Background: The analysis of longitudinal birth cohorts with micro-arrayed allergen molecules has provided interesting information about the evolution of IgE sensitization in children. However, so far no cross-sectional study has been performed comparing IgE sensitization profiles in children with and without symptoms of allergy. Furthermore, no data are available regarding molecular IgE sensitization profiles in children from Russia. Methods: We recruited two groups of age-and gender-matched children, one (Group 1: n = 103; 12.24 ± 2.23 years; male/female: 58/45) with symptoms and a second (Group 2: n = 97; 12.78 ± 2.23 years; male/female: 53/44), without symptoms of allergy according to international ISAAC questionnaire. Children were further studied regarding symptoms of allergy (rhinitis, asthma, atopic dermatitis) according to international guidelines, and skin prick testing with a panel of aeroallergen extracts was performed before sera were analyzed in an investigator-blinded manner for IgE specific to more than 160 micro-arrayed allergen molecules using ImmunoCAP ISAC technology. Results: IgE sensitization = or >0.3 ISU to at least one of the micro-arrayed allergen molecules was found in 100% of the symptomatic children and in 36% of the asymptomatic children. Symptomatic and asymptomatic children showed a comparable IgE sensitization profile; however, frequencies of IgE sensitization and IgE levels to the individual allergen molecules were higher in the symptomatic children. Aeroallergen sensitization was dominated by sensitization to major birch pollen allergen, Bet v 1, and major cat allergen, Fel d 1. Food allergen sensitization was due to cross-sensitization to PR10 pollen and food allergens whereas genuine peanut sensitization was absent.
More than 30% of the world population suffers from allergy. Allergic individuals are characterized by the production of immunoglobulin E (IgE) antibodies against innocuous environmental allergens. Upon allergen recognition IgE mediates allergen-specific immediate and late-phase allergic inflammation in different organs. The identification of the disease-causing allergens by demonstrating the presence of allergen-specific IgE is the key to precision medicine in allergy because it allows tailoring different forms of prevention and treatment according to the sensitization profiles of individual allergic patients. More than 30 years ago molecular cloning started to accelerate the identification of the disease-causing allergen molecules and enabled their production as recombinant molecules. Based on recombinant allergen molecules, molecular allergy diagnosis was introduced into clinical practice and allowed dissecting the molecular sensitization profiles of allergic patients. In 2002 it was demonstrated that microarray technology allows assembling large numbers of allergen molecules on chips for the rapid serological testing of IgE sensitizations with small volumes of serum. Since then microarrayed allergens have revolutionized research and diagnosis in allergy, but several unmet needs remain. Here we show that detection of IgE- and IgG-reactivity to a panel of respiratory allergens microarrayed onto silicon elements is more sensitive than glass-based chips. We discuss the advantages of silicon-based allergen microarrays and how this technology will allow addressing hitherto unmet needs in microarray-based allergy diagnosis. Importantly, it described how the assembly of silicon microarray elements may create different microarray formats for suiting different diagnostic applications such as quick testing of single patients, medium scale testing and fully automated large scale testing.
Обоснование. В патогенезе и развитии атопического дерматита (АтД) важную роль играют генетическая предрасположенность, двухфазный иммунный ответ, дисбаланс T1- и Т2-лимфоцитов, нарушение функции эпидермального барьера, участие триггерных факторов, различных антигенов. В последнее время активно изучаются генотипы, эндотипы заболевания, а также взаимосвязь генетических факторов, особенностей патогенеза и клинической картины АтД, которая определяет фенотип заболевания. Цель. Изучить клинические особенности различных фенотипов АтД. Материалы и методы. Проведено открытое проспективное исследование, в котором приняли участие 86 пациентов со среднетяжелым и тяжелым течением АтД, в том числе 25 детей в возрасте от 2 до 18 лет и 61 взрослый в возрасте от 19 до 54 лет. Пациенты наблюдались в отделении аллергологии и иммунопатологии кожи ФГБУ ГНЦ Институт иммунологии ФМБА России в период с 2012 по 2016 г. Период наблюдения за пациентами составил не менее 1 года. Критериями отбора данной группы послужили возможность сбора полноценного анамнеза, проведение оптимального аллергологического обследования, оценки тяжести течения заболевания и ответа на проводимую терапию, адекватность выполнения пациентами рекомендаций врача, включая соблюдение элиминационных мероприятий, диеты, рациональный уход за кожей, а также применение наружной терапии. Все 86 пациентов данной группы получали стандартную терапию в соответствии с современными российскими и международными клиническими рекомендациями. В течение периода наблюдения проводили оценку степени тяжести заболевания на основании индексов SCORAD и IGA, эффективности наружной терапии и частоты развития нежелательных явлений. Результаты. Установлены основные критерии для определения клинических фенотипов АтД по показателям тяжести течения: степень тяжести заболевания (на основании индексов SCORAD, IGA) частота и длительность обострений возраст дебюта заболевания вторичная инфекция кожи сопутствующие респираторные аллергические заболевания и сенсибилизация к различным группам аллергенов резистентность к терапии. Рецидивирующее течение АтД заболевания и резистентность к стандартной терапии топическими глюкокортикостероидами отмечались у 8 (32) детей и 20 (32,7) взрослых. Результаты углубленного обследования репрезентативной выборки пациентов позволили выделить несколько фенотипов АтД: изолированный неосложненный АтД - у 15 пациентов АтД, осложненный вторичной инфекцией и сенсибилизацией к бактериальным или грибковым аллергенам, - у 7 пациентов АтД, сопровождающийся сопутствующими респираторными аллергическими заболеваниями и сенсибилизацией к пищевым и ингаляционным аллергенам, - у 29 пациентов АтД крайне тяжелого течения, сопровождающийся вторичной инфекцией, респираторными аллергическими заболеваниями и поливалентной сенсибилизацией, резистентностью к терапии, - у 36 пациентов. Заключение. Выделение клинического фенотипа позволяет дифференцировать пациентов в зависимости от клинических характеристик и особенностей течения АтД, что может быть полезным для понимания этиопатогенеза заболевания у конкретного пациента и позволит разработать персонифицированные подходы к диагностике и лечению АтД.Genetic predisposition, twophase immune response, T1 and T2 lymphocytes dysbalance, epidermal barrier dysfunction, trigger factors, antigens play an important role in the atopic dermatitis pathogenesis. Recently, genotypes, phenotypes of the disease, as well as the relationship of genetic factors, pathogenesis and clinical features of AD, which determine the phenotype of the disease, are actively studied. The purpose of this research was to evaluate the clinical features of different AD phenotypes. Materials and methods. The research was conducted as an open prospective study. 86 patients suffered from moderate and severe AD, including 25 children aged 2 to 18 years and 61 adults aged 19 to 54 years were involved. Patients in the skin allergy and immunopathology department of The Institute of Immunology of the FMBA of Russia in the period from 2012 to 2016 were observed. The followup period was at least 1 year. The inclusion criteria of this group were the ability to collect a full anamnesis, the allergological examination, assessment of the severity of the disease and the response to the therapy, the adequacy of the fulfilment of the doctors recommendations by the patients, including compliance with elimination measures, diet, rational skin care, as well as the use of topical treatment. All patients received standard therapy according to Russian and international clinical guidelines. The severity of the disease was assessed on the basis of SCORAD and IGA scales, effectiveness of topical treatment and adverse events frequency. Results. The main criteria for determining of AD clinical phenotypes were established: severity of the disease (based on SCORAD, IGA) frequency and duration of exacerbations age of onset of the disease secondary skin infection concomitant respiratory allergic diseases and sensitization to different groups of allergens resistance to therapy. Recurrent course of AD and resistance to standard topical corticosteroids therapy were observed in 8 (32) children and in 20 (32.7) adults. The results of examination of representative sample of patients allowed to identify and characterize several AD phenotypes: isolated uncomplicated AD - in 15 of patients AD complicated by secondary infection and the presence of sensitization to bacterial or fungal allergens - in 7 of patients AD accompanied by the concomitant respiratory allergic diseases and the presence of sensitization to food and respiratory allergens - in 29 of patients extremely severe AD, accompanied by secondary infection, respiratory allergic diseases and polyvalent sensitization, resistance to therapy - in 36 of patients. Conclusion. Identification of the clinical phenotype allows to determine the patients on the grounds of the clinical characteristics and AD features, which can be useful for understanding the etiopathogenesis of the disease in a particular patient and can be the basis for development of personalized approaches to the diagnosis and treatment of AD.
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