在抗血栓治疗期间患有血栓性抗脂综合征的患者出血的危险因素
Pedro Gaspar1,2,3, Prabal Mittal4,5, Hannah Cohen4,5
1Department of Internal Medicine, Hospital Santa Maria, Unidade Local de Saúde Santa Maria, Lisbon, Portugal.
Lupus
|February 20, 2025
概括
患有血栓性抗脂综合征 (tAPS) 的患者接受抗血栓性治疗时面临出血风险. 血小板缺血是这些患者出血的最强的独立危险因素.
科学领域:
- 血液学 血液学 血液学
- 血栓形成研究研究
- 抗脂综合征是什么
背景情况:
- 血栓性抗脂综合征 (tAPS) 需要进行抗血栓性治疗.
- 在接受治疗的TAPS患者中,出血是严重的并发症.
- 识别出血风险因素对于患者管理至关重要.
研究的目的:
- 为了确定在接受抗血栓治疗的TAPS患者中出血的患病率.
- 在这个队列中确定与任何出血和重大出血相关的风险因素.
主要方法:
- 对197名被诊断患有TAPS的患者进行了单中心追溯分析.
- 根据ISTH标准分类为主要或任何出血的出血事件.
- 后勤回归用于分析出血事件的风险因素.
主要成果:
- 40.6%的患者经历出血,其中22.8%是严重出血事件.
- 二次性APS,复发性血栓形成和高强度抗凝药与出血有关.
- 血小板缺血被确定为任何和重大出血的最强的独立风险因素.
结论:
- 患有二次性APS,复发性血栓形成或接受联合抗血栓治疗的患者患出血风险增加.
- 血小板缺血显著增加了TAPS患者出血的风险.
- 针对性监测和管理策略对于血小板缺血 tAPS 患者是有必要的.
相关概念视频
Anticoagulant Drugs: Low-Molecular-Weight Heparins
593
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
593
Disorders of Hemostasis
680
Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
680
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
455
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
455
Clot Retraction and Fibrinolysis
3.5K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
3.5K
Extrinsic and Intrinsic Pathways of Hemostasis
4.8K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
4.8K
Formation of the Platelet Plug
3.8K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
3.8K


