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ME/CFS AUSTRALIA (SA) INC
Registered Charity 698
Mailing address:
GPO Box 383,
Adelaide,
South Australia 5001
Office:
266 Port Road,
Hindmarsh,
South Australia 5007
Ph: (08) 8346 3237
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FIBROMYALGIA HELP: Contact Fibromyalgia SA at the Arthritis Foundation of SA 118 Richmond Road, Marleston 5033 Ph: (08) 8379 5711 |
ME/CFS Australia (SA) Inc supports the needs of sufferers of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and related illnesses. We do this by providing services and information to members.
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ME/CFS Australia (SA) Inc aims to keep members informed of the various research projects, diets, medications, therapies etc. All communication, both verbal and written, is merely to disseminate information and not to make recommendations or directives.
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Congress on CFS
Page 1: Diagnosis
Page 2: Observations
Page 3: Treatment
Page 4: Posters
Page 5: GW Syndrome
Talking Point
March 2000
In this issue:
Pat
carries the torch
Health management
World CFS Congress
‘Cures’
Second World Congress on CFS and related disorders
Brussels, September 9-12 1999
This is the second part of a review by Dr Rosamund Vallings. Part one was published in the December 1999 issue of Talking Point.
Diagnosis
Alterations in HPA axis function were proposed by J Gaab (Germany) as a shared pathway linking aetiological and perpetuating processes with observed physiological changes, such as immune function and central activation. Plasma cortisol, free cortisol and ACTH responses in response to stress and exercise were measured in CFS patients and controls. There was evidence for a lower “set-point” of HPA activity. There was no reduction in glucocorticoid secretion and no evidence for reduced glucocorticoid activity, and the changes in HPA activity are therefore likely to be central.
B Hyde (Canada) reviewed the technological investigation of ME/CFS. He stressed the difficulties that many would have in accessing these tests. 25% of patients with acute onset tested positive by PCR for enteroviruses, while none did who had had gradual onset. Only 10% of his patients had a positive tilt table test. Red blood cell volume was reduced in 66% of patients, meaning enormous implication for oxygen carriage. Blood volume was reduced on average to 60% of normal. He confirmed that immunological tests are expensive and difficult.
Tim Roberts and the Newcastle, NSW team had investigated erythrocyte oxidative damage in CFS. These patients had increased levels of methaemoglobin and malondiahyde as markers of oxidative stress and had increased mean erythrocyte volume compared to controls. Erythrocyte distribution risk was a primary factor differentiating controls and subgroups of those with CFS. These parameters were associated with symptoms expression and symptom indices in the patients. The data suggest that oxidative stress maybe a contributor in the pathology of a subset of CFS patients. This may indicate persistent underlying intracellular infection. Antioxidant therapy may therefore be useful in some CFS patients.
Pituitary function was studied by G Moorkens and his team (Antwerp). Comprehensive hormone testing was performed in 73 patients with 21 controls. Significant changes in growth hormone (GH) secretion were demonstrated during insulin tolerance testing and nocturnal GH secretion. Increase in visceral fat (measured by CT scan), a characteristic of GH deficiency, was clearly demonstrated. It is possible that this decrease in GH in CFS is related to poor sleep.
| Page 2: Clinical Observations |  |
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