Клинико-патогенетические факторы риска инсульта у пациентов с неуточненным (криптогенным) патогенетическим вариантом ишемического инсульта согласно критериям TOAST

Обоснование. Как показывают последни е научные исследования, для криптогенного ишемического инсульта (ИИ) характерна гетерогенность этиопатогенетических механизмов, что указывает на актуальность поиска потенциальных факторов риска развития криптогенного ИИ, в т. ч. клинико-генетических.
Цель исследования — исследовать ассоциации генетических маркеров, влияющих на спонтанную и индуцированную агрегацию тромбоцитов (АТ), клинико-лабораторных показателей у пациентов с неуточненным характером ИИ согласно критериям TOAST для выявления потенциальных клинико-генетических факторов риска и более глубокого понимания патогенетических механизмов заболевания.
Материалы и методы. В исследование включено 196 пациентов с неуточненным патогенетическим вариантом ИИ. Исследованы ассоциации полиморфизмов генов ITGB3, GPIba, TBXA2R, ITGA2, PLA2G7, HMOX1, PTGS1, PTGS2, ADRA2A, ABCB1, PEAR1 и межгенной области 9p21.3 с клинико-лабораторными параметрами.
Результаты. Носительство генотипа G/G rs1062535 ITGA2 ассоциировалось с достоверно более низкими показателями спонтанной АТ по сравнению с пациентами с генотипами G/A+A/A. У пациентов с генотипом С/С PLA2G7 уровень спонтанной АТ (ОП %) являлся значимо (p = 0,041) более низким по сравнению с пациентами с генотипами T/C+T/T. У пациентов с генотипом С/С rs4523 TBXA2R определялся достоверно (p < 0,050) ниже показатель АТ, инду цированной аденозиндифосфатом, по сравнению с пациентами с генотипами C/T+T/T. У пациентов с генотипом С/С rs5918 ITGB3 достоверно более низкий показатель АТ, индуцированной адреналином, по сравнению с пациентами с генотипами T/T+T/C. У пациентов с генотипом A/A rs1062535 ITGA2 уровень АТ, индуцированной ристомицином, достоверно (p < 0,050) выше по сравнению с пациентами с генотипами G/G+G/A.
Заключение. Носительство генотипов G/A+A/A ITGA2, T/C+T/T PLA2G7, C/T+T/T TBXA2R, A/A ITGA2 может быть использовано как потенциальный маркер течения ИИ неуточненного патогенетического варианта.

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