"COVID-19和慢性病毒性肝炎患者血小板的超结构变化"
Ayat SalahEldin Mohamed Hassan1, Sahar Samir Abdelmaksoud Abo Gaziah2, Hieba Gamal Ezzelregal Awad3
1Department of Electron Microscopy, Theodore Bilharz Research Institute, Giza, Egypt.
Ultrastructural pathology
|April 15, 2024
概括
COVID-19和慢性病毒性肝炎感染显著影响血小板,导致激活和亡变化. 血小板因子-4 (PF-4) 水平表明疾病的严重程度,与凝血标志物相关.
科学领域:
- 血液学 血液学 血液学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 凝血障碍是COVID-19的一个重要后果.
- 慢性病毒性肝炎感染通常会导致凝血因子缺陷,血小板缺陷和血小板功能障碍.
- 与SARS-CoV-2和慢性病毒性肝炎的双重感染是可信的,特别是在特有地区.
研究的目的:
- 为了研究COVID-19患者的血小板超结构变化.
- 量化血清中的血小板因子-4 (PF-4),费里丁,C反应蛋白 (CRP) 和D-二次体的水平.
- 评估同时存在的慢性病毒性肝炎对这些参数的影响.
主要方法:
- 对COVID-19患者 (n=60),COVID-19患有慢性病毒性肝炎患者 (n=20) 和健康对照组 (n=20) 的比较分析.
- 电子显微镜用于评估血小板的超结构形态.
- 血清生物化学试验用于PF-4,费里丁,CRP和D-二元量的量化.
主要成果:
- 在所有患者组中都观察到超结构性血小板激活.
- 慢性病毒性肝炎患者表现出血小板超结构性亡变化.
- 在中度至严重的COVID-19中显著增加PF-4水平 (P<0.001),预测截止值为17 ng/ml.
- PF-4与费里丁,CRP和D-二聚体 (P<0.001) 有正相关性,与血小板和颗粒数 (P<0.001) 有负相关性.
- 患有双重感染的患者表现出轻微的COVID-19症状,PF-4水平与轻微的COVID-19病例相似.
结论:
- 血小板激活和超结构性变化在COVID-19凝血病和慢性病毒性肝炎中至关重要.
- 升高的PF-4作为COVID-19严重程度的敏感生物标志物,与关键的炎症和凝血标志物相关.
- 双重病毒感染对血小板功能造成重大负担,强调需要警的凝血监测.
相关概念视频
Structure and Function of Platelets
1.1K
The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
1.1K
Formation of the Platelet Plug
6.0K
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...
6.0K
Anticoagulant Drugs: Low-Molecular-Weight Heparins
689
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...
689
Disorders of Hemostasis
881
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.
881


