Патогенетические механизмы нарушения функции щитовидной железы при COVID-19
Настоящий обзор суммирует сведения об основных патогенетических механизмах нарушения функции щитовидной железы (ЩЖ), ассоциированных с COVID-19. На сегодняшний день в литературе имеются указания на прямой механизм повреждения тиреоцитов и тиреотрофов посредством связывания SARS-CoV-2 с мембранными белками (ангиотензинпревращающий фермент-2, трансмембранная протеаза серина-2, нейропилин-1, интегриновые и обонятельные рецепторы) на поверхности клеток. К настоящему моменту опубликованы данные, подтверждающие наличие SARS-CoV-2 в образце ткани ЩЖ. Вместе с тем рассматривается возможность непрямого (иммуноопосредованного) поражения ЩЖ, связанного с развитием гипервоспалительного синдрома, гиперцитокинемией и цитотоксическими эффектами Т-клеток. Накапливается все больше данных о случаях деструктивных тиреоидитов и манифестации аутоиммунных заболеваний ЩЖ у пациентов с COVID-19. Дополнительно известно, что на показатели тиреоидного статуса могут влиять препараты, применяемые для лечения новой коронавирусной инфекции, в частности глюкокортикостероиды и гепарины. Уточнение патогенетических аспектов дисфункции ЩЖ, вызванной SARS-CoV-2, может иметь клиническое значение для выбора тактики ведения пациентов как в острый, так и постковидный периоды инфекции.
Ключевые слова: COVID‑19, SARS-CoV-2, щитовидная железа, ТТГ, ангиотензинпревращающий фермент 2, цитокиновый шторм, глюкокортикостероиды, Т-клетки
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