Note: This report was originally published in two parts by CFS-NEWS Electronic Newsletter on October 28 and 29, 1999. Copyright © 1999 - Roger Burns. It is reprinted here with permission.
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Brussels Conference -- Dr. Rosamund Vallings' Report

[Dr. Vallings is a general practitioner from Bucklands Beach, Auckland, New Zealand. Her practice is mostly CFS patients and she has seen about 1,500 patients with the illness. This is her report on the Brussels CFS World Congress held on Sept. 9-12 1999.]

[Please remember, regardless of what you may read in these reports, to be sure to consult your licensed health care practitioner about your own health care.]

Second World Congress on Chronic Fatigue Syndrome and Related Disorders

Brussels, 9-12 September, 1999

Reviewed by:

Rosamund Vallings MB BS
Auckland, New Zealand

From 9-12 September, 1999, I was privileged to attend the Second World Congress on Chronic Fatigue Syndrome and related disorders. This was hosted and efficiently organised by Professor Kenny de Meirleir and his team from the Vrije Universiteit Brussels. On the first afternoon we attended a pre-conference symposium on Gulf War Illness. Then followed 2 intensive days of presentations of scientific papers coupled with posters displaying a wide range of scientific endeavour and new ideas. The conference was well attended by physicians, researchers, health workers and patients from all around the globe. There was ample opportunity for mixing and mingling at the regularly scheduled breaks, and as always this is the time for sharing of ideas and networking for future interaction. We were also treated to a relaxing social programme coupled with wonderful weather in which to enjoy Brussels at its best.

In the following report I have tried to follow the conference format, when the sessions were categorised according to various disciplines.


The conference opened with a keynote address by Neil McGregor, from Newcastle, Australia, who gave an overview of the current biochemical research in Australia, followed by a discussion of the biochemistry of chronic pain and fatigue. In their studies, no single virus has been implicated in Chronic Fatigue Syndrome (CFS) and 75% of patients, compared to 14% of controls, showed elevated RnaseL activity. The metabolic events associated with chronic pain differ from those associated with chronic fatigue. Chronic pain was associated with reductions in serum sodium, changes in urinary volume and output of amino and organic acids, increases in levels of markers of tissue damage (ALT, AST), and increase in the tyrosine/leucine ratio, representing alterations in protein turnover. Chronic fatigue was associated with alterations in urinary excretion of amino and organic acids associated with the tricarboxylic acid cycle.

Symptom expression relates to cytokine activity, urine volume and chemistry. The mechanism for chronic pain was clarified as related to catabolism (enhanced proteolysis) in muscles. We take amino acids from muscles as we fight infection and this leads to muscle protein depletion. A number of the urinary metabolites are altered in CFS, which provide evidence for proteolysis.

The urinary volume is increased in pain and fatigue states, and this can lead to reduced blood pressure and blood volume, coupled with loss of metabolites. This phenomenon is helped by added salt in the diet and the use of blood pressure raising medication. Antidepressants are found to be helpful by improving kidney function leading to reduction in urinary output, improved metabolism and reduction in fatigue.

McGregor then talked about myofascial pain, which occurs in 60-70% of CFS patients. Intensity of symptoms was found to correlate with carriage of toxin-producing coagulase negative staphylococci. This maybe a secondary contributory bacterial phenomenon. The presence of the toxin correlated positively with cytokine levels and symptom expression.

This discussion was furthered by Henry Butt, another of the Newcastle team. He discussed the association of the staphylococcal membrane-damaging toxin and chronic fatigue/pain. 90% of 73 patients reviewed were found to be positive for the membrane-damaging toxin with almost nil being found in controls. Pain severity was found to correlate with level of toxin and significant alterations in urinary metabolites. In particular, tyrosine was elevated and leucine decreased signifying altered proteolysis. Cognitive function also correlated with toxin levels. It was recommended that nose, throat and low vaginal swabs should be taken when staph infection is suspected. If pain improves with antibiotic use, this may help confirm diagnosis.

Hugh Dunstan, Newcastle, then discussed the development of laboratory-based tests in relation to essential fatty acids (EFAs) and cholesterol. He reiterated the heterogeneity of CFS and the fact that we may never therefore have a yes/no definitive test for CFS per se. His research has shown that CFS patients had significantly different profiles of fatty acids and sterols compared with controls.

The most important factors in discriminating controls from CFS patients were decreased elaidic acid and increased stearic acid. CFS patients also had low levels of cholesterol, which affects cell membrane integrity and function, steroid hormone synthesis, energy metabolism and bile production. The CFS patients could be subgrouped according to their lipid profiles. (e.g. different profiles in those with acute onset compared with those with gradual onset). Some of the changes maybe due to viral reactivation or secondary infection.

The assessment of fatty acids and sterols in fasting plasma samples can indicate EFA deficits, suggest appropriate types of EFAs for supplementation, indicate potential cholesterol deficit associated anomalies, provide evidence for mitochondrial dysfunction and categorise CFS patients into biochemical subgroups. This can help to devise individually tailored management protocols.

Visual processing disablility (scotopic vision) had been researched by Tim Roberts, Newcastle. The fact that patients with visual problems reported feeling better after taking antibiotics or amino acids led to a study investigating the possibility that biochemical anomalies in CFS correlated with visual processing anomalies. Urine excretion data revealed a number of biochemical abnormalities associated with symptom expression. These patients were shown to have Scotopic Sensitivity/Ihrlen Syndrome (SSIS) and it seems likely that there are specific biochemical markers. Hydroxyproline and proline were found to be significantly elevated. The lipid profiles also help in diagnosis and there was correlation with those suffering from conditions such as dyslexia and ADD with SSIS.

Children with reading difficulties (e.g. dyslexia) can be helped by the use of Ihrlen's filters. It is postulated that this approach maybe useful in CFS also, where there seems to be inadequate visual processing linked to dyslexia, with blurring and movement of print, and problems in the magno-cellular perceptual system. Use of coloured lenses or cellophane or coloured background to the computer screen, can have a major impact in improved reading ability and decrease in headaches. Different patients are found to need different colours. Amino acid supplementation and use of antioxidants may also be helpful. Pathogen elucidation and elimination can also be useful.

H.Kuratsune from Osaka, Japan and his team have studied acetylcarnitine (ACC) levels for some time now, and have found that the majority of patients do have depleted serum levels. There is clear correlation between acetylcarnitine levels and rating score of fatigue in CFS. Acetylcarnitine is found (in mice) to be involved in the biosynthesis of major neurotransmitters like glutamate, aspartate and GABA. Acetylcarnitine metabolism and cerebral blood flow has been found to be deficient in Brodman's areas 9 and 24 - areas of the brain associated with executive functions, such as affective and motivational behaviour and attentive and autonomic functions.


This session began with an overview by LeBleu (Montpellier, France) of the interferon-activated 2-5a/RnaseL pathway. Interferons have been characterised as mediators of a broad range of defence mechanisms particularly against viruses. Further evidence shows their involvement in immune regulation, cell growth and differentiation control.

In CFS the RnaseL is a low molecular weight variety (normal is high molecular weight). The whole pathway is upregulated. RnaseL comprises 741 amino acids.

Robert Suhadolnik from Philadelphia continued to confirm his work that the RnaseL pathway is upregulated in CFS and has continued to demonstrate the presence of a low molecular weight (LMW) form of this enzyme in peripheral blood mononuclear cells (PBMC) in CFS. 2 independent experimental methods were used to demonstrate the presence of this enzyme. Both methods demonstrated significantly statistical agreement with clinical diagnosis and showed a high degree of specificity and sensitivity. The levels of the LMW RnaseL correlated with Karnofsky scores. The presence of the LMW was independent of the duration of the CFS, and the CFS patients could be identified accurately. The drug Ampligen has been found to normalise the pattern.

K. De Meirleir also found the presence of LMW RnaseL in 680 of 705 patients studied. A more pronounced RnaseL dysfunction correlated with the 1988 definition for CFS - and this may relate to the more acute viral onset stressed in that definition. But RnaseL dysfunction also correlates significantly with those fulfilling the Fukuda definition. Presence of the abnormal enzyme also correlated with increased incidence of bronchial hyperactivity. Favourable outcome after ampligen treatment is inversely correlated with the presence of LMW RnaseL.


The immunology session began with an overview of the immunological abnormalities in CFS by Nancy Klimas (Miami). There is always a trigger factor with 60-80% cases having acute onset with viral infection (e.g. EBV, CMV, Q fever, RRV etc.). There maybe genetic predisposition. Psycho-neuro-immune mediators are important factors (e.g. stress preceding the illness is evident in 67% of patients).

The immune response is antigen driven and there is evidence of chronic immune activation, although the immune system is not wholly activated. Cytokines are the immune system's messengers and 3 types were described: cytotoxic/antiviral, promoters of antibody production and pro-inflammatory (which mediate inflammatory responses). The latter can affect sleep, which both the brain and immune systems require to function efficiently. There are changes in cytokine expression over time depending on illness severity. TNF( receptor expression increases with flares of illness, and type 2 expression is increasingly evident as illness persists.

There are also indirect effects on the immune system such as soluble mediators, which act on many tissues, and influences from the brain and endocrine system. Longterm stress will lead to immune dysfunction, such as reduced CD8 cells, decreased NK function and changes in T cells. Depression also causes changes in immune function.

CFS is a model of neuro-endocrine-immune interaction with immune activation, autonomic changes and alterations in the HPA axis. The immune system is both a cause and effect interacting with the autonomic nervous system and the HPA axis. This suggests antigen exposure. Immune therapies, which shift the cytokine pattern to type 1 expression, should be considered.

Allergy in CFS was then discussed by J Brostoff (London). 25% of the population do suffer from intolerances/allergy and the % is the same in CFS. He explained that food and inhalant sensitivity could lead to many health problems. Symptoms of intolerance include conditions such as migraine, irritable bowel, arthralgia and chronic fatigue. He recommended the value of trying elimination diets in helping establish whether or not a patient had intolerance. An interesting point was that diabetics rarely have allergies, and this may represent gene exclusion. He mentioned the effects of "exorphins" (external morphine-like substances) such as chocolate, which can have effects such as gut problems, addictive potential and psychological sequelae.

Multiple chemical sensitivity (MCS) which can be acute or lifelong was discussed. There is considerable overlap in symptoms with asthma, CFS, fibromyalgia, depression, somatisation disorder, hyperventilation syndrome. This presents problems with a case definition.

Hyperventilation syndrome occurs as a result of a patient with CFS being ill for a long time. There are many symptoms such as blurred vision, tachycardia, chest pain, pins and needles and yawning. He thinks the respiratory alkalosis leads to magnesium depletion, then muscle spasm. Noise sensitivity and vivid dreams often ensue.

Lambrecht from Ghent, Belgium presented work on the clinical, immunological and neuro-imaging correlations in those with CFS. This was a very thorough investigation incorporating a wide range of medical and immunological investigations, Karnofsky performance ratings, pulmonary and exercises function, MRI and SPECT scanning. Physicians without knowledge of the clinical history evaluated the neuroSPECTscans. 294 defects were found in 148 patients. Karnofsky scores correlated negatively with significant SPECT anomalies. Immune parameters were also positively correlated with scan results. 17 out of 30 patients had significant abnormalities on MRI, with 10 times the number of lesions than in controls. The findings illustrate the multisystem involvement and disability in CFS supporting encephalomyelitic pathogenesis.

Byron Hyde (Canada) then discussed his findings in 16 CFS patients. He too found there were persisting major immunological abnormalities and a subgroup had associated abnormal brain SPECTscans. He then looked at the effects of the drug Isoprinosine on the immune markers in this subgroup. He found some of these patients had marked improvement in symptoms, with associated improvement in cytokine parameters and NK cell numbers. Improvement did not show in the placebo group.

Nickel allergy was discussed by B.Regland (Goteborg) as a possible marker for hyper-reactivity in women with CFS. Of those who reacted adversely to an anti-staphylococcus vaccine used in treatment, 81% were found to be allergic to nickel (which was not present in the vaccine). Incidence of nickel allergy in healthy controls was 25%. This was postulated as a possible area for further research. L.Sterz (Prague) looked at the presence of hypersensitivity to dental and environmental metals in those with CFS. He suggests that metal-driven inflammation may affect the HPA axis and indirectly symptoms characterising chronic fatigue. Lymphocyte changes were shown in response to presence of mercury and nickel, and these improved in some patients when amalgam was removed. V. Stejskal (Stockholm) had also found significant numbers of metal-specific lymphocytes in the blood of patients with a CFS-like syndrome. This may be a genetic effect.


Garth Nicolson (California) discussed diagnosis and treatment of cell-invasive mycoplasmal infections in CFS and related diseases. Consideration was given as to whether these infections are causative, cofactors or opportunistic. Mycoplasma penetrates right into the cells and plays havoc with the mitochondria. This leads to many symptoms. The most reliable and highly sensitive method of detection is by forensic PCR. 50% of those suffering from Gulf War Illness (GWI) and family members with similar symptoms had evidence of mycoplasmal infections inside the leucocytes. In non-deployed healthy adults the incidence was 0 - 6%. M.Fermentans was the most common species found.

Successful treatment of positive patients with longterm antibiotics was reviewed. Relapse was common in early cycles of treatment, but after up to seven 6-week cycles, those who were symptom free tested negative to mycoplasma. 60% CFS/FM patients tested positive for mycoplasma compared to 6% of controls. Rheumatoid arthritic patients also tested 45% positive. It was concluded that treatment of these chronic conditions with antibiotics, oxidative therapy and nutritional supplements had potential for slow recovery. There were warnings about not using penicillin because of the increasing risk of reactions, including anaphylaxis.

Henry Butt (Newcastle) had investigated the changes in the distribution of anaerobic and aerobic bacteria, as well as the biochemical composition of faeces from patients with chronic fatigue and pain disorders. He found marked quantitative changes in both aerobic and anaerobic faecal microflora, with distributions significantly different to controls. These alterations may adversely affect the symbiotic benefits that normally occur between microbes and host. 60% CFS patients have gastrointestinal problems. The lipid composition of the stools in CFS showed significant correlation with gastrointestinal symptoms and changes in the distribution of gut flora. As a result, the clinician can evaluate gut dysfunction and devise individually tailored protocols.

It was interesting to note that less than 15% CFS patients had candida in the faeces and none had evidence of overgrowth.

A further presentation on the effects of the coagulase negative staphylococcal membrane producing toxin by Hugh Dunstan (New castle, Australia) hypothesised that an occult pathogen maybe an aetiological agent contributing to the sustenance of fatigue and pain. Alterations in urine excretion and microbiology in CFS were investigated. Patients had multiple anomalies in amino and organic acid homeostasis, and it was possible to subgroup the CFS patients according to symptoms and characteristic urinary profile. The imbalances suggested active muscle catabolism, which was directly related to pain severity. The carriage of toxin producing coagulase negative staphylococci was strongly correlated to the catabolic response and pain severity.

Rickettsial infection had been found to have a possible link with CFS by C.Jadin (Johannesburg) following on the work of P.Bottero from Paris. There is similar clinical presentation between CFS, a number of auto-immune conditions and Rickettsial disease. When strains of rickettsia have been isolated, all patients in her clinic are treated with cyclical courses of antibiotics such as tetracyclines over several months. Good results are claimed.

W.A.Nix from Germany studied a group of 69 CFS patients who had proneness towards infections. 16 were found to have elevated titres for various viruses. In all patients a single-fibre electromyography (SFEMG) study was performed to ascertain whether there was a muscle membrane defect or neuromuscular transmission defect causing fatigue.

SFEMG studies did not show abnormalities in either group of patients leading to the assumption that these defects are not likely to be the cause of the muscle fatigue in CFS.


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% 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% 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 sub-groups of those with CFS. These parameters were associated with symptom 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 maybe 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.


S. Bastien (California) tested for motor abnormalities associated with neuropsychologically compromised CFS patients. She used an extensive neuropsychological battery, and found most motor tests were impaired bilaterally. On the majority of motor indicators, the dominant hand performance was worse than the non-dominant. Male results were slightly different to the females. The results support the patient complaints of clumsiness, dropping things, weakness and slowed motor co-ordination.

Fluctuations in fatigue were described as a result of a French fatigue questionnaire by J.Cabane (Paris). Among the 10 patients, none had permanent fatigue and all had more than one period of fatigue per 24 hours. Various rhythms of fatigue were noted such as monthly, weekly and daily.

Memory impairment was examined by John de Luca (New Jersey) to see whether there is deficient learning of information in CFS as opposed to deficit in retrieval from long-term storage. A well controlled study was described. The results implied that the primary problem in CFS results from deficient acquisition as the patients required significantly more trials to learn a word list than did healthy controls, but there was also some deficient retrieval from longterm storage.

J.Hardt (Mainz, Germany) reported on the work undertaken in 3 countries to compare the quality of life of CFS patients. Remarkable similarity in self-rated functional status suggests homogeneity in CFS patients in USA, Germany and UK.

Byron Hyde (Canada) reported on 4 patients who fell ill with CFS and 4 who fell ill with MS immediately after recombinant Hepatitis B immunisation. The onset in the 8 patients was identical, but the CFS group were distinguishable, as SPECTscan changes were evident with normal MRIs, while demyelinating lesions were evident in the MS patients. The question was raised as to whether the effects after immunisation were coincidental or causal. As a result of similar worries in France this type of vaccine for children has been withdrawn. However it was pointed out that we should not forget the enormous and important benefits in preventative immunisation programmes.

Altered perception of muscle force in patients with CFS was discussed by W.Nix (Germany). CFS patients perceived that it was more difficult to generate a given force output than normals, and although the recovery phase was slower in the CFS patients, they could in fact perform as well as the controls. Its seems therefore that the fatigue could be perceptual and the possibility was raised that mental fatigue sets in earlier than the physical fatigue.

A significant degree of functional impairment was demonstrated in CFS patients surveyed by N.Posner and his team in Queensland. They used the SF36 and found particularly that these patients had significant physical role limitation. 8 dimensions were assessed and the means for each were markedly lower than the population norms. The least differences were in the mental health and emotional role limitation dimensions. Results were dissimilar from most other disease profiles, particularly depression, and indicate a very significant degree of functional impairment. Support needs should thus be recognised.

K. Rowe (Melbourne) looked at whether the symptom complex of adult CFS occurs in adolescents. She studied 189 young people with defined onset of fatigue with a symptom complex lasting at least 6 months. 85% of patients had an illness following an acute viral illness. Factor analysis was used with the data from the clinical group. Symptoms reported were consistent across all subjects, and while the symptoms in CFS were similar to adults, prolonged fatigue after exercise, headache, concentration difficulties, disturbed sleep, abdominal pain and myalgia were particularly evident. Somatization disorder was not a likely alternative because of low response frequencies of such symptoms.

Two papers on exercise capacity in CFS were then presented. P.deBecker (Brussels) et al found that CFS patients were limited in their capacity to perform physical activities Females were on average more impaired than males. Exercise parameters were generally down with a mean working capacity of approximately 55% of normal. C. Sargent (Adelaide, SA) found that CFS patients were not deconditioned and a graded exercise training programme would seem unwarranted in treatment. These patients had normal exercise capacity with abnormal lactic acid accumulation demonstrated from the beginning of the exercise.


Treatment of rickettsial and chlamydial infections with macrolides and/or cyclines was discussed by P.Bottero (Paris) Symptoms may be accentuated initially due to release of bacterial toxins, but this can be combatted by the use of anti-inflammatory drugs. The drugs are used cyclically and may be needed for one to two years to obtain positive outcome. Overall results were not discussed.

Treatment with the drug Isoprinosine (an immune modulator with anti-viral properties) was outlined by B.Hyde (Canada), who described this drug as having been available for 30 years without encountering any serious side effects. Patients studied were widely and thoroughly investigated, and a group of 16 CFS patients with abnormal SPECTscans was treated using placebo control over a 7 month period. 7 patients improved on the drug, 7 remained unchanged and 2 deteriorated when on placebo, with improvement once the drug was reinstated. Improvements in general health and energy were modest but significant. All those who improved were happy to continue. Thinking and memory improved, ataxia decreased, headaches decreased, there was less clumsiness and better motor function. In particular, ability to attend social functions increased. Only one patient experienced side effects, which were bad headaches.

N. Klimas (Miami) discussed further her work showing alteration of type1/type2 cytokine patterns following adoptive immunotherapy using expanded lymph node cells. 13 patients with strict inclusion criteria were studied. Lymph nodes were removed and cells were then cultured for 10-12 days and reinfused into the donor who was monitored for safety and possible clinical benefit. No adverse events were recorded. 2 patients had unsuitable fibrotic lymph nodes, so were not included. For the remaining 11 who underwent successful expansion and reinfusion, there were favourable clinical and immunological results. It is hoped that further trials will follow.

Three studies regarding the use of the drug Ampligen were then reported. Ampligen is a biological response modifier with antiviral and immunomodulatory effects. D.Strayer (USA) had compared twice or thrice weekly infusions in order to optimize the dosing schedule. 111 patients were studied. Activity and safety of the 2 dosing schedules were compared and it was found that thrice weekly dosing offers no advantage over a twice weekly schedule. There were slightly more adverse events in the thrice weekly group, mainly myalgia and flu-like symptoms. A pharmaco-economic analysis intervention in CFS was presented by W.Carter (USA) looking at the savings on concommitant medications and hospitalisation in the treated and untreated groups. Although the cost of the drug is extremely high, considerable savings were shown to be made in these areas, which it seems could have some thrust in convincing government agencies of the potential of this drug, particularly more so if patients could eventually return to the workforce.

Finally, K de Meirleir presented his work on the Ampligen study in Belgium. 44 severely affected patients under 60 had been given the drug for 24 weeks and compared to 16 untreated controls. Infusions were given twice weekly starting with 200mg and increasing to 400mg. There was significant improvement in bicycle-exercise testing, increased Karnofsky scores, reduction in cognitive impairment, alleviation of many of the CFS symptoms and improved general health perception, significant improvement in day to day function and no serious adverse events.


A wide variety of posters were displayed and the following represents a brief overview of some of the important findings.


P. de Becker (Brussels) looked at mode of disease onset in CFS. 74% patients had acute onset with progressive disease in 26%. Infectious agents seem to play an important role in the onset of CFS with other factors such as immune dysregulation involved in the perpetuation of the illness. He also did a 6 month follow up in CFS patients. He found that health stayed unchanged or deteriorated measured by several parameters. Especially, physical capacity seemed to get worse over time. Only a small number of patients were followed over this relatively short period of time. 1248 patients were studied in a further poster by de Becker, and in almost all patients all symptoms of the Holmes criteria occurred. Other symptoms noted were: dyspnoea, lightheadedness, gastro-intestinal complaints, cold extremities, decreased libido and disequalibrium. They found the Fukuda definition less stringent and therefore less suitable for scientific homogeneity.

E. Fitzgibbon (Galway, Ireland) had used the SF36 in a postal survey of 123 CFS patients. There was 77% response rate. With a mean duration of illness of 5 years, 66% were improving, 29% were static and the remainder were worse. 26% described themselves as almost back to normal with 60% back to fulltime work or study. The females had worse general health and reported more symptoms. Quality of life was lower in all domains measured by the SF36 than norms, and the overall results were unique compared to data from other disease groups.

In the UK the diagnosis of CFS seems better accepted than Multiple Chemical Sensitivity as pointed out by D.Jones. 78 patients had completed questionnaires demonstrating the difficulties in diagnosis and the complexity of this condition. Many possible causes were cited. She had also followed up 45 patients who attributed their CFS-like illness to use of cotrimoxazole.

Midlife and elderly women's vulnerability to CFS was discussed by M.van Moffaert (Ghent, Belgium). It seems many underlying health disorders and sociological factors increase the vulnerability to both CFS and multisomatoform disorders.


Prevalence of bronchial hyper-responsiveness in CFS was observed by K.Bervoets (Brussels). A high incidence was observed irrespective of smoking habits. This finding cannot be explained by the expiratory muscle effort involved in the histamine provocation procedure, as there was no significant difference between baseline spirometry and expiratory muscle strength between CFS patients and controls. E.Brouns furthered this work by looking to see if there was correlation between cellular immunity and bronchial hyper-reactivity in CFS. These patients were significantly found to have an increased number of activated T-cells and a decreased number of cytotoxic T-cells.

RnaseL testing was done in 136 German patients by L.Habets. RnaseL dysfunction was found in most patients with a correlation between the RnaseL/LMW RnaseL ratio and disease symptoms. M.Reynders (Brussels) found that the large amount of LMW RnaseL correlates with higher levels of IFN gamma, which has antiviral properties. Normal NK cell numbers with high LMW/HMW ratio correlate with high IL-12 levels in CFS patients compared with controls. IL-12 has been shown to be a potent inducer of IFN gamma secretion by both resting and activated T and NK cells in humans.


D. Racciati (Italy) et al observed an alteration in the antioxidative enzyme activities of skeletal muscle, and alterations of fatty acid composition and fluidity of membrane in muscles in CFS and FM patients. No similar abnormalities were found in controls. The oxidative muscle damage could represent the consequence of an impaired oxidative/antioxidative system and could possible correlate with the increased muscle fatiguability in CFS.


4 case reports by A.D.Hock (Germany) brought up the possibility that Vitamin D and parathormone disturbance should not be overlooked as a possible cause of chronic fatigue. The symptoms are very similar and this is a treatable disorder.

S. Meghan (Boston) as leader of a group of female health care workers with CFS stressed the importance of considering that as this illness seemed to be "predominantly female" we should not overlook the impact of the endocrine system as a likely factor in potentiating CFS.

Clinical Observations

Symptom patterns in adolescents with CFS were again addressed by K. Rowe (Melbourne). 189 young people were studied. 3 subgroups were identified according to severity. The more severe group had greater fatigue and pain, the moderately severe group having more neurocognitive symptoms and the least severe having more headaches, nausea and abdominal pain. Investigation of these subgroups may assist with management.

The pregnancy experiences of women with CFS were explored by R.Vallings (Auckland, NZ). Most women found the experiences positive, but the importance of family and partner support was emphasised together with an understanding of CFS by the obstetric personnel involved.

Data were collected by P. de Becker and de Meirleir (Brussels) on 1248 patients attending a clinic complaining of chronic fatigue. The patients were subgrouped after thorough review according to whether they had CFS or chronic fatigue from other disease causes. Frequency and severity of symptoms were more marked in the CFS group. The physical capacity of the CFS patients was lower and they seemed to be more debilitated. In another paper they also found that 4.5% of a large cohort of patients reported that their illness came on following surgery with an accompanying transfusion. None had developed Hepatitis C or other possible transfusion-transmitted infection. The findings do point to a possible transmissable cause in this subset of CFS patients. They therefore advise CFS patients not to offer to be blood donors. Blood transfusions also should be given when strictly necessary. While looking at possible opportunistic infections, they concluded that mycoplasmas might be partially responsible for some of the signs and symptoms in CFS. They also seem to be implicated in the T-cell activation observed in these patients.

CFS patients suffer significantly from psychomotor dysfunction, which may contribute to the global disability in the syndrome. (L. Lambrecht, Ghent). Rehabilitation methods including biofeedback and progressive aerobic training and restoring psychomotor abilities may constitute an important part of management. Low prevalence of autonomic dysfunction was found in this group of patients. The same team had evaluated neuropsychological impairment using numerous different tests and found that the Purdue pegboard turned out to be the most affected test. Visual memory span was affected and 20% of the patients were depressed according to the Beck depression inventory. When they reviewed SPECTscans in CFS patients, 189 aberrations were found in 65 patients.

O. Zachrisson (Sweden) found a high prevalence of irritable bowel syndrome in CFS and FM patients (61%) and a further 19% had other GI symptoms. A common pathogenic mechanism such as disturbed microflora in the gut was suggested.


L. Barker (Essex UK) described an 8 week group programme for CFS patients was followed up by questionnaire/audit, and results demonstrated that 71% patients improved, with a number returning to work or college. It is hoped therefore to develop outpatient services to provide a comprehensive management approach to the illness.

P. Bottero (Paris) demonstrated the immunology of Rickettsial diseases (small intracellular gram-negative bacteria). It seems that rickettsiae penetrate and persist in the macrophages and diminish their function. Accompanying immunological changes also occur.


4 papers on Gulf War Illness (GWI) were presented as part of the opening symposium.

Peckerman and Natelson (Orange USA) presented figures to familiarise us with the situation in the USA. 16.8% of returning veterans surveyed had medical problems. The rate of Chronic Fatigue in this group was 5.2% compared to 1.2% of veterans in non-active service. Of those diagnosed as suffering from GWI 50% fitted the criteria for a diagnosis of CFS. It was hypothesised that those suffering from GWI have poor control of cardiovascular stress. Cardiovascular regulation was studied using various approaches. BP tended to fall during speech and mental arithmetic tests with no difference in pressor tests. During the speech test the peripheral resistance did not budge as it should. 3 possible issues were raised: Is this: (1) related to the cause of fatigue, (2) a marker of illness or (3) a premorbid condition? The greatest physiological consequences, impacting central and peripheral control systems, occurred in veterans who sustained exposure to both chemical and severe psychological war stresses.

Using factor analysis, Paul Levene (Washington) also concluded that the identification of a cluster of neurologic symptoms in a large sample (7000) of deployed Gulf War vets that could not be found in non-deployed vets supports the possibility that environmental factors could be responsible for some of the complaints of Gulf War veterans.

M. Hooper (UK) described the Gulf War as the most toxic war in all military history. Up to 17 vaccines were given, many disinfectants were used (e.g. in insect control), many chemical warfare agents were in the area, "uranium" weapons were used creating toxic dust, biological weaponry was in the area (e.g. brucella, smallpox, viruses) and many other chemical agents (smoke, oilfires) were prevalent. Birth defects have now been found to be a major factor in Iraqi veterans' families. Risks of leukaemia, other cancers, neurotoxic effects and possible effects on sperm are also becoming evident.

G. Nicolson pointed out that there is as yet no case definition for GWI, but the signs and symptoms loosely fit the CFS definition. Using Forensic PCR Hybridization it was found that 45% GWI patients showed evidence of mycoplasmal infections in the leucocytes but not in the plasma or serum. When comparing CFS patients, 70% of them were found positive for mycoplasma. A variety of mycoplasma species were found. These infections could be causative, cofactors or opportunistic. These infections maybe a major source of morbidity in these related illnesses. There is some evidence of possible transmission to family members. Possible other transmittable bacterial and viral infections maybe involved.

Treatment with appropriate antibiotics and nutritional support can result in improvement in these chronic conditions, though not in every case. It is possible that GWI is to a large degree due to multiple exposure to chemical, radiological and biological agents that can cause immune depression, multiple infections, and multifactorial illnesses, which may be treatable.

[Thanks to Dr. Rosamund Vallings for this report. Please remember, regardless of what you may read in these reports, be sure to consult your licensed health care practitioner about your own health care.]
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