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Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflam... (Kruger et al, 2022)

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Proteomics of fibrin amyloid microclots in long COVID/post-acute sequelae of COVID-19 (PASC) shows many entrapped pro-inflammatory molecules that may also contribute to a failed fibrinolytic system

Abstract

Background
Post-acute sequelae of COVID-19 (PASC), also now known as long COVID, has become a major global health and economic burden. Previously, we provided evidence that there is a significant insoluble fibrin amyloid microclot load in the circulation of individuals with long COVID, and that these microclots entrap a substantial number of inflammatory molecules, including those that might prevent clot breakdown. Scientifically, the most challenging aspect of this debilitating condition is that traditional pathology tests such as a serum CRP (C-reactive protein) may not show any significant abnormal inflammatory markers, albeit these tests measure only the soluble inflammatory molecules. Elevated, or abnormal soluble biomarkers such as IL-6, D-Dimer or fibrinogen indicate an increased risk for thrombosis or a host immune response in COVID-19. The absence of biomarkers in standard pathology tests, result in a significant amount of confusion for patients and clinicians, as patients are extremely sick or even bed-ridden but with no regular identifiable reason for their disease. Biomarkers that are currently available cannot detect the molecules present in the microclots we identified and are therefore unable to confirm their presence or the mechanisms that drive their formation.

Methods
Here we analysed the protein content of double-digested microclots of 99 long COVID patients and 29 healthy controls. The patients suffering from long COVID reported their symptoms through a questionnaire completed by themselves or their attending physician.

Results
Our long COVID cohort’s symptoms were found to be in line with global findings, where the most prevalent symptoms were constant fatigue (74%,) cognitive impairment (71%) and depression and anxiety (30%). Our most noteworthy findings were a reduced level of plasma Kallikrein compared to our controls, an increased level of platelet factor 4 (PF4) von Willebrand factor (VWF), and a marginally increased level of α-2 antiplasmin (α-2-AP). We also found a significant presence of antibodies entrapped inside these microclots.

Conclusion
Our results confirm the presence of pro-inflammatory molecules that may also contribute to a failed fibrinolysis phenomenon, which could possibly explain why individuals with long COVID suffer from chronic fatigue, dyspnoea, or cognitive impairment. In addition, significant platelet hyperactivation was noted. Hyperactivation will result in the granular content of platelets being shed into the circulation, including PF4. Overall, our results provide further evidence of both a failed fibrinolytic system in long COVID/PASC and the entrapment of many proteins whose presence might otherwise go unrecorded. These findings might have significant implications for individuals with pre-existing comorbidities, including cardiovascular disease and type 2 diabetes.

The study: https://cardiab.biomedcentral.com/articles/10.1186/s12933-022-01623-4
 

Wishful

Senior Member
Messages
5,852
Location
Alberta
I thought of an experiment that might be useful for the microclot theory: take samples from different parts of the body and compare numbers of microclots. For example, are there more microclots coming out of the brain than going in? Maybe they are originating in one organ, or certain muscle groups (maybe test before/after exertion). Maybe they originate where the blood connects to the lymphatic system.
 

SWAlexander

Senior Member
Messages
1,985
Maybe they originate where the blood connects to the lymphatic system.
May I add a guess?
The lymphatic system is very well guarded but here is one direct entry where chyle enters the thoracic section.
That means this is a close cycle between hypothalamus, amygdala, thalamus, and hippocampus.
I would not dismiss the possibility of microclots impacting also the thyroid (TSH).
Reason: I have von Willebrand Factor and since I had Covid in 2020 I have Antiphospholipid syndrome (APS) and thrombosis, my TSH, especially T3 is extremely high.
There are nearly endless symptoms related to the malfunction of lymphatic system. One of them is exhaustion.
 
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