Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Inf

Discussion in 'Fibromyalgia Main Forum' started by RatsWife, Mar 7, 2007.

  1. RatsWife

    RatsWife New Member


    Has anyone else looked into this causation for our FM, etc.?

    Personally I have noted that my blood viscosity has changed markedly over the last decade or so. Once it flowed quickly into tubes when I'd go to a lab for blood work, now it flows like molasses in the winter.

    Please let me know if I've done something inappropriate by posting this url.

    Thank you!
    (FM diagnosed Jan 07)


  2. bwilkins

    bwilkins New Member

    I have just recently had blood work done also and I had the same results as you. I asked the nurse why my blood seemed so thick? She said maybe you didn't drink enough water today. My blood use to flow quickly also. I too have fibromyalgia for 7 years.
  3. RatsWife

    RatsWife New Member

    You, too? It's not good except that you've noticed a change, too, like I have. I can recall going to a blood drive at a local community college around 1991 or so, and when they pricked my finger the blood squirted so powerfully it got all over the front of the tech's lab coat. She freaked out, too. I'm sure she didn't rest easy until all the tests were done on my contributions to the drive. Today I sit and sit and sit while the tubes slowly fill up. It's truly completely different.

    Thanks for replying, B!
  4. AllWXRider

    AllWXRider New Member

    Dr. William Wong N.D. says that Fibrin (a protien based blood clotting factor) is used to quarentine off an area of infection until the body is able to deal with it. Common areas are muscles. Lack of blood flow causes ischemic pain. This is often the cause of FM.

    The body then uses systemic enzymes made mostly by the liver to break down the fibrin and restore blood flow.

    Toxic metals, other chemicals and age can interfere with our enzyme production. Systemic enzymes are also made by healthy bacteria (Probiotics) in the gut. Healthy bacteria is often killed off by anti-biotic use.

    Enzymes are made of an amino acid + a metal ion. Toxic metals attach themselves to antagonistic metals and the resulting enzymes create the wrong reactions and sometimes don't work at all.

    Systemic enzymes:
    Cleanse the blood
    Dissolve fibrin blockages
    Dissolve the isoprin protien bond of certain viruses
    Modulate the immune system
    Assist in digestion
  5. RatsWife

    RatsWife New Member

    Where do I find out more, please? A good friend is always trying to get me to use enzymes to improve nutrition. Are these the same enzymes?

  6. ulala

    ulala New Member

    I'm posting the article that you made a link to if you don't mind?

    I have CFS/FM and several years ago ended up with a blood clot in my calf. A year or two later I got to Dr. Holtorf at the FFC in Torrance, Ca. and he did a blood test for clotting that showed that I should be tested for Factor V Leiden, which is a genetic clotting mutation (mentioned in the article below). He just kind of skimmed over that fact but did put me on heparin. I felt much better while on it. One problem for me with the heparin is that the shots that I gave myself in my stomach caused brusing and some swelling. A bruised and swollen stomach is not very attractive.

    Since then I had another blood test and found that I am a Factor V Leiden homozygote, which means that I inherited the gene from both parents. This is very unusual and puts me at an 80% greater risk of getting a stroke than the average person.

    I've run out of the heparin and can't get it re-filled until I see Dr. Holtofrr again. I still hate the bruised stomach. The heparin made me feel much better. Thanks for reminding me. I'm going to make an appointment with him now!

    I think there is a lot to this theory. Have you tried heparin or been tested for hypercoaguability?

    Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness
    PART 1

    Read these related articles:
    Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness - PART 2
    Hypercoagulation & Heparin - A Second Look.

    Interview with David Berg

    David Berg is the Director and Cofounder, with Lois Hill Berg, of HEMEX Laboratories. Along with Dr. Harold Harrison and several clinical collaborators, they have developed the idea of the hypercoagulation/ immune system activation of coagulation theory in chronic diseases, a proposed cause of Chronic Fatigue Syndrome and Fibromyalgia, and have proposed an appropriate treatment that reduces many related symptoms. Mr. Berg has a M.S. degree in clinical pathology and laboratory medicine, and has been in practice for 35 years. HEMEX Laboratories offers testing and consultative services relating to the diagnosis, treatment, and monitoring of hematological, clotting and/or bleeding disorders.

    We first became involved with research in chronic illnesses while we were performing re search regarding hypercoagulability - related infertility in women with one of the local infertility specialists here in Phoenix, AZ. We found that a hypercoagulable state, presumably due to a coagulation protein defect, existed in many women who were infertile and/or who had recurrent spontaneous abortions. Our colleague Dr. Couvaras observed that when he put women on low dose heparin in order to maintain pregnancy, some with CFS/FM-like symptoms, pelvic pain, and migraine-like headaches had amelioration of their symptoms. He asked us “Why?” As a result, we performed a retrospective study on 30 of these obstetric patients with chronic illness symptoms, and determined that all had coagulation system activation. As the hypercoagulability was decreased by heparin injections, the chronic illness symptoms diminished. This was the first clue to the connection between coagulation and chronic illnesses. These findings were published as a poster at the 1998 AACFS meeting in Cambridge, MA.

    We subsequently refined our test panel for low level activation of coagulation to include Prothrombin fragment 1+2 (F1+2), thrombin/antithrombin complexes (T/AT) and Platelet Activation by Flow Cytometry assays. Thus, the ISAC or Immune System Activation of Coagulation panel consisting of fibrinogen (FIB), soluble fibrin monomer (SFM), F1+2, T/AT, and PA by Flow was born. With our partner and Medical Director, Dr. Harold Harrison and several clinical collaborators, we then designed and conducted a prospective, multi-center, blinded, case control, associative study of non-obstetric CFS/FM patients and controls, with centers in New York, Houston, and Phoenix. When the code was broken, identifying patients and controls, we were able to identify most of the CFS/FM patients based on having two or more positive test results out of the five assays in the ISAC panel. It was the first definitive evidence that, indeed, chronic illnesses have a demonstrable basis in the blood coagulation system. This study was published in the international journal Blood Coagulation & Fibrinolysis, 1999, 10:435-438. In another associative cohort study published in Blood Coagulation & Fibrinolysis, 2000, 11:673-678, we determined that Gulf War illness has similar findings of low level activation of coagulation.

    In November, 1999, Dr. Joe Brewer (an Infectious Disease specialist in Kansas City) and I developed a model of pathogen activation of the immune and coagulation systems. The model proposes that the end result of such pathogenmediated activation is increased blood viscosity due to 1) an underlying coagulation regulatory protein defect, and 2) activation of the coagulation system by the pathogen. As the blood viscosity increases, the diminished blood flow creates hypoxia (lack of oxygen) and nutrient deprivation within various areas of the body. This is like trying to start your car in Wisconsin in the winter with 60- weight engine oil. This model explains the multi-organ symptomatology and also explains why the low dose heparin therapy is effective by increasing blood flow as the blood viscosity decreases. Thus, patients gain relief from their symptoms with this therapy.

    The model states that coagulation activation generates thrombin, which converts fibrinogen to soluble fibrin monomer (SFM). Soluble fibrin becomes deposited in the micro-circulation (capillaries) as fibrin or fibrinoid-like deposition, blocking oxygen and nutrients transfer to parenchymal tissues. Many pathogens activate the immune system. These include viruses (such as EBV, CMV, HHV6 & others), bacteria (mycoplasma, chlamydia, borrelia, etc), fungi (such as candida), etc. These pathogens are anaerobes, i.e., they live and reproduce in an oxygen deprived cellular matrix or environment. That’s why fibrin deposition becomes important to the survival of the pathogens because it produces decreased oxygen in cells and tissues. One of the biggest challenges to a clinician is to figure out what pathogens are present in the patient, and therefore the most appropriate therapies against these pathogens. The average CFS/FM patient may have anywhere from one to seven pathogens that need eradication.

    Positivity of two or more tests in the ISAC panel occurs in more than 80% of all patients tested. However, the longer a patient has been ill (many years), the less activation is needed by the pathogens for survival, and therefore fewer tests may be positive. Someone who has been ill for 10 years or more may only have one test positive in the panel. The ISAC panel also works very well for monitoring anticoagulant therapy between 4-6 weeks after therapy has started. It indicates whether or not there is enough heparin being given to the patient, the overall patient improvement and the reaction of the body to the pathogens, such as a Herxheimer-like reaction (relapse from infections or reactivation of pathogens).

    In addition to the pathogens that can activate the immune system, metals (e.g. mercury, lead, aluminum), exogenous toxins, chemicals, allergens, physical trauma, vaccinations, and/or biological warfare agents can also activate the immune system. This may lead to secondary infections, which may also trigger coagulation activation. If the coagulation mechanism does not shut down properly, then there is continued thrombin generation and soluble fibrin formation, resulting in increased blood viscosity and decreased blood flow.

    When you look for a genetic basis in this model, one can test for seven different regulatory proteins of the coagulation mechanism plus homocysteine in a panel we call the HTRP (Hereditary Thrombosis Risk Panel). In July 2001, at the International Society of Thrombosis and Hemostasis meeting in Paris, we presented data from a retrospective study of over 400 chronically ill patients, 83% had one or more demonstrable coagulation protein defects. Forty percent of the patients had a thrombophilia defect (decreased protein C, decreased protein S, decreased anti-thrombin, APC resistance/factor V Leiden positivity, or increased prothrombin/prothrombin gene mutation positivity). 39% of the patients have defects in the fibrinolytic system (hypofibrinolysis due to elevated lipoprotein (a) - Lp(a) and/or PAI1-plasminogen activator inhibitor-1. 21% of these patients had a defect in both the thrombophilia and hypofibrinolysis marker groups. This means that not only do they form fibrin easily, but also they are compromised in the ability to clean up the fibrin deposition.

    Let’s put this in plain English. When a pathogen(s) gains a foothold, especially in the endothelial cells in the blood vessels (as well as other cells), the bug(s) can be protected by the coagulation mechanism of fibrin deposition on top of the infected cells. Half of the patients form fibrin very fast, becoming fibrin(oid) deposition. Half of the patients have an inability to clean up the fibrin, and therefore continue to have oxygen and nutrient starvation of tissues for a long time. For example, if the fibrin deposition occurs in a muscle, it says “ouch,” and you have a tender point as in Fibromyalgia. If it is in the placenta, the placenta is compromised by fibrin deposition and the baby aborts. As blood viscosity increases and blood flow is reduced throughout the body, the patient becomes hypo-this and hypo-that, such as hypothyroid, hypo-HPAaxis, hypo-estrogen, etc. The use of low dose heparin restores blood flow throughout the body and hormones from the endocrine system tend to normalize. Thus, the blood flow issue becomes one of the most important issues of chronic illnesses. Unfortunately there is no easy test to measure blood flow, only the effects of blood flow.

    If you consider the movie “Braveheart” (1000 AD) and you went to battle and were wounded, you probably would have bled to death unless you clotted fast. By clotting fast, you saved your own life and passed on this new trait to your children. This hypothesis may explain how these coagulation defects were genetically selected during the last 2000 years in Europe. Life expectancy back then was only 30-40 years. With our life expectancy now of 80+ years, these traits are no longer beneficial, but rather deleterious to our health. It was the Spanish, French, British, Germans, Italians, Scandinavians, etc. (Europeans) that colonized the Americas. This explains why most of the chronically ill patients are white people of European decent. Therefore we have a genetic basis in the coagulation system for chronic illnesses that is very straightforward.

    The model of reduced blood flow from increased blood viscosity due to activation of coagulation accompanied by a coagulation protein defect gives a scientific basis for a contribution to the pathophysiology of chronic illness. It also gives a measurable or quantifiable, objective aspect to testing the blood of patients with these diseases. It is no longer “all in your head”, but rather in your “blood.” It’s not rocket science, but a simple, logical explanation for what’s going on in many chronically ill patients.

    HEMEX Laboratories provides testing services and consultative interpretations to clinicians and physicians throughout the United States. For more information, technical reprints, and/or patient information, please see their website at www. hemex.com

  7. ulala

    ulala New Member

    Besides heparin nattokinase and lumbrokinase help clear the blood of fibrin.

    Low Level Activation of Coagulation with Coagulopathies in the Etiology of CFS / FM and Chronic Illnesses. An Explanatory Model Revisited1. DE BERG1, LH BERG1 and HH.HARRISON1,2; 1HEMEX Laboratories, Phoenix, Az, 2Univ AZ College of Medicine.

    INTRODUCTION: Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) may be considered a Chronic Illnesses (CI). A MODEL of Low Level Activation of Coagulation in CFS / FM as a variant of Antiphospholipid Syndrome (APS) was first published in 19991.

    The purpose of this presentation is to give additional supporting data to the 1999 hypothesis about the subthrombotic process termed ISAC (Immune System Activation of Coagulation) which results in low level activation of coagulation in CI patients, how the subthrombotic condition is effected by a coagulation protein defect and how this model of disease is involved on the cellular level in many different and seemingly unrelated disease processes.

    MODEL: A pathogen (infection) plus a coagulation defect allows excess thrombin generation, converting fibrinogen to soluble fibrin. Soluble fibrin increases plasma viscosity and may decrease blood flow.

    Soluble fibrin may be deposited on the capillary wall as fibrin deposition, slowing oxygen and nutrients transfer to the tissues and as well as waste products from reentering the blood stream.

    DISCUSSION: In the initial cohort of 54 patients and 23 controls, 92% of the patients had a demonstrable hypercoagulable state or low level activation of coagulation. Subsequent cohorts have yielded from 78 - 92% coagulation activation as defined as two or more of the five ISAC (Immune System Activation of Coagulation) markers being positive.

    After testing over 3000 patients with a variety of chronic illnesses, a coagulopathy (coagulation protein defect) has been found in over 80% of these patients. Genetic studies have shown a 2 to ~ 10 fold increase of coagulation protein defects over the general population rates in CFS/FM and chronic illnesses2.

    A coagulation regulation protein defect allows accumulation of fibrin (fibrin deposition) on the blood capillary walls due to the lack of proper control of the clotting mechanism.

    This may be due to either a thrombophilic defect (forms fibrin too easily) or a fibrinolytic defect (cannot clean up fibrin easily). These data allow for the discussion of a coagulation protein defect as being permissive and/or predispositional in chronic illnesses. Around 20% of patients tested have both a thrombophilic and fibrinolytic defect.

    When a defect is present, a precipitating event (infection, trauma, etc) leads to coagulation activation. The inflammatory response and coagulation activation are the components of the host defense mechanism. If the body can wall off a pathogenic invader with fibrin, it can prevent a systemic infection.

    Because of a regulatory protein inappropriate action at some point in the sequence of events to control the fibrin formation, thrombin generation continues at a low level which keeps the coagulation mechanism activated in this low level state.

    This is the important paradigm shift from a thrombotic process (a blood clot) to an ongoing subthrombotic condition, as found in chronic illnesses.
    Supporting evidence comes from several sources. Pathogens, such as Epstein Barr virus (EBV), Cytomegalovirus (CMV), Human Herpes Virus 6 (HHV6), Mycoplasma (many species), Chlamydia pneumonia, tick borne disease (Borrelia [Lyme], Babesia, Bartonella, Ehrlichea), Human Herpes 1, 2 & 3, Staphylococcus, Streptococcus, parasites, and many more pathogens, have the capability of triggering the coagulation mechanism.

    Many of these pathogens have amino acid sequences that induce cross reacting antibodies against the protective proteins on the blood vessel walls. B2GPI and Annexin V are two protective proteins on the inside of the capillary that keep coagulation proteins from binding to the endothelial cells (EC) and generating thrombin.

    In 2000, CMV was shown to have two 19 amino acid sequences on its outer coat that induce anti-B2-GlycoProtein I (B2GPI) antibodies3. These findings suggest a mechanism of induction of autoimmune AntiPhosphoLipid antibodies after incidental exposure to viruses.

    Since pathogens can induce the formation of these cross reacting antibodies, they can generate fibrin deposition over the ECs which are infected. Staph, Strep, CMV, EBV, HHV6
    are just a few of these pathogens that have these capabilities4.

    This gives support to the proposed 1999 model of CFS / FM being a variant of APS.
    Cross reacting antibodies strip the protective proteins that cover endothelial cells and allow binding of the coagulation cascade proteins and thrombin generation. Thrombin (IIa) generation results in the formation of Soluble Fibrin Monomers (SFM) from Fibrinogen (FIB)5. Continuing low level thrombin generation converts SFM into Soluble Fibrin Protofibrils (SFP). [See photomicrographs]

    When there is a burst of Thrombin (trauma), IIa activates Factor XIII which in turn cross-links SFPs into insoluble fibrin, i.e., a blood clot. Since SFPs are a method by which the body can wall off pathogens, SFPs have a protective mission in the blood [See diagram].

    Soluble Fibrin deposited on EC can delay oxygen and nutrient delivery to tissues around capillaries as hypothesized in 1999.

    Nemerson6 reported in the International Society Thrombosis & Hemostasis meeting (July, 2003, Birmingham, England) that 1 micron (1 Fm) of fibrin deposition changes the oxygen diffusion time, from RBC through the capillary wall to the local tissue, from 2 seconds (normal diffusion) to greater than 5 minutes. [See diagram]

    This fibrin deposition not only creates local hypoxia, but also blocks nutrients and hormones from getting into the tissues easily as well as slowing down the process of waste removal from the tissues.

    The fibrin deposition model explains the local tissue hypoxia found in many disease entities, including Fibromyalgia. Lindman, et al7, in 1995 showed swollen endothelial cells in muscle biopsies from trapezius muscles in myalgia patients.

    They concluded that capillary derangements might be caused by disturbances in the muscle microcirculation, hypoxia or ischemia. “This might severely affect the microcirculation of the muscle by diminishing the exchange of gases and substrates between the capillaries and the surrounding tissues”. Park et al8 (1998), using P-31, detected metabolic abnormalities in muscles of patients with Fibromyalgia.

    These metabolic abnormalities are consistent with weakness and fatigue in FM patients. This included significant decrease in ATP and ADP with increased AMP in patients over controls.

    These findings were corroborated by several other similar studies. Park concluded that inadequate circulation and oxygenation leads to reduced tissue oxygenation, resulting in decreased ATP synthesis.

    Jeschonneck, et al9, presented evidence in 2001 that Fibromyalgia is local hypoxia. They found chemical changes secondary to local hypoxia (\ATP, \ADP and [AMP), “moth-eaten fibers”, “disturbed” blood flow, higher RBC concentration, reduced RBC flow and increased RBC rouleau, decreased skin temperature, vasoconstriction of unknown pathophysiology, swollen endothelial cells and local muscle pain associated with local muscle hypoxia.

    The end result is ischemia and pain. These findings could be easily explained by fibrin deposition proposed in the unifying coagulation activation model listed above.
    In addition to the build up of SFM and SFPs on the capillary walls, Soluble Fibrin may create another problem for the patient.

    Increased SFM in the plasma may increase the plasma viscosity. Increased plasma viscosity decreases blood flow. Decreased blood flow may cause some end organ dysfunction. This may explain the Raynaud’s phenomenon of cold hands and/or cold feet.

    Unpublished data indicate that increased SFM in the plasma may result in very low Sedimentation Rates, e.g., values between 0 - 4.

    Thus, besides blocking oxygen and nutrients from entering the tissues and waste removal in a timely manner, blood flow is compromised by increased Soluble Fibrin. This may contribute to positive tilt table tests in CFS / FM patients.

    Recent studies involving arthritis confirm the local and systemic activation of coagulation and fibrinolysis defects. So, et al10, (2003) showed that patients with arthritic joint disease have increased plasma and joint coagulation activation (F1+2, T/ATs, D-Dimers) as compared to healthy volunteers.

    These activation markers were highest in RA patients. Increased fibrinolysis inhibitors (Thrombin Activated Fibrinolytic Inhibitor-TAFI) in the joints permits ongoing coagulation activation and blocks the removal of subsequent fibrin deposition.

    The use of low dose heparin therapy may reverse the fibrin deposition and allow for potential treatment of pathogens.
    Clinical evidence of this subthrombotic pathophysiology as it relates to patient symptoms comes from the apparent efficacy of anticoagulant therapy in these patients.

    In a retrospective study from one
    clinical practice11, a cohort of 60 CFS/FM patients was given 5000 units of sq heparin BID along with other therapies. The time on heparin ranged from 3 to 20 months with a average of 8 months of therapy. Each patient received a clinical assessment score before and after treatment as an outcomes evaluation. The average improvement (scale 1-10) was 8.5 (85%). The coagulation activation testing (ISAC panel) was positive in 78.3% of the patients at baseline and showed improvement on repeat testing.

    Thus the ISAC panel is useful also for monitoring effectiveness of heparin therapy in CFS/FM patients.

    SUMMARY: CFS, FM and other Chronic Illnesses may have a common etiology which is the subthrombotic process termed ISAC (Immune System Activation of Coagulation) which results in low level activation of coagulation. This has been described as a subset of AntiPhosphoLipid Antibody syndrome (APS).

    A permissive or predispositional coagulation regulatory protein defect allows for ongoing thrombin generation from pathogen(s) activation.

    Thrombin converts fibrinogen to soluble fibrin which may be deposited on capillary walls. Increased soluble fibrin increases plasma viscosity, decreasing blood flow throughout the body.

    Fibrin deposition slows oxygen and nutrient delivery to local tissues, creating hypoxia, ischemia and decreasing ATP production within the cells.

    The same process inhibits cellular metabolic wastes from reentering the blood stream for disposal.

    Low dose heparin therapy (not warfarin) decreases thrombin generation and soluble fibrin production, improves blood flow, allows for fibrinolysis to clean up fibrin deposition, and allows the return of an anticoagulant environment (instead of a procoagulant environment) in the capillaries.

    Other therapies may be indicated based on the hereditary coagulation defect(s) found in the patient.

    [This Message was Edited on 03/07/2007]
  8. RatsWife

    RatsWife New Member

    No. I've never been tested and with all the hassle I'm having with doctors on top of being so irritable and tired all the time, I don't know if I can add this to the fight. I'm getting together my medical history so it travels with me now and not rests with scattered other sources -- although it concerns me that most of them have destroyed my records before 2000 already. Don't really understand how they can be allowed to do that in this modern age of technology where whole libraries can be stored on a chip the size of a postage stamp. When I get the remaining records, I think I will ask my current PCP. Thanks for substantiating with your situation.
  9. bigmama2

    bigmama2 New Member

    hi guys- thanks for the great info. i am looking into this. my fibrinogen level is 415, which is at the very high end of normal lab range. my dr said under 275 is better.
    i will prob start natto eventually.

    take care
  10. elliespad

    elliespad Member

    When I went on Heparin Injections, ALL my muscle pain disappeared COMPLETELY. It was shocking really, as I usually have a level 7-8 pain. After one month, my doc switched me over to Lumbrkinase (enzymes from earthworms) and my pain gradually returned.

    I have used Digestive and Systemic enzymes over the years and they have never done much, if anything, for my pain. Maybe if I took REALLY HIGH doses, hmmm.
  11. Mikie

    Mikie Moderator

    My doc and I tried the injections empirically because people with longstanding chronic infections usually suffer fibrin overgrowth in the blood. The injections caused HUGE immune reactions and Herxing as the pathogens lost their hiding places--fibrin/platelet clumps. My legs felt warmer after each injection and the injections got rid of a large numb spot I had had on my leg.

    I believe getting rid of the excess fibrin is an important part of an overall treatment regimen.

    Love, Mikie
  12. AllWXRider

    AllWXRider New Member

    If you google Vitalzym or Virastop you'll find plenty of competitive sources.

    Dr. Wong says to start w/ 1 per day and increase the dose by +1 each week. He says your body will notice when it starts working.

    My mom's dosage was 6/ day.

    "Forbearance" is up to 2/day [Virastop]. See her posts on this forum.
  13. ulala

    ulala New Member

    back on the heparin shots if they were making you feel so much better? Will your doctor switch you back?

    Does anyone know if there is another form of heparin that is similar to the injections that does the same thing? I think there are lonzengers but I don't know if they have the same effects.

    I'm finding it difficult to find a doctor who will prescribe heparin for me. Although Dr. Holtorf prescribed it for me not even knowing that I was a Factor V Leiden homozygote (he did a preliminary blood test that showed that I was at risk for Factor V Leiden and should be tested for it). A third follow-up appointment with him is $345.00 which at this time is expensive for me.

    The evidence seems very clear of the connection between CFS/FM and hypercoagulation. I read in another article that hypercoagulation can be responsible for positive tilt table tests which ties in to the cardiac problems.
  14. ulala

    ulala New Member

    keep their patients records for ten years. I thought that was the law. Are your medical records missing? It's best to get copies of records soon after seeing a doctor.

    In my experience it almost seems that some doctors take it personally if you ask for copies of your meical records. If you have copies you're going for a second opinion and their fragile, large egos will be offended.
  15. ulala

    ulala New Member

    below is a paragraph from an article written by Dr. Jospeh H. Brewer

    "Chronic Active Human Herpesvirus-6 (HHV-6) Infection: A New Disease Paradigm

    Another interesting treatment concept involves the use of anti-coagulants. Given the issue of activated coagulation pathways in these patients (endothelial cell tropism and vasculopathy), anti-coagulation may improve oxygen delivery and help with the symptoms that have been caused by a hypercoaguable state and fibrin deposition (99).

    One study has demonstrated symptom improvements in CFS patients treated with heparin (99). Several studies have shown that herpes viruses attach to cell surfaces via heparan sulfate receptors and that exogenous heparin can block this interaction and viral infectivity (100, 101).

    Thus, heparin may have some antiviral properties for
    herpes viruses. Patients with hereditary hypercoaguable syndromes (thrombophilia or hypofibrinolysis) may be at further risk for substantial hypercoaguable related problems and require anticoagulation. One evolving concept involves blocking viral activation (antiviral agents or immune modulation such as TF) combined with anticoagulants (heparin or coumadin).

    A model for a hypercoaguable state in patients with active HHV-6 infection and possible management strategies of the patient with a hypercoaguable state and associated active HHV-6 infection are outlined in Table 2 and 3."

  16. RatsWife

    RatsWife New Member

    I just didn't know they destroyed them EVER. I worked in record keeping in the past (the way back past...) microfiching records for healthcare practices. Alas, my records are gone before 2000. I asked two of the doctors if they would write up what they recalled to put into my records but they both declined saying they didn't remember enough to warrant the attempt.

    What I can discern now is confirmation that the practices where I have the most trouble with appointments, followups and referrals are the ones who aren't providing the copies I've requested -- not sure why the staff at these practices are so unfriendly and disorganized but here's more evidence of it. It's not the physicians or nurses or PAs.

    I've resolved to garner copies of my records on an annual basis now, at the very least. If I'm sent to a specialist, then I might ask for copies while I'm there.

    How much of a med history can pharmacies provide I wonder?

    I haven't encountered anyone getting offended but of course the bulk of my requests went to practices I no longer visit for any number of reasons, including personality conflicts, and I'm not concerned about their feelings getting hurt.

    I'm allergic to aspirin. Even so, would they address the hypercoagulation, does anyone think? I can take them for a few days, skip a week or so, then take them again, etc. I'd think about trying if they do affect blood viscosity.
  17. ulala

    ulala New Member

    losing your records. Can you get to a doctor now to have your blood checked for hypercoagulation? Coumadin thins the blood but doen't afftect the fibrin.

    There are two over the counter products, nattokinase and lumbrokinase. They both clear fibrin from the blood. If you do a search for natural blood thinners you should find some info. I think that garlic is a blood thinner. I'm allergic to garlic. For some reason it affects my eyes. If you're allergic to aspirin you shouldn't take it.

    Best wishes! Keep after your records because if you don't iseems they can get lost easily!
  18. SpiroSpero

    SpiroSpero New Member

    Hi all,

    Could anyone sum up what should be tested in order to find out if you have coagulation issues? You would help me so much.



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