Platelet Changes Causes Blood Clots in COVID-19

Patients with severe COVID-19 are noted to have a higher tendency to form blood clots inside the blood vessels. These blood clots can block the flow of blood and lead to organ dysfunction. The blood clots can form in both arteries and veins.

A study from Ireland available as a preprint from Medrxiv described the changes in platelet activity in COVID-19 patients.

Platelets

Platelets are the smallest type of blood cell. They are responsible for the formation of blood clots whenever there is a break or cut in blood vessels.

Whenever there is a skin laceration or blood vessel damage, the platelets are there to start clot formation to prevent further blood loss.

In disease states, the platelets can form a clot that can block blood flow to the heart and the brain. That is why people who are at risk are given platelet inhibitors like aspirin and clopidogrel to prevent heart attacks and strokes.

Blausen_0740_Platelets
Platelets Change Once Activated Get More Sticky

Platelets in COVID-19

The study, COVID-19 induces a hyperactive phenotype in circulating platelets, discovered several alterations in platelet number, size, and activity among patients with COVID-19 

The Platelet: Neutrophil ratio is Decreased

White blood cells or WBCs fight infection. They increase in number in most diseases.  Platelets also increase in number during infections. The rise in both platelets and neutrophils follows a certain ratio.

The Platelet-neutrophil ratio can be obtained from the result of a standard blood test, the Complete blood count, or CBC.

COVID-19 patients are noted to have a lower than normal platelet: neutrophil ratio. This means that fewer platelets than neutrophils are being produced as a response to COVID-19.

COVID-19 patients have bigger platelets.

They found that COVID-19 patients have larger platelets. This can also be seen in the CBC as the Mean Platelet Volume or MPV.

The MPV is a measure of the size of the platelets. The bigger size accommodates a higher amount of signaling molecules or cytokines inside that promote clot formation. They are Platelet Factor 4, sP-selectin, and TPO.

Platelet Factor 4

Blood vessels prevent clotting by secreting a heparin-like substance in its lining. This ensures that unwanted clots are not formed that may block the blood flow.

The Platelet Factor 4 or PF4 neutralizes this heparin-like substance to promote clot formation that may happen when blood vessels are cut like in surgeries or injuries.

The higher amount of PF4 makes the blood of COVID-19 patients more coagulable.

 sP-Selectin

In a healthy environment, the platelets do not stick to the endothelium or the inner lining of the blood vessels. When a situation calls for blood clot formation, the sP-selectin is secreted by the platelets.

The sP-selectin is a cell adhesion molecule that is found on the surface of the platelets. When get activated, the platelets get sticky and start to clump together at the site where they are needed.

 

Platelet_Response_Animation
The Ligands, Denoted By Letter L, Is A Signal For Platelets (P) To Migrate Towards The Wound (Site A). As More Platelets Gather Around The Opening, They Produce More Ligands To Amplify The Response. The Platelets Congregate Around The Wound To Create A Cap To Stop Blood Flow Out Of The Tissue. Cytokines Act As Ligands In This Gif.

 

Thrombopoietin

Thrombopoietin or TPO is a hormone mainly produced by the liver and the kidneys. TPO induces more platelet production. It can also be found on the surface of the platelets.

Typically, once inside the platelets, the TPO gets destroyed, and it stops the growth of the platelets.  In COVID-19 patients, the TPO persists inside the cells and allows continued growth.

In this case, the increase in the platelet size is seen in the MPV, as discussed above. The larger platelet size also accommodates more cytokines inside like the PF4 and sP-selectin.

Adenosine Diphosphate is higher in COVID-19.

Adenosine Diphosphate or ADP changes into adenosine triphosphate or ATP. ATP is the energy source of cellular functions.

In this study, the ADP is used as a surrogate marker for the levels of ATP. Higher ADP means higher ATP, which is needed by the hyperactive platelets in COVID-19 patients.

Summary of the Study

Putting them together, this study found that COVID-19 induces lower amounts of platelets but are larger than usual. The increase in size allows the platelets to contain more substances that promote widespread and faster blood clot formation.

The formation of clots is systemic. This explains why many seriously ill COVID-19 patients develop multiple organ dysfunction and sometimes failure and death.

In the end, the study authors recommend that more studies be made to know the types of platelets prone to these changes to refine treatment strategies for better COVID-19 outcomes.

A healthy body, Platelets, and COVID-19

The vast majority of people who are healthy and acquire COVID-19 get better.

People who develop severe COVID-19 illness have chronic medical problems like diabetes, hypertension, and obesity.

The three conditions have one thing in common. They damage the endothelium or the inner lining of the blood vessels. Just like COVID-19 affects the blood vessels.

The human body is well designed to protect itself against several aggressors and invaders like the SARS-CoV-2 virus.

However, if the immune system and endothelium are subpar, then the body’s defenses will be inadequate to meet the challenge of COVID-19. It won’t take much to tip the scales.

The best way to lower the risk of getting very ill with COVID-19 is to maintain a healthy body with physical activity and a healthy low sugar diet.

Knowledge about Covid-19 is rapidly evolving. Information may update as new researches are done. Stay current by subscribing. Feel free to share.

Don’t Get Sick!

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Image Credit: Platelets in action By Bbowen23 – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=49174575

Activated platelets Blausen.com staff (2014). " Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. – Own work, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=28223979

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