Have you had a clot or labs that show a hypercoagulative state?

[SWAlexander]

My ESR was 2 in my last lab work. The highest it has been was 9 in 2008, and it looks to slowly lower with the years.

My coagulation labs have always been normal. I had one specific coagulation panel back in 2006 (I was mild back then) with normal values for:
- PFA 100 COL/EPI
- D-DIMER
- Factor V
- Euglobulin lysis
- Fibrinogen/Prothrombin/Thrombin times and ratios...


I think so, but I don't get why, since usually we have low ESR.
Rouleaux occurs when there are high protein levels in the blood (like fibrinogen) and it produces a high sedimentation rate. Hyperviscosity is what lowers ESR.

What is an erythrocyte sedimentation rate (ESR)?
An erythrocyte sedimentation rate (ESR) is a type of blood test that measures how quickly erythrocytes (red blood cells) settle at the bottom of a test tube that contains a blood sample. Normally, red blood cells settle relatively slowly. A faster-than-normal rate may indicate inflammation in the body. Inflammation is part of your immune response system. It can be a reaction to an infection or injury. Inflammation may also be a sign of a chronic disease, an immune disorder, or other medical condition.
https://medlineplus.gov/lab-tests/erythrocyte-sedimentation-rate-esr/

 

[Akasha]

What is an erythrocyte sedimentation rate (ESR)?

What I mean is I haven't seen my ESR going up and I guess some of my labs have been in the middle of a crash.
If Rouleaux occurs in a crash our ESR should be high, right? Maybe we are talking the type of crash where we are completely shut down in the middle of the floor? How did they take the samples then?
I'm just thinking out loud...

 

[Shanti1]

I had a 23andME test last December and it alerted me to a blood clotting disorder. I asked the doctor if I could be tested to discover which one, but was told that 'there is no point'.

I started experiencing a number of small blood clots from the age of 15 throughout my adult life (4 years before the severe infection that triggered ME) and these would cause painful swellings until they burst, leaving a large bruise the size of a saucer. In recent years, I have had a stroke in the basal ganglia, a number of TIAs, and most unpleasantly of all, a blood clot in the retinal artery a few months ago that has damaged my sight. It was after this that the doctor declined to test for a blood clotting disorder that is also evidenced by early death in my family, according to the death certificates that I have traced back to 1837.

I filled in the poll but because I had genetic testing that indicated a blood clotting disorder I ticked the coagulation box even though the doctor declined to test. Hope that is okay.

Thank you for contributing to the poll, I'm always amazed by people's experiences with the medical system. It just seems irrational not to run coagulation testing on you. Obviously, you have hypercoagulation, but I think the more we know about the specifics of our individual condition, the better chance we have of finding the right therapies and being able to monitor them.

I think so, but I don't get why, since usually we have low ESR.
Rouleaux occurs when there are high protein levels in the blood (like fibrinogen) and it produces a high sedimentation rate. Hyperviscosity is what lowers ESR.

What I mean is I haven't seen my ESR going up and I guess some of my labs have been in the middle of a crash.
If Rouleaux occurs in a crash our ESR should be high, right? Maybe we are talking the type of crash where we are completely shut down in the middle of the floor? How did they take the samples then?
I'm just thinking out loud...

It is a bit contradictary isn't it with some studies showing we have lower than average ESR, and yet, if there is hypercoagulation, you would think it would be higher, and that it would elevate more if there are rouleaux during a crash.

What is consistent with a low ESR is the low RBC defomability leading to hyperviscosity. I wouldn't be surprised if there is a subset of pwME who have higher ESR due to a hypercoagulation state and that it overcomes the low ESR driven by low RBC deformation.

As the rouleaux formation has only, to my knowledge, been reported by Joshua, and we have little info, it is speculative. It sounds like it may not be consistent with your experience and labs. Unfortunately, there is little data on any of this and the data we do have has gaps in it, so we are left speculating

 

[Lieselotte]

A related topic...I listened to a seminar by Dr Holtorf talking about coagulation deformities.
Basically, Immune activation of coagulation builds fibrin around infectious pathogens.
This makes it harder for the body to access the pathogen and kill it, and also blocks tissues from oxygen and other nutrients.

Dr. Holtorf uses Heparin quite a bit for this.

Here are the testing measures (notice, no ESR here):

• Thrombotic Marker Panel
• D-dimer
• Soluble fibrin monomer
• Prothrombin Fragment 1+2
• Thrombin antithrombin complex
• PAI-1 number (activity degrades quickly)
• PAI-1 4G/5G genetic test (4G/4G (about 15% incidence) and 4G/5G have up to a 10 fold increase risk of thrombotic event and IAC)(also increased CA risk)
• Protein C/S activity
• Elevated fibrinogen
• Low PTT
• Low PTT, elevated fibrinogen, increased LP(a) and high homocystine make more likely

Here's a presentation with the information, starting slide 58.
https://restorativemedicine.org/wp-content/uploads/2017/01/4Holtorf_-Lyme-CFS.pdf

 

[SWAlexander]

Lieselotte: "Immune activation of coagulation builds fibrin around infectious pathogens." Thank you.

This is the big and unanswered question for me:
What is building fibrin and how fast and for how long the hold on to infectious pathogens?
What is the culprit for daily reoccurring and sporadic inflammation? Could it be that von Willebrand Factor (vWF) or infection quiet down while sleeping?

A question to all. I would appreciate all suggestion and expertise.
After 7 hour sleep I feel no inflammation - I have good energy.
About 1-2 hours later I feel inflammation. Is this the time coagulation/infection reaches the brain?
High sensitivity in the head around the cranial bones (fontanel area) - even the hair roots hurt in this area and cloudy vision begins.
Then, energy is now way down, pain in the legs and arms (thrombosis) and sometimes brain fog follows.
Very cold hands an feet.
Temperature: 36.3
Blood pressure:
SYS 113
DIA 63
Puls 75
Oxidant 96

 

[Akasha]

Immune activation of coagulation builds fibrin around infectious pathogens.

This would explain a lot.

What is building fibrin and how fast and for how long the hold on to infectious pathogens?

And this is the mechanism that I assume doesn't work properly and enters a vicious cycle.

I hope someone with more expertise can give you answers...

 

[Shanti1]

A related topic...I listened to a seminar by Dr Holtorf talking about coagulation deformities.
Basically, Immune activation of coagulation builds fibrin around infectious pathogens.
This makes it harder for the body to access the pathogen and kill it, and also blocks tissues from oxygen and other nutrients.

And this is the mechanism that I assume doesn't work properly and enters a vicious cycle.

What an interesting topic! The slide posted above references a 2011 talk by Dr. David Berg on "The Role of Hypercoagulation and Biofilm". I'm not sure what is in that talk but I linked to a similar type of interview with Dr. Berg below. Although compelling, I think it is important to recognize that this a working model in which some aspects have scientific evidence and some aspects are theorized.

For example, Berg's work shows that many pwME have increased markers of coagulation. We also know that pathogens can activate coagulation to varying degrees. It seems probable that pathogen-induced hyperviscosity contributes to ME/CFS symptoms. What there seems to be less evidence for is the formation of pathogen-containing, fibrin-capped biofilms in the microcirculation/capillaries, at least I couldn't find anything. If anyone finds something, please post. I'm not saying it doesn't happen, but it may be theory, not fact.

I did find studies on oral bacteria incorporating themselves into atherosclerotic plaque inside the wall of the artery. This is a different process and doesn't occur in the microcirculation where it would block nutrient exchange. I put those studies below. It is interesting, though, that atherosclerosis does change microcirculation and oxygen delivery by decreasing blood flow (reduced nitric oxide) and capillary density (decreased VEGF).

Interview with David Berg
https://cfsremission.com/treatment/...emex-protocol-and-dave-berg/dave-berg-talk-4/

In November, 1999, Dr. Joe Brewer (an Infectious Disease specialist in Kansas City) and I developed a model of pathogen activation of the immune and coagulation systems. The model proposes that the end result of such pathogen-mediated activation is increased blood viscosity due to 1) an underlying coagulation regulatory protein defect, and 2) activation of the coagulation system by the pathogen.

As the blood viscosity increases, the diminished blood flow creates hypoxia (lack of oxygen) and nutrient deprivation within various areas of the body. This is like trying to start your car in Wisconsin in the winter with 60- weight engine oil. This model explains the multi-organ symptomatology and also explains why the low dose heparin therapy is effective by increasing blood flow as the blood viscosity decreases. Thus, patients gain relief from their symptoms with this therapy.

When a pathogen(s) gains a foothold, especially in the endothelial cells in the blood vessels (as well as other cells), the bug(s) can be protected by the coagulation mechanism of fibrin deposition on top of the infected cells.

Bacteria are integrated into atherosclerotic plaques (this is inside the blood vessel wall as opposed to a biofilm on the surface of the blood vessel wall)

Bacterial invasion of vascular cell types: vascular infectology and atherogenesis (Kazarov 2012)The evidence of a polybacterial infectious component of the atheromatous lesions opens the doors for exploration of the new field of vascular infectology and for the study of atherosclerosis microbiome.

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The presence of biofilm structures in atherosclerotic plaques of arteries from legs amputated as a complication of diabetic foot ulcers (Snow 2016) While the presence of bacterial biofilm structures in atherosclerotic plaque does not prove that biofilm is the proximate cause of atherosclerosis, it could contribute to the persistent inflammation associated with it.

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This study looks at bacteria in thombi, which originate from intravascular atherosclerotic plaque​

Oral Bacterial Signatures in Cerebral Thrombi of Patients With Acute Ischemic Stroke Treated With Thrombectomy (Patrakka 2019) This is the first study showing the common presence of bacterial DNA from viridans streptococci in aspired thrombi of patients with acute ischemic stroke. Streptococcal bacteria, mostly of oral origin, may contribute to the progression and thrombotic events of cerebrovascular diseases.

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[Lieselotte]

What an interesting topic! The slide posted above references a 2011 talk by Dr. David Berg on "The Role of Hypercoagulation and Biofilm". I'm not sure what is in that talk but I linked to a similar type of interview with Dr. Berg below. Although compelling, I think it is important to recognize that this a working model in which some aspects have scientific evidence and some aspects are theorized.

In the talks I listened to, there were a few doctors using heparin (maybe some other anti-coagulants, but my memory fails me) for patients with this theorized condition. They said it really helps to make all the other treatments work better because the pathogens can be reached and also nutrients can get into the body more readily. I think if someone has all the markers above for this coagulation defect, it might be worth a shot trying it out.

 

[Shanti1]

I think if someone has all the markers above for this coagulation defect, it might be worth a shot trying it out.

I definitely agree. If someone has coagulation markers, regardless of how it ends up working, it is worth trying. To be honest, I try almost everything I can. Most things make me feel worse, I few do nothing, but over the years I've come across a few things that have really helped me.

 

[Treeman]

I don't have any tests done, but my blood clots quickly. When I've gone to give blood, sometimes it won't come out when the needles in my arm. When I get a cut, there is little bleeding. Could this be an indication?

 

[junkcrap50]

What there seems to be less evidence for is the formation of pathogen-containing, fibrin-capped biofilms in the microcirculation/capillaries, at least I couldn't find anything. If anyone finds something, please post. I'm not saying it doesn't happen, but it may be theory, not fact.

I haven't found any yet either. I want to know if any of these microclots or coagulation problems could cease to stop floating around in circulation after a few years of ME/CFS and if they eventually stick somewhere or get stuck in a microcapillary. Once far away from the initial infection or trigger, maybe the microclots stop being produced. Long Covid patients are still relatively early in their illness.

 

[Shanti1]

I don't have any tests done, but my blood clots quickly. When I've gone to give blood, sometimes it won't come out when the needles in my arm. When I get a cut, there is little bleeding. Could this be an indication?

If the blood is actually clotting in the needle /tube and that is what is preventing the blood donation from starting or completing, I would say that is evidence of hypercoagulation. This is in contrast to the blood not coming out due to a collapsed vein/small veins/missing the vein etc.

 

[andyguitar]

What there seems to be less evidence for is the formation of pathogen-containing, fibrin-capped biofilms in the microcirculation/capillaries, at least I couldn't find anything. If anyone finds something, please post. I'm not saying it doesn't happen, but it may be theory, not fact.

Some blood samples from LC patients being treated at Dr Jaeger's clinic have gone to the Max Planck institute so maybe they will be able to say if there is any evidence of the pathogen (corona virus) being trapped inside.

 

[Shanti1]

Some blood samples from LC patients being treated at Dr Jaeger's clinic have gone to the Max Planck institute so maybe they will be able to say if there is any evidence of the pathogen (corona virus) being trapped inside.

I wouldn't be surprised if it is found. I just found this:

https://pubmed.ncbi.nlm.nih.gov/20676107/ During systemic infection, activation of coagulation fosters compartmentalization of bacteria in liver microvessels and reduces bacterial invasion into tissue. In the absence of a pathogen challenge, neutrophil-derived serine proteases and nucleosomes can contribute to large-vessel thrombosis, the main trigger of myocardial infarction and stroke. The ability of coagulation to suppress pathogen dissemination indicates that microvessel thrombosis represents a physiological tool of host defense.

I'm wondering more about Berg's theory of biofilm formation on the capillary walls with fibrin cap.

 

[SlamDancin]

I definitely agree. If someone has coagulation markers, regardless of how it ends up working, it is worth trying. To be honest, I try almost everything I can. Most things make me feel worse, I few do nothing, but over the years I've come across a few things that have really helped me.

If you don’t mind sharing, I’m similar when it comes to trying countless supplements and medications over the years to find very few helpful ones, what have you found helpful?

 

[Shanti1]

If you don’t mind sharing, I’m similar when it comes to trying countless supplements and medications over the years to find very few helpful ones, what have you found helpful?

Valacyclovir, Oxymaitrine, Desmopressin, B1, and Supplemental Oxygen.
Also was helped by some natural antimicrobials in 2015 to clear intestinal candida.
That's it! Anything you found that has helped you?

 

[Akasha]

Some blood samples from LC patients being treated at Dr Jaeger's clinic have gone to the Max Planck institute so maybe they will be able to say if there is any evidence of the pathogen (corona virus) being trapped inside.

Resia Pretorius said the spike protein was found inside the clots, not the whole pathogen. I think this Is what initiates the reaction.

I've heard (through the grapevine, so I don't have much confidence) that the Long-Covid cases induced by the vaccine also had clots, and that the Mulheim research group also found the spike protein inside. This could be huge. It would explain the subtype of pwMe that got sick after vaccination (I know I'm jumping into too many conclusions here, but let me dream a little).

I don't know a lot about different types of vaccines, but I'm sure not all vaccines have the property of doing this.
But this could also mean that it is not a recurrent infection what causes this process, just its debris or the distant protein formation by a latent virus would be enough.

I think this is a really interesting topic to follow closely for the next months.

 

[Martin aka paused||M.E.]

Hello,
please remember that these are preliminary findings. I just shared it with permission bc I have many researchers as followers. Afaik Pretorius was interesting this finding. But also keep in mind that there may be subgroups who suffer from completely different pathologies.

 

[BrightCandle]

Resia Pretorius said the spike protein was found inside the clots, not the whole pathogen. I think this Is what initiates the reaction.

I've heard (through the grapevine, so I don't have much confidence) that the Long-Covid cases induced by the vaccine also had clots, and that the Mulheim research group also found the spike protein inside. This could be huge. It would explain the subtype of pwMe that got sick after vaccination (I know I'm jumping into too many conclusions here, but let me dream a little).

Almost all of them work the same way by introducing the spike. One of the easiest way to show why most people don't have the problem is that the virus is mostly in the muscle and never gets into the blood in any quantity, that is why the shoulder muscle is chosen. However if you hit a blood vessel then it gets forced into the blood at pressure and that seems to be the cause of the clotting problems that kill people along with other side effects. The relative rarity of vaccine induced injuries of pwME could simply be explained by the blood vessel being a rare thing and many countries are now aspirating the injections too which avoids most of the incidents too.

 

[Strawberry]

Would these markers be something a hematology clinic would test for? I just got a referral to an oncology/hematology clinic.

All my former lab results are gone due to a cruel boss…. I need to know where to start over in testing.