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Abstract
The basis for the development of atopic dermatitis (AtD) is a complex interaction between genetic disorders, environmental factors, lack of the skin barrier and immunological disorders. In view of the importance of immunological disorders in the etiopathogenesis of atopic dermatitis, the study of these parameters in patients with AtD is a necessary aspect to assess the severity of the course, prognosis of complications and recurrence. Purpose. Comprehensive assessment of clinical and immunological parameters in adolescents with atopic dermatitis. Materials and methods. The study included examination of 28 patients with atopic dermatitis aged from 12 to 16 years, with disease duration from 10 to 15 years, which included analysis of complaints and anamnesis data, evaluation of disease severity on the SCORAD scale, General clinical and immunological studies. The peculiarities of cellular and humoral immunity in the relapse stage were determined. The main indicators of phagocytic activity of blood neutrophils were also investigated. Results. In the analysis of anamnestic data of patients, a history of diseases associated with atopia in 16 (57.1%) of 28 adolescents (AtD, bronchial asthma in relatives of the first and second line of kinship) was revealed. When assessing the disease severity on a scale of SCORAD, prevailed patients with moderate to severe atopic dermatitis over — 19 (67,9%) patients, the average score of the assessment of the severity of AtD amounted to 29.3 ± 1,25. The conducted immunological examination with assessment of cellular and humoral immunity showed significant changes in immunological reactivity in patients with AtD. On the part of the cellular immunity level it is necessary to note a clear decrease in CD3+ and CD8 + , as well as an increase in the subpopulation of T-lymphocytes — CD4 + and b-lymphocytes — CD20 + in most patients compared to normal indicators characteristic of this age group. Compared to healthy adolescents, there were high rates of IRA and NK cells (CD16 + ). In all patients there was an increase in immunoglobulin M and G, a high content of immunoglobulin E. The formation of secondary immunodeficiency, manifested by a decrease in phagocytic activity of leukocytes and incomplete phagocytosis, which is a factor predisposing to the development of pyoderma. Conclusion. Changes in immune status in patients with AtD are expressed by imbalance of population Of T-lymphocytes, increase of various classes of immunoglobulins and considerable oppression of practically all indicators of functional activity of neutrophils of blood.
Highlights
Атопический дерматит (АтД) — хроническое воспалительное заболевание кожи, которое затрагивает более 20% населения развитых стран всего земного шара [1]
Distribution of patients with ATD by sex depending on the severity of the course
Kawasaki H, Nagao K, Kubo A, Hata T, Shimizu A, Mizuno H, et al Altered stratum corneum barrier and enhanced percutaneous immune responses in filaggrin-null mice
Summary
ФГБОУ ВО «Рязанский государственный медицинский университет им. академика И. В работе проводилось обследование 28 пациентов с АтД в возрасте от 12 до 16 лет, c длительностью заболевания от 10 до 15 лет, которое включало в себя анализ жалоб и анамнестических данных, оценку тяжести заболевания по шкале SCORAD, общеклинические и иммунологическое исследования. Проведенное иммунологическое обследование с оценкой клеточного и гуморального звеньев иммунитета показало значимые изменения иммунологической реактивности у пациентов с АтД. Со стороны клеточного звена иммунитета необходимо отметить явное снижение показателей СD3+ и СD8+, а также повышение субпопуляции Т-лимфоцитов — СD4+ и В-лимфоцитов — СD20+ у большинства пациентов по сравнению с нормальными показателями, характерными для данной возрастной группы. Изменения иммунного статуса у больных АтД выражаются дисбалансом популяции Т-лимфоцитов, повышением различных классов иммуноглобулинов и значительным угнетением практически всех показателей функциональной активности нейтрофилов крови. Статья поступила 03.02.2018 г., принята к печати 05.03.2018 г
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