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Journal of Health and Social Sciences


Italian Society for Psychotherapy, Interdisciplinary Health and Social Development





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The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a new coronavirus disease (COVID-19), which is highly contagious and its pathogenesis has not been fully elucidated. In COVID-19, the inflammation and blood coagulation systems are excessively activated. SARS-CoV- 2 damages endothelial cells and pneumocytes, which leads to disruption of hemostasis in SARS. Thromboembolism is the main cause of mortality in patients with COVID-19. Clots, including pulmonary embolism (PE) and deep vein thrombosis (DVT), ranging from minor to fatal complications of the SARS-CoV-2 infection are known. Individuals with pre-existing diseases are more susceptible to the development of blood clots and poor outcomes. High levels of circulating cytokines and D-dimer (DD) are influential biomarkers of poor outcomes in COVID-19. The latter occurs as a result of hyperfibrinolysis and hypercoagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viral envelope proteins, including SARS-CoV. Due to this function penetration of viruses into the host cell occurs. In addition, plasmin is involved in the pathophysiology of acute respiratory distress syndrome (ARDS) in SARS and promotes the secretion of cytokines, such as IL-6 and TNF, from activated macrophages. The focus of existing treatment to alleviate fibrinolysis in patients with COVID-19 is the use of systemic fibrinolytic therapy given thrombotic pathology in severe forms of COVID-19 which may lead to death. However, fibrinolytic therapy may be harmful in the advanced stages of COVID-19, when the status of disseminated intravascular coagulation (DIC) changes from suppressed fibrinolysis to its enhancement during the progression of the disease. This narrative review aims to elucidate the pathogenesis of COVID-19, which will further help in precise diagnosis and treatment.


SARS-CoV-2; COVID-19; Inflammation; Blood Coagulation; Thromboembolism; Circulating Cytokines; D-dimer


Medical Sciences

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Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

Publisher Citation

Dubey L, Lytvyn H, Dorosh O, Dubey N, Kozlova O, Pruc M, Kubikowska N, Szarpak L, Batra K, Chirico F, Nucera G, Doan S, Shevtsiv U. The Pathogenesis of COVID-19: Hypercoagulation and D-dimer in Thrombotic Complications. J Health Soc Sci. 2023; 8(1): 45–58. Doi: 10.19204/2023/thpt4

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