Hypercoagulation: The CFS/FM Plot Thickens

Very interesting article on "sticky blood" and how it can contribute to Lyme disease. This is not exactly a new article (it's from 2001), but is still something that chronicly-ill Lyme and other immuno-compromised patients should know about.

This article was found on:

Melissa Kaplan's
Chronic Neuroimmune Diseases
Information on CFS, FM, MCS, Lyme Disease, Thyroid, and more...
Last updated February 27, 2012

Hypercoagulation
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.

Read more:
http://www.anapsid.org/cnd/diffdx/hypercoagulation.html