This is a summary, written by members of the CITF Secretariat, of:

Nazy I, Jevtic SD, Moore JC, Huynh A, Smith JW, Kelton JG, Arnold DM. Platelet-activating immune complexes identified in critically ill COVID-19 patients suspected of heparin-induced thrombocytopenia. J Thromb Haemost. 2021 Feb 27. DOI: 10.1111/jth.15283.

The results and/or conclusions contained in the research do not necessarily reflect the views of all CITF members.

Dr. Ishac Nazy and the McMaster Platelet Immunology Laboratory have found some of the reasons behind why some patients with severe COVID-19 have blood clots. The team found that blood from critically ill COVID-19 patients contains molecules that can activate cells involved in blood clotting. This study was supported by the Canadian Institutes of Health Research (CIHR) and the COVID-19 Immunity Task Force (CITF).

COVID-19 is an infectious viral disease which can present as a mild to moderate respiratory illness, or in some cases, can lead to hospitalization and even death. Blood clots are a troubling complication in patients with severe cases of COVID-19, as they can cause long-lasting damage to organs. It is unclear, however, how these blood clots form.

Dr. Nazy and his group tested 10 critically ill COVID-19 patients that were suspected of a disease called heparin-induced thrombocytopenia (HIT), which causes blood clots. Through testing, this disease was ruled out. They then retested these samples and found SARS-CoV-2 antibodies. This finding, together with other tests, indicate that critically ill COVID-19 patients have immune complexes formed that can stimulate blood clotting.

These insights into blood clotting mechanisms in patients with severe forms of SARS-CoV-2 infection can help to better inform treatments, such as blood thinners, for hospitalized COVID-19 patients. This is increasingly important with the recent information regarding the clotting complication in a few patients who have received the AstraZeneca vaccine in several European countries. The mechanisms of clotting could potentially be similar in response to the infection by the virus or by the vaccines.