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Pathways that contribute to hypercoagulation in patients with severe SARS-CoV-2

 


Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a new RNA virus in the betacoronavirus family. Members of the coronavirus family adapt to the human host and effectively transmit from person to person through the respiratory pathways. 7 different Coronavirus The incubation period, infectivity, and severity of the disease vary and have so far affected humankind. They are MERS-CoV> SARS-CoV> SARS-CoV-2> HKU1 ≃NL63≃OC43≃229E in order of mortality.

Of these, SARS-CoV-2 is unique and has a relatively long incubation time. Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 occurred in Wuhan, China, and now progresses to an unprecedented rate of pandemic, with significant morbidity and mortality worldwide. Is causing. Apart from its ability to cause acute respiratory failure, the virus can also cause hemostatic imbalance. This is a serious problem for patients with moderate to severe illness. These disorders cause hypercoagulation and disseminated intravascular coagulation (DIC), which can lead to organ failure, heart and kidney complications, and stroke.

Over the last few weeks, coagulopathy has surfaced as one of the major complications of severe COVID-19 patients. Notably, over 70% of COVID-19-related deaths are due to coagulation-related complications such as pulmonary embolism, multiple organ failure, and stroke, which have been confirmed at autopsy.

A study by researchers at the University of South Carolina School of Medicine, Penn State University, and the Graduate School of Medical Education in Chandigarh, India, focused on hypoxic-related roles and investigated possible mechanisms of coagulation disorders. .. Activation of coagulation factors; Cytokine storm, Activation of neutrophils, and release of neutrophil extracellular traps.This study is published in the journal Review of medical virology.

In this study, researchers briefly reviewed how multifactorial pathology and molecular reactions affect the coagulation and fibrinolytic systems of COVID-19 patients.

Mechanism of activation of coagulopathy in severe acute respiratory syndrome coronavirus 2 infection. Image Credits: John Wiley & Sons, Inc.

Mechanism of activation of coagulopathy in severe acute respiratory syndrome coronavirus 2 infection. Image Credits: John Wiley & Sons, Inc.

“Cytokine storms” cause a devastating inflammatory response in severe COVID-19

A typical SARS-CoV-2 infection lasts about 20 days. The first infection presents a series of clinical symptoms that extend to sore throat, dry cough, fever, muscle aches, and gastrointestinal symptoms such as nausea, loss of appetite, and diarrhea. Some infected patients also have a temporary loss of odor and taste.

As the infection progresses in the second or third week, the patient has signs of dyspnea, various hematological signs such as lymphopenia and neutropenia, pulmonary embolism, coagulation abnormalities such as blood thickening, Rarely shows some neurological symptoms.

Patients with severe COVID-19 can develop a condition called a “cytokine storm.” In this condition, cytokines released by monocytes, lymphocytes, and alveolar macrophages that come into contact with the virus cause a destructive inflammatory response.

Liver damage associated with cytokine storms and increased D-dimer due to the virus alter blood coagulation factors and cause DIC. Patients with fatal infections present with acute respiratory distress syndrome, myocardial injury, stroke, and multiple organ dysfunction in the final stages of infection.

Anti-inflammatory drugs reduce the effects of cytokine storms and minimize serious illness

In this unprecedented pandemic situation caused by new viruses, the literature on the SARS-CoV-2 virus is evolving rapidly every day. Using current understanding, researchers have proposed a mechanism that can cause coagulopathy in patients with COVID-19.

According to their findings, the virus enters its receptor, binds to it, and then attaches to the upper respiratory tract and lung tissue. Inflammation and hypoxia caused by the infection lead to the release of TF, IL6, and other chemokines, attracting more lymphocytes and neutrophils to the lungs. Reactive immune molecules leak into the circulation, activating platelets and thrombin and triggering the coagulation process. This induces the microthrombosis process, leading to multiple organ failure due to PE, DIC, and starvation of oxygen and nutrients.

Researchers say that symptomatic treatment with anti-inflammatory therapy and close monitoring of platelet count and D-dimer and fibrinogen levels help mitigate the effects of cytokine storms and help diagnose PE early in patients with COVID-19. thinking about. In addition, antiviral candidates such as remdesivir and hydroxychloroquine, which target viral invasion and replication, can reduce recovery time and reduce mortality. The team hopes that future research will help to better understand the different pathways that contribute to thrombus formation in patients with SARS-CoV-2 infection.

“Future observations and studies play an important role in drawing clear images in understanding the physiological, molecular, and cellular signaling pathways that contribute to SARS-CoV-2 related thrombosis. I will do it.

Source

Pujhari, S., Paul, S., Ahluwalia, J. and Rasgon, JL (2020), Severe Acute Respiratory Syndrome Coronavirus 2 coagulopathy. RevMed Virol. doi: 10.1002 / rmv.2177, https://onlinelibrary.wiley.com/doi/10.1002/rmv.2177

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