CFS and/or FM as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis, 1999, Berg et al

[Sly Saint]

Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis


Abstract

Chronic Fatigue and/or Fibromyalgia have long been diseases without definition. An explanatory model of coagulation activation has been demonstrated through use of the ISAC panel of five tests, including, Fibrinogen, Prothrombin Fragment 1+2, Thrombin/ AntiThrombin Complexes, Soluble Fibrin Monomer, and Platelet Activation by flow cytometry. These tests show low level coagulation activation from immunoglobulins (Igs) as demonstrated by Anti-B2GPI antibodies, which allows classification of these diseases as a type of antiphospholipid antibody syndrome. The ISAC panel allows testing for diagnosis as well as monitoring for anticoagulation protocols in these patients.


https://pubmed.ncbi.nlm.nih.gov/10695770/

Conclusions:
CFS and/or FM patients who have a hereditary deficiency for thrombophilia or hypofibrinolysis may be unable to control thrombin generation properly. We have found that three out of four CFS and/or FM patients have a genetic deficiency (unpublisheddata). Certain pathogens induce the immune system generation of APL antibodie s and can be a triggering mechanism
for APS. Once antibodies are formed, protective proteins are dislodged from endothelial cells, exposing PS. Coagulation proteins bind on exposed PS surfaces, generating thrombin on the EC surface.

Excess thrombin converts fibrinogen to SFM, which may be deposited on the EC surface and/or circulate in the plasma. Fibrin deposition leads to decreased oxygen, nutrient and cellular passage to tissues around the microcirculation. This hypercoagulable state may cause localized pathology in many tissues, yielding the systemic compromises and symptoms characteristic of the CFS-FM complex.

Since this hypercoagulable state does
not necessarily result in a thrombosis, but rather in fibrin deposition, we suggest that an alternative name for this Antiphospholipidantibody process would be immune system activation of coagulation (ISAC) instead of antibody-mediated thrombosis [18]. Once
this hypercoagulable state is detected, appropriate anticoagulant therapies may be given to relieve patient symptoms. These studies will be presented in a separate report.

 

[Mij]

This article is from 1999. I had the ISAC panel done and it was normal. I didn't have the genetic profile done b/c I didn't feel it applied to me.

David Berg is not a medical person. He or his wife was the owner of Hemex Lab that did the tests.

 

[DokaGirl]

This article is from 1999. I had the ISAC panel done and it was normal. I didn't have the genetic profile done b/c I didn't feel it applied to me.

David Berg is not a medical person. He or his wife was the owner of Hemex Lab that did the tests.

Yes. Came across this back then as well. Didn't do the testing.

Many of my blood draws are difficult, and I've been told my blood is thick or sticky. This despite extra hydration before blood tests.


This puts me in mind of Leslie O. Simpson's research, which includes work on blood viscosity:

https://me-pedia.org/wiki/Leslie_Simpson

ETA: Maybe I missed this on MEPedia, the book by Dr. Simpson: Blood Viscosity Factors: The Missing Dimension in Medicine ISBN 10: 0615254578 Pub. Mumford Institute Inc.

 

[Mij]

@DokaGirl

My doctor attended a workshop in Arizona in 2002 where Hemex Lab was located and met David Berg. There were also a few other doctors that treated ME patients at that workshop. David Berg flat out told my doctor that I had HHV6 reactivation based on my test results. My tests were normal, except for Fragmin that was slightly elevated.

A few of us here got tested and the test results came back normal.