The risk of thrombosis and arterial and venous thromboembolic complications seen in 30% of hospitalized subjects due to NCP has been reported in many studies, which can be explained by the prolonged inflammatory response, decreased physical activity during infection, and reduced oxygen levels in the circulation. Some reports raise the alarm regarding this complication, such as increased thromboembolism incidence despite prophylaxis [9], sevenfold increase in large vessel stroke in some patients who experienced either no or mild COVID-19 symptoms [10], cerebral infarct occurrence in NCP diagnosed patients with thrombocytopenia, coagulopathy, and increased anticardiolipin antibodies [11]. which is very worrying and needs further investigation of the molecular basis of this phenomenon.
In the literature, lung thromboembolism as well as thrombus in different localizations has been reported in NCP cases [12,13]. Sharon et al. also detected fibrin thrombi in small vessels and capillaries and argued that it would be beneficial to use agents that also treat thrombotic and microangiopathic effects caused by the virus [14].
According to the observations of some physicians in Turkey, it is suspected that genetic factors are affecting the course of NCP because of cases who are relatives and have similar severe clinical complications despite living in different provinces. Again, in these observations, the presence of young people who died at a young age and with a severe clinic was observed, although they did not have a sub-disease. Additionally, the existence of asymptomatic NCP-positive young and old people one more time confirms the genetic predisposition hypothesis.
Clinical observation of intensive care unit (ICU) physicians from all over the world indicates that NCP-diagnosed patients are very hypercoagulable and that there is a high rate of micro-pulmonary embolism between patients. There is also the possibility that some patients had already pulmonary embolism before hospitalisation who were not responsive to prophylactic doses of heparins during their hospital stay [15]. Additionally, many other studies indicate that abnormal coagulation results are (especially elevated D-dimer) common in NCP-related deaths [16-19]. Considering all of the abovementioned factors, it is possible that one of the possible susceptibility factors of severe NCP is genetic predisposition to thrombophilia, and it was considered that there can be a relation between well-known single nucleotide polymorphisms of FII, FV and PAI-1 genes and investigated in the current study.
There are many studies showing [20] relationships between genetic thrombophilia factors (FV, PAI-1, etc.) and disseminated intravascular coagulation, which is frequently seen in severe NCP and is often associated with mortality [21]. Gralinski et al. investigated the viral pathogenesis of SARS-coronavirus disease and suggested that PAI-1 plays a protective role against infection [22].
According to Fatma Berri et al. [23], 6-aminocaproic acid can protect against influenza, as plasminogen contributes to inflammation caused by influenza. The application of aggressive anticoagulation by using inexpensive antithrombotic drugs is very attractive [15], but finding genetic markers before using it is essential, and such markers would be very important for the determination of people who are susceptible to severe NCP primary infection.