What is it about?

Soon after the onset of the COVID-19 pandemic, it was noted that enhanced blood clotting (thrombosis or embolism) frequently occurred as life-threatening complication in severely ill patients. This complex disorder involves an intense inflammatory response and a strong stimulation of blood clotting, and was named therefore “thromboinflammation”. In previous papers, the authors raised a hypothesis that the natural protein α2-macroglobulin (α2-M) which has been conserved over 500 million years of evolution in many species including humans, might contribute to the protection of children from a severe course in COVID-19. The ancient protein α2-M can be found in all body fluids and is capable by a unique mechanism to trap and neutralize a vast spectrum of functional proteins, including several proteins thought to be involved in COVID-19 thromboinflammation. An important element of progress in clinical care is the implementation of evidence-based medicine (EBM), which means integrating the best available research evidence with clinical expertise and patient values. However, in the case of COVID-19 thromboinflammation, the best available evidence appears to be still insufficient.

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Why is it important?

The usual therapy of thrombosis with substances which attenuate blood coagulation, i.e., anticoagulants, also known as “blood thinners”, is not sufficiently effective in COVID-19 thromboinflammation. Thus, there is the need to seek further options. The authors suggest that a potential protective role of proteins such as α2-M should be explored.

Perspectives

New insights into the mechanisms behind thromboinflammation and the impact of proteins such as α2-M might be helpful for understanding and treating also other complex disorders such as bacterial sepsis.

Rainer Seitz

Read the Original

This page is a summary of: “Thromboinflammation in COVID-19: can α2-macroglobulin help to control the fire?”: Comment from Seitz et al., Journal of Thrombosis and Haemostasis, March 2023, Elsevier,
DOI: 10.1016/j.jtha.2023.01.005.
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