Hypercoagulation Linked to Chronic
Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness.
Read these related articles
Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness. -
Hypercoagulation & Heparin - A
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.
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, Sjogrens Syndrome, Lyme Disease.
Model - A Paradigm Shift
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.
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.
are not chronically ill unless there is a coagulation regulatory protein defect
as seen in Thrombophilia or Hypofibrinolysis.
information on how hypercoagulation links to
Chronic Fatigue, Fibromyalgia, MS,
Infertility, Chronic Illness see the interview with David Berg.
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