hughes syndrome and chronic fatigue

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.