Researchers identify why Covid-19 patients develop life-treating clots

Piece written by Dawn O'Shea for Univadis Medical News, 22 Jun 2021

Researchers from the Royal College of Surgeons in Ireland have identified how and why some COVID-19 patients develop life-threatening clots.

The team analysed blood samples from patients with COVID-19 in the Beaumont Hospital Intensive Care Unit in Dublin.

They found that the balance between von Willebrand Factor (VWF) and its regulator, ADAMTS13 is severely disrupted in patients with severe COVID-19.

When compared to control groups, COVID-19 patients had higher levels of the pro-clotting VWF and lower levels of the anti-clotting ADAMTS13. Furthermore, the researchers identified other changes in proteins that caused the reduction of ADAMTS13.

* Rose Cottage doc - VWF is a blood glycoprotein which is involved in haemostasis - a process to prevent and stop bleeding. It is the first stage of wound healing. This involves coagulation- blood changing from a liquid to a gel. Intact blood vessels are central to moderating blood's tendency to form clots. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiate the maintenance of haemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. These processes seal the hole until tissues are repaired.

So essentially too high levels of VWF will cause clot formation.

Increased plasma levels of VWF are seen in many cardiovascular, cancers, and connective tissue diseases which have a higher risk of blood clots and are presumed to arise from adverse changes to the endothelium, and may predict an increased risk of thrombosis. (So more evidence that Covid-19 is an endothelial disease) *

“Our research helps provide insights into the mechanisms that cause severe blood clots in patients with COVID-19, which is critical to developing more effective treatments,” said Dr Jamie O’Sullivan, study co-author and research lecturer at the Irish Centre for Vascular Biology at the RCSI.

“While more research is needed to determine whether targets aimed at correcting the levels of ADAMTS13 and VWF may be a successful therapeutic intervention, it is important that we continue to develop therapies for patients with COVID-19. COVID-19 vaccines will continue to be unavailable to many people throughout the world, and it is important that we provide effective treatments to them and to those with breakthrough infections.”


Ward SE, Fogarty H, Karampini E, Lavin M, Schneppenheim S, Dittmer R, Morrin H, Glavey S, Ni Cheallaigh C, Bergin C, Martin-Loeches I, Mallon PW, Curley GF, Baker RI, Budde U, O'Sullivan JM, O' Donnell JS; Irish COVID-19 Vasculopathy Study (iCVS) investigators. ADAMTS13 regulation of VWF multimer distribution in severe COVID-19. J Thromb Haemost. 2021 May 30. doi: 10.1111/jth.15409. Epub ahead of print. PMID: 34053187.

34 views0 comments

Recent Posts

See All