Newbie, Question On Blood Tests

Discussion in 'Fibromyalgia Main Forum' started by forensicsgirl, Jul 1, 2003.

  1. forensicsgirl

    forensicsgirl New Member

    I was seeing a neurologist for tremors, he ran a hypercoagulation profile and I came back with:

    Lupus Interpretation (Detected)
    Phospholipid Neutral (Confirmed)
    DRVVT (High)
    Hexagonal Phase Neut (Confirmed)
    PTT (LAC) (High)

    I am seeing a hematologist this week, but just wanted to get some background info. Does anyone have any information on the above and what it means in "layman" terms. I also suffer from Type 2 Diabetes and Osteoarthritis.

    Thanks for any and all help!
  2. Applyn59

    Applyn59 New Member

    Can't help you but there has been so much
    discussion on here lately on hypercoagulation.
    There is a website called Hemex that explains
    a lot.

    Gee, he ran all that without you asking?
    What did he tell you about it.
    I know the last one is about how thin or thick
    your blood is. My mother had a blood clot
    and was put on blood thinners and that
    is the test they kept running to make sure
    her blood level was okay. I think it tests the
    ability of your blood to clot.

    Here's some info from this site:

    Hypercoagulation Theory Viable Explanation f...

    Monday, March 4, 2002

    Hypercoagulation Theory Viable Explanation for Some CFS & FM Symptoms
    by David Berg 10-05-2001
    Editor’s Note: The following is a transcript discussion with David Berg, provided exclusively to David Berg is the Director and Cofounder with Lois Hill Berg, of HEMEX Laboratories. Mr. Berg helped develop the Hypercoagulation theory, a proposed cause of CFS and FM symptoms. He has a M.S. degree in clinical pathology and laboratory medicine, and has been in practice for 35years. He recommends patients discuss the following information with their physicians.
    Berg: We first became involved with research in chronic illnesses in 1992. At that time, Dr. John Couvaras, an infertility specialist in Phoenix, AZ, and HEMEX, began to research infertility in women. We found a hypercoagulable state due to a coagulation protein defect, existing in women that we tested who were infertile and/or had recurrent spontaneous abortions. In 1996, Dr. Couvaras noted that when he put women on low dose heparin in order to become pregnant, the CFS/FM symptoms, pelvic pain, and migraine-like headaches diminished. He asked us, “why?” As a result of this scientific curiosity, we performed a retrospective study on 30 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 AACSF meeting in Cambridge.
    This study led to a major, multi-center, blinded, patient or control study with centers in New York, Houston, and Phoenix. When the code was broken, identifying patients and controls, we were able to identify a patient based on two or more positive test results out of the five assays in the ISAC panel. It was the first definitive proof that indeed chronic illnesses have a basis in the blood system. This was published in the international journal Blood Coagulation & Fibrinolysis, 1999, 10:435-438. In another study published in Blood Coagulation & Fibrinolysis, 2000, 11:673-678, it was determined that Gulf War illness has the same mechanism and positive findings.
    In November 1999, myself and Dr. Joe Brewer (an Infectious Disease specialist in Kansas City) developed the model of a pathogen activating the immune and coagulation systems which is now known as the Immune System Activation of Coagulation or ISAC. The end result is increased blood viscosity which is due to 1) a regulatory protein defect and 2) activation of the coagulation system by the pathogen. As the blood viscosity increases, the blood flow diminishes throughout the body, creating anoxia (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 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 microcirculation (capillaries) as fibrin or fibrinoid-like deposition, blocking oxygen and nutrients to nearby 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 of a clinician faces is to figure out what pathogens are present in the patient, and therefore determine the most appropriate therapies against these pathogens. The average CFS/FM patient has 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 are positive. Someone who may be 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 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, parasites, physical trauma, vaccinations, (anthrax, measles, mumps) and/or biological warfare agents can also activate or poison the immune system. This may lead to secondary infections, which 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 eight different regulatory proteins of the coagulation mechanism in a panel we call the HTRP (Hereditary Thrombosis Risk) panel. In July 2001, at the international meeting of ISTH, we presented data that in a retrospective study of 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 400+ patients have defects in the fibrinolytic system (hypofibrinolysis due to elevated lipoprotein (a) - Lp(a) and / or PAI1-plasminogen activator inhibitor 1). Unfortunately, 21% of these patients had a defect in both groups. This means that not only do they form fibrin easily, but also they cannot clean up the fibrin deposition generated.
    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 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 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 baby starves, the baby dies, 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-HPA axis, hypo-estrogen, etc. Restoring the blood flow by 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,” and you went to battle during the middle ages, 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 explains how these coagulation defects occurred over 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 from a coagulation protein defect gives a scientific basis for chronic illness. It also gives a measurable or quantifiable aspect to testing a patient’s blood for 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 chronically ill patients.
    HEMEX Laboratories offers testing and consultative services relating to the diagnosis, treatment, and monitoring of hematological, clotting and/or bleeding disorders. HEMEX provides services and interpretations to clinicians and physicians throughout the United States