Department of Pathophysiology, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz, Poland.
Department of Anesthesia and Intensive Care, IRCCS-ISMETT, Palermo, Italy.
Adv Exp Med Biol. 2021;1352:73-86. doi: 10.1007/978-3-030-85109-5_5.
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has recently and rapidly emerged and developed into a global pandemic. Through the renin-angiotensin system, the virus may impact the lung circulation, but the expression on endothelium may conduct to its activation and further systemic damage. While precise mechanisms underlying these phenomena remain to be further clarified, the understanding of the disease, its clinical course, as well as its immunological and hematological implications is of paramount importance in this phase of the pandemic.
This review summarizes the evidence gathered until 12 June; electronic databases were screened for pertinent reports on coronavirus and inflammatory and hematological changes. Search was conducted by two independent investigators; keywords used were "SARS-CoV-2," "COVID-19," "inflammation," "immunological," and "therapy."
The viral infection is able to trigger an excessive immune response in predisposed individuals, which can result in a "cytokine storm" that presents an hyperinflammation state able to determine tissue damage and vascular damage. An explosive production of proinflammatory cytokines such as TNF-α IL-1β and others occurs, greatly exaggerating the generation of molecule-damaging reactive oxygen species. These changes are often followed by alterations in hematological parameters. Elucidating those changes in SARS-CoV-2-infected patients could help to understand the pathophysiology of disease and may provide early clues to diagnosis. Several studies have shown that hematological parameters are markers of disease severity and suggest that they mediate disease progression. According to the available literature, the primary hematological symptoms-associated COVID-19, and which distinguish patients with severe disease from patients with nonsevere disease, are lymphocytopenia, thrombocytopenia, and a significant increase in D-dimer levels.
SARS-CoV-2 infection triggers a complex response altering inflammatory, hematological, and coagulation parameters. Measuring these alterations at certain time points may help identify patients at high risk of disease progression and monitor the disease severity.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的感染最近迅速发展成为全球大流行。该病毒可能通过肾素-血管紧张素系统影响肺循环,但在血管内皮的表达可能导致其激活和进一步的全身损伤。虽然这些现象的确切机制仍有待进一步阐明,但在大流行的这一阶段,了解疾病、其临床过程以及其免疫学和血液学意义至关重要。
本综述总结了截至 6 月 12 日收集的证据;电子数据库筛选了有关冠状病毒和炎症及血液变化的相关报告。搜索由两名独立调查员进行;使用的关键词是“SARS-CoV-2”、“COVID-19”、“炎症”、“免疫”和“治疗”。
病毒感染能够在易感染个体中引发过度的免疫反应,从而导致“细胞因子风暴”,即呈现出能够导致组织损伤和血管损伤的过度炎症状态。大量促炎细胞因子如 TNF-α、IL-1β 等的爆发性产生,极大地夸大了分子损伤性活性氧的产生。这些变化通常伴随着血液学参数的改变。阐明 SARS-CoV-2 感染患者的这些变化有助于了解疾病的病理生理学,并可能为早期诊断提供线索。几项研究表明,血液学参数是疾病严重程度的标志物,并提示它们介导疾病进展。根据现有文献,与 COVID-19 相关的主要血液学症状,以及将重症患者与非重症患者区分开来的症状,是淋巴细胞减少症、血小板减少症和 D-二聚体水平的显著升高。
SARS-CoV-2 感染会引发复杂的反应,改变炎症、血液学和凝血参数。在某些时间点测量这些变化可能有助于识别疾病进展风险较高的患者,并监测疾病的严重程度。