Recent papers below.
As some will know, I am very interested in PCa-related coagulation. I believe that control of microclots may prevent metastasis (& further mets in those who have some.) Clot control can also prevent DVTs & fatal pulmonary embolisms.
The D-dimer test is very useful when a clot is suspected. Zero (or as close to zero as the test can measure) means no clot. Nattokinase can be used to speed-up to the removal of unwanted clots.
~10 years ago I had a double DVT in my left leg. After 3 months of Coumadin/Warfarin one vein was clear but the other one was not. My doctor gave me permission to switch to nattokinase, knowing that I would come back if it didn't work. It worked very well - at least in terms of D-dimer ( I don't know the status of the 2nd vein - my doctor said that some of them never clear.)
Nattokinase is similar to plasmin, which the body uses to clean up clots. Plasmin is necessarily slow; nattokinase is much faster. Plasmin can't keep up with clots that keep growing. Warfarin does not dissolve clots - it merely increases clotting time. This theoretically allows plasmin to dissolve a clot faster than it is growing. This is why people are on Warfarin for 3 months, 6 months or forever. The downside of Warfarin, since it inhibits vitamin K, is that bones get weaker & arteries become calcified. Also, one might bleed-out after a serious injury.
A seconday effect of nattokinase is that fibrinogen levels fall.
"Fibrinogen (factor I) is a glycoprotein complex that circulates in the blood of vertebrates. During tissue and vascular injury, it is converted enzymatically by thrombin to fibrin and then to a fibrin-based blood clot." (Wikipedia [1])
We want fibrinogen to low, albeit in the 'normal' range (IMO). Unfortunately, fibrinogen is also an acute-phase protein:
"Acute-phase proteins (APPs) are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation." [2]
Cancer is an inflammatory condition.
"... high pretreatment plasma fibrinogen levels can predict poorer {overall survival} and {cancer-specific survival} in patients with urological cancers" [3]
& so men with PCa can be on a hair-trigger for a blood clot.
... end of preamble ...
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There are 45 PubMed hits for <"covid-19" coagulation>. All since March 13!
The oldest paper [4] reported on 183 consecutive patients:
D-dimer (<0.50 µg/mL) was 0.61 for survivors & 2.12 for those who died.
Fibrinogen (2-4 g/L) was 4.21 for survivors & 5.16 for those who died.
FDP (fibrin degradation product) (<5 µg/mL) was 4.0 for survivors & 7.6 for those who died.
From Italy (4/21/20) [5]:
"Cases showed significantly higher fibrinogen and D-dimer plasma levels versus healthy controls ... Interestingly enough, markedly hypercoagulable thromboelastometry profiles were observed in COVID-19 patients, as reflected by shorter Clot Formation Time (CFT) in INTEM ... and EXTEM ... and higher Maximum Clot Firmness (MCF) in INTEM, EXTEM and FIBTEM ... In conclusion, COVID-19 patients with acute respiratory failure present a severe hypercoagulability rather than consumptive coagulopathy. Fibrin formation and polymerization may predispose to thrombosis and correlate with a worse outcome."
From China (4/20/20) [6]:
"Coronavirus has an extensive tissue distribution, causing a high number of proinflammatory cytokines to be released, promoting a systemic inflammatory response syndrome (SIRS), accelerating cell death in the lungs, livers, heart, kidneys and the adrenal parenchymal organs, which can ultimately lead to multiple organ dysfunction syndrome (MODS) . As inflammatory reactions occur in the all organs of the body, the microvascular system is damaged, leading to abnormal activation of the coagulation system, which pathologically manifests as generalised small vessel vasculitis and extensive microthrombosis"
The paper contains 17 'Recommendations'.
For those wanting more info, here is the link to the 45 PubMed hits: [7].
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In my case, to maintain D-dimer at the lowest level, I take 6 caps of 2,000 FUs.
It's tough to know what a prophylactic dose is when one can't get out for a D-dimer test. But I think that all PCa patients should consider it.
Incidentally, some doctors put COVID-19 patients admitted to hospital on a blood thinner. As mentioned above, they are anticoagulation agents rather than blood "thinners". Whereas nattokinase is a fibrin dissolver.
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Incidentally (from the Washington Post):
"When the novel coronavirus first hit, the Centers for Disease Control and Prevention and others put people with asthma at the top of their lists of those who might be the most vulnerable. But European researchers writing in the journal Lancet noted it was “striking” how underrepresented asthma patients had been. Earlier this month, when New York state released data about the top chronic health problems of those who died of covid-19, asthma was not among them. Instead, they were almost all cardiovascular conditions."
IMO, this is due to the absence/presence of a favorable receptor for the virus.
Many who do not feel ill enough to go to a hospital, die suddenly at home. There needs to be triage procedure that takes into account coagulation factors. & everyone with a pre-existing condition such as a malignancy should be assumed to be at risk. IMO
I hope the above wasn't too upsetting, but I'd hate to hear of an unnecessary death in this group.
-Patrick
[1] en.wikipedia.org/wiki/Fibri...
[2] en.wikipedia.org/wiki/Acute...
[3] pubmed.ncbi.nlm.nih.gov/307...
[4] ncbi.nlm.nih.gov/pmc/articl...
[5] pubmed.ncbi.nlm.nih.gov/323...
Melatonin as potential Covid-19 adjuvant treatment
