How To Increase Platelet Count In COVID Patients? What Is Thrombocytopenia?

Authors: Ananya Varma

Platelets are said to play an important role in inflammatory signalling. Here is why it is important to keep a check of Platelet count in COVID patients. 

Given that COVID-19 is a relatively novel disease, newer research continues to emerge into its characteristics with scientists now linking rapidly decreasing platelets to be a symptom of the infectious virus. Genetically linked to the 2002 SARS-CoV-1 virus, research has now drawn a link between Thrombocytopenia (a condition with low platelets) to the severity of a COVID-19 infection. Here is why it is important to keep a check of Platelet count in COVID patients. 

Platelet Count in COVID patients

As per a recent study, Platelets are said to play an important role in inflammatory signaling as well as in the infectious response of Coronavirus. An analysis of 7,613 COVID-19 patients revealed that patients with severe COVID had a lower platelet count than those with the non-severe disease. Moreover, mild Thrombocytopenia was also detected in those who had severe cases of COVID-19, that is those patients with a lower platelet count. 

Thrombocytopenia & COVID

A normal platelet count in human body ranges from 150,000 to 450,000 platelets per microliter of blood. Having less than 150,000 platelets is known as Thrombocytopenia. Older research has shown that of the patients affected by the 2003 SARS epidemic, 20–55% had Thrombocytopenia and these patients experienced greater morbidity/mortality. In a similar way, Thrombocytopenia has also been detected in 5–41.7% of COVID-19 patients and mild Thrombocytopenia has been detected in 58–95% of severe cases of COVID-19. Notably, severely affected patients had a platelet count only 23 ×109/L to 31 ×109/L lower than those with the non-severe disease.

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Thrombocytopenia following Pfizer and Moderna SARS‐CoV‐2 vaccination

Authors: Eun‐Ju Lee, 1 Douglas B. Cines, 2 Terry Gernsheimer, 3 Craig Kessler, 4 Marc Michel, 5 Michael D. Tarantino, 6 John W. Semple, 7 Donald M. Arnold, 8 Bertrand Godeau, 5 Michele P. Lambert, 9 , 10 and James B. Bussel 11

Cases of apparent secondary immune thrombocytopenia (ITP) after SARS‐CoV‐2 vaccination with both the Pfizer and Moderna versions have been reported and reached public attention. Public alarm was heightened following the death of the first identified patient from an intracranial hemorrhage, which was reported on the Internet, then in USA Today 1 and then in The New York Times. 2 Described below, we have collected a series of cases of very low platelet counts occurring within 2 weeks of vaccination in order to enhance our understanding of the possible relationship, if any, between SARS‐CoV‐2 vaccination and development of ITP with implications for surveillance and management.

Twenty case reports of patients with thrombocytopenia following vaccination, 17 without pre‐existing thrombocytopenia and 14 with reported bleeding symptoms prior to hospitalization were identified upon review of data available from the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), agencies of the U.S. Department of Health and Human Services (HHS) Vaccine Adverse Events Reporting System (VAERS), published reports, 3 and via direct communication with patients and treating providers. These cases were investigated as suspicious for new onset, post‐vaccination secondary ITP; we could not exclude exacerbation of clinically undetected ITP. Search terms relating to “decreased platelet count”, “immune thrombocytopenia”, “hemorrhage”, “petechiae”, and “contusion” were utilized to identify cases reported in VAERS.

The reports describing 19 of 20 patients included age (range 22–73 years old; median 41 years) and gender (11 females and 8 males). Nine received the Pfizer vaccine and 11 received the Moderna vaccine. All 20 patients were hospitalized and most patients presented with petechiae, bruising or mucosal bleeding (gingival, vaginal, epistaxis) with onset of symptoms between 1–23 days (median 5 days) post vaccination. Platelet counts at presentation were available for all 20 cases with the majority being at or below 10 × 109/L (range 1–36 × 109/L; median 2 × 109/L).

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Platelet Gene Expression and Function in COVID-19 Patients

Authors: Bhanu Kanth Manne (University of Utah, United States) Frederik Denorme (Molecular Medicine Program, University of Utah, United States), Elizabeth Middleton (University of Utah, United States), Irina Portier (University of Utah, United States) Jesse Rowley (University of Utah, United, States) Chris Stubben (University of Utah, United States) Aaron Petrey (University of Utah, United States) Neal Tolley (University of Utah, United States) Li Guo (University of Utah, United States) Mark Cody (University of Utah, United States) Andrew Weyrich (University of Utah, United States) Christian Yost (Department of Pediatrics, University of Utah, United States) Matthew Rondina (University of Utah Health Sciences Center, United States) Robert Campbell (University of Utah, United States).


There is an urgent need to understand the pathogenesis of coronavirus disease 2019 (COVID-19). In particular, thrombotic complications in
patients with COVID-19 are common and contribute to organ failure and mortality. Patients with severe COVID-19 present with hemostatic
abnormalities that mimic disseminated intravascular coagulopathy associated with sepsis with the major difference being increased risk of
thrombosis rather than bleeding. However, whether SARS-CoV-2 infection alters platelet function to contribute to the pathophysiology of COVID19 remains unknown. In this study, we report altered platelet gene expression and functional responses in patients infected with SARS-CoV-2.
RNA sequencing demonstrated distinct changes in the gene expression profile of circulating platelets of COVID-19 patients. Pathway analysis
revealed differential gene expression changes in pathways associated with protein ubiquitination, antigen presentation and mitochondrial
dysfunction. The receptor for SARS-CoV-2 binding, ACE2, was not detected by mRNA or protein in platelets. Surprisingly, mRNA from the SARSCoV-2 N1 gene was detected in platelets from 2/25 COVID-19 patients, suggesting platelets may take-up SARS-COV-2 mRNA independent of
ACE2. Resting platelets from COVID-19 patients had increased P-selectin expression basally and upon activation. Circulating platelet-neutrophil, –
monocyte, and -T-cell aggregates were all significantly elevated in COVID-19 patients compared to healthy donors. Furthermore, platelets from
COVID-19 patients aggregated faster and showed increased spreading on both fibrinogen and collagen. The increase in platelet activation and
aggregation could partially be attributed to increased MAPK pathway activation and thromboxane generation. These findings demonstrate that
SARS-CoV-2 infection is associated with platelet hyperreactivity which may contribute to COVID-19 pathophysiology.

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SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19

Authors: Si Zhang 1Yangyang Liu 2Xiaofang Wang 2Li Yang 3Haishan Li 4Yuyan Wang 5Mengduan Liu 2Xiaoyan Zhao 2Youhua Xie 5Yan Yang 6Shenghui Zhang 7Zhichao Fan 8Jianzeng Dong 2Zhenghong Yuan 5Zhongren Ding 2Yi Zhang 9Liang Hu 10


Background: Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.

Methods: Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl3-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo.

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The Impact of COVID-19 Disease on Platelets and Coagulation

Authors: Geoffrey D Wool 1Jonathan L Miller 2


Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patients. COVID-19 also leads to arterial thrombotic events (including strokes and ischemic limbs) as well as microvascular thrombotic disorders (as frequently documented at autopsy in the pulmonary vascular beds). COVID-19 patients often have mild thrombocytopenia and appear to have increased platelet consumption, together with a corresponding increase in platelet production. Disseminated intravascular coagulopathy (DIC) and severe bleeding events are uncommon in COVID-19 patients. Here, we review the current state of knowledge of COVID-19 and hemostasis.

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Dr. Charles Hoffe issues Vaccine warning… Deep dive on endothelial damage to blood vessels…

Author: Dr. Charles Hoffe

in a Coronavirus, that spike protein becomes part of the viral capsule. In other words, the cell wall around the virus, called the viral capsule. But it’s not in the virus. It’s in your cells. So it therefore becomes part of the cell wall of your vascular endothelium. Which means that these cells that line your blood vessels, which are supposed to be smooth so that blood flows smoothly, now have these little spikey bits sticking out.

So it is absolutely inevitable that blood clots will form. Because your blood platelets circulate around in your blood vessels. And the purpose of blood platelets is to detect a damaged vessel and block that vessel to stop bleeding. So when the platelet comes through the capillary, it suddenly hits all these all these Covid spikes that are jutting into the inside of the vessel, it is absolutely inevitable that a blood clot will form to block that vessel. That’s how platelets work.

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