Atopic dermatitis

Atopic dermatitis - acute, subacute or chronic recurrent inflammation of the epidermis and dermis, characterized by pronounced itching, has a certain age dynamics.

The term "atopic dermatitis" was first proposed in 1923 by Subzberger for the diseased skin, accompanied by increased sensitization to various allergens. In the anamnesis or in close relatives often allergic diseases are found (hay fever, allergic rhinitis, bronchial asthma). This definition is conditional and there is no generally accepted definition of atopic dermatitis in the scientific literature, since the term is not applicable to any clearly delineated clinical situation, but to a heterogeneous group of patients with chronic superficial inflammation of the skin. Synonyms of atopic dermatitis are atonic - eczema, constitutional eczema, allergic dermatitis, neurodermatitis, prurigo Rciibe, exudative-catarrhal diathesis, allergic diathesis, children's eczema. The variety of terms reflects the phase transformation of skin elements and the chronic recurrent course of the disease.

[1], [2], [3], [4]

Epidemiology

Atopic dermatitis occurs in all countries, in people of both sexes and in different age categories.

The incidence of atopic diseases is increasing. They affect approximately 5 to 20% of the population, most often expressed as allergic rhinitis and atopic dermatitis (approximately 50%) and significantly less in the form of bronchial asthma. Atopic dermatitis is manifested in most cases already in infancy, often between 2 and 3 months of life. The disease can occur in later childhood. According to scientists, atopic dermatitis is on the eighth place in the frequency of all dermatoses in persons under 25 years of age. The disease occurs in infancy, early childhood, in adolescents and adults. Male subjects are more likely to get sick in infancy and childhood, and women in older children and adults. Primary manifestations of atopic dermatitis after the period of puberty are relatively rare.

[5], [6], [7], [8], [9], [10], [11], [12]

Causes of the atopic dermatitis

Atopic dermatitis primarily affects children in developed countries; At least 5% of children in the United States are affected by this disease. Like asthma, this may be due to the pro-allergic or pro-inflammatory immune response of the T-cells. Such reactions are most often observed in developed countries with a tendency toward small families, where the hygienic state of the premises where early vaccination is performed is better, which protects children from infections and allergens, but suppresses the pro-allergic reaction of T-cells and leads to tolerance.

Atopic dermatitis develops under the influence of environmental factors provoking immunological, usually allergic (for example, IgE-mediated) reactions in people with an increased genetic predisposition. Causative factors include food products (milk, eggs, soybean, wheat, peanuts, fish), inhalation allergens (dust mites, mold, dandruff) and colonization of Staphylococcus aureus on the skin due to a lack of endogenous antimicrobial peptides. Atopic dermatitis often has a genetic component, therefore it is of a family nature.

Kaposi's herpetiform eczema is a common form of herpes simplex that occurs in patients with atopic dermatitis. Typical groups of vesicles are formed not only in places of rashes, but also on healthy skin. After a few days, the temperature rises and adenopathy develops. Rashes are often infected with staphylococcus aureus. Sometimes viremia develops and infection of the internal organs, which can lead to death. As with other herpetic infections, relapse is possible.

Fungal and non-herpetic viral skin infections, such as warts and molluscum contagiosum, can also complicate atopic dermatitis.

Exogenous (biological, physical and chemical) and endogenous (GI, nervous system, genetic predisposition, immune disorders) factors take part in the development of atopic dermatitis. The leading role in the pathogenesis of atopic dermatitis belongs to a hereditary predisposition. 70% of children with atopic dermatitis have a high serum IgE level, which is controlled by the IL-4 gene. If the population risk of atopic dermatitis is 11.3%, then it is 44.8% in children. In patients with atopic dermatitis, family atopy occurs 3-5 times more often than in healthy ones. Mainly there is a connection with atonic diseases along the mother's line (60-70%), more rarely - along the line of the father (18-22%). It has been established that atopic dermatitis develops in 81% of children, if both parents suffer from atopic dermatitis and 56% when only one parent suffers. According to some scientists, atopic dermatitis is inherited by polygenic type.

According to modern views, the most important place in the functioning of the immune system belongs to T cells with helper activity and a decrease in the number and functional activity of T supressors. Immunopathogenesis of atopic dermatitis can be represented as follows: as a result of the violation of the integrity of biological membranes, antigen penetration (bacteria, viruses, chemicals, etc.) occurs in the internal environment of the organism and recognition of these antigens by antigen-presenting cells - APC (macrophages, Langerhans cells, keratocytes and leukocytes) , which activate T-lymphocytes, and there is an intensification of the process of differentiation of T-helper cells of the first and second order. The key point is calcineurin (or calcium-dependent phosphatase), under the influence of which the nucleotide factor of activated T-lymphocytes is nucleated to the core. As a result of the ego, activation of T-helper cells of the second order, which synthesize and secretion of proinflammatory cytokines-interleukins (IL 4, IL 5, IL 13, etc.) occurs. IL 4 is the main factor for the induction of IgE synthesis. There is also an increase in the production of specific IgE antibodies. Later, with the participation of mast cells, which produce histamine, serotonin, bradykinin and other biologically active substances, the early phase of the hyperergic reaction develops. Further, in the absence of treatment, the IgE-dependent late phase develops, characterized by infiltration of the skin with T lymphocytes, determining the timing of the allergic process.

In the formation of atopic dermatitis, great importance is attached to the functional state of the gastrointestinal tract. Dysfunction of the gastrin regulation link was found, consisting of imperfect parietal digestion, insufficient activity of enzymes in the treatment of chyme, etc. In children of the first year of life, the frequent cause of atopic dermatitis is the consumption of chicken eggs, proteins, cow's milk, cereals. The course of atopic dermatitis is aggravated by the development of dysbacteriosis due to the uncontrolled intake of antibiotics, corticosteroids, the presence of foci of chronic infection, allergic diseases (asthma, rhinitis), dismetabolic nephropathies, and helminthiases.

The value of the inheritance type for atopic dermatitis

The type of inheritance in all the details is not yet clear, not related to a separate gene. The effect of the HLA system is also apparently absent. The probability of disease for a child who has one of the parents with atopy is estimated at 25-30%. If both parents are atopics, it significantly increases and is 60%. Probably a polygenic type of inheritance. Not inherited atopic disease is inherited, but predisposition to atopic reaction of various systems. Approximately 60-70% of patients have a positive family anamnesis for atopy. For this reason, careful collection of family and individual history with atopic diseases is of diagnostic importance for determining atopic dermatitis. In addition to hereditary predisposition, an important role is played also by exogenous, individually realized factors. Among the environmental factors provoking atopic diseases of the respiratory tract or intestines, the importance is not only inhalation (home dust mites, plant pollen, animal hair) or food allergens (often together with allergic urticaria) - such as milk protein, fruit, eggs, fish , preservatives, but also individual factors such as stress or accompanying psycho-vegetative and psychosomatic disorders.

Approximately 30% of cases are vulgar ichthyosis, with even greater frequency - dry skin (asteatosis, sebostasis) with altered lipid content and increased water permeability (violation of the barrier function). Many patients have a typical ichthytic palm with a pronounced linear pattern - hyperlinaearance. Vitiligo is more common in patients with atopic dermatitis, and alopecia in these patients has an unfavorable prognosis (atopic type of alopecia). Remarkable also is the formation, although very rare, of eye anomalies, such as atopic cataracts, especially in young people, less often keratoconus. There is a connection with dyshidrosis, dyshidrotic eczema of the palms and urticaria. The connection with migraine is discussed, but it is not considered to be reliably established.

[13], [14], [15], [16], [17], [18]

Risk factors

In recent years there has been an increase in the incidence of atopic dermatitis. This, apparently, is due to the frequent use of allergenic foods, vaccination. The use of various drugs, in particular antibiotics, and environmental pollution.

[19], [20], [21], [22], [23]

Pathogenesis

Atopic dermatitis is a hereditary disease of a multifactorial nature with a genetically determined deficit of the function of suppressor T-lymphocytes, a simultaneous partial blockade of beta-adrenergic receptors and a B-dependent IgE-globulin mechanism of pathological immune responses. The main symptom is itching. Skin lesions vary from mild erythema to severe lichen. The diagnosis is substantiated anamnesticheski and clinically. In treatment, moisturizing creams, topical glucocorticoids are used. In addition, it is necessary to avoid allergic and irritating factors.

Atopic dermatitis is characterized by age-related variability, chronic recurrent course, itchy inflammatory skin lesions with true polymorphism (erythema, papules, vesicles), lichenification; symmetrical topography of rashes, which depends on evolutionary dynamics; often combined with functional disorders of the nervous system, impaired immunity, atopic injuries of respiratory organs.

Atopic dermatitis (ATD) is an IgE-dependent (exogenous 70-80% of cases) or lgE-independent (endogenous in 20-30% of cases). LgE-dependent is better studied; lgEindependent atopic dermatitis is an idiopathic and without a family predisposition of the disease.

Among dermatological diseases, atopic dermatitis due to the completely unexplained etiopathogenesis, chronic course and related therapeutic problems occupies a special place in dermatology. There are about a hundred signs of this disease in the literature. Unlike English and French literature, in which the term "atopic dermatitis" or "atopic eczema" has been established, the terms "atopic eczema", "endogenous eczema", "diffuse neurodermatitis", "atopic neurodermatitis" are more often used in German sources. Such terminological kaleidoscope complicates the work of practical doctors and creates confusion in identifying the disease. It is recommended to adhere to two equivalent and unambiguous terms: "atopic dermatitis" and "atopic neurodermatitis", although the English-language manuals on dermatology often use the name "atopic eczema".

The difficulty in applying the concept of "atopic disease" is that with allergic rhinitis, allergic conjunctivitis and allergic bronchial asthma, it is a question of IgE-mediated allergic reactions of immediate type (type I by Coombs and Gell), and in atopic dermatitis, there is a complex interaction of several immunological and non-immunological factors, which are partially unknown. From this fact, there are also existing difficulties to terminology up to the present day. The name neurodermatitis, proposed by Brocq in 1891, indicates a presumptive pathogenetic connection with the nervous system, since severe itching was seen as a factor triggering the disease. The synonyms used for this constitutional or atopic neurodermatitis indicate, in particular, the pathogenetic significance of familial or hereditary factors, while the names of atopic eczema, endogenous eczema, or constitutional eczema focus more on eczematous eruptions.

Immunological theory attracts more attention, but the phenomena that cause the reaction have yet to be identified. There are anomalies of both humoral and cell-mediated immunity. Obviously, IgE is stimulated by specific antigens. It is located on mast cells and causes the release of inflammatory mediators from them. In favor of cell-mediated factors is evidence of susceptibility to viral infections and their recurrence, including herpes simplex, molluscum contagiosum and warts. Patients are often resistant to sensitization of dinitrochlorobenzene. The presence of a reduced number of T-lymphocytes may indicate a lack of important T-cell subpopulations that control the production of immunoglobulin by B cells and plasmocytes so that IgE production levels are high. In addition, phagocytic activity is reduced and the chemotaxis of neutrophils and monocytes is impaired. Another factor supporting the immunological basis is the presence of a significant amount of staphylococci in both the patient and the healthy skin of patients with atopic dermatitis.

Beta-adrenergic theory is supported by a number of abnormal skin responses. These include an excessive constrictor response of cutaneous vessels, white dermographism, delayed blanching for cholinergic stimuli, and a paradoxical response to the use of nicotinic acid. Reduced cAMP levels can increase the release of mediators from mast cells and basophils.

Violations of humoral immunity

Persons with hereditary predisposition to atopy react to contact with environmental substances (allergens) by sensitization of the immediate type. Such sensitization is confirmed by urticar reaction of the immediate type during the intracutaneous test. Immunologically, it is an immediate allergic reaction (type I to Coombs & Gell). A healthy person does not react to contact with such substances found in the environment. However, the essence of atopic dermatitis can not be reduced only to one such allergic reaction method of the atopic organism.

Patients already during the early childhood by skin test are found positive reactions of immediate type to food and inhalant allergens. The number of positive skin reactions is from 50 to 90%. Patients with allergic bronchial asthma or allergic rhinitis are more likely to have positive intracutaneous reactions to inhaled allergens, in particular home dust, house dust mites (Dermatophagoides pteronyssinus), plant pollen or animal allergens (wool and animal dander). Human dander and sweat proteins can also act as allergens. Although the causative role of inhalant allergens as agents of deterioration of atopic dermatitis is not yet clear, it is known to any dermatologist that seasonal exacerbation of allergic rhinitis is accompanied by a worsening of cutaneous manifestations, and vice versa. Food allergens (protein in milk, fish, flour, fruits, vegetables) also often give positive test responses, although they do not always coincide with clinical symptoms. In addition, mothers often note the fact that itching and inflammatory skin reactions in their babies are often provoked by certain foods (such as milk or citrus fruits). Prospective studies show that feeding the baby with maternal, and not cow's milk, in the first weeks of life has a positive effect on atopic children; so in the first months of life it is recommended that mother's milk. In addition, external contact with the pollen of plants can cause inflammatory skin reactions and provoke pollen vulvitis in young girls.

So, in general, despite the fact that the pathogenetic significance of immediate reactions for the development of atopic dermatitis has not yet been fully appreciated, a number of data speak in his favor. Relevant intradermal and in vitro tests (RAST) are also indicated, and the test responses should be considered critically, in conjunction with the overall clinical picture, which may serve as an occasion for possible further activities such as exposure tests or elimination diet.

The definition of IgE is currently carried out most often through the PRIST method. In most patients with severe atopic dermatitis, serum IgE is elevated. Elevated levels of IgE are recorded especially with simultaneous manifestations in the respiratory tract (allergic asthma, allergic rhinitis). However, since in some individual patients with advanced skin lesions, the IgE level may be normal, its determination, except for cases of suspected hyper-IgE syndrome, has no pathognomonic significance, especially as in other inflammatory dermatoses, serum IgE levels increase. Therefore, the absence of IgE in the serum does not mean that there is no atopic dermatitis. Remarkable is also a decrease in the increased IgE indices during remission of the disease.

In recent years, thanks to modern immunological methods, a better understanding of the regulation of IgE formation has been achieved. Certain cytokines that are generated by activated T-lymphocytes, in particular interleukin-4 (IL-4) and interferon-7 (INF-y), are involved in a complex network of regulatory signals for IgE synthesis via B lymphocytes. Further research in this area could show therapeutic implications if the overproduction of IgE could be inhibited.

The RAST method provides the physician with a method for proving in vitro the presence of allergen-specific antibodies to the patient's blood serum. In this way, the presence of IgE antibodies to a range of inhaled and food allergens can be demonstrated. Atopic dermatitis, RAST or ATS are positive in a large percentage of cases; these techniques can prove the presence of circulating antibodies to environmental allergens that were not covered by the intracutaneous test.

[24], [25], [26], [27]

Disturbances of cellular immunity

In patients with atopic dermatitis, in addition to violations of humoral immunity, there is a weakening of cellular immunity. It is noteworthy that such patients are susceptible to viral, bacterial and fungal skin infections. These infections, on the one hand, are more common in atopics, and on the other hand, they are more severe. As complications of this kind are known eczema verrucatum, eczema molluscatum, eczema coxsaccium, as well as impetigo contagiosa and tinea corporis. In severe atopic dermatitis, an obvious reduction in erythrocyte rosette formation, a change in the response of T-lymphocytes to mitogens, a decrease in in vitro stimulation of lymphocytes with bacterial and mycotic antigens, and a decrease in propensity to contact sensitization (however, with a high prevalence of contact allergy to nickel), a decrease in the number or activity of natural killer cells. The severity of the disease correlates with a decrease in suppressor T-lymphocytes. It is known from practice that patients have a slight tendency to develop contact dermatitis after topical application of medications. Finally, defects of neutrophil granulocytes (chemotaxis, phagocytosis) and monocytes (chemotaxis) are proved. Eosinophils increase and react more strongly to stress. Obviously, the number of IgE-bearing lymphocytes is also increased. Interpretation of these data is rather complicated. The hypothesis is based on the assumption that the excessive formation of IgE in patients with atopic dermatitis is due to the secretory deficiency of IgA, especially in the first three months of life, and it can not be compensated because of a deficiency of suppressor T-lymphocytes. In this sense, the original cause defect should be sought in the T-lymphocyte system. It can be imagined that as a result of impaired inhibition of T-lymphocyte activity, inflammatory changes in the skin can develop spontaneously, as occurs with contact allergic dermatitis. The results of the latest research also support this hypothesis.

IgE-bearing antigen-presenting cells in the epidermis, that is, Langerhans cells, also play a significant role in the onset of skin changes in atopic dermatitis. It is suggested that antigen-specific IgE molecules bound on the surface of the Langerhans epidermal cells through the high affinity receptor, aeroallergens (home dust mites antigens from the skin surface) and food allergens interact through the bloodstream. Then they, like other contact allergens, are presented by Langerhans cells to allergen-specific lymphocytes, which cause an inflammatory allergic reaction of the eczematous type. This new concept of the pathogenesis of atopic dermatitis forms a bridge between the humoral (IgE-mediated) and cellular links of the immune response and is clinically confirmed in that epicutane tests with inhalant allergens (eg plant pollen) in patients with atopic dermatitis, in contrast to healthy persons, can lead to an eczematous skin reaction in the area of the test.

[28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38]

Violations of the autonomic nervous system

The best known is white dermographism, that is, narrowing of the vessels after mechanical stress on the skin in its apparently unchanged areas. In addition, after the application of the nicotinic acid ester reactively there is not erythema, but anemia due to contraction of capillaries (white reaction). Injection of cholinergic pharmacological agents, such as acetylcholine, also results in white skin color at the injection site. Of course, white dermographism is uncharacteristic for inflamed skin areas. The tendency to vascular contraction in such patients is also manifested with a relatively low temperature of the skin of the fingers and a strong contraction of the vessels after exposure to cold. It is for sure not known whether this is an abnormal sensitivity of alpha-adrenergic stimulation of muscle fibers. In connection with this, the theory of Szentivanzy about beta-adrenergic blockade became known. The inhibition of beta receptor activity results in a reduced reactive rise of cAMP of cells with an increased tendency to form inflammatory mediators. Violation of the balance between alpha and beta adrenergic receptors can probably also explain the increased sensitivity of smooth muscle cells in the zone of blood vessels and pilomotors. The absence of cAMP-induced inhibition of antibody synthesis can lead to an increase in their formation. In addition, the underlying cause may be the basis of pharmacological and immunobiological disorders.

Sebostase (asteatosis)

Reducing the production of sebaceous glands is a typical phenomenon for patients with atopic dermatitis. Skin is dry and sensitive, it is prone to frequent drying and / or showering to further drying and itching. Hence the low inclination of such patients to diseases of the seborrheic circle, such as vulgar acne, rosacea or seborrheic eczema, is also understandable. In the basis of dryness and skin sensitivity, there are probably also disorders in the formation of epidermal lipids (ceramides) or a violation in the metabolism of essential fatty acids (deficiency of 8-6-dezaturase), which may have immunological consequences. An anomaly in the metabolism of essential fatty acids is based on the recommended diet with the content of y-linoleic acids.

Infringement of a sweating

Such violations are not proven for certain. Rather, there are sweating disorders. Many patients complain of severe itching with sweating. It is possible that sweating is impeded by disorders in the stratum corneum (hyperkeratosis and parakeratosis), so that sweat after exiting the excretory ducts of the sweat glands into the surrounding skin initiates inflammatory reactions (sweating-delay syndrome). Sweat also contains IgE and mediators of inflammation and can cause reactions of reflex reddening and hives.

Climatic allergens

As the reasons for the development of atopic dermatitis, so-called climatic allergens were also considered. In mountains at an altitude of more than 1500 m above sea level or on the coast of the North Sea, patients often feel very good, but the underlying pathophysiological processes are difficult to generalize. In addition to allergic factors, the level of insolation and the state of mental relaxation can be important.

[39], [40], [41], [42], [43]

Neuropsychological factors

They play a very important role. The effect of stress or other psychological factors can be represented through the adenylcyclase-cAMP system. Patients with atopic dermatitis often represent individuals of asthenic type, have a level of education above the average, are prone to selfishness, self-doubt, conflict situations such as "mother-child" in which the dominant mother is, suffer from frustration, aggression or suppressed states of fear. It remains an open question what is primary here, and what is secondary. However, highly itchy skin manifestations can also participate in the formation of personality and affect sensitively, especially in children, on their development and school success.

Bacteria

Patients with atopic dermatitis are prone to staphylococcal skin lesions and may have an increased amount of staphylococcal IgE antibodies in the serum. The pathogenetic significance of this fact has not been elucidated, but it must be taken into account in the course of treatment.

Summarizing the above, it should be noted that modern data indicate the immunological basis of atopic dermatitis. Atopic specific T helper cells can play a pathogenetic role by producing and releasing cytokines relevant for allergic inflammation, such as IL-4, IL-5 and other factors. It is suggested that eosinophils play a major role as effector cells mediating a pathogenetically significant late-phase reaction that is associated with significant destruction of the surrounding tissue. Accordingly, significant preactivation of peripheral blood eosinophils in patients with atopic dermatitis was found, which leads to increased sensitivity of these cells to certain stimuli, such as IL-5. Toxic proteins, such as the eosinophilic cationic protein contained in the matrix and nucleus of secondary eosinophil granules, can play an important role in spreading the allergic inflammatory process both indirectly and directly, due to its immunomodulatory properties.

In patients with atopic dermatitis, the content of "eosinophils-long-livers" is increased, which in vitro have a long decay period and are less prone to apoptosis. Long-term in vitro growth was stimulated by IL-5 and GM-CSF; the content of both mediators is increased with atopic dermatitis. Eosinophils with a prolonged life cycle may be a characteristic feature of atopic dermatitis, since eosinophils from patients with hypereosinophilic syndrome do not exhibit similar properties in vitro.

The pathogenetic role of eosinophils in atopic dermatitis is confirmed by the detection of proteins contained in their granules in the eczematous skin of patients. Moreover, current data indicate a significant correlation between the activity of the disease and the accumulation (deposition) of the contents of the eosinophilic granule:

• serum eosinophilic cationic protein levels in patients with atopic dermatitis were significantly increased;
• the levels of the eosinophilic cationic protein were correlated with the activity of the disease;
• Clinical improvement was associated with both a decrease in the clinical evaluation of disease activity and a decrease in the level of the eosinophilic cationic protein.

These data clearly indicate that activated eosinophils are involved in the allergic inflammatory process in atopic dermatitis. Consequently, a change in the activity of eosinophils may be an important criterion in the selection of pharmacological agents for the treatment of atopic dermatitis in the future.

The first and main aspect of the pathogenesis of atopic dermatitis is allergic dermatitis. Intradermal or cutaneous administration of various allergens in most patients with atopic dermatitis, having only skin lesions, received 80% of positive reactions. The following allergens play the main role in atopic dermatitis: air allergens (house dust mite, mildew, animal hair, pollen), living agents (staphylococci, dermatophytes, pitirosporum orbicular), contact allergens (aeroallergens, nickel, chromium, insecticides), food allergens. Of all specific aeroallergens, house dust mite allergens can cause a specific inflammatory response in most patients with atopic dermatitis, especially in individuals over 21 years of age. Food products are important allergens in atopic dermatitis in early childhood.

[44], [45], [46], [47], [48], [49], [50], [51], [52]

Histopathology

The histopathological picture of the disease depends on its type. In the presence of exudative foci in the infancy period, the same phenomena are observed as in allergic contact dermatitis: spongiosis and spongiotic blisters, beginning acanthosis with hyper- and parakeratosis and serum inclusions, as well as a dermal perivascular infiltrate from lymphocytes and histocytes with exocytosis. In lichenized foci, the epidermis is acanthotically thickened 3-5 times and has a disturbance of keratinization (hyperkeratosis); the papillary body is hypertrophic and permeated with inflammatory cells (lymphocytes, histiocytes). Remarkable is the presence, as in psoriasis, of a large number of mast cells, which is explained by the increased content of histamine in chronic lichenificated foci.

Symptoms of the atopic dermatitis

Atopic dermatitis usually begins in infancy - up to 3 months. During the acute phase of the disease, which lasts 1-2 months, the face develops red, crusty foci that spread to the neck, scalp, limbs and abdomen. During the chronic phase, scratching and rubbing cause skin lesions (typical foci - erythematous spots and papules against the background of lichenification). The foci usually appear in the elbow folds, popliteal fossa, on the eyelids, neck and wrists. The lesions gradually dry out, causing xerosis. In adolescents and adults, the main symptom is intense itching, which is intensified by exposure to allergens, dry air, sweating, stress and wearing of wool clothes.

[53], [54], [55], [56], [57], [58]

Forms

Distinguish the following clinical and morphological forms of atopic dermatitis: exudative, erythematous-squamous, erythematous-squamous with lichenification, lichenoid and pruriginous. This division of atopic dermatitis is more acceptable for a practical doctor

Exudative form is more common in infancy. This form is clinically manifested by bright edematous erythema, against which there are small flat papules and microvesicles. In the foci of lesion marked exudation and scaly-cortical layers are noted. The process in the initial period is localized on the face, in the region of the cheeks, then spreads to other areas of varying intensity. Often joins a secondary infection.

Erythematous-squamous form is observed during early childhood. Elements of the rash are erythema and flakes, which form single or multiple erythematous-squamous lesions. Against this background, often there are individual small papules, vesicles, hemorrhagic crusts, excoriation. Subjectively, there is an itch of varying intensity. Foci, as a rule, are localized on the flexor surfaces of the limbs, the anterior and lateral surfaces of the neck, the back of the hands.

Erythematous-squamous form with lichenification usually occurs in the childhood period.

With this form against the background of the erythematous-squamous lesion, there are strongly itchy lichen papular rashes. The lesion focus is lichenified, the skin is dry, covered with small-scale scales, there are hemorrhagic crusts and excoriation. Elements of the rash are localized in the elbows, on the neck, and in the face in the popliteal fossa. Often joins a secondary infection.

The vesiculosis -cross-like form of atopic dermatitis is formed on the 3-5th month of life and is characterized by the appearance on the background of erythema of microvesicles with serous contents. Microvesicles are opened with the formation of serous "wells" - point erosions, simultaneously marked by intense itching of affected areas of the skin. The process is most pronounced on the skin of the cheeks, trunk and extremities.

The lichenoid form occurs in adolescence and adolescence and has clear foci with pronounced lichenification and infiltration, lichenoid papules with a shiny surface. On the surface of the lesion, hemorrhagic crusts and excoriations are noted. Due to painful itching, sleep disturbance, irritability and other neurological disorders are noted. Foci of lesion are localized on the face (around the eyes, eyelids), neck, elbow folds.

The pruriginous form (prurigo Gebra) is characterized by the appearance on the upper and lower limbs, in the neck, gluteal and lumbar regions of isolated itchy papules the size of a pea.

By the prevalence of the skin process, a limited, widespread and diffuse atopic dermatitis is isolated.

With limited atopic dermatitis (lichen Vidal), lesions are limited to elbows or knee folds, the area of the rear of the wrists or wrist joints, anterior or posterior surfaces of the neck. Itching is mild, with rare attacks (see chronic simple diarrhea).

With widespread atopic dermatitis, lesions occupy more than 5% of the skin area, the skin-pathological process extends to the limbs, trunk, and head. There is dry skin, intense itching, pungent or small-plate peeling. With diffuse atopic dermatitis, the whole surface of the skin is lesioned, with the exception of the palms and nasolabial triangle, biopsy itching, severe dryness of the skin.

[59], [60]

Complications and consequences

They are mainly due to secondary infections or illiterate therapy (a rigid diet with secondary manifestations of deficiency, side effects of glucocorticoids). Reported violations in growth in children with severe atopic dermatitis. In infections, a certain role is played by violations of the function of leukocytes and lymphocytes, and also that skin manifestations in patients after months of treatment with external glucocorticoids become more sensitive to infections. Staphylococcus aureus is often found on the skin of such patients.

Secondary bacterial infection

It is expressed in impetiginization of foci due to Staphylococcus aureus. Yellow impetiparous crusts on dermal manifestations with an unpleasant odor - a typical picture, which, together with a painful increase in lymph nodes, makes it possible to diagnose. Furuncles, erysipelas and otitis externa are quite rare.

[61], [62], [63], [64], [65], [66], [67], [68], [69], [70]

Secondary viral infections

The broken barrier function of the skin in such patients makes it more sensitive to infections caused by viruses. This applies primarily to infections caused by the herpes simplex virus (eczema herpeticatum). At present, there is also a report on the transfer of the smallpox virus. This disease begins acutely with fever and a corresponding deterioration in the general condition. Numerous vesicles appear in the skin at the same stage of development. Practically important is a smear from the bottom of the vial to prove the presence of epithelial giant cells (Tzank-test). Sometimes the presence of the pathogen should be proved by electron microscopy, negative contrast, immunofluorescence, PCR, or viral culture. Viral infections caused by the virus Molluscum contaginosum (eczema molluscatum) or human papillomavirus (HPV) (eczema verrucatum) are easily diagnosed. In particular, with warts in the field of paronychia and on soles in children, one should think about atopy. Viral infection Coxsack in the zone of atopic dermatitis (eczema coxsaccium) is very rare.

Secondary fungal infection

It is interesting that it is rare, mostly in adults, more often in the form of dermatomycosis and is observed when more figuriform erythematous-squamous eruptions with appropriate glucocorticoid therapy do not pass. At present, in particular, the pathogenetic role of contact allergy on Malassezia spp is discussed in atopic dermatitis of the scalp and occipital region. Malassezia spp is considered as the cause of deterioration in atopic dermatitis in this area. In favor of this value is the success of the local treatment with ketoconazole (nizoral).

The prevalence of skin lesions is different: localized lesions (limited lesions in the ulnar and popliteal folds or on the wrists and wrists, perioral lichenification); widespread defeat; universal lesion (erythroderma).

In terms of severity (severe, moderate, relatively light) atopic dermatitis is divided on the basis of the prevalence of skin lesions, the duration of the disease, the frequency of relapses and the duration of remission.

The most important provocative factors causing exacerbation in atopic dermatitis are dry skin, heat, sweating, cold, exercise, temperature changes, infections, allergic contact dermatitis, agitation, stress, food allergy, aeroallergens, combs, concomitant diseases (scabies).

Diagnostics of the atopic dermatitis

The diagnosis of atopic dermatitis is established on the basis of clinical signs. Atopic dermatitis is often difficult to distinguish from other forms of dermatitis (eg, seborrheic eczema, contact dermatitis, numular eczema, psoriasis), although atopic history and localization of lesions indicate a diagnosis. Psoriasis is usually localized on the extensor surfaces, it can affect the nails and is characterized by small-plate scaling. Seborrheic eczema most often affects the skin of the face (nasolabial folds, eyebrows, nose bridge, scalp). Coin-like eczema does not occur in places of folds, and lichenification is rare. Allergens in atopic dermatitis can be detected by skin tests or by determining IgE levels of specific antibodies. Atopic dermatitis can be accompanied by other skin diseases.

There are two groups of diagnostic criteria (basic or mandatory, and additional or secondary signs) that help in diagnosing atopic dermatitis.

Obligatory criteria of atopic dermatitis

1. Itching of the skin.
2. Typical morphology and localization of rashes: in childhood - defeat of facial skin, extensor sites of limbs, trunk; in adults - lichenification on the flex sites of the limbs.
3. Atopy in the anamnesis or hereditary predisposition to atopy.
4. Chronic recurrent course with exacerbations in spring and in the autumn-winter season.

Although the diagnosis of atopic dermatitis seems fairly straightforward, there are borderline cases and some other skin conditions in atopic individuals, so it is important to adhere to the above diagnostic criteria. For the diagnosis, it is necessary, as a minimum, the presence of three main and three additional characteristics.

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Additional signs of atopic dermatitis

Clinical signs

• Xeroderma or ichthyosis
• Follicular keratosis
• Heilit
• Darkening of the eye skin
• Nonspecific dermatitis of hands and feet
• Keratoconus
• Anterior subcapsular cataract

Immunological signs

• Elevated serum total IgE
• Food intolerance
• Inclination to skin infections

Pathophysiological features

• White dermographism
• Itching with sweating
• Pale or erythema of the face
• Intolerance to lipid solvents and wool

The European Task Force on Atopic Dermatitis (1993) developed a method for scoring the severity of this disease: the index SCORAD (The SCORAD Index).

In atopic dermatitis, the diagnosis is primarily aimed at identifying a causal relationship with various allergens, which play a leading role in the development of skin inflammation. It is important to collect an allergological history that includes the history of skin lesion development, family allergological history, the presence of atopic respiratory manifestations, concomitant skin diseases, the presence of risk factors in the anamnesis (during pregnancy and childbirth, the nature of feeding, the presence of infection in infancy, the use of antibacterial drugs in the early childhood, concomitant diseases and foci of focal infection, drug intolerance). Allergological examination involves the setting of skin tests (without exacerbation and in the absence of antihistamine therapy) and provocative tests. With torpid recurrent dermatosis and common skin lesions, specific IgE and IgG 4 antibodies to non-infectious allergens are determined using MAST (multiple allergosorbent test) or PACT (radioallergosorbent test), and other paraclinical and special instrumental studies are also conducted.

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Scheme of examination of patients with atopic dermatitis

Laboratory and instrumental methods of research

• General blood analysis
• Biochemical blood test (total protein, bilirubin, AlT, AsT, urea, creatinine, fibrinogen, C-reactive protein, glucose)
• General urine analysis
• Immunological examination (IgE, a subpopulation of lymphocytes)
• Bacteriological study of feces (on dysbacteriosis)
• Esophagogastroduodeno-fibroscopy
• Electrocardiogram
• X-ray examination of the paranasal sinuses

Allergological examination

• Allergic anamnesis
• Skin tests with atopic allergens
• Determination of specific IgE antibodies to atopic allergens (MAST, PACT)
• Provocative tests (nasal, conjunctival) - if necessary

Additional research

• Ultrasound of internal organs, small pelvis - according to indications
• X-ray examination - according to indications
• Skin biopsy - according to indications

Consultations of specialists

• Allergist
• Therapist (pediatrician)
• Gastroenterologist
• Otolaryngologist
• Neuropsychiatrist
• Endocrinologist

With red flat lichen, there are typical papules of violet color with a shiny surface and an umbilical impression in the center; characteristic of the existence of a Wickham grid in the form of whitish-gray dots and stripes; lesions of mucous membranes are observed.

In patients with Prurigus, the papules are located on the extensor sites of the limbs; elements are isolated from each other; enlarged lymph nodes; there is no atopy in the anamnesis.

With mushroom mycosis the foci of lichenification are less pronounced, there are no remissions in the summer.

Chronic eczema is characterized by polymorphism of rashes, vesicles, wetness, red dermographism.

Differential diagnosis

Atopic dermatitis must be differentiated with the following diseases: limited neurodermatitis, lichen planus, Prerigo Gebra, mushroom mycosis, chronic eczema.

For limited neurodermatitis (depriving Vidal) is characterized by a lack of atopy in the anamnesis, the onset of the disease in the adult period of life; absence of dependence of exacerbations from action of allergens; localized lesion; presence of three zones in the lesion: central lichenification, lichenoid papular rash and dyschromic zone; accompanying diseases precede skin rashes; the level of total IgE in the blood serum is normal; skin tests are negative.

Treatment of the atopic dermatitis

The course of atopic dermatitis in children often improves to 5 years, although exacerbations occur in adolescence and adulthood. The longest course of the disease is most likely in girls and patients with serious diseases, with early development of the disease, with concomitant rhinitis or asthma. However, even in these patients who have atopic dermatitis completely disappears by the age of 30. Atopic dermatitis can have long-term psychological consequences, as children face a problem during adulthood. In patients with a prolonged course of the disease, cataracts may develop by the age of 20-30.

Treatment is usually done at home, but patients with exfoliative dermatitis, panniculitis, or herpetiform eczema may need to be hospitalized.

Supportive treatment of atopic dermatitis

Skin care is primarily done by moisturizing. When bathing and washing hands, use warm (not hot) water, and also reduce the use of soap, as it dries the skin and can cause irritation. Help the bath with colloidal compounds.

Moisturizing oils, petroleum jelly or vegetable oils can help when applied immediately after bathing. An alternative is the constant use of moist dressings for severe lesions. To remove the itching should apply creams and ointments containing tar.

To alleviate the itching, antihistamines are used

For example: hydroxyzine 25 mg orally 3-4 times a day (children - 0.5 mg / kg every 6 hours or 2 mg / kg 1 time a day before bedtime) and diphenhydramine 25-50 mg orally before bedtime. Light sedative H2 blockers, such as loratadine, fexofenadine and cetirizine, can be used, although their effectiveness has not yet been fully proven. Doxepin, a tricyclic antidepressant also with blocking activity of H1 and H2 receptors can be used at a dose of 25-50 mg orally at night, but it is not recommended for children younger than 12 years. To minimize excoriation and secondary infection, the nails should be cut short.

Preventing provoking factors

Reduce the impact of antigens can be, using synthetic fiber cushions and dense mattress covers, often changing bed linens. In addition, you should replace the furniture, upholstered with cloth, remove soft toys, carpets, get rid of pets. Antistaphylococcal antibiotics not only external (mupirocin, fusidic acid), but also systemic (dicloxacillin, cephalexin, erythromycin, all 250 mg 4 times a day) applications can control the colonization of S. Aureus and are prescribed to patients with severe disease resistant to treatment. Significant dietary changes to eliminate reactions to allergenic foods are not required, since this is not an effective measure. Food allergy rarely persists in adulthood.

Glucocorticoids and atopic dermatitis

Glucocorticoids are the basis of therapy. Creams or ointments applied 2 times a day are effective for most patients with mild or moderate form of the disease. Emollients can be used between glucocorticoid applications, and mixed with them to reduce the amount of corticosteroid required for application to the affected area. Systemic glucocorticoids (prednisone 60 mg or for children 1 mg / kg orally once a day for 7-14 days) are prescribed for extensive lesions and resistance to another type of therapy, but they should be avoided whenever possible, as the disease often recurs and the local treatment is safer. Systemic glucocorticoids should not be given to babies, because this can cause suppression of the adrenal glands.

Other treatments for atopic dermatitis

Tacrolimus and pimecrolimus - Tlymphocytic inhibitors, are effective for the treatment of atopic dermatitis. They should be used when the use of glucocorticoids does not produce a result or causes side effects, such as skin atrophy, streaking or adrenal suppression. Tacrolimus and pimecrolimus are applied twice daily, burning and tingling after application are temporary and decrease after a few days. Rarely does the skin redden.

Phototherapy is useful for extensive atopic dermatitis

The natural effect of the sun improves the condition of patients. Alternatively, use of ultraviolet A (UVA) or B (UVB) radiation may be used. Therapy UVA with psoralenom is designed to treat extensive atopic dermatitis. Side effects include non-melanocytic skin cancer and lentiginosis; for this reason, phototherapy using psoralen and ultraviolet radiation from the Adapazon is rarely prescribed for the treatment of children or adolescents.

Systemic immune modulators, effective, at least for the treatment of some patients, include cyclosporine, gammainterferon, mycophenolate, methotrexate and azathioprine. All of them have an anti-inflammatory effect, are prescribed for patients who have atopic dermatitis, in the absence of reaction to phototherapy.

When herpetiform eczema is prescribed acyclovir, infants 10-20 mg / kg every 8 hours; older children and adults with a moderate form of the disease 200 mg orally 5 times a day.

Prevention

The main areas of prevention - adherence to the diet, especially pregnant and lactating mothers, breast-feeding children. Particular attention should be paid to limiting the effects of inhalation allergens, reducing contact with chemicals in everyday life, preventing colds and infectious diseases, and the prescription of antibiotics.

Genetic consultation; restrictions in food (dietary measures in children and adults for clinically proven cases for a certain period of time); Avoidance of aeroallergens (exclude contact with cats, dogs, horses, cows, pigs, do not start pets, exclude smoking in the house, use extracts in the kitchen, exclude contact with plants that form pollen); against household dust mites - thorough cleaning of carpets and wet cleaning of the apartment; removal from the bedroom of carpets, curtains, collecting dust; use of pillows with polyester filling, frequent washing of bed linen; elimination of sources of dust accumulation, including TV and computer); against dry skin - smearing the skin with creams after bathing, bathing oils, humidifying the premises (maintaining a relative humidity of about 40%); avoiding overheating, sweating, heavy physical exercises; avoiding woolen coarse clothing and synthetic fabrics, "impermeable" fabrics; dispensary observation (information for patients with atopic dermatitis and the recording of these patients); teaching parents of patients with atopic dermatitis in children.

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Forecast

The prognosis of atopic dermatitis and the quality of life of the patient and one hundred families largely depend on the reliable knowledge they obtained about the causes of skin rash, itching, careful implementation of all the doctor's recommendations and prevention.

Due to possible secondary infections in young children, the prognosis should be made with caution. In general, the intensity of the disease after the first year of life is somewhat reduced. Skin manifestations become less, and by the 30th year of life they almost disappear. The association with other atopic lesions, such as bronchial asthma and allergic rhinitis, is individual and not entirely clear. Patients who also suffer from these diseases report that sometimes a spontaneous improvement in skin manifestations worsens the condition of the lungs or nose and vice versa.

It is quite difficult to make a forecast in each individual case.

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