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Hughes Syndrome and Chronic Fatigue Syndrome
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Hughes Syndrome and Chronic Fatigue Syndrome

© MMII,  Ken Lassesen, M.S.

 In 1999, I had sudden onset CFS while I was employed by Microsoft. Microsoft offers self-insured medical insurance that is extremely liberal -- for all practical purposes there was no deductible or restrictions on any tests that my MD wish to try – of course, living in the US meant a wealth of private facilities and laboratories. As a result of this blessing, not only did I go into full remission from CFS but my wife and two daughters had an accurate diagnosis of their odd symptoms and rational treatment started.


Our class of CFS appears to be a variant of Hughes Syndrome (formerly called Antiphospholipid antibody syndrome (APS)). The first paper on this variant was published in 1999 by David Berg and others[i]. Add to this blessing, our existing family practice MD believed that CFS was very real and that she had no treatment for it – but she was willing to listen, learn and cooperate if I could present hard, peer-review research.  I was her first CFS patient that she had seen 2 weeks before onset and 2 weeks after onset – very dramatically illustrating the changes. I was also her first patient to become symptom free.

Hughes Syndrome

Hughes syndrome is caused by antibodies that result in deficiency of certain enzymes, such as annexin V. These enzymes normally form a shield around certain phospholipid molecules that blocks their entry into coagulation (clotting) reactions. In the Hughes syndrome, the formation of this shield is disrupted by these abnormal antibodies. Without the shield, there is an increased quantity of phospholipid molecules on cell membranes, speeding up coagulation reactions and causing the abnormal blood clotting characteristic of the Hughes syndrome.


In terms of CFS, this “sticky” blood means that oxygen delivery to the brain and to the body is reduced. Many of the cognitive characteristics of hypoxia or acute altitude sickness are also seen with CFS – for example, insomnia. “Sticky” blood also mean reduced nutrients to the body and impeded removal of toxins – for example, higher level of carbon monoxide and increase in lactic acid concentration.


What causes these antibodies? Many different type of infections have been implicated – including viral (EBV), mycoplasma, chlamydia, rickettsia and even helicobacter pylori[ii]. It is interesting to note that many of these infections prosper in a low oxygen environment, so the disruption of coagulation has probably been beneficial to these infections’ desire for low oxygen.


Family Experience

Eventually my entire family had the “Immune System Activation of Coagulation” panel (ISAC) done at Hemex laboratories, which was followed by Hereditary Thrombosis Risk Panel when the first tests returned positive results . Our physician also sent blood to a local laboratory and received equivalent readings – but the local laboratory did not provide the services of a hematologist that Hemex offered. Although each of us presented differently – one with acute temperature sensitivity, another with salicylate sensitivity (a teenager was honestly allergic to green vegetables!), another with slow onset over 18 years and myself with acute onset – we all appear to have the same root cause, and all of us had inherited coagulation defects. Coagulation defects usually mean that we produce less than the normal amount of enzymes to break down coagulation when it forms.


The equation became simple:

·        More than normal tendency to coagulate

·        Less than normal ability to remove coagulation


How did we proceed? We wanted to do three things:

·        Eliminate the infection(s) that cause the antibodies

·        Eliminate items that triggers coagulation

·        Get assistance in reducing coagulation

Eliminate the infections

For myself, treatment patient #1, we shot blind – we adapted the protocols of Prof. Garth Nicolson, USA and Cecile Jadin, MD, South Africa. For 18 months we changed monthly between different tetracyclines, macrolides and levaquinpotentating them with bromelain and serrapetase. Our test of effectiveness was monitoring the jarod-herxheimer reaction that occurred. Our criteria to stop was having no JH reaction to any antibiotics for 3 months with high dosages of potentators.


For our youngest daughter, 12 years old, we recently did the CFS Panel PCR tests (at ) and found two infections: Mycoplasma Fermentus and Chlamydia Pneumonia. These had survived a 6 month course of antibiotics that ended 9 months earlier. She is back on antibiotics (Biaxin).


For my wife, she was positive for helicobacter pylori and suffered a horrible jarod-herxheimer from its treatment – she was unable to walk and frequently had to crawl to the washroom. She preserved through the JH reaction and started to slowly and progressively improved. The results of her last CFS Panel PCR test shows an EBV infection – which is being treated by transfer factor and olive leaf extract (a protease inhibitor).

Eliminate coagulation triggers

Many things make people with CFS sick – the why has usually been a mystery. Since we understood the probable mechanism, we could start looking for a model of why. This is what we found using Medline to search medical literature:


Temperature Sensitivity

“Sticky” blood means that heat regulation is impeded, so Raynaud’s syndrome makes sense. Our 12 year old became sick at 70F was a bit of a mystery until we found out that heat stroke triggers a coagulation cascade very early[iii].  This also would explain why all of us have sub-normal temperatures: the body’s response to prevent a coagulation cascade. So keep cool and do not allow yourself to overheat!


Anaphylaxis and Chemical Sensitivity

Hughes syndrome is documented to have unusual anaphylaxis associated with it.[iv] With a little bit of research we discovered that allergic reactions can also involve coagulation cascade – in fact, the coagulation cascade can be triggered without the normal allergic reactions[v]. A recent article clearly demonstrated that items like perfume may trigger anaphylaxis[vi]. The result is clear: a reaction that would normally produce a little coagulation in a normal person may provoke a massive coagulation cascade with Hughes Syndrome.


This was demonstrated clinically with my wife and 12 year old in January 2002: 17 days after a perfume exposure that triggered a relapse, a new ISAC panel was done with the result showing a 2 and 1 standard deviation jump in an already abnormally high Prothrombin Fragments 1+2. This measure has a half-life of 30 minutes and indicates how much coagulation is occurring – in short, a LOT! So avoid your allergies and possible allergies -- anti-allergy medicines do NOT affect coagulation cascades.


A normal response to infection is coagulation. The chronic infections that are responsible for the antibodies also cause coagulation. Eliminating chronic infections (which may not produce other symptoms) is likely not an option but a necessity. PCR tests are the most sensitive test – especially for detecting infections that are not in the blood stream.


Adrenaline, commonly produced by stress, has a very interesting effect on many of these infections – New Scientist reported a 4000x growth over 24 hours with mycoplasma and chlamydia when adrenaline is present. Research from Australia found that a mycoplasma infection will cause viral infection re-activation (producing “mono” that never goes away).


Reducing Coagulation

Modern medical science has a very small toolkit for treating the complex process of coagulation. If you take the wrong item, not only do you have no benefit, but may be putting your life at risk. Most “blood thinners” (especially herbals and aspirin) affect only platelet activity and have a high bleeding risk. For platelet activity we use only grape-seed extract for three reasons: no bleeding risk, longer half-life than aspirin and all of the same benefits.


Other anti-coagulants or blood flow enhancers that we have used are:

  • Lovenox – Prescription, low molecular weight heparin – safer than heparin. 3-4000 UI /day
  • Tumeric – the kitchen spice. 1-2 grams per day
  • Piracetam (and other Nootropics) imported from Europe[vii]
  • Alpha-Lipoic Acid
  • Niacin – the cheap type that makes you lobster red (and clear your mind!)
  • Lipotor – Prescription Statin[viii]
  • Bromelain
  • Serrapetase

The list above is what is effective for our specific condition and based on our ISAC results. Always consult with your MD on supplements, and research carefully the risks.


Gastrointestinal Problems

One of the greatest enlightenments for gastrointestinal problems was the discovery that stomach lining renews itself regularly and that it depends on adequate blood flow for a healthy renewal. The reduction of gastrointestinal problems with improvement of coagulation, and the worsening of the problems after a deterioration (for example a coagulation cascade triggered by chemical sensitivity)  now made sense – and gave hope for continued improvement.

Where are we?

Of the four of us, my 19 yr old is normal on the ISAC panel now (after lovenox and antibiotics). I am symptomless but with some high readings on my ISAC panel which is still being treated with a new PCR panel for infections scheduled soon . My wife improved slowly but progressively, has stopped having what appear to have been Transient Ischemic Attacks, has normal (instead of low) blood pressure, reduction of MCS sensitivity and more physical activities. For my 12 year old, we have seen a return of her prior brightness. The coagulation cascade in January, 2002 (due to perfume) has caused a relapse with both of them – but we know why and are actively working on undoing it. Knowing the enemy and how it works makes life a lot less stressful and gives firm hope for the future.


We know that not every one with CFS will not have a variant Hughes Syndrome – but we, and our MD(based on her testing of other patients), believe that over 70% of CFS patients does have this treatable condition.


[i] D. Berg, L. H. Berg, J. Couvaras and H. Harrison, Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis. Blood Coagul Fibrinolysis. 1999 Oct;10(7):435-8

[ii] Cicconi V, Carloni E, Franceschi F, Nocente R, Silveri NG, Manna R, Servidei S, Bentivoglio AR, Gasbarrini A, Gasbarrini G. Disappearance of antiphospholipid antibodies syndrome after Helicobacter pylori eradication. Am J Med 2001 Aug;111(2):163-4

[iii] O'Donnel, T., Jr. “Acute heat stroke. Epidemiologic, biochemical, renal, and coagulation studies”. Journal of the American Medical Association, 1975, 234, 824-828,

Bouchama A, Bridey F, Hammami MM, Lacombe C, al-Shail E, al-Ohali Y, Combe F, al-Sedairy S, de Prost D. Activation of coagulation and fibrinolysis in heatstroke. Thromb Haemost 1996 Dec;76(6):909-915

[iv] Armentia A, Barber D, Lombardero M, Martin Santos JM, Martin Gil FJ, Arranz Pena ML, Callejo A, Salcedo G, Sanchez-Monge R. Anaphylaxis associated with antiphospholipid syndrome. Ann Allergy Asthma Immunol 2001 Jul;87(1):54-9

[v] Dahl R, Venge P. Activation of blood coagulation during inhalation challenge tests. Allergy 1981 Feb;36(2):129-33;

Pandit HB, Spillert CR, Shih RD. Determination of hypercoagulable state in acute bronchospasm. J Am Osteopath Assoc 1999 Apr;99(4):203-6.

[vi] James E. Lessenger, Occupational Acute Anaphylactic Reaction to Assault by Perfume Spray in the Face, J Am Board Fam Pract 14(2):137-140, 2001

[vii] Szelies B, Mielke R, Kessler J, Heiss WD. Restitution of alpha-topography by piracetam in post-stroke aphasia. Int J Clin Pharmacol Ther. 2001 Apr;39(4):152-7.

Handschu R, Garling A, Heuschmann PU, Kolominsky-Rabas PL, Erbguth F, Neundorfer B. Acute stroke management in the local general hospital. Stroke. 2001 Apr;32(4):866-70.

Martinez-Vila E, Sieira PI. Current status and perspectives of neuroprotection in ischemic stroke treatment . Cerebrovasc Dis. 2001;11 Suppl 1:60-70.

Kessler J, Thiel A, Karbe H, Heiss WD. Piracetam improves activated blood flow and facilitates rehabilitation of poststroke aphasic patients. Stroke. 2000 Sep;31(9):2112-6.

[viii] Meroni PL, Raschi E, Testoni C, Tincani A, Balestrieri G, Molteni R, Khamashta MA, Tremoli E, Camera M. Statins prevent endothelial cell activation induced by antiphospholipid (anti-beta2-glycoprotein I) antibodies: effect on the proadhesive and proinflammatory phenotype. Arthritis Rheum. 2001 Dec;44(12):2870-8.



Original 2001 WebSite as PDF for download

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