The term “atopy” comes from the Greek word “atopos”, which means strange. AD predisposes to diseases such as bronchial asthma, hay fever, eczema, neurodermatitis, allergic gastritis, migraine, multiple organ types of pathologies.
Blood pressure is detected in 10-20% of children. Atopic diseases are based on hypersensitivity to natural allergens, mediated by class E immunoglobulins, less often IgG4 subclass .
It was found that the synthesis of IgE is controlled by the genes of the 14th chromosome. In addition, a locus (5q31) was isolated on the 5th chromosome, which also controls the synthesis of interleukin 4 and the total IgE content in the blood. The presence of several gene loci, one way or another connected with the development of atopy, allows us to attribute it to polygenic pathology. WITH
One should take into account the very significant contribution of external environmental factors to the development of atopic diseases and, as an indispensable condition, the presence of allergens in the environment.
Therefore, atopy is a polygenically inherited disease in the development of which the regulatory gene for the synthesis of immunoglobulin E plays the role of the main gene.
The hereditary predisposition to atopy, in addition to the tendency to increased synthesis of Ig E and (or Ig G4), is also determined by the insufficient function of the receptor apparatus of immunocompetent cells – a deficiency of beta-2 adrenergic receptors, excessive secretion of mediators of allergic inflammation, and increased sensitivity to various tissues.
v Genetically determined hyperproduction of Jg E.
v Deficiency blocking Jg G. reagents
v Functional, and often quantitative, insufficiency of cells belonging to helper subpopulations of Th1 and Th2 lymphocytes, as well as insufficiency of T-suppressors with a decrease in their functional activity.
v The ability of target cells to respond to allergen contact with increased production of histamine, leukotrienes, prostaglandins, and other allergy mediators.
v A defined immunophenotype (gallotype) of HLA.
v Transient or persistent deficiency of SJgA and JgA in the blood.
v Low production of gamma interferon by leukocytes.
v Hyperproduction of interleukin by 5 lymphocytes in vitro.
v Deficiency of mast cell b-2 receptors, eosinophils, lymphocytes.
v Vagotonia and bronchial hyperreactivity.
v Violation of tryptophan metabolism.
v An increase in the relative content of polyunsaturated fatty acids (in particular, arachidonic acid) in the lipid structures of cell membranes.
v Positive evidence of a family allergic history.
Manifestations of atopic reactions are subject to a certain age dependence .
It is believed that toxic erythema is the equivalent of atopy in newborns, however, this has not yet been conclusively proven. Erythroderma, similar to Leiner’s erythroderma, in a child of the first year of life is more reliably caused by atopic reactions. The presence of allergic dermatitis in young children, even with an increased plasma level of Ig E, still does not allow attributing it to the manifestations of atopic diathesis. The likelihood of atopy in a child increases if, along with allergic dermatitis, he has repeated attacks of obstructive bronchitis and recurrent gastrointestinal disorders.
The development of bronchial asthma, allergic, rhinitis and conjunctivitis, becomes possible in the second year of life. At an older age, physical stress contributes to the development of bronchial asthma, in addition to specific sensitization .
Prevention of the development of atopic diseases is possible only on the basis of timely identification of predisposition, signs of sensitization of the body.
The presence of atopic diseases in the family justifies the feasibility of birth planning, since children born in the summer months and early autumn are more at risk of developing these diseases than those born in late autumn or winter.
The presence of signs of a food or other allergy in a pregnant woman serves as the basis for the appointment of an elimination diet, which, when selecting it, should take into account the possibility of cross-reactions due to the commonality of antigenic structures with similar food composition. A similar diet should be followed by a nursing mother.
The promotion of natural feeding is one of the factors that reduce the nutritional sensitization of a child.
A very serious risk factor for the implementation of an atopic predisposition is considered to be the unfavorable environmental situation inside the home and beyond.
All children with atopic diathesis should be under the supervision of a local pediatrician and allergist. In this case, children are divided into groups:
? Group 1 (attention) – children at increased risk of manifestation of allergic diathesis, when both parents, mother or siblings suffer from allergic diseases.
Preventive therapy is to monitor the diet and regimen of the child, to provide maximum protection against food, household, drug allergens.
Support for natural feeding. Hardening, gymnastics, prevention of rickets and anemia. Preventive vaccinations are carried out according to the generally accepted scheme against the background of the complete exclusion of food allergens from the diet of a child and a nursing mother.
? Group 2 – children with minimal skin manifestations of allergic diathesis (exclude food allergies). They rarely get sick, quickly recover after acute respiratory viral infections, they do not have obstructive syndrome.
Preventive therapy includes a hypoallergenic diet, food diary. Treatment of allergic dermatitis. Preventive vaccinations are carried out 3 months after the disappearance of skin manifestations and in good general condition with the appointment of antihistamines before and after vaccination.
? Group 3 – children with manifestations of atopic dermatitis, eczema. With SARS, they have “wheezing” breathing, there are signs of bronchial hyperreactivity. They are early switched to mixed or artificial feeding.
Preventive therapy requires the implementation of the same measures as in children of group 2, as well as the rehabilitation of foci of chronic infection. Anti-relapse courses include antihistamines (astemizole, clarithin). Treatment in sanatoriums is recommended. With ARVI, the use of interferon is necessary. Preventive vaccinations are carried out no earlier than 6 months after the onset of remission (including the administration of ADS-M toxoid) and with the advisory participation of an immunologist (allergist).
? Group 4 – children with common, torpid-flowing forms of eczema and neurodermatitis. They have a history of spastic bronchitis. Rhinitis and rhinoconjunctivitis are frequent. Foci of chronic infection are detected (most often hypertrophic tonsillitis, adenoids, eosinophilia in a nasal secret).
Preventive therapy provides the same measures, but children should take courses of anti-relapse treatment in a hospital. As anti-relapse therapy, Intal, Ketotifen, Xidifon, Polyenol is recommended for use. The question of prophylactic vaccinations is decided individually with the participation of an immunologist (allergist).
? Group 5 – children with severe manifestations of atopic dermatitis, recurrent obstructive bronchitis, bronchial asthma, multiple organ allergies.
Preventive therapy includes the same measures, as well as the use of cromoglycate sodium (intal) or nedocromil (tiled), ketotifen, xidifon in adverse seasons. At the age of 3 years, the issue of carrying out specific hyposensitization can be decided. For preventive purposes during the period of remission, the introduction of histaglobulin can be used. In recent years, it is proposed to conduct courses of interferon.
Atopic children are contraindicated with aspirin, indomethacin, ibuprofen, amidopyrine, as aspirin sensitization may occur. It is acceptable to use paracetamol, sodium salicylate.
Drug treatment of atopic diseases should be carried out only if a child with atopic diathesis has clinical symptoms and intercurrent diseases (the appointment of interferon, antihistamines, corticosteroids).
The minimum follow-up period is 3 years. If atopic diseases have not occurred during this period, children can be deregistered.
Children assigned to group 5 are not deregistered and must be transferred to the teenager’s office for further observation, even if they have persistent long-term remission.