Катастрофический антифосфолипидный синдром: прототип аутоиммунного тромбовоспаления

Антифосфолипидный синдром (АФС) определяется как «аутоиммунное тромбовоспалительное заболевание, характеризующееся увеличением риска тромбозов с локализацией в венозных и артериальных сосудистых бассейнах, тромботическим повреждением микрососудов, плацентарной недостаточностью, цитопенией, поражением кожи, клапанов сердца, нефропатией, легочными геморрагиями и др.». Наряду с клиническими симптомами кардинальным признаком АФС являются антитела к фосфолипид-связывающим белкам и фосфолипидам, включая волчаночный антикоагулянт, антитела к кардиолипину и антитела к β2-гликопротеину I, подчеркивающие ведущий аутоиммунный механизм патогенеза этой патологии. АФС рассматривается как важная проблема современной медицины, находящаяся на стыке ревматологии и гематологии. Отличительной особенностью АФС является гетерогенность, которая проявляется как на клиническом (фенотипы, варианты течения), так и на патогенетическом уровне (молекулярные эндотипы). Особое внимание привлечено к потенциально летальной форме АФС, проявляющейся фулминантным развитием мультиорганного тромбоза, которая впервые описана Рональдом Ашерсоном (Ronald A. Asherson) в 1992 г. и названа «катастрофической» формой АФС (КАФС). В настоящее время активно обсуждаются подходы к персонифицированной терапии АФС с использованием искусственного интеллекта и на этой основе – реализации концепции «лечение до достижения цели» (treat-to- target), направленной на достижение ремиссии. Последнюю при АФС следует рассматривать как отсутствие рецидивов тромбозов. Реализация этой стратеги при иммуновоспалительных ревматических заболеваниях во многом стала возможной благодаря разработке и внедрению широкого спектра генно-инженерных биологических препаратов, представляющих собой моноклональные антитела или гибридные молекулы, селективно модулирующие ключевые механизмы иммунопатогенеза. Рассмотрены клиническое формы КАФС и патогенетические механизмы АФС и на этой основе – новые возможности лечения КАФС с использованием анти-В-клеточной терапии, CAR-T-клеточной терапии, ингибиторов комплемента и перспективы профилактики тромбозов, связанных с коморбидной кардиометаболической патологией.

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