Discussion:
This study was conducted with the aim of investigating the occurrence of coagulation disorders in COVID-19 patients and determining its relationship with the disease outcome. The results indicated that the prevalence of coagulation disorders was significantly higher in the deceased patients as compared to the surviving ones. Moreover, a positive correlation was observed between serum D-dimer level and mortality risk. Therefore, the level of D-dimer can be used as a prognostic risk factor in patients with COVID-19.
In their study, Tang et al. (2020) attempted to determine the poor prognosis of COVID-19 patients based on the aberrant coagulation parameters in the first 28 days of hospitalization. Their findings revealed that during these 28 days, elevated D-dimer level, prolonged PT, and higher age were associated with the highest levels of mortality while higher platelet counts were associated with the lowest levels of mortality (8). The findings of their study regarding the relationship of elevated D-dimer, PT, and age with mortality are consistent with the findings of the present study.
The results of the meta-analytic study conducted by Lippi et al. demonstrated that the platelet count in patients afflicted with COVID-19 was significantly lower than normal. Moreover, they found that the risk of being afflicted with thrombocytopenia was 5 times more in patients suffering from severe forms of COVID-29 as compared to normal patients (9). However, this finding is not in line with our finding. This inconsistency might be related to the fact that we checked the patients’ platelet counts only at the beginning of the study while it is possible for patients to develop thrombocytopenia during hospitalization, which was not investigated at all in the current study.
In Brazil, Dolhnikoff et al. conducted a pathological study on 10 deceased patients (5 male and 5 female cases with the mean age of 67.8 years). Pathological observations were indicative of higher incidence of coagulation disorders among patients in critical condition. They also showed that renal microthrombosis was more prevalent among these patients (10).
In a retrospective study, whose findings tuned out to be in line with ours, Yin et al. (2020) compared the coagulation status and clinical characteristics of patients with SARS-CoV-2-induced severe pneumonia (COVID group) and those of the patients with non-SARS-CoV-2-induced severe pneumonia (non-COVID group). They observed that severe forms of COVID-19 were usually accompanied by coagulation disorders. Therefore, they suggested that higher levels of D-dimer can be helpful in deciding whether to use anticoagulant therapy or not (11).
In the present study, 87% of the patients had elevated D-dimer levels. In line with our finding in this regard, Yao et al. (2020) also observed elevated D-dimer levels in 74.6% of the total patients under investigation. In their study too, D-dimer level significantly increased as the severity of COVID-19 symptoms increased. This finding was confirmed by the clinical observations and CT results. In their study, the hospital mortality rate was 6.9%%. Furthermore, the mean D-dimer level in the deceased patients was significantly higher than that of the surviving patients. Moreover, hospital mortality rate was predicted based on the D-dimer level of higher than 2.14 mg/L with the sensitivity of 88.2% and specificity of 71.3% (12). This level for D-dimer in the current study was found to be 450 μg/dL. Thrombocytopenia and elevated D-dimer level can be explained by the over-activation of coagulation cascades and platelets. Viral infections induce systemic inflammatory response and cause imbalance in procoagulant and anticoagulant hemostatic mechanisms (13). Multiple pathogenic mechanisms are involved here which include endothelial dysfunction, increase in von Willebrand factor, Toll-like receptor activation, and the activation of tissue factor pathway (13). After recognizing the antigen, platelets become activated and interact with it. White blood cells are also activated and clot formation is accelerated (14). Platelets are the main mediators of inflammation and detect infectious agents via perceiving the interaction of cell-surface receptors and pathogens as well as the activation of, and interaction among, macrophages, monocytes, endothelial cells, platelets, and lymphocytes. Therefore, they play an important role in the prognostic effect of viral infections (15).