CFIDS and FMS Support Group of DFW

Blood Related Disorders in CFS/FMS

Recent research reveals that many patients with Chronic Fatigue Syndrome (CFS), Fibromyalgia (FMS), and other chronic illnesses may have one or more of the three conditions listed above. Understanding these conditions can help explain many symptoms, and treating them can lead to improvement - even recovery.

Hypercoagulation (Thick Blood)

Dr. David Berg of Hemex Laboratories has been studying the hypercoagulation (thick blood) often found in patients with CFS, FMS, Myofascial Pain Syndrome, Osteonecrosis, and fetal loss.

What Makes It Thick? 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 protects us 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 activate 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, MPS and other chronic conditions, continuous generation of low levels of thrombin can occur. This results in hypercoagulation (thick blood), as opposed to clot formation.

What Is The Underlying Cause? There are at least three possible causes:

  1. Viruses, bacteria and/or parasites can activate certain antibodies in the immune system, which trigger the production of thrombin, generating SFM and resulting in fibrin deposits.
  2. Genetic coagulation defects can lead to hypercoagulation.
  3. Chemical exposure can result in changes that trigger the coagulation process.

What Are The Results?

  1. When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is comprised.
  2. The fibrin coating the capillaries and producing thick blood can make viruses and bacteria less accessible to treatment.
  3. Thicker blood is harder to pump.
  4. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in Irritable Bowel Disease. If the bowel is deprived of blood, it will sluff off its contents.
  5. 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.

How Common Is It? 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. Studies show that between 79% and 92% of CFS and/or FMS patients have hypercoagulation defect. A standard coagulation work up most likely will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive.

What About Treatment? In a 1998 study, heparin was given to seven FMS and nine CFS patients with hypercoagulation. Of the seven FMS patients, one reported some improvement, three moderate, and 3 significant; of the nine CFS patients, four reported moderate improvement and five significant.

Recently, Dr. Berg learned the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner like heparin is prescribed one month before beginning antibiotics for bacteria (like mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (like HHV6, CMV and EBV). the heparin is continued throughout, and 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. [Editor's note: Transfer Factor contains anti-bodies to various pathogens. It comes from cows that have been exposed to the pathogens and developed the needed antibodies. Also, note that Paul Cheney, M.D., PhD, is researching the use of undenatured whey to treat mycoplasma, HHV6, etc.]

CFS/FMS patients who have been ill more than ten years may show only one abnormality - or none - on the ISAC test. But a trial of heparin, 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. But 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.

Dr. Berg (from Hemex), Dr. Knox (from one of the top HHV6 labs, and Dr. Brewer (who develops transfer factor), recently conferred and discovered they were all on the same page, so to speak. Dr. Brewer has developed a transfer factor designed for CFS: unconfirmed reports state it contains specific IgG and IgM antibodies to HHV6, CMV, etc. Dr. Brewer has tested many of his HHV6 positive CFS patients, and all have hypercoagulation. Beginning this year, many patients began receiving both heparin and transfer factor, with some dramatic successes.

The work of these doctors holds great promise for understanding and treating CFS and FMS.

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Low Circulating Blood Volume

In 1998, Dr. David Bell and Dr. David Streeten conducted a study on blood volume in 19 CFS patients. The average patient had only 70% of normal blood volume, and six had only half. A sudden loss of half of one's blood typically causes shock and is fatal.

Standard methods of restoring blood volume have met with limited or short-term success, including fluids, salt and Florinef.

The study also measured red blood cell mass, which was significantly reduced in 84% of patients. This has serious implications, since red blood cells carry oxygen throughout the body, including the brain.

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Blood Pressure Abnormalities

Bell and Streeten suspected the low blood volume was a factor in another problem: blood pressure abnormalities. Their new study on this topic was published in July. It examined the orthostatic intolerance (worsened symptoms upon standing) common in CFS. Fifteen CFS patients had their blood pressure and heart rate monitored every minute for 30 minutes while lying down, and then for 60 minutes while standing still. Pronounced abnormalities in pulse and/or blood pressure were noted in 73% of CFS patients and none of the controls. Affected patients were given military anti-shock trousers (MAST) to wear, and their reading normalized within ten minutes. (The MAST garment provides lower body compression.)

Orthostatic intolerance involves the pooling of blood in the legs and a lack of blood to the brain. The underlying mechanism is a condition called dysautonomia - a dysfunction of the autonomic nervous system that controls involuntary functions, including pulse rate and blood pressure.

Dr. Bell described a comparable test that can be done anywhere with a blood pressure cuff. The full protocol is in the Co-Cure archives. (Search using "Streeten" to find it.) Lay down for 10 minutes and have your pressure and pulse checked every five minutes. Then stand for 30 minutes without moving or leaning, taking readings again every five minutes.

When healthy people stand, there might be a slight rise in pulse, but overall their pressure and pulse remain constant. Many CFS patients experience one or more of the five following types of orthostatic irregularities while standing:

  1. Orthostatic systolic hypotension: a fall in systolic BP (upper number) of 20 or more.
  2. Orthostatic diastolic hypotension: a fall in diastolic BP of 10 or more - least likely finding.
  3. Orthostatic postural tachycardia: an increase in heart rate or 28 or a pulse of more than 100 - 120. Also known as POTS, this is a very common finding.
  4. Orthostatic narrowing of pulse pressure: a fall in the difference between systolic and diastolic to 18 or lower. When the pulse pressure drops much below 20, it's difficult to even detect a pulse. This is technically a state of circulatory shock.

    Sources: Co-Cure archives and the article "No Other Illness Like This One" by Joan S. Livingston, originally published on About.com's Chronic Fatigue Syndrome/Fibromyalgia site at About.com. Reprinted with permission.

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    New Study

    Nancy Klimas, M.D., a well known CFS researcher in Miami, has received a grant to study the interactions of blood volume, autonomic dysfunction and pro-inflammatory cytokines. Also under study will be the drug EPO (erythropoietin), used to increase red blood cell mass and facilitate an increase in the blood's oxygen carrying capacity. (EPO is a naturally occurring hormone that can be synthesized as a drug.)

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    Update 01/10/05. For questions or comments concerning this site, please contact Lori or Deborah.

    Copyright © 1999-2005 by the CFIDS/FMS Support Group of DFW. All rights reserved. 

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