Nội dung được dịch bởi AI, chỉ mang tính chất tham khảo
Kích hoạt tiểu cầu và cơ chế hình thành tắc mạch trong bệnh nhân COVID-19 nặng. Các cơ chế thay thế về hoạt động của hệ thống đông máu
Tóm tắt
Bài tổng quan này nhấn mạnh cơ chế phát triển tình trạng đông máu quá mức và tắc mạch trong các dạng COVID-19 nặng. Việc đưa virus SARS-CoV-2 vào cơ thể ký chủ được thực hiện thông qua sự tương tác giữa protein đột biến S và enzyme chuyển đổi angiotensin ACE-2, nằm ở tế bào phổi loại 2, nội mạc mạch máu, thận, gan và các cơ quan khác. Trong trường hợp bệnh nhân COVID-19 có tình trạng nghiêm trọng, cả hệ miễn dịch không đặc hiệu và miễn dịch thích nghi đều được kích hoạt. Sự kích thích hệ thống bổ sung với sự xuất hiện của các đoạn C3a, C3b và C5a, cùng với phức hợp tấn công màng (MAC) tạo ra điều kiện cho sự phát triển của tình trạng đông máu quá mức. Sự tham gia của hệ thống renin-angiotensin-aldosterone trong quá trình này và sự xuất hiện của angiotensin 2 (Ang-2) càng làm tăng cường bản chất của tình trạng đông máu quá mức. Khi virus SARS-CoV-2 xâm nhập vào tế bào, phản ứng bảo vệ của hệ thống miễn dịch thích ứng có thể chuyển thành phản ứng bệnh lý (cơn bão cytokine phát triển), đặc trưng bởi mức độ cao của các cytokine tiền viêm (IL-1α, IL-6, IL-8, TNF-α, IL-17, v.v.) và các chemokine (CCL-2, CCL-11, v.v.), điều này cuối cùng dẫn đến sự phát triển của chứng thuyên tắc huyết khối hoặc còn gọi là miễn dịch huyết khối ở những bệnh nhân COVID-19 nặng. Bệnh nhân có tổn thương nặng hơn có thể phát triển tình trạng tương tự như DIC. Đồng thời, bệnh nhân COVID-19 có tình trạng giảm tiểu cầu nhẹ và mức độ fibrinogen, D dimer và sản phẩm phân hủy fibrinogen (FDP) tăng cao, cho thấy sự hình thành huyết khối mãnh liệt, cũng như thời gian prothrombin ngắn (PT) và thời gian hoạt hóa thromboplastin một phần (APTT), do mức độ FVIII tăng cao. Trong COVID-19, bên cạnh con đường đông máu cổ điển, một con đường thay thế (bỏ qua thrombin) về sự điều chỉnh hệ thống đông máu và hình thành huyết khối xuất hiện, chủ yếu liên quan đến ảnh hưởng của protein đột biến S (PS, PROS1) của virus SARS-CoV-2 và protease giống papain (PROS1). Protein S tác động trực tiếp đến sự chuyển đổi fibrinogen thành fibrin, cũng như sự kích hoạt của các yếu tố đông máu huyết tương riêng lẻ. Con đường thay thế của quá trình đông máu cũng do việc kích hoạt hệ thống bổ sung thông qua con đường lectin với sự bao gồm của các metalloproteinases MASP-1, -2 và -3. Ngoài ra, protein S kích hoạt tPA, có thể kèm theo tăng phân hủy fibrin. Ở những bệnh nhân COVID-19 nặng, tiểu cầu đóng vai trò quan trọng trong việc xuất hiện các biến chứng thuyên tắc huyết khối. Trong quá trình phản ứng giải phóng, tiểu cầu được giải phóng từ bào tương vào máu chứa các tiểu cầu α-granules và dense granules chứa cytokine và chemokine viêm, điều này làm tăng cường cơn bão cytokine và do đó, sự hình thành huyết khối. Bằng cách tác động lên protein đột biến S, tiểu cầu tăng cường con đường thay thế điều chỉnh hệ thống đông máu và hình thành huyết khối.
Từ khóa
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