Persistent clotting protein pathology in Long COVID/PASC is accompanied by increased levels of antiplasmin, 2021, Pretorius et al

Sly Saint

Senior Member (Voting Rights)
"
Inflammatory micro clots in blood of individuals suffering from Long COVID
Date:
October 4, 2021
Source:
Stellenbosch University
Summary:
Researchers have found an overload of various inflammatory molecules, 'trapped' inside insoluble microscopic blood clots (micro clots), in the blood of individuals suffering from Long COVID."
https://www.sciencedaily.com/releases/2021/10/211004104134.htm

eta:
Is this what's behind long Covid? Sufferers have 'micro blood clots' that may stop oxygen flowing around the body properly
 
https://cardiab.biomedcentral.com/articles/10.1186/s12933-021-01359-7
Open Access


Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin


Background
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, the cause of coronavirus disease 2019 (COVID-19), is characterized by acute clinical pathologies, including various coagulopathies that may be accompanied by hypercoagulation and platelet hyperactivation. Recently, a new COVID-19 phenotype has been noted in patients after they have ostensibly recovered from acute COVID-19 symptoms. This new syndrome is commonly termed Long COVID/Post-Acute Sequelae of COVID-19 (PASC). Here we refer to it as Long COVID/PASC.

Lingering symptoms persist for as much as 6 months (or longer) after acute infection, where COVID-19 survivors complain of recurring fatigue or muscle weakness, being out of breath, sleep difficulties, and anxiety or depression. Given that blood clots can block microcapillaries and thereby inhibit oxygen exchange, we here investigate if the lingering symptoms that individuals with Long COVID/PASC manifest might be due to the presence of persistent circulating plasma microclots that are resistant to fibrinolysis.

Methods
We use techniques including proteomics and fluorescence microscopy to study plasma samples from healthy individuals, individuals with Type 2 Diabetes Mellitus (T2DM), with acute COVID-19, and those with Long COVID/PASC symptoms.

Results
We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation. After a second trypsinization, the persistent pellet deposits (microclots) were solubilized.

We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.

Conclusions
Clotting pathologies in both acute COVID-19 infection and in Long COVID/PASC might benefit from following a regime of continued anticlotting therapy to support the fibrinolytic system function.
 
Last edited:
I vaguely remember research that suggested ME could be helped by anticlotting drugs but can't think of the details.

It was a theory from 1999 that pwME and now pwLyme and MCAS (add on more) were/are in a hypercoagulative (thick blood) state where injecting heparin dissolves fibrin.

So the theory goes that a hypercoagulable state starves cells of oxygen and nutrients.
 
Last edited:
@Adam pwme posted video clip of Dr Asad Khan BBC interview on Apheresis and microclots.

(Apologies not a good day but I have some questions)

Am I posting a relevant/best thread?
Is venous oxygen saturation testing he mentioned easy to do. Any ME studies use this measure?
This is H.E.L.P Apheresis? Only available Germany?
What is the assessment/opinion of the level of effective collaboration in any direction MECFS-LC?
 
@Adam pwme posted video clip of Dr Asad Khan BBC interview on Apheresis and microclots.

(Apologies not a good day but I have some questions)

Am I posting a relevant/best thread?
Is venous oxygen saturation testing he mentioned easy to do. Any ME studies use this measure?
This is H.E.L.P Apheresis? Only available Germany?
What is the assessment/opinion of the level of effective collaboration in any direction MECFS-LC?

Also interesting from the BBC clip of dr Assad Khan was that the clots were not picked up by tests such as fibrin and d-dimer.
 
Edit - removed unnecessary section (brain fail)

In the clip above of Dr Khan on BBC news he says that “a simple bedside test called a venous oxygen saturation can demonstrate how ill we are”

For those like me who don’t know what that is: https://www.ncbi.nlm.nih.gov/books/NBK564395/
Venous oxygen saturation (SvO2) is a measure of the oxygen content of the blood returning to the right side of the heart after perfusing the entire body. When the oxygen supply is insufficient to meet the metabolic demands of the tissues, an abnormal SvO2 ensues and reflects an inadequacy in the systemic oxygenation. SvO2 is, therefore, dependent on oxygen delivery and oxygen extraction.

Venous oximetry is used in certain clinical settings of hemodynamic instability, such as in critical illnesses, perioperative periods of major surgeries, heart failure, and sepsis. The venous blood in the pulmonary artery represents oxygen extraction in the whole body and is called mixed venous oxygen saturation (SmvO2). It was measured using a pulmonary artery catheter (PAC). A second, less invasive method of measuring SvO2 is via a central venous catheter (CVC) positioned in the superior vena cava and is called the central venous oxygen saturation (ScvO2).
 
Last edited:
This may be of interest. Comment posted on the YouTube video. Link to the paper below.
Long COVID similarity to ME/CFS continues. For ME/CFS, a subset was found to have the same situation in 1998/1999. Documented in this study "Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis" 1999. I was one and fully recovered with appropriate treatment.

https://pubmed.ncbi.nlm.nih.gov/10695770/
 
Last edited by a moderator:
You know those air fresheners in public buildings that are triggered by opening the door to the toilets?

Every time the door of the staffroom is opened in one of the fatigue clinics, it should trigger a recording of Dr Khan's "It is a myth" statement.
 
This looks interesting. I remember reading years ago about a patient with ME/CFS who figured out he really had some sort of clotting problem. It would not be surprising if this was a subset of ME/CFS, now also appearing in long covid (perhaps more prominently due to specific effects of the SARS-2 virus).
 
Last edited:
Back
Top