Mujibur Rahman, Nadira Naznin Rakhi
Department of Biotechnology and Genetic Engineering, Bangabandhu Sheikh
Mujibur Rahman Science and Technology University, Gopalganj, Bangladesh.
*Correspondence:nadiranrakhi@gmail.com;
+8801515241201
Key Word: COVID-19, blood coagulopathy, D-dimer, embolism,
thrombosis
To the editor
Coronavirus Disease 2019 (COVID-19) primarily being considered as a
respiratory illness has been showing a highly diverse and anomalous
array of symptoms since its origin in December 2019. The death toll has
already surpassed 327,821 with more than 4.99 million confirmed cases
worldwide1, while the pathophysiology of COVID-19 is
still obscure. At present, concerns are mounting over the increasing
reports of blood coagulation accompanied by organ dysfunction among the
COVID-19 patients. The disease tends to cause a hyper- and rapid
coagulable state allegedly leading to pulmonary embolism and deep vein
thrombosis especially among the severe cases of
COVID-192. However, predisposition to both venous and
arterial thromboembolism causing acute pulmonary embolism (PE),
deep-vein thrombosis (DVT), ischemic stroke, myocardial infarction and
systemic arterial embolism has also been reported. So, the experts are
claiming that COVID-19 causes an eminent change in coagulation function,
which is directly associated with disease severity3.
Even a study showed that 71.4% of non-survivor COVID-19 patients meet
the diagnostic criteria for disseminated intravascular coagulation (DIC)
compared to only 0.6% of the survivors4.
However, that study also reported an elevated level of D-dimer protein
among COVID-19 cases, which is produced as the result of fibrinolysis
following a thrombotic event and associated with the risk of Acute
Respiratory Distress Syndrome (ARDS)5. Besides,
D-dimer protein was reported significantly higher among the severe cases
and the patients requiring intensive care compared to patients with mild
symptoms6. A meta-analysis on 1015 cases showed a
notable difference in D-dimer level along with prothrombin time between
severe and mild cases, but not in case of platelet count (PLT) and
activated partial thromboplastin time (aPTT)7. Most
importantly, the level of D-dimer and other fibrin degradation protein
of non-survivor cases significantly differ from
survivors4 and considered as the major cause of
mortality. Therefore, the spike in the level of D- dimer protein
provides evidence of abnormal coagulation with the prognostic value,
which can be used to evaluate the severity and adverse outcome among
patients with community-acquired pneumonia as well as
COVID-198. Moreover, the level of D-dimer has been
reported to be dependent on the ethnic groups, which may explain the
differential racial susceptibility to COVID-19 severity evident across
the world9.
However, patients’ immobilization during treatment, presence of
cardiovascular disease and damage of endothelial cells by viral
infection/mechanical procedure has been reported to cause a higher
incidence of venous thromboembolism among hospitalized
patients10, which is even more threatening for
COVID-19 susceptible individuals with underlying comorbidities including
cardiovascular diseases. Because co-morbidity provokes the COVID-19
severity thus hospitalization, which may lead to thrombotic
complications and vice-versa11.
So, the differences in coagulopathy, especially D-dimer level among
severe and non-severe cases surely urge immediate attention to the
current diagnosis and treatment strategy. Besides, both thrombotic
complications of COVID-19 and its risk factors need to be addressed to
adapt a more effective management strategy.