1999 Clinical and Scientific Meeting

Phillip Clifton Bligh2, Suzanne Niblett1, Leigh Hoskin2, R Hugh Dunstan1, Greg Fulcher2, Neil McGregor1,4, Julie Dunsmore3, Timothy K Roberts1, Henry L Butt1, Katrina King1, Iven Klineberg4

1 Collaborative Pain Research Unit,
Bioanalytical Research Group,
Dept of Biological Sciences,
University of Newcastle,
Callaghan, NSW 2308
Australia
2 Royal North Shore Hospital,
CFS Research Unit,
Dept of Endocrinology,
Royal North Shore Hospital,
St Leonards,
NSW 2065
3 Royal North Shore Hospital,
CFS Research Unit,
Dept of Health Promotion and Education,
Royal North Shore Hospital,
St Leonards,
NSW 2065
4 Neurobiology Research Unit,
Centre for Oral Health Research,
University of Sydney,
Westmead Hospital
Westmead,
NSW 2084

Biochemical Abnormalities in Chronic Fatigue Syndrome

Chronic fatigue syndrome is defined as a disorder in which the subject has unexplained prolonged fatigue, often worse after minimal exercise, frequently associated with impaired sleeping, painful muscles, intermittently swollen lymph glands and impaired cognitive function. The pathogenesis has eluded explanation. The bioanalytical research group of the University of Newcastle has developed methodology for examining excretion of amino acids and organic acids into the urine. In collaboration with the Department of Endocrinology at the Royal North Shore Hospital, the overnight urine excretion rate of a number of amino acids and organic acids was measured in 100 patients with chronic fatigue syndrome, and in 83 age- and sex-matched normal controls.

The excretion rate of the metabolites was measured in units/minute. The most striking differences between patients with chronic fatigue syndrome and controls was a reduction in urine asparagine (p<0.0001) and a reduction in urine succinic acid (p<0.0003) in patients with chronic fatigue syndrome.

The excretion of urinary asparagine and succinic acid was highly correlated (p<0.00001). Urinary tyrosine (p<0.04) and urinary 3-methyl histidine (p<0.03) were significantly increased in patients with chronic fatigue syndrome. The urinary excretion of tyrosine, a protein catabolism marker, was associated with symptoms of fatigue, muscle pain, lymph node pain and cognitive disturbance.

The overnight excretion of succinic acid was correlated with the fasting plasma glucose (p<0.002). It is not known at present whether urine excretion rates of succinic acid and asparagine are correlated with serum concentrations of these metabolites or whether renal tubular function independently influences the urine excretion rates, and if so, whether renal tubular function is itself altered in chronic fatigue syndrome.

It is possible that urine asparagine excretion rates are low because of reduced entry of asparagine into the circulation, and thence into the urine. If the rate of entry of asparagine into the circulation is reduced, this could come about because of more rapid metabolism of asparagine in cells or because total body stores of asparagine are depleted. Further work is necessary to define these issues.

 

Alison Hunter Memorial Foundation
PO Box 6132 North Sydney 2059 Australia
Phone/Fax +61 2 9958 6285

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