face takes on a characteristic appearance, defined as an “atopic face”: the eyelids are hyperpigmented, their skin is flaky, the skin folds are emphasized and the eyebrows are combed out.
The teenage stage is accompanied by pronounced lichenification, dryness and flaking of the skin. The rash consists of dry, scaly, erythematous papules and large numbers of lichenified plaques. The skin is predominantly affected on the face, neck, shoulders, back, flexor surfaces of the limbs in the area of natural folds, the back surfaces of the hands, feet, fingers and toes.
Adolescents may experience a priginous form of atopic dermatitis, which is characterized by severe itching and multiple follicular papules. They have a spherical shape, a dense consistency, and numerous scattered excoriations are located on their surface. The rash is combined with severe lichenification.
With a mild course of atopic dermatitis, limited skin lesions, slight erythema or lichenification, mild itching of the skin, and rare exacerbations are noted - 1-2 times a year.
In moderate cases, there is a widespread nature of skin lesions with moderate exudation, hyperemia and / or lichenification, moderate itching, more frequent exacerbations - 3-4 times a year.
A severe course is characterized by a diffuse nature of skin lesions, hyperemia and/or lichenification, constant itching and an almost continuous recurrent course.
To assess the severity of atopic dermatitis in allergology, the international SCORAD system is used. It evaluates several parameters.
Parameter A- prevalence of the skin process, i.e. area of skin affected (%). For assessment, you can use the palm rule (the area of the palmar surface of the hand is taken to be equal to 1% of the total surface of the body).
Parameter B- intensity clinical symptoms. To do this, the severity of 6 signs is calculated (erythema, edema/papule, crusts/wetting, excoriation, lichenification, dry skin). Each sign is scored from 0 to 3 points: 0 - absent, 1 - mildly expressed, 2 - moderately expressed, 3 - severely expressed. Symptom assessment is carried out on the area of skin where the lesions are most pronounced.
Parameter C- subjective signs (itching, sleep disturbance). Scored from 0 to 10 points.
SCORAD index = A/5 + 7B/2 + C. Its values can range from 0 (no skin lesions) to 103 points (maximum manifestations of the disease). Light form SCORAD course - less than 20 points, moderate - 20-40 points; severe form - more than 40 points.
Atopic dermatitis can occur in the form of several clinical and etiological variants (Table 14).
Laboratory diagnostics. IN general analysis eosinophilia is observed in the blood; when a secondary infection occurs on the skin, leukocytosis and accelerated ESR are observed. The immunogram determines increased level IgE. To identify a causally significant allergen outside of an exacerbation of the skin process, specific allergological diagnostics (skin tests with allergens) are carried out. If necessary, they resort to an elimination-provocative diet, which is especially informative in children in the first years of life.
Treatment. Therapeutic measures should be comprehensive and include a hypoallergenic lifestyle, diet, drug therapy in the form of local and systemic treatment.
In the apartment where a child with atopic dermatitis lives, it is necessary to maintain the air temperature no higher than +20... +22 ° C and a relative humidity of 50-60% (overheating increases the itching of the skin).
Table 14.Clinical and etiological variants of atonic dermatitis at children
|
With predominant food sensitization |
With predominant tick-borne sensitization |
With predominant fungal sensitization |
|
Association of exacerbation with the intake of certain foods; early start when switching to artificial or mixed feeding |
Exacerbations:
|
Exacerbations:
|
|
Positive clinical dynamics when prescribing an elimination diet |
Ineffectiveness of the elimination diet. Positive effect when changing place of residence |
Effectiveness of targeted elimination interventions and diet |
|
Detection of sensitization to food allergens (positive skin tests to food allergens, high content of allergen-specific IgE antibodies in the blood serum) |
Detection of sensitization to house dust mite allergens and complex house dust allergen (positive skin tests, high content of allergen-specific IgE antibodies in blood serum) |
Detection of sensitization to fungal allergens (positive skin tests, high levels of allergen-specific IgE antibodies in the blood serum) |
Much attention should be paid to creating a hypoallergenic lifestyle with the elimination of causally significant or potential allergens and nonspecific irritants. To this end, it is necessary to take measures to eliminate sources of accumulation of house dust in which mites, which are allergens, live: do wet cleaning daily, remove carpets, drapes, books, and, if possible, use acaricides.
You should not keep pets, birds, fish, or raise houseplants, since animal hair, bird feathers, dry fish food, as well as fungal spores found in flower pots are allergic genes. Contact with plants that produce pollen should be avoided.
No less important is the reduction in the child’s exposure to nonspecific irritants (elimination of smoking in the house, use of a hood in the kitchen, lack of contact with household chemicals).
The most important element in the complex treatment of atopic dermatitis is diet. Products that are causally significant allergens are excluded from the diet (Table 15). They are identified based on a survey of parents and the child, data from a special allergological examination, taking into account the analysis of a food diary.
Table 15.Classification of food products according to the degree of allergenic activity
Drug therapy for atopic dermatitis includes local and general treatment.
Currently, stepwise therapy of the disease is used.
Stage I (dry skin): moisturizers, elimination measures;
Stage II (mild or moderate symptoms of the disease): local glucocorticosteroids of low and moderate activity, 2nd generation antihistamines, calcineurin inhibitors (local immunomodulators);
Stage III (moderate and severe symptoms of the disease): local glucocorticosteroids of moderate and high activity, 2nd generation antihistamines, calcineurin inhibitors;
Stage IV (severe atopic dermatitis that cannot be treated): immunosuppressants, 2nd generation antihistamines, phototherapy.
Local treatment is an obligatory part complex therapy atopic dermatitis. It should be carried out differentiatedly, taking into account pathological changes skin.
The initial therapy drugs for moderate and severe forms of the disease are local glucocorticoids (MGCs). Taking into account concentration active substance There are several classes of MGCs (Table 16).
Table 16.Classification of local glucocorticoids by degree
activity
For mild and moderate atopic dermatitis, class I and II MGCs are used. In severe cases of the disease, treatment begins with class III drugs. In children under 14 years of age, class IV MHC should not be used. MHAs have limited use on sensitive areas of the skin: face, neck, genitals, and skin folds.
Strong drugs are prescribed in a short course for 3 days, weak ones - for 7 days. If the clinical manifestations of the disease decrease and if its course is undulating, it is possible to continue treatment with MHA in an intermittent course (usually 2 times a week) in combination with nutrients.
The drugs are applied to the skin once a day. It is not advisable to dilute them with indifferent ointments, since this is accompanied by a significant decrease in the therapeutic activity of the drugs.
Local glucocorticoids should not be used for a long time, as they cause the development of local side effects such as stretch marks, skin atrophy, telangiectasia.
Minimum side effect have non-fluorinated MHAs ( elocom, advantan). Of these, elocom has an advantage in efficiency compared to advantan.
For atopic dermatitis complicated by a bacterial infection on the skin, it is recommended combination drugs containing corticosteroids and antibiotics: hydrocortisone with oxytetracycline, betamethasone with gentamicin. In recent years, a combination of a broad-spectrum antibiotic has been widely used - fusidic acid with betamethasone (fucicort) or with hydrocortisone (fucidin D).
For fungal infections, a combination of MHA with antifungal agents is indicated ( miconazole). Combination preparations containing a glucocorticoid, an antibiotic and an antifungal agent have a triple effect (antiallergic, antimicrobial, antimycotic) (betamethasone + gentamicin + clotrimazole).
For local treatment atopic dermatitis with mild and moderate course of the disease, local immunomodulators are used. They prevent disease progression, reduce the frequency and severity of exacerbations, and reduce the need for MGCs. These include non-steroidal drugs pimecrolimus And tacrolimus in the form of 1% cream. They are used for a long time, for 1.5-3 months or more on all areas of the skin.
In some cases, an alternative to MHA and local immunomodulators may be tar preparations. However, at present they are practically not used due to the slow development of the anti-inflammatory effect, pronounced cosmetic defect and possible carcinogenic risk.
Has an anti-inflammatory effect and restores the structure of damaged epithelium D-Panthenol. It can be used from the first weeks of a child’s life on any area of the skin.
Can be used as drugs that improve skin regeneration and restore damaged epithelium. bepanthen, solcoseryl.
They have a pronounced antipruritic effect 5-10% benzocaine solution, 0.5-2% menthol solution, 5% procaine solution.
The modern standard of local therapy for atopic dermatitis includes nourishing and moisturizing agents. They are used daily, their effect lasts for about 6 hours, so they should be applied to the skin regularly, including after each wash or bath (the skin should remain soft throughout the day). They are indicated both during the period of exacerbation of the disease and during the period of remission.
Ointments and creams restore damaged epithelium more effectively than lotions. Every 3-4 weeks, a change of nourishing and moisturizing products is necessary.
Traditional care products, especially those based on lanolin and vegetable oils, have a number of disadvantages: they create an impermeable film and often cause allergic reactions. In addition, their efficiency is low.
More promising use modern means medicinal dermatological cosmetics (Table 17). The most common are the special dermatological laboratory "Bioderma" (program "Atoderm"), the laboratory "Uriage" (program for dry and atopic skin), the laboratory "Aven" (program for atopic skin).
To cleanse the skin, it is advisable to take daily cool baths (+32...+35 °C) lasting 10 minutes. Baths are preferable to showers. Baths are carried out with products that have a soft detergent base (pH 5.5) that does not contain alkali. For the same purpose, medicinal dermatological cosmetics are recommended. After bathing, the skin is only blotted without wiping it dry.
Basic therapy general treatment atopic dermatitis are antihistamines (Table 18).
1st generation antihistamines have a number of significant disadvantages: to achieve the desired therapeutic effect, they must be prescribed in large doses. In addition, they cause lethargy, drowsiness, and reduce attention. In this regard, they should not be used for a long time and are used in case of exacerbation of the process in short courses at night.
Table 17.Dermatological cosmetics for skin care with atopic dermatitis
|
Program |
Hydration |
Anti-inflammatory |
||
|
Atoderm program (Bioderma laboratory) |
copper - zinc gel copper - zinc |
atoderm RR Hydrabio cream Thermal water Uriage (spray) Hydrolipidic cream |
atoderm RR Cream emollient Cream Estrem |
Cream atoderm Spray copper - zinc Cream copper - zinc Prirised cream Prirised gel |
|
Program for dry and atopic skin (Uriage laboratory) |
copper - zinc gel copper - zinc |
Thermal Uriage (spray) Hydrolipidic cream |
Cream emollient Cream Extrem |
Spray copper - zinc Cream copper - zinc Cream squat Gel squat |
Table 18.Modern antihistamine drugs
2nd generation antihistamines are more effective. They can also be used during the daytime.
In order to stabilize the membranes of mast cells, cromones are prescribed - nalcrom, membrane stabilizing drugs: ketotifen, vitamin E, dimephosphone, xidifon, antioxidants ( vitamins A, C, polyunsaturated fatty acids), vitamins and B 15, zinc and iron preparations. Anti-leukotriene drugs are effective ( montelukast, zafirlukast and etc.).
To normalize the function of the gastrointestinal tract and intestinal biocenosis, enzyme preparations are indicated ( festal, mezim-forte, pancitrate, creon) and factors that promote colonization of the intestine with normal microflora (probiotics - lactobacterin, bifidobacteria, enterol, bactisubtil and etc.; prebiotics - inulin, fructooligosaccharides, galactooligosaccharides; synbiotics - fructooligosaccharides + bifidobacteria, lacthiol + lactobacilli, etc.).
Enterosorbents are systematically used to absorb food allergens: activated carbon, smecta, polypephan, belosorb.
Systemic glucocorticoids and immunosuppressive therapy are used in severe cases and insufficient effectiveness of all other treatment methods.
Prevention.Primary prevention must be carried out during fetal development and continue after the birth of the child.
High antigen loads during pregnancy (abuse of highly allergenic foods, one-sided carbohydrate nutrition, irrational use of medications, gestosis, exposure to occupational allergens) significantly increase the risk of atopic dermatitis in a child.
In the first year of a child’s life, breastfeeding, rational nutrition of the nursing mother, proper introduction of supplementary feeding, and a hypoallergenic lifestyle are important.
Primary prevention of atopic dermatitis also includes avoiding smoking during pregnancy and in the house where the child is, eliminating contact of a pregnant woman and child with pets, and reducing children’s contact with chemicals in the home.
Secondary prevention is to prevent relapses. When breastfeeding, the severity of the disease can be significantly reduced by the mother following a hypoallergenic diet and taking probiotics. Their use in a child is important. If impossible breastfeeding The use of hypoallergenic mixtures is recommended. In the future, the main principle of diet therapy remains the exclusion of the cause-significant allergen from the diet.
In the system of preventive measures, great importance is given to the hygienic maintenance of the premises (using air conditioning in hot weather, using a vacuum cleaner during cleaning, etc.), ensuring a hypoallergenic lifestyle, and educating the child and family.
An essential part of secondary prevention is skin care (proper use of nourishing and moisturizing products and medicinal drugs, applying sunscreen in sunny weather, taking a cool shower every day, using a washcloth made of terry cloth for washing, which does not allow intense friction of the skin, wearing clothes made of cotton fabrics, silk, linen, excluding items made from wool and animal fur from the wardrobe, regularly changing bedding linen, use of synthetic fillers for bedding. During an exacerbation, the child is advised to sleep in cotton gloves and socks, cut his nails short, and use liquid detergents for washing.
