Prothrombotic status in COVID‑19 with diabetes mellitus (Review)

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has caused an important social and health impact worldwide and the coronavirus disease-19 (COVID-19) has elicited devastating economy problems. The pathogenesis of SARS-CoV-2 infection is a complex mechanism and is considered to be the result of a challenging interaction, in which host and virus immune responses are the key elements. In this process, several inflammatory pathways are involved, and their initiation can have multiple consequences with a considerable impact on evolution, such as hyperinflammation and cytokine storm, thereby promoting activation of the coagulation system and fibrinolytic activity suppression. It is commonly recognized that COVID-19 severity involves multiple factors, including diabetes which increases the risk of developing different complications. This could be as a result of the low-grade inflammation as well as the innate and adaptive immune response dysfunction that is observed in patients with diabetes mellitus. In patients with diabetes, multiple metabolic disturbances which have a major impact in disturbing the balance between coagulation and fibrinolysis were discovered, thus the risk for thrombotic events is increased. Diabetes has been recognized as an important severity prognosis factor in COVID-19 cases and considering there is a significant association between diabetes and prothrombotic status, it could be responsible for the increased risk of thrombotic events with a worse prognosis.

Keywords: coronavirus disease-19 infection; diabetes mellitus; prothrombotic status.

Figure 1

Impact of SARS-CoV-2 infection on immune cells and the consequences on the coagulation process. Multiple immune cells are the target of SARS-CoV-2, such as macrophages, monocytes, endothelial cells, dendritic cells, T-cells and NK cells. Following the cells activation, the viral particles stimulate multiple inflammatory pathways, producing large quantity of chemokines and cytokines, which leads to cytokine storm. The cytokine storm changes the balance between coagulation and fibrinolysis, elevating the levels of vWF, TF, angiotensin II, PAI-1 and the platelet adhesion and aggregation (27,51). SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; NK, natural killer; vWF, von Willebrand factor; CCL, C-C motif chemokine ligand; CXCL, C-X-C motif chemokine ligand; TF, tissue factor; PAI-1, plasminogen activator inhibitor-1.