Лекарственная гиперчувствительность: молекулярные механизмы и современные подходы к диагностике


DOI: https://dx.doi.org/10.18565/nephrology.2019.2.58-68

К.А. Айтбаев, И.Т. Муркамилов, В.В. Фомин, А.Д. Алымкулова, М.Т. Талайбеков, Ж.А. Муркамилова

1) Научно-исследовательский институт молекулярной биологии и медицины, Бишкек, Кыргызстан; 2) Кыргызская государственная медицинская академия им. И.К. Ахунбаева, Бишкек, Кыргызстан; 3) Кыргызско-Российский Славянский университет им. первого Президента России Б.Н. Ельцина, Бишкек, Кыргызстан; 4) ФГБОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова», Москва, Россия; 5) Центр семейной медицины № 7, Бишкек, Кыргызстан
Клинические проявления лекарственной гиперчувствительности (ЛГ) могут варьироваться в диапазоне от мягких кожных реакций (например, макулопапулезная экзантема и крапивница) до тяжелых системных реакций, таких как анафилаксия, обусловленная лекарствами эозинофилия с системными симптомами (DRESS – drug reactions with eosinophilia and systemic symptoms)/индуцированный лекарствами синдром гиперчувствительности (DIHS), или синдром Стивенса–Джонсона (SJS – Stevens–Johnson syndrome)/токсический эпидермальный некролиз (TEN – toxic epidermal necrolysis). В современных фармакогеномных исследованиях сделаны важные шаги по предотвращению некоторых форм лекарственной ЛГ путем идентификации соответствующих генетических вариантов, особенно тех, которые кодируют ферменты, метаболизирующие лекарственные средства и антигены лейкоцитов человека (HLA – human leucocyte antigens). Кроме того, успехи в области иммунологической генетики позволили выдвинуть новые концепции механизмов развития ЛГ. В результате чего модели презентации лекарств, объясняющих, каким образом небольшие лекарственные антигены могут взаимодействовать с молекулами HLA (human leucocyte antigens) и T-клеточного рецептора (TCR) при ЛГ, значительно дополнились и сегодня включают помимо теории гаптена концепцию «фармакологического взаимодействия», модель измененного пептидного репертуара и модель измененного репертуара TCR. Широкий спектр клинических проявлений ЛГ и участие различных лекарственных средств в ее развитии, а также многообразие патогенетических механизмов делают диагностику и управление ЛГ чрезвычайно сложным. В настоящем обзоре освещены последние достижения в изучении молекулярных механизмов развития ЛГ и кратко рассмотрены современные подходы к ее диагностике.
Ключевые слова: лекарственная гиперчувствительность, анафилаксия, молекулярные механизмы, модели презентации лекарств, диагностика
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Об авторах / Для корреспонденции

Айтбаев К.А. – д.м.н., профессор, заведующий лабораторией патологической физиологии НИИ молекулярной биологии и медицины; Бишкек, Кыргызстан.
Муркамилов И.Т. – к.м.н., нефролог, и.о. доцента кафедры факультетской терапии КГМА им. И.К. Ахунбаева; Бишкек, Кыргызстан.
Е-mail: murkamilov.i@mail.ru
Фомин В.В. – д.м.н., профессор, член-корреспондент РАН, проректор по клинической работе и дополнительному профессиональному образованию, директор клиники факультетской терапии им. В.Н. Виноградова, заведующий кафедрой факультетской терапии № 1, ФГАОУ ВО «Первый МГМУ им. И.М. Сеченова» МЗ РФ; Москва, Россия.
Алымкулова А.Д. – научный сотрудник лаборатории патологической физиологии НИИ молекулярной биологии и медицины; Бишкек, Кыргызстан.
Талайбеков М.Т. – аспирант кафедры оториноларингологии КРСУ им. Б.Н. Ельцина; Бишкек, Кыргызстан.
Муркамилова Ж.А. – врач-терапевт, Центр семейной медицины № 7; Бишкек, Кыргызстан.

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