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Causes of atopic dermatitis in children
Last reviewed: 23.04.2024
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The causes of atopic dermatitis in children are diverse. The occurrence of the disease is significantly influenced by sex, climatic and geographical features, technogenic level, the state of the economy and the quality of life of the population.
Due to the high prevalence and steady increase in the incidence among children, atopic dermatitis occupies one of the leading places in the overall structure of allergic diseases. Based on the results of studies conducted in 155 clinical centers around the world (ISAAC-International study of asthma and allergy in childhood), the incidence of atopic dermatitis among children is between 10 and 46%. Epidemiological studies in the ISAAC program (1989-1995) showed that in Russia and CIS countries the prevalence of atopic dermatitis in children varies from 5.2 to 15.5%. In further studies, a direct correlation was found between the prevalence of atopic dermatitis and the degree and nature of environmental contamination.
The quality of life
Atopic dermatitis, preserving its clinical manifestations for many years, has an adverse effect on the physical and mental development of children, changes their habitual way of life, contributes to the formation of psychosomatic disorders, leads to social maladaptation, difficulties in choosing a profession and creating a family. In this case, the relationships in the family of sick children are often violated: the labor losses of parents are increased, problems arise in the formation of the environment surrounding the child, the material costs associated with the arrangement of life, the observance of the regime and the diet, etc. Are increased. Patients suffer not only pathological skin processes and itching, but also limitations in daily activity (physical, social, professional), which drastically reduces the quality of life.
Risk factors and causes of atopic dermatitis in children
Atopic dermatitis develops, as a rule, in persons with a genetic predisposition to atopy under the influence of factors of the external and internal environment. Among the risk factors for atopic dermatitis in children, the leading role is played by endogenous factors (heredity, atopy, skin hyperreactivity), which in combination with various exogenous factors lead to clinical manifestation of the disease.
Causes of atopic dermatitis in children (Kaznacheeva LF, 2002)
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Unmanaged |
Conditional causes |
Managed causes (factors that form in a family environment) |
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Genetic predisposition to atopy. Climatogeographical factors |
Antenatal. |
Dietary (especially feeding, family food traditions, etc.). |
Endogenous causes of atopic dermatitis in children
In 80% of children suffering from atopic dermatitis, a family history of an allergic family (neurodermatitis, food allergy, pollinosis, bronchial asthma, recurrent allergic reactions) is noted. And more often the connection with atopic diseases is traced on the mother's line (60-70%), less often - along the line of the father (18-22%). At present only polygenic inheritance of atopy is established. In the presence of atopic diseases in both parents, the risk of developing atopic dermatitis in a child is 60-80%, in one parent - 45-56%. The risk of developing atopic dermatitis in children whose parents are healthy reaches 10-20%.
In addition to genetically determined IgE-dependent inflammation of the skin, the atopic genotype may be due to non-immune genetic determinants, for example, increased synthesis of mast cells of pro-inflammatory substances. Such selective induction (excitation) of mast cells is accompanied by hyperreactivity of the skin, which in the end can become the main realizing factor of the disease. There is also the possibility of a broken immune response (similar to atopic genotype) or spontaneous mutation resulting from exposure to various stressful situations (diseases, chemical and physical agents, psychological stress, etc.).
Exogenous causes of atopic dermatitis in children
Among the exogenous causes of atopic dermatitis in children, triggers (causative factors) and factors aggravating the action of triggers are singled out. In the role of triggers, substances of an allergenic nature (food, domestic, pollen, etc.) can act as well as non-allergenic factors (psychoemotional loads, changes in the meteorological situation, etc.).
Depending on the age of the children, the various etiological causes of atopic dermatitis in children are the role of triggers or the "culprits" of atopic inflammation of the skin. Thus, in young children in 80-90% of cases, the disease occurs due to food allergy. According to the literature, the degree of sensitizing potential of various products can be high, medium or weak, but in most cases, food allergies at an early age are provoked by proteins of cow's milk, cereals, eggs, fish and soy.
Why does the skin become the target organ of the allergic reaction, and atopic dermatitis is the earliest clinical marker of atopy in young children? Probably, the anatomical and physiological characteristics of children of this age can predispose to the development of allergic reactions, namely:
- a huge resorptive surface of the intestine;
- reduced activity of a number of digestive enzymes (lipase, disaccharidase, amylase, protease, trypsin, etc.);
- peculiar structure of the skin, subcutaneous fat layer and blood vessels (extremely thin layer of epidermis, richly vascularized dermis proper, a large number of elastic fibers, loose subcutaneous fat layer);
- low production of diamino oxidase (histaminase), arylsulfatase A and B, phospholipase E, which are contained in eosinophils and are involved in the inactivation of mediators of allergy;
- vegetative imbalance with insufficient sympathicotonia (dominance of cholinergic processes);
- prevalence of mineralocorticoid production over glucocorticoids;
- reduced production of IgA and its secretory component - IgAS;
- age-related dysfunction of the adrenergic cyclic system of nucleotides: reduced synthesis of adenylate cyclase and cAMP, prostaglandins;
- peculiar structural structure of the bilayer of plasma membranes: increased content of arachidonic acid (a precursor of prostaglandins), leukotrienes, thromboxane and the associated increase in the level of platelet activating factor.
It is obvious that with unjustifiably massive antigenic load and hereditary predisposition these age features can lead to the realization of atopic disease.
As children grow, food allergy gradually loses its dominant importance, and at the age of 3-7 years, triggers of allergic inflammation are household (synthetic detergents, library dust), tick-borne (Dermatophagoides Farinae and D. Pteronissinus), pollen (grasses, trees and weeds) allergens. Children of 5-7 years old are sensitized to epidermal allergens (dog, rabbit, cat, sheep, etc.), and their impact through the damaged skin can be very intense.
A special group of causes of atopic dermatitis in children are bacterial, fungal, vaccinal allergens, which usually act in association with other allergens, potentiating individual links of allergic inflammation.
In recent years, many authors have noted the enormous importance in the development and progression of atopic dermatitis of the enterotoxin superantigen Staphylococcus aureus, the colonization of which is observed in almost 90% of patients. Secretion of staphylococcus toxins, superantigens, stimulates the production of inflammatory mediators by T cells and macrophages, which exacerbates or maintains skin inflammation. Local production on the surface of the skin of staphylococcal enterotoxin can cause IgE-mediated release of histamine from mast cells, thus triggering the mechanism of atopic inflammation.
Approximately 1/3 of patients with atopic dermatitis cause mold and yeast fungi - Alternaria, Aspergillus, Mucor, Candida, Pénicillium, Cladosporium, which usually develop a superficial fungal infection. It is believed that, in addition to the actual infection, an allergic reaction of the immediate or delayed type to the components of the fungus can play a role in maintaining atopic inflammation in this case.
In young children, the cause of atopic dermatitis in children is sometimes a viral infection caused by Herpes simplex.
Sometimes vaccination (especially live vaccines), triggered without taking into account the clinical and immunological status and appropriate prevention, may be the starting factor of the clinical manifestation of the disease.
In a number of reasons, atopic dermatitis in children can be drugs, more often antibiotics (penicillins, macrolides), sulfonamides, vitamins, acetylsalicylic acid (aspirin), metamizole sodium (analgin), etc.
Non-allergic causes of atopic dermatitis in children include psychoemotional loads, sudden changes in weather conditions, tobacco smoke, food additives, etc. However, the mechanisms of their participation in the development of atopic dermatitis remain unclear.
The group of exogenous causes of atopic dermatitis in children, aggravating the effect of triggers, includes climatic and geographical zones with extreme temperatures and increased insolation, anthropogenic pollution of the environment, exposure to xenobiotics (industrial pollution, pesticides, household chemicals, medicines, etc.). ).
In the maintenance of allergic inflammation, especially in infants and young children, factors such as a violation of diet, diet regime and skin care rules are important.
Among the household causes of atopic dermatitis in children, enhancing the effect of triggers, we can distinguish the following: poor hygiene of the home (dry air, low humidity, collectors of house dust and mites, etc.), synthetic detergents, keeping pets (dogs, cats, rabbits, birds, fish), passive smoking.
All this leads to increased dryness of the skin and mucous membranes, a decrease in their bactericidal properties, inhibition of phagocytosis and increased permeability for allergens.
A stable trigger effect is also exerted by chronic infections in the family (microbial proteins can selectively stimulate the production of T-helper type 2), psychological conflicts (form astheno-neurotic reactions, hyperreactivity syndrome), disorders of the central and autonomic nervous system, somatic diseases (lung, GIT, kidney), psychosomatic and metabolic disorders.
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Pathogenesis of atopic dermatitis in children
In a multifactorial pathogenesis of atopic dermatitis, the leading role is played by immune disorders. It is generally recognized that the genetic development of the disease is based on a genetically determined immune response characterized by a predominance of T helper type 2 activity, which leads to hyperproduction of total IgE and specific IgE in response to environmental allergens.
Differences in the immune response at the atopic and non-atopic (normal) type are determined by the function of T-cell subpopulations that inhibit the corresponding pools of memory T cells. A population of memory T cells with constant antigen stimulation can direct the T-cell (CD4 +) response of the body along the way of producing T-helper type 1 (Th1 or type 2 (Th2) .The first way is characteristic for persons without atopy, the second for atopy. Patients with atopic dermatitis, the predominance of Th2 activity is accompanied by a high level of interleukins (IL-4 and IL-5), which induce the production of total IgE, against a background of decreased production of interferon-γ.
The role of the immune trigger mechanism in atopic dermatitis is the interaction of antigens with specific antibodies on the surface of mast cells, which in children (especially young children) are concentrated in a large number in the dermis and subcutaneous fat layer. In turn, non-immune relevants increase allergic inflammation through non-specific initiation of synthesis and release of pro-inflammatory mediators of allergy, such as histamine, neuropeptides, cytokines.
As a result of disruption of the integrity of biological membranes, antigens penetrate into the internal environment of the organism -> representation of antigens by macrophages on the molecule of the main histocompatibility complex of class II (GKGSN) and subsequent expression of antigens by Langerhans cells, keratinocytes, endothelium and leukocytes -> local activation of T lymphocytes with enhancement the process of differentiation of T-helpers (CD4 +) along the Th2-like pathway -> activation of the synthesis and secretion of proinflammatory cytokines (IL-2, IL-4, IL-5, TNF-a, TNF-y, MCSF) -> IgE and specific IgE with further fixation of Fc fragments of the latter to specific receptors on mast cells and basophils -> increase in the number of dendritic and mast cells in the dermis -> impaired prostaglandin metabolism -> colonization of S. Aureus and their production of superantigens -> realization of allergic inflammation with the predominant localization in the skin.
Although immune disorders are at the core of the pathogenesis of atopic dermatitis, the activation of immunocompetent cells is controlled by neuroimmune interactions, whose biochemical substrates are neuropeptides (substance P, neurotensins, calcitoninogen-like peptide) produced by nerve fiber endings (C-fibers). In response to various stimuli (extreme temperature, pressure, fear, overexcitation, etc.), neuropeptides are isolated in C-fibers, resulting in vasodilation, manifested by erythema (axon reflex). The involvement of the peptidergic nervous system in the manifestation of atopic dermatitis is due to the anatomical connection between the cells of Langerhans, blood vessels and C-fibers.
Thus, atopic dermatitis in children causes is very different, so the clinical manifestation of the disease develops as a result of the combined effects on the body of genetic factors, triggers and factors that enhance their effects.