I have a number of posts on abnormal coagulation & the need to monitor with D-dimer tests - & the use of nattokinase to speed clot elimination. Currently, doctors wait until cancer patients get a DVT or pulmonary embolism, etc. Those who do not die on the way to the ER are then put on anticoagulants.
In other words, there are no prophylactic meds, so docs do not screen for patients at risk - or even look for active clots.
"Incidental pulmonary embolism (IPE) is a common finding on computed tomography (CT). IPE is frequent in oncologic patients undergoing staging CT."
You can't really ignore a pulmonary embolism when it is accidentally found.
"The overall frequency of {incidental pulmonary embolism} in oncologic patients was 3.36%" However, "The highest frequency was found in prostate cancer (8.59% ...)" Wow!
"The highest frequency of IPE {incidental pulmonary embolism} was identified in prostate cancer patients. It has been shown previously that patients with prostate cancer are at higher risk of thromboembolic diseases, with the highest risk for those receiving endocrine therapy. Moreover, it was stated that prostate cancer itself, prostate cancer treatments, and selection mechanisms all contribute to an increased risk of thromboembolic events. Beyond that, the high frequency of IPE in the present study might be caused by the fact that prostate cancer staging CTs are mainly performed at the metastasized tumor stage compared to other tumor entities, which harbors in itself a higher risk of IPE."
As I say, a D-dimer test may identify a growing clot. If the number is zero, there is no clot. D-dimer may be elevated for other reasons, but where there is high risk of a clot, one should consider taking nattokinase. In my opinion. I'm not a doctor, etc, etc."
One might take a daily 2,000 FU cap & hope for the best, or double up, but sometimes a therapeutic dose has to be much higher. I have to take 6 caps to keep D-dimer in check. i.e. that is my maintenance dose.
Nattokinase is not a "blood thinner" (nor are aspirin & omega-3). It is similar to the plasmin enzyme that (very slowly) dissolves fibrin. Nattokinase speeds up the process & the aim is to outpace the accretion of fibrin.
Aspirin inhibits the aggregation of platelets. It does this at the lowest dose & there is no point in taking a higher dose. There is nothing to monitor. It is not guaranteed to prevent clots - i.e. an accumulation of fibrin. The clumping together of platelets at the site of a clot is the first step. It is followed-up by the conversion of fibrinogen to fibrin, & accumulation, at the site.
Omega-3 [DHA/EPA] are important in that they compete for space in the lipid rafts of cells. As such, they create a more favorable omega-3:6 ratio. Arachidonic acid [AA] (an omega-6) is pro-coagulation & pro-inflammation. EPA/DHA are the reverse. It's good to have a favorable EPA/DHA:AA ratio in the raft, but that will not necassarily prevent clots. One should not take more than the highest recommended dose. Once again, there is nothing to monitor.
Patrick thanks for this. Do you think it is a good idea to take lowest dose aspirin and Natto because they work differently or Natto only. I can’t get a regular d dimer test in UK so am flying blind but taking 4000 FU Natto
Personally, I do not use aspirin since it can be a problem for the stomach & kidneys. Would the FDA approve it today? It's grandfathered because it has been around for over 120 years. That is half the time that the U.S. has been a country!
For those who tolerate low-dose aspirin, I believe it to be useful,
Nattokinase does not stop coagulation. It cleans it up after the fact. I'm OK with that. But it does mean having to to know that clotting has occurred. Hence the D-dimer test.
I was wondering how in these Covid times or for those otherwise unable to get D-dimer tested, what would be a good strategy? You are doubling-up. Fair enough for maintenance. But what about an initial washout period? A month at quadruple the dose? I couldn't say.
Be on the lookout for leg discomfort. Warmth at the affected area. Perhaps a hint of water retention. & of course, breathing issues. Note that anticoagulants do not dissolve clots. They simply give plasmin a chance to dissolve the clot by slowing down coagulation. Speeding-up the destruction of the clot is a better strategy IMO.
Once again, I'm not a doc. I don't want anyone in the ER saying: "But Patrick said ... " LOL
It's a dismal prospect to be on Warfarin for the rest of one's life, with the attendant bone loss & arterial calcification. Your friend was lucky to avoid that.
Best, -Patrick
I wonder what the age adjusted risk would be? Avg PCa patient is in his 60s or 70s? What is the general population risk for that age? And what is the oncology patient risk at that age?
Is the risk normal if you are NED and much higher if on chemo or ADT or?
One can study the probability distributions & assess one's risk - or monitor D-dimer.
What concerns me as much as the possibility of a lethal clot to the lungs, is that micro-clots may facilitate the migration of cancer cells to favorable sites. One may already have metastatic cancer, but I think it a good idea to inhibit further mets & tumor burden.
I am currently on Eliquis for this. Started having problems breathing after 8th chemo round. Did a CT of lungs and was diagnosed with multiple bilateral PE. After a month and a half of blood thinners I am getting back to normal. Dr. First though it was Anemia causing the breathing problems. Be safe fellow members!!
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
Greater consumption of healthful plant-based foods associated with modestly higher scores in quality-of-life among patients with PCa
