Lishs mom
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Member # 2344
posted
One of the current fads, that has recently resurfaced, is that Lyme disease cure is aided with blood thinning agents. In some cases Lyme disease can cause clotting or thickening which can cause other significant issues to arrise (heart and brain health). Since lyme bacteria prefers to be in the tissue (hence difficult to get positive PCR tests), it probably is not hiding in fibrous materials in the blood, so some statements about lyme hiding in the thick blood have no scientific basis. Lyme however does loves collagen and fibrous (*not to be confused with fibrinogen) tissue in the deep areas of the body where the blood can not reach.
Fibrogen (see www.fibrogen.com for more information on fibrogen) is a biotech material quite different from Fibrinogen. Fibrinogen affects clotting. There has been some confusion in some of the lyme circles, and mis information has been stated. Remember, when you read things, prior to passing them on, do a litmus test to make sure they are correct.
When concerned about high levels of Fibrinogen, the following tests are necessary. These tests check coagulation abnormalities:
prolonged prothrombin time (PTT)
activated partial thromboplastin time
thrombin time;
Platelet count
Packed cell volumes
Schistocytes on a peripheral blood smear
There are other tests which also can help determine blood health, and the requirements for blood thinning agents:
US-CRP - an ultra sensitive C-Reactive protien which is used to determin inflammation within the body.
Homocysteine (Hcy)- an amino acid. a High Hcy level is often related to future development of heart problems, and also associated with low Vit. B6 and B12 levels, and kidney disease.
DO NOT intiate blood thinning treatment without the aid of your physician and understand the risks of the medications before starting these procedures and without at least the proper baseline tests (PT, PTT, PCV, Platelet counts, WBV)
Some risks that I am aware of (and Im sure there are others):
Thromboembolism (cause of strokes) : This can happen when anticoagulants are given following heparin therapy. Solutions: Long-term therapy with low-molecular-weight heparin may help until the underlying cause can be brought under control
Internal Bleeding: Intracranial bleeding (10-68% mortality) Increased gut bleeding, increased bleeds from bruising.
Drug interactions with: quinolones, Rifamipin, Thyroid hormones, pennicillins, Metronidazole,Fluvoxamine,Ethanol,Diflunisal,Antifungal agents,Acetaminophen
posted
Do you know anything about levels of protein C activity and plasminogen? At my request, a doc ordered a hypercoagulation test. It was not the HEMEX panel that other people seem to be getting.
On the results the levels of these two were marked H, for high, just above the top of the normal range. Said nothing about the significance of plasminogen, but said that increase in protein c activity was of unknown hemostatic consequence.
So, they didn't seem to find anything amiss.
However, I found an interesting article which indicates that increased level of plasminogen facilitates borrelia invasion of organs (not dealing with our borrelia spp but probably similar). Not good, in other words, to have increased level of plasminogen. So, is this innate characteristic of my blood or is this something that infection causes, as a way of enhancing its activity? Not expecting you to know the answer, just thinking out loud. Here is the abstract for the article:
(Note that free full text available at pubmed.)
Infect Immun. 2001 Sep;69(9):5832-9.
Delayed invasion of the kidney and brain by Borrelia crocidurae in plasminogen-deficient mice.
Nordstrand A, Shamaei-Tousi A, Ny A, Bergstrom S.
Department of Molecular Biology, Department of Medical Biosciences, Umea University, S-90187 Umea, Sweden.
Borrelia crocidurae is an etiologic agent of relapsing fever in Africa and is transmitted to humans by the bite of soft ticks of the genus Ornithodoros. The role of the plasminogen (Plg) activation system for the pathogenicity of B. crocidurae was investigated by infection of Plg-deficient (plg(-/-)) and Plg wild-type (plg(+/+)) mice. No differences in spirochetemia were observed between the plg(-/-) and plg(+/+) mice. However, signs indicative of brain invasion, such as neurological symptoms and/or histopathological changes, were more common in plg(+/+) mice. Quantitative immunohistochemical analysis demonstrated infection of spirochetes in kidney interstitium and brain as soon as 2 days postinoculation. Lower numbers of extravascular spirochetes in plg(-/-) mice during the first days of infection suggested a less efficient invasion mechanism in these mice than in the plg(+/+) mice. The invasion of the kidneys in plg(-/-) mice produced no significant inflammation, as seen by quantitative immunohistochemistry of the CD45 common leukocyte marker. However, significant kidney inflammation was observed with infection in the plg(+/+) mice. In brain, inflammation was more severe in plg(+/+) mice than in plg(-/-) mice, and the numbers of CD45(+) cells increased significantly with duration of infection in the plg(+/+) mice. The results show that invasion of brain and kidney occurs as early as 2 days after inoculation. Also, Plg is not required for establishment of spirochetemia by the organism, whereas it is involved in the invasion of organs.
PMID: 11500461 [PubMed - indexed for MEDLINE]
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
Here is an interesting excerpt quoted from the above article:
"The mechanism by which Borrelia species enter blood and invade organs is still largely unknown. In higher vertebrates, plasminogen (Plg), the key component of the fibrinolytic system, can be converted to plasmin, a broad-spectrum serine protease, by the tissue-type Plg activator and the urokinase-type Plg activator (uPA) (6).
In addition to fibrinolysis, plasmin-mediated proteolysis has been associated with many other biological processes, e.g., macrophage migration, tumor cell invasion, angiogenesis, and atherosclerosis (6). In vitro, a number of invasive bacteria have the ability to interact with the Plg activation system by binding plasmin(ogen) to the bacterial surface and/or by expressing endogenous Plg activators (12, 26).
The activation of surface-bound Plg to plasmin is suggested to be a mechanism that enhances their ability to penetrate endothelium and tissue barriers. In addition, Plg binding may result in direct pathological effects due to the proteolytic activity of plasmin.
Interestingly, besides the implication of Plg binding in bacterial pathogenicity, a recent study by Fischer and colleagues suggests that the binding of a pathological prion protein to Plg is of importance for pathogenicity in transmissible spongiform encephalopathies (20)."
Posts: 8430 | From Not available | Registered: Oct 2000
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Lishs mom
Frequent Contributor (1K+ posts)
Member # 2344
posted
Increased in protein c activity is usually correlated with an inflammatory condition (lyme?)
Regarding the plasminogen, I dont know if its is a cause or a by product. Increased plasmin is often correlated with the increase of amino acid Homocysteine from my understanding. This is usually again, a result of an inflammatory condition and can relate to bacteremia, virus, or other conditions. (This is my understanding, and I could be wrong)
I do know that these things seem to be common wiht lyme patients, but still there is a huge question of which came first....but my guess is it is a better marker of your body fighting something that is causing inflammatory response, rather than the cause...
Posts: 1918 | From Central, Oregon | Registered: Apr 2002
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posted
My daughter has had clotting problems since her second picc line. She recently tested deficient in protein S, which, according to the hematologist is a rare genetic blood clotting disorder. I found information indicating that vitamin K deficiency, cancer and SEVERE INFection also can cause this deficiency. He knew nothing about that possibility, warned me about internet information, but promised to keep an open mind as we moved forward with testing her father and me, one of whom should have this same deficiency. I just received my results, which were normal. Her father will be next. We shall see.......
Posts: 422 | From Herndon, Virginia | Registered: Oct 2005
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posted
I was going to post about this topic tonight. My kids (15 & 19) will be starting Heparin in a couple of weeks.
Both had extensive testing done recently and there were abnormal results. These are the tests that were done:
Factor V Leiden PAI-1 gene MTHFR gene (both C677T, A1298C allelles) Prothrombin Gene IIb/IIIa polymorphism of platelet glycoprotein gene Resistance to activated protein C Homocysteine Methylmalonic acid Proteins C, S (total and free) Antithrombin III Fasting serum insulin Fasting serum c-peptide Factor VIII Factor XI Anticardiolipin antibodies IgG and IgM Lupus Anticoagulant Fibrinogen Plasminogen activator inhibitor activity (PAI-Fx) Lp(a)
They originally had the testing done because they have Intracranial Hypertension and blood disorders is one of the causes. They are seeing a hematologist at Children's Hospital.
-------------------- Peggy
~ ~ Hope is a powerful medicine. ~ ~ Posts: 2775 | From MN | Registered: Apr 2001
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Jellybelly
Frequent Contributor (1K+ posts)
Member # 7142
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I don't know that I would call it a "fad"?!? or that it has currently resurfaced? I was put on heparin about 5 1/2 years ago, and there is tons of research to back it.
There is a study out of Japan that found heparin to erradicate Babesia all on it's own by inhibiting it, and it is suspected heparin may do the same for Lyme.
National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
We examined the inhibitory effects of three heparins on the growth of Babesia parasites. The multiplication of Babesia bovis, B. bigemina, B. equi, and B. caballi in in vitro cultures and that of B. microti in vivo were significantly inhibited in the presence of heparins, as determined by light microscopy. Treatment with various concentrations of heparin showed complete clearance of the intracellular parasites. Interestingly, a higher percentage of abnormally multidividing B. bovis parasites was observed in the presence of low concentrations of heparin. Furthermore, fluorescein isothiocyanate-labeled heparin was preferably found on the surfaces of extracellular merozoites, as detected by confocal laser scanning microscopy. These findings indicate that the heparin covers the surfaces of babesial merozoites and inhibits their subsequent invasion of erythrocytes.
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
Please note that it is extremely important to obtain an accurate diagnosis before trying to find a cure. Many diseases and conditions share common symptoms: if you treat yourself for the wrong illness or a specific symptom of a complex disease, you may delay legitimate treatment of a serious underlying problem. In other words, the greatest danger in self-treatment may be self-diagnosis. If you do not know what you really have, you can not treat it!
Knowing how difficult it is to weed out misinformation and piece together countless facts in order to see the "big picture", we now provide simple online access to The Analyst�. Used by doctors and patients alike, The Analyst� is a computerized diagnostic tool that sits on a vast accumulation of knowledge and research. By combining thousands of connections between signs, symptoms, risk factors, conditions and treatments, The Analyst� will help to build an accurate picture of your current health status, the risks you are running and courses of action (including appropriate lab testing) that should be considered. Full information is available here.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn's disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner. Each patient must be treated individually.
KEY Weak or unproven link Strong or generally accepted link Proven definite or direct link Highly recommended
I had been knocking on deaths door with Lyme and Mycoplasma. I was treated with heparin for 3 years and have achieved about a 95% remission and have remained there for over 2 years. I have used very micro doses and I do mean micro doses of ABX, like 2.5 mgs of minocycline for periods of about 6 weeks. By far the most major portion of my treatment was treating the hypercoagulation with heparin.
Yes there are things to be aware of when your doc prescribes heparin, but for most it is a very safe treatment. Bleeding is not much of a worry because, ONE heparin is so stable and has a VERY short half life and TWO the doses given are absolutely miniscule.
My daughter was on heparin for 2 years and gave birth to her first child while on heparin. None of her doctors were worried about it's safety. She even had an epidural. All she had to do was not take another doae after labor started.
Here is a website with LOTS of information on why treating hypercoagulation IS important and info on heparin as well as natural alternatives and their safety.
As usual you would want to talk to your LLMD, but then you can't even get heparin without talking to your LLMD. So that point is kind of moot.
One last thing. Fibrin will coat the viens making it nearly impossible for ABX or any other supplements, natural or otherwise to reach the tissues where the Lyme is hiding. ABX start in the blood and hopefully get to the tissues, but if fibrin is working like a Teflon barrier, success will be limited or at the very least slower.
PS: To Lishmom, You are correct it is fibrinogen, I don't know what the heck the other stuff is that you mentioned "fibrogen". We are talking FIBRIN though.
Some of the tests that you recommended are useful in testing for this form of hypercoagulation, but others are useless when you are talking high fibrin levels. For example platelets won't tell you anything about ISAC Syndrome/hypercoaglation as related to an active infection. Sure EVERYONE should have their platelets checked, but that won't tell you if you have excess fibrin. Did you know you can be a bleeder and still have ISAC Syndrome? A PTT on the other hand can be a clue for a doctor who understands this for of hypercoauglation.
There are also numerous natural alternatives to heparin that are now being used.
You might want to get out the litmus paper:}
Posts: 1251 | From california | Registered: Apr 2005
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
Talking f i b r i n now - : One of the more known mechanisms the microbes use to create anergy is hypercoagulation. The microbes tend to live in the endothelium, where the food is most abundant. They trigger the host's coagulation mechanism to lay down a layer of fibrin on top of them to evade recognition by the immune system, etc.
There is a much simpler way and a very painless way than shooting yourself with heparin. You could try Rechtsregulat.
According to Dr. K., Rechtsregulat "has outperformed the s.c. injection of heparin in our trials." He is well acquainted with Hemex, etc., but has discontinued heparin for patients. Also, apparently patients became allergic to heparin after a short while - especially using the more affordable on.
posted
Pseudoginseng and serrapeptase are some good natural anticoagulants that don't increase risk of bleeding like heparin does. Serrapeptase is also supposed to help break down fibrin and scar tissue in the body. I took a supplement with pseudoginseng in it, and it helped me with Lyme Disease tremendously and it aided the tissue penetration of the other medicinals I was taking.
Farah
Posts: 208 | From New Mexico | Registered: Dec 2005
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SForsgren
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posted
I went down the Recht-Regulat route and in less than 2 months can see a HUGE change in the color of my blood and ease of blood draw. From dark dark almost black to bright bright red. I think it is potentially good stuff.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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Lishs mom
Frequent Contributor (1K+ posts)
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posted
Jelly belly, I see I used a word that maybe I should NOT have used. FAD is not necessarily bad in my understanding, obviously to some it is, so for that I am sorry. I am not against the treatment, in fact I too have used it and found it helpful.
However, when a lyme patient is helped by the heparin therapy or warfarin, or whatever the choice to thin blood it is because there was a need to do so. What I have run into recently is phone calls of people telling me a friend said they should go in with them on a bulk order (but not ordered by a physician) on blood thinning agents. I have had 6 phone calls in the past two weeks about this from different people. They dont do the proper tests to identify if it is an issue, nor do they have a physician to help them determine if it is a good idea and this is where it becomes a problem.
Heparin or warfarin therapy is often necessary, however, not ok for all people. Hence, when I saw some things floating around and started recieving phone calls, I thought it would be wise that people understand its not a cureall, and it does require good evaluations such as what PAB has shown.
Posts: 1918 | From Central, Oregon | Registered: Apr 2002
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P.S. Serrapeptase that Farah mentioned above is not a plant-derived enzyme. It is an enzyme created by a bacteria from the silk worm. If you want to go the plant way, this is not the enzyme to go for.
Posts: 9834 | From Washington State | Registered: Oct 2000
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kgg
Frequent Contributor (1K+ posts)
Member # 5867
posted
Thank you Gigi! Now I remember why I didn't order this before, it as soy in it. Oh well . . .
Karen
Posts: 1845 | From Maine | Registered: Jun 2004
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posted
I have tried over over again to get my doc to recognize, even brought the info for him. Last time my blood, hypercoagulation, undoubtedly. She could barely get it through the needle was so thick took long time. My doc pays no attention when tell him probably could paint the walls with it so thick. BTW/I drink over gallon water a day. So, this should not be. Unless underlying problem. I probably have active CMV now. Bad bought with Uveitis which is linked to Lyme & CMV. Hard work to save my vision. He still has done nothing. Good Luck with any of you who need help or to get right meds. I keep getting worse with only band-aid meds.
Eye Inst. was extremely concerned when dxed with Uveitis. After ER fiasco, got herpes virus in eye along with the 3 abrasion from them trying to get pressure results. Did 10 times with pen like instrument. He did not change tip which nor did he know what he was doing. Then eye cut, talk about pain for days with all the. On 9 eye drops. You would think that would wake doc up. Yet, he is only doc on my list who believes in Lyme or FM/Cfids. Sorta stuck with Primary Doc. Used most saving being mis dxed for more yrs. than can count. Now no income basically living off what little savings left for roof over my head. Unable now to go out on my own. Some good info & is true. Jelly, does here research well. Thanks for some things I was not aware of & I work on this crud too many hrs. With no 1 to listen.... Take Care All Kerry
Posts: 746 | From Clearwater/fl/Pinellas | Registered: Jun 2003
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posted
So sorry, kerry. Wish I could do something to help. Not in a good place myself. Seems like it is taking forever for the medical establishment to get this right.
Your eye ordeal was bad. I once refused to let them do that test, because it had already been done recently by another doc. This was not received with good grace. Even plumbers behave better toward customers than a lot of medical people do. My initial reaction now to any testing, especially invasive, is to say no unless there is a really good case made for it. Does not please the docs. But I notice they have testing biases. When in doubt, order another test, or order the same tests you have already had. Even if you bring a whole pile of previous test results, try and get them to actually look at 'em! Putting a name on something and testing seems to have a higher priority than action on treating. After they have a name and lots of tests results, bang goes their interest in you.
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I have tried over over again to get my doc to recognize, even brought the info for him. ![[group hug]](graemlins/grouphug.gif)
Kerry
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