Are Enzymes a Key to COVID Endothelial Injury?

Are Enzymes a Key to COVID Endothelial Injury? by Dr. Joseph Mercola for Mercola

Enzymes catalyze many biological reactions in your body. They regulate the rate of these chemical reactions, speeding them up so necessary functions like digestion, muscle contractions and other aspects of cellular metabolism can occur.¹

Enzymes are also emerging as key players in COVID-19, as studies suggest damage to the endothelium, which are cells covering blood vessels, is contributing to the development of blood clots, or thrombosis, in the blood vessels of severely ill COVID-19 patients.² Enzymes may turn out to be the missing link in helping to break up clusters of clotting proteins involved in this dangerous thrombosis.

Endothelium Damage Found in Critically Ill COVID-19 Cases

After noticing blackened fingers and toes — signs of what appeared to be microvascular thrombosis, or tiny blood clots in small blood vessels — in COVID-19 patients in advanced stages of the disease, physicians at the Yale School of Medicine began running clotting tests on their patients.³

Levels of Von Willebrand factor (VWF), a clotting protein released by endothelial cells, were found to be significantly elevated, which suggested to hematologist Alfred Lee that damaged endothelial cells may be releasing large quantities of VWF, leading to clots.⁴ This prompted the team to screen for additional markers of endothelial cell and platelet activation in critically and noncritically ill COVID-19 patients.

The study, which was conducted in April 2020, included 68 hospitalized patients with COVID-19 and 13 asymptomatic controls. VWF antigen was significantly elevated in COVID-19 patients admitted to the intensive care unit (ICU) compared to non-ICU COVID-19 patients,⁵ as was soluble platelet selectin (sP-selectin), which is sometimes used as a biomarker for infection and mortality.⁶

Specifically, mean VWF was 565% among ICU patients and 278% among non-ICU patients while soluble P-selectin was 15.9 ng/mL compared to 11.2 ng/mL.⁷ “Our findings show that endotheliopathy is present in COVID-19 and is likely to be associated with critical illness and death. Early identification of endotheliopathy and strategies to mitigate its progression might improve outcomes in COVID-19,” the researchers concluded.⁸

Likely not coincidentally, endothelial dysfunction is also associated with insulin resistance and plays a role in the vascular complications of diabetes,⁹ as well as being involved in obesity and high blood pressure,¹⁰ conditions that raise the risk of severe COVID19.

Even mild obesity may raise the risk of COVID-19 severity — COVID-19 patients with mild obesity had a 2.5 times greater risk of respiratory failure and a five times greater risk of being admitted to an ICU compared to nonobese patients. Those with a BMI of 35 and over were also 12 times more likely to die from COVID-19.¹¹

Another study looking into the impact of coexisting health conditions like high blood pressure, heart disease and diabetes on COVID-19 outcomes found they’re linked to “poorer clinical outcomes,” such as admission to an intensive care unit, a need for invasive ventilation or death.¹²

It’s possible that the endothelial damage in all of these conditions plays a role in worsening COVID-19 outcomes, but it’s unclear which comes first — endothelial damage or COVID-19.

Endothelial Cells Are the ‘Main Target’ of SARS-CoV-2

Imperial College London cardiologist Thomas Lüscher told The Scientist that the endothelium is the main target of SARS-CoV-2, the virus that causes COVID-19.¹³ Under healthy conditions, blood cells can pass through the endothelium lining blood vessels, but when exposed to viral infections and other inflammatory agents, the endothelium becomes sticky and releases VWF.

The end result is a cascade of clotting and inflammation, both characteristics of severe COVID-19. According to a case report published April 8, 2020, “A hallmark of severe COVID-19 is coagulopathy, with 71.4% of patients who die of COVID-19 meeting … criteria for disseminated intravascular coagulation (DIC) while only 0.6% of patients who survive meet these criteria.”¹⁴

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