The CFS/FM Plot Thickens
Melissa Kaplan, The Carousel Network News, 8(5), 2001
A simplified introduction into hypercoagulable state...
Research conducted by Dr. David Berg and others at Hemex Laboratories1 has found hypercoagulation to be a factor in many patients with chronic fatigue syndrome (CFS), fibromyalgia (FM), myofascial pain syndrome (MPS), and other disorders such as osteonecrosis (bone loss due to inadequate blood supply), and fetal loss.
Hypercoagulation (thickened blood) results from fibrin being deposited in small blood vessels. Fibrin is the body's natural bandaid: strands of fibrin form across a defect (wound, tear) in the walls of blood vessels, forming a mesh that holds platelets and blood cells. This beneficial clotting of cellular matter and fibrin strands plugs the leak, so to speak, holding things together until the body starts to repair itself.
Fibrin production is the last stage in a complex clotting process. The process itself starts off with the release of thrombin which in turn results in the production of soluble fibrin monomer (SFM), a sticky protein that increases blood viscosity. This leads to the deposit of fibrin on the endothelial cells that line the wall of the blood vessels. Under the normal conditions, it takes only a single burst of thrombin to generate a large amount of SFM which in turns produces sufficient amounts of fibrin to clot the defect. Testing of many patients diagnosed with CFS, FM, MPS shows that the thrombin-SFM-fibrin process is not working properly. Instead of a single burst of thrombin producing the amount of SFM needed, the thrombin keeps being produced at low levels. Instead of clots being formed, however, the result is that blood becomes increasingly thickened. The body's own ability to thin blood and break up clots is impaired because the fibrin smothering the endothelial cells prevents those cells from releasing heparans.
There are two different ways this scenario can be played out. The first is thrombinphilia, "thrombin loving", where the body keeps producing thrombin because the normal control that would prevent excessive or inappropriate thrombin generation fail, do not exist, or have somehow been overridden so the body keeps producing thrombin at low levels. The controller is anti-thrombin (AT). AT combines with thrombin to form thrombin/anti-thrombin (T/AT). Normally, when the endothelial cells release heparans, the release activates the AT, which acts slowly to reduce the thrombin. Not enough AT may be produced, or the amount may not be enough to keep up with the continuous thrombin production. Another possible cause is hypofibrinolysis, where too little heparans, the body's natural clot busters, is produced or circulated. So, in the (simplified) three part process (thrombin, antithrombin, heparans), one or more parts is dysregulated or rendered insufficient, leading to hypercoagulation.
Berg states that there are at least three possible causes for this thrombin malfunction:
The results of this thickened blood are widespread, due to the role blood plays as the major transport of nutrients and oxygen throughout the body:
Some of the symptoms associated with hypercoagulation will surprise few with CFS and/or FM: brainfog, cognitive dysfunction, digestion problems, fatigue, and generalize malaise.
Because this hypercoagulability does not result in an immediate thrombosis (100% occlusion), but rather in fibrin deposition (50-95%), Berg, et al.2 suggest that an appropriate name for this antiphospholipid antibody process would be Immune System Activation of Coagulation (ISAC) syndrome.
Those who have had CFS/FM for more than 10 years may show only one abnormality - or none - on the ISAC test. However, a trial course of heparin, especially if done in conjunction with the antibiotic or transfer factor, may result in more abnormalities showing up in subsequent testing. Berg suspects that this is because the organisms buried beneath the fibrin sludge layer needn't be as active so they cease triggering the coagulation process. As the heparin starts clearing out the sludge and restores cell-to-cell communication, the organisms reactivate and step up their attack, once again triggering coagulation. Most patients, when re-tested one month into the heparin treatment, show more abnormalities on the ISAC test. This indicates progress is being made. This also means that, with the reactivation and the die-off of organisms that starts once antibiotic/antiviral treatment is started, patients may experience a herxheimer effect: feeling sicker before feeling better.
of the Minds
Resources and References
Related ICD-9 Codes:
In researching this article, I relied extensively on the Hemex Laboratories, Inc. website.
a personal note...
A month into the heparin shots, I got retested. The full results weren't back by the time of my follow-up appointment, but the fibrinogen was and it was even higher, indicating a need to increase my dose from 0.3 BID to 0.4 BID.
I was tested for HHV6 4+ years ago, with negative results. I was tested again six months ago, this time using ViraCor's HHV6 test. Unfortunately, the Th2 part of my immune system is so elevated that the test result came back with one word: hemotoxic. The antibodies killed their cell culture. Since this is not uncommon in cases of CFS with this type of Th2 imbalance (and in those who have been taking Transfer Factor), ViraCor developed a new test. My results on that, too, was negative. My physician feels that that may not be conclusive so has be taking Transfer Factor anyway, but a less expensive version of it. The one I am taking is sold through a multilevel marketing company, which doesn't thrill us, but the product is good. (Note: This is before I found out that the TF is patented by Animune.com and they have another authorized manufacturer selling it, for less, under the Source Natural Wellness Cell Response name. See footnote 5 above for more information.)
Each bottle of Transfer Factor from 4Life (item #24010) contains 90 200 mg capsules and costs $37.95 each ($379.50 for ten bottles - ask about their 12 bottles for the price of 10 offer if you will need to buy that many or want to share an order with someone). Taxes and shipping costs are added to the product price. The company also makes a Transfer Factor Plus product (60 300 mg capsules, $53.95/bottle). I asked my doctor about using TF Plus rather than the regular TF; he said that many patients seem to have an adverser reaction to it so he recommends using the regular TF. Dosing starts at one capsule, once a day, gradually increasing to one capsule three times a day. (Note that prices and product availability change over time, and new products and protocols emerge as ongoing research changes our understanding of the disease and treatment process.)
Even though my Lp(a) was within normal ranges, because of its apparent assistance in busting clots, my doctor has me taking 200-500 mg of bromelain daily, along with the Transfer Factor and heparin.
For information on the labs doing the CFS immune panel and other testing useful in diagnosing the scope of problems in those with CFS and/or FM, see my Testing Laboratories page.
When musing about this with some friends knowledgeable about herbs, one reminded me that artemesinin, a factor found in the plant Artemesia (wormwood), has anti-thrombin factors, resulting in thinning the blood. I have been taking artemesinin to help combat babesiosis, an infection caused by the Babesia organism, frequently found in people who have been infected by Borrelia, the organism that causes Lyme disease (neuroborreliosis). So, without affecting the underlying cause(s) of this hypercoagulation disorder, the artemesinin is thus far the only thing I have tried that is at least superficially thinning my blood.
I recently came across nattokinase, a naturally occurring fibrolytic enzyme found in soy. I won't be taking it as it is far more expensive than artemesia, but if you are one of that small group who did not respond to the heparin/transfer factor/antibiotic/bromelain protocol for hypercoagulation, you might want to look into nattokinase as a work-around to the continuing hypercoagulation.
My doctor, who has done the testing and prescribed this protocol for a number of patients, is finding that a few get worse on the heparain, even at lower than the recommended 0.3-0.4 cc/day, and about one third experience no improvement at all. He is going to try to figure out if there is anything in the HEMEX or other tests that may be used to help predict which patients may fall into the worse or no-change treatment response categories.
Since the time I was doing the heparin protocol, the treatment for hypercoagulable state has evolved, with many patients doing better on higher doses of heparin given sublingually, rather than injected. In discussing the more normal bleeding with my doctor, we decided that I will try heparin again, this time orally. As of this date, I have started the new heparin protocol. I will take the HEMEX test again in three weeks to see if there is any improvement over my last panel.
Evaluation of the hypercoagulable state: Whom to screen, how to test and treat, Postgraduate Medicine, 2000
Hypercoagulable States, MedlinePlus (NIH)
Hypercoagulable States, University of Florida
TEG® Tests vs Standard Coagulation Tests, Haemoscope Corporation
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