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Faulty blood clotting mechanism may explain COVID-19 severity

Byindianadmin

Apr 24, 2020
Faulty blood clotting mechanism may explain COVID-19 severity

One of the things we know about COVID-19 so far is that people who already have certain conditions are more likely to have a severe form of the disease. New research helps to explain why and points to an impaired blood clotting system.

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Research suggests an impaired blood clotting mechanism helps explain why some people have more severe forms of COVID-19.

The conditions that raise the risk of COVID-19 severity are high blood pressure, diabetes, heart disease, cerebrovascular disease, respiratory conditions such as chronic obstructive pulmonary disease (COPD), and conditions affecting the kidneys.

Researchers are still investigating the precise reasons and mechanisms for why these conditions make COVID-19 outcomes so much worse.

The authors of a new review study — appearing in the journal Physiological Reviews — note that hemorrhage or bleeding disorders are among the leading causes of death for these patients.

Dr. Hong-Long Ji, from the University of Texas Health Science Center at Tyler, and his colleagues further suggest in their study that the hyperactivity of the body’s anticoagulant response may be to blame for these bleeding dysfunctions.

An overactive anticlotting system, in other words, may be what causes excessive bleeding in COVID-19.

This overactivity of the body’s attempts to remove blood clots is known as hyperfibrinolysis. Fibrinolysis is “an enzymatic system […] that serves to localize and limit clot formation,” according to research.

In fibrinolysis, a clotting protein called fibrin is broken down, or degraded, through a process that two opposing “forces” drive. These opposite drivers “regulate pro and con the conversion of plasminogen to plasmin, the active enzyme that dissolves the fibrin clot into soluble fibrin degradation products.”

In their paper, Dr. Ji and team note that people with severe COVID-19 also present with fibrin degradation products and reduced platelets, which can be an indi

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