Obeagu Emmanuel Ifeanyi, Obeagu Getrude Uzoma, Aja Patrick Maduabuchi, Okoroiwu G I A, Ubosi N I, Pius Theophilus, Ashiru Muhammad, Akaba Kingsley, Adias Teddy Charles
Department of Medical Laboratory Science, Kampala International University.
School of Nursing Science, Kampala International University.
Ann Med Surg (Lond). 2024 Jun 20;86(8):4634-4642. doi: 10.1097/MS9.0000000000002302. eCollection 2024 Aug.
The COVID-19 pandemic has brought to light the intricate relationship between platelets, soluble platelet selectin (sP-selectin), and disease pathogenesis. Platelets, traditionally recognized for their role in hemostasis, have emerged as key contributors to the immunothrombotic complications observed in COVID-19 patients. Concurrently, elevated levels of sP-selectin, indicative of platelet activation and endothelial injury, have been consistently identified in COVID-19 patients and have shown associations with disease severity and adverse outcomes. This multifaceted connection underscores the pivotal role of platelets and sP-selectin in orchestrating thromboinflammation, vascular dysfunction, and disease progression in COVID-19. Platelet activation triggers the release of inflammatory mediators and promotes platelet-leukocyte interactions, amplifying the systemic inflammatory response and exacerbating endothelial injury. Additionally, platelet-derived factors contribute to microvascular thrombosis, further exacerbating tissue damage and organ dysfunction in severe COVID-19. Elevated sP-selectin levels serve as biomarkers for disease severity and prognostication, aiding in risk stratification and early identification of patients at higher risk of adverse outcomes. Therapeutic strategies targeting platelet dysfunction and sP-selectin-mediated pathways hold promise in mitigating thromboinflammation and improving outcomes in COVID-19 patients. Antiplatelet agents, platelet inhibitors, and anti-inflammatory therapies represent potential interventions to attenuate platelet activation, inhibit platelet-leukocyte interactions, and alleviate endothelial dysfunction. A comprehensive understanding of the multifaceted connection between platelets, sP-selectin, and COVID-19 pathogenesis offers opportunities for tailored therapeutic approaches aimed at mitigating thromboinflammation and improving patient outcomes in this complex and challenging clinical setting.
新冠疫情揭示了血小板、可溶性血小板选择素（sP-选择素）与疾病发病机制之间的复杂关系。血小板传统上因在止血中的作用而被认可，现已成为新冠患者免疫血栓并发症的关键促成因素。同时，在新冠患者中一直发现sP-选择素水平升高，这表明血小板活化和内皮损伤，并且已显示其与疾病严重程度和不良结局相关。这种多方面的联系强调了血小板和sP-选择素在新冠中协调血栓炎症、血管功能障碍和疾病进展方面的关键作用。血小板活化触发炎症介质的释放并促进血小板与白细胞的相互作用，放大全身炎症反应并加剧内皮损伤。此外，血小板衍生因子导致微血管血栓形成，在重症新冠中进一步加剧组织损伤和器官功能障碍。sP-选择素水平升高可作为疾病严重程度和预后的生物标志物，有助于进行风险分层并早期识别不良结局风险较高的患者。针对血小板功能障碍和sP-选择素介导途径的治疗策略有望减轻血栓炎症并改善新冠患者的结局。抗血小板药物、血小板抑制剂和抗炎疗法是减轻血小板活化、抑制血小板与白细胞相互作用以及缓解内皮功能障碍的潜在干预措施。全面了解血小板、sP-选择素与新冠发病机制之间的多方面联系，为在这种复杂且具有挑战性的临床环境中采取旨在减轻血栓炎症和改善患者结局的量身定制治疗方法提供了机会。
