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Microclots may be responsible for symptoms associated with Long COVID

Long COVID: Coagulopathies and Microclots

Months after recovering from initial SARS-CoV-2 infection, many people still fight debilitating symptoms with what we call Long COVID. But what is it that allows some people to recover within a couple of weeks while others suffer from long-term symptoms for months or even years? Scientist Resia Pretorius, head of the science department at Stellenbosh University in South Africa, believes that microclot formation found in the blood of acute COVID and Long COVID patients may be a key to unlocking the Long COVID mystery.

Clotting Mechanisms in a Healthy Body

To better understand what microclots are and what their presence means, let’s take a closer look at how a healthy body works when it comes to clotting. When you cut your finger, a clot forms to seal the wound, creating the scab that you see. However, damage can occur to the blood vessels inside your body from a simple bump into a table. When this damage occurs, the body springs into action. Platelets immediately swarm to the area of damage, adhering to the cut edges of the vessel. In addition to platelets, clotting factors in the body cause fibrin to stick and seal the damage. The platelets and fibrin work to form a plug (or clot) that stops the bleeding until the vessel heals. But once the vessel heals, what happens to the clot?

While the damage heals, alpha (2)-antiplasmin in the body helps to maintain the clot. However, once the vessel heals, the body uses an activator to trigger plasmin in the clot to begin the breakdown process. This material works similarly to an internal self-destruct button within the clot. The relationship between plasmin and antiplasmin within the body is an essential balancing act when it comes to internal healing and clot removal.

What Can Occur in the Blood of COVID and Long COVID Patients?

The research from Pretorius shows that there is an overload of inflammatory molecules trapped inside insoluble microclots in patients with acute COVID, as well as those with Long COVID. It appears that there are hyperactivated platelets and high levels of alpha (2)-antiplasmin in the body. These levels work to not only increase the formation of clots due to inflammation but also prevent the breakdown of these microclots. As these clots build up and circulate through the body, they can block small blood vessels, such as microcapillaries. This blockage can reduce the delivery of oxygen to tissues within the body. This creates hypoxia and, without the oxygen the tissues need, debilitating symptoms can occur, such as those we see in Long COVID. In addition, these microclots can also increase the risk of stroke and heart attacks, even in young patients.

How Do We Diagnose Microclots?

When looking for these clots, traditional tests for clotting issues, such as fibrinogen and D-dimer, often show normal results. Because these tests show elevated results due to the breakdown of clots, Long COVID patients are not showing positive as the elevated rates of alpha (2)-antiplasmin are not allowing for any clot breakdown. According to UK respiratory physician Dr. Asad Khan, the best test to look for these microclots may be a simple blood oxygen test that looks at the amount of oxygen traveling in the blood. If your oxygen levels are low, you may have clots limiting oxygen transport in the blood.

Treatment for Long COVID Microclots

Treatment for these microclots focuses on the breakdown of the clots as well as addressing the hyperactivated platelets. Anticlotting therapy is a traditional treatment method for blood clots. However this requires close monitoring in order to minimize the risk of excess bleeding. Unfortunately, these microclots can often be difficult to break down and they do not always respond to this traditional treatment.

Researchers in Germany are evaluating another treatment option that is showing success. This treatment is heparin-mediated extracorporeal LDL-cholesterol precipitation (HELP) apheresis. Currently offered by Dr. Beate Jaegar, HELP apheresis works similar to a dialysis machine. Blood from one arm enters the machine. The machine removes the clots and then returns the blood into the other arm. While the treatment appears promising, more research is necessary before HELP apheresis becomes a mainstream treatment option.

A recent preprint from Pretorius and her team shows that a combination antiplatelet and anticoagulant therapy for those with microclots provided significant Long COVID symptom improvement, as well as a reduction in the microclots. While research is ongoing, this treatment option is very promising.

6 thoughts on “Long COVID: Coagulopathies and Microclots”

  1. Would love the opportunity to take part in the anticoagulant study I’ve had problems with circulation for months, I have been gaslighted by my doctor who won’t even entertain the idea of microclots or new research / studies on long covid as I’m sure many have.
    I’m at my wits end with feeling constantly unwell.
    Would be more than happy to take part.
    It’s great work that your doing and very much needed here in the UK 🇬🇧

  2. Thank you for all the very useful information on your site.
    In reference to microclots, could nattokinase (K1), from Japanese natto, assist in dissolving clots? From WebMD: There’s some early evidence that nattokinase may have benefits for heart and artery health. One study shows that a nattokinase supplement lowers the risk of blood clots after long plane flights. It may help reduce narrowing of the arteries.
    https://www.webmd.com/vitamins-and-supplements/nattokinase-uses-and-risks

  3. I can see why this looks like a great discovery, and indeed some Long Covid patients have improved with the anticoagulant anti platelet therapy. However ME/CFS patients have micro clots too, and when Ron Davis at Stanford School of Medicine stressed ME/CFS cells (in vitro) with their blood serum, the cells ‘pooped out’ of energy very quickly compared to controls that are stressed.

    As far as I am aware if there was micro clots in the serum in that test it won’t effect the cells being observed because there’s no tiny capillaries in the test to block flow or (endothelial interference)

    Interestingly when Ron Davis’s team put healthy controls cells into ME/CFS blood serum, their cells ‘pooped out’ fast too!

    And when ME/CFS cells were put into healthy control blood serum, the cells ’woke up’ and behaved like healthy controls cells. Meaning there’s something in the blood serum of ME/CFS patients that’s putting cells to sleep. It could be micro clots, but I think they would have seen that in the test.

    I think it’s an autoantibody or even something from the innate immune system attacking cells that produce excess energy, perhaps targeting a receptor on the cells or a metabolite produced by cellular exertion. This in turn puts the cells into a Cellular Defence Response like seen in sickness behaviour

    As for Long Covid I think some patients have ME/CFS and others their condition mimics it. Those with ‘Post Exertional Malaise’ probably actually have ME/CFS

    As for the finding of more micro clots in Long Covid that’s most probably because the ME/CFS patients used to compare to, have had the disease much longer. As it is known that the ME/CFS immune system changes after 3 years, the hyperactive state reduces to an under-active state (but the patient remains ill) . This would explain why there’s less micro clots. i.e. because they are clumping around inflammatory molecules. And after 3 years there’s less of them, so less micro clots. Yet like I mentioned no improvement

    The similarities between Long Covid and ME/CFS are startling, especially the rare condition ‘Post Exertional Malaise’ the whole thing is truly quite baffling

  4. This echos the work of David Berg, Hemex labs, for ME/CFS some 20+ years ago. See https://cfsremission.com/treatment/thick-blood-clots-dimension-of-cfs-etc/hemex-protocol-and-dave-berg/

    Of special interest is that he found that different clusters of individuals had SNP mutations which were normally tolerated by an individual well, but in some circumstances they stop being sufficient (epigenetics).

    DNA analysis of all of the individuals may improve insight and allow more targeted treatment. He found that I had the PROTHROMBIN G20210A (FACTOR II MUTATION) and that lead to explicit treatment.

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