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).