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Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness.


Read these related articles
Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness. - PART 1
Hypercoagulation & Heparin - A Second Look.

The following is a brief summary of the work of David Berg of Hemex Laboratory in Phoenix, Arizona, linking an immune activated hypercoagulation mechanism to a wide range of chronic conditions.

Immune System Activation of Coagulation ( I S A C ) :Chronic Illnesses Due to a Coagulation Protein Defect

Infertility (Recurrent Fetal Loss), TIA, Osteonecrosis of the Jaw, Chronic Fatigue Syndrome/Fibromyalgia (CFS/FM), Crohn's Disease, IBD, Multiple Sclerosis, Sjogren’s Syndrome, Lyme Disease.

The Model - A Paradigm Shift

The model proposes that a majority of individuals diagnosed with chronic illnesses, based on clinical criteria, may be potentially classified as “Anti Phospholipid Antibody Syndrome” (APS) with the endothelial cell (EC) as the disease target. These patients have a hypercoagulable state demonstrated by increased markers of coagulation activation and increased blood viscosity due to the generation of Soluble Fibrin Monomer (SFM). The CFS/FM process may be triggered by a variety of pathogens (CMV, HHV6, Mycoplasma, Ch1, pneumonia, etc.), resulting in pathogen-mediated immune activation that induces antibodies which cross-react with BC protective proteins B2GP1 & Annexin V. These antibodies dislodge the protective proteins from EC surfaces, exposing PhosphatidylSerine (PS) on the EC surfaces in capillary beds. Pathogens induce inflammatory responses which include cytokine modulation of EC to down-regulate the antithrombotic environment (Thrombomodulin, tPA) in favor of prothrombotic expression of Tissue Factor (TF). TF and PS exposure allows binding of the coagulation tenase and prothrombinase complexes to EC surfaces.

This results in thrombin generation leading to SFM formation. SFM dimerizes easily, increasing blood viscosity and precipitating out on EC surfaces as fibrin(old) deposition, creating local ischemia and pathology, blocking nutrient and oxygen delivery in the microcirculation. A hereditary defect in a coagulation regulatory protein, such as protein C, protein S, Factor VL, prothrombin gene mutation, PAI-1, Lp(a), or elevated homocysteine is predispositional in greater than 755 of patients. Because this hypercoaguability does not result in an immediate thrombosis (100% occlusion), but rather in fibrin deposition (50-95%), we suggest that an appropriate name for this antiphospholipid antibody process to be Immune System Activation of Coagulation (ISAX) syndrome. This model provides an explanation for the therapeutic benefits reported with low dose anticoagulant therapy (heparin or warfarin) in the majority of chronically ill patients.

People are not chronically ill unless there is a coagulation regulatory protein defect as seen in Thrombophilia or Hypofibrinolysis.

More information on how hypercoagulation links to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness see the interview with David Berg.

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