This characteristic is unusual and seems specific to COVID‐19 infections, especially in their severe form. Viral infections can trigger acquired thrombophilia, which can then lead to thrombotic complications. We investigate for the presence of acquired thrombophilia, which could participate in this phenomenon, and report its prevalence. We also wonder if these thrombophilias participate in the bad prognosis of severe COVID‐19 infections.
Compared to baseline, the COVID-19 patients had elevated levels of tissue factor, a protein found in blood that initiates the clotting process. Patients also had reduced levels of protein S, an anticoagulant that helps prevent blood clotting.
The researchers concluded that lung inflammation caused by COVID-19 is what leads to a decrease in protein S. This inflammation also causes immune and possible endothelial cell activation, which leads to increased tissue factor protein.
Assess a high prevalence of positive tests detecting thrombophilia in COVID‐19 infections. However, in our series, these acquired thrombophilias are not correlated with the severity of the disease nor with the occurrence of thrombotic events. Albeit the strong thrombotic tendency in COVID‐19 infections, the presence of frequent acquired thrombophilia may be part of the inflammation storm of COVID‐19 and should not systematically modify our strategy on prophylactic anticoagulant treatment, which is already revised upwards in this pathological condition.
Blood clots are ‘consumptive’, in that the explosive coagulation reaction consumes free soluble coagulation proteins by incorporating them into the growing clot, lowering their concentration in the circulation. This depletion of coagulation factors in part accounts for the continued bleeding that accompanies clot-precipitated blood vessel ruptures and haemorrhagic strokes. One of the many coagulation factors that are depleted during exuberant clotting is the anticoagulant protein S . This protein is present in the blood at a concentration of ~300 nM (~60% bound to the complement factor C4BP), where it normally acts in concert with activated protein C to degrade factor Va and factor VIIIa and thereby terminate the coagulation reaction4. It is an essential inhibitory node in the coagulation cascade, as congenital PROS1 deficiencies in people can lead to profound coagulopathies, and complete Pros1 deficiency in mice is embryonically lethal owing to catastrophic blood clotting and associated haemorrhages.
The study additionally showed that protein S levels remained low in some patients even after they tested negative for COVID-19, which suggests that blood clotting issues may persist after infection and long-term monitoring of thrombotic risk may be necessary.
Wood says this preliminary data could be a cause for concern. Certain viruses like HIV are linked to a long-term deficiency in protein S, which causes an ongoing risk of thrombosis in patients. It is not yet known if COVID-19 could cause a similar persisting protein S deficiency.