1998 Clinical and Scientific Meeting

Neil R. McGregor, R. Hugh Dunstan [1] , Mark Donohoe [2], Timothy K. Roberts [1], Henry L. Butt [3], Jennifer A. Watkins [1], Raymond N. Murdoch [1]

Collaborative Pain Research Unit: Neurobiology Research Unit
University of Sydney, Westmead Hospital, Westmead
NSW 2084, Australia;
1 Bioanalytical Research Group
The University of Newcastle
Callaghan
NSW 2308, Australia;
2 Environmental Medical Centre
Mosman
NSW 2088, Australia
3 Division of Microbiology and Infectious Diseases
Hunter Area Pathology Service
Newcastle
NSW 2308, Australia.

Assessment of Lipid Homeostasis in Sudden and Gradual Onset CFS Patients

A study was undertaken in 60 chronic fatigue syndrome (CFS) patients and 39 age and sex-matched non-CFS control subjects. Plasma saponified lipid products were assessed using capillary gas chromatography - mass spectrometry (GC-MS) to measure qualitative changes in plasma lipid profiles. The major lipid anomalies observed in the CFS patients were reductions in trans-9-octadecenoate (CFS 0.99% vs Controls 0.74%) and cholesterol (CFS 4.13 mmole L-1 vs Controls 3.51 mmole L-1).

Twenty of the CFS patients reported an acute viral-like infection at onset and were assessed for Epstein-Barr virus (EBV) and Cytomegalovirus (CMV) whereas the remaining 40 CFS patients reported a gradual onset. None of the sudden onset patients had immunological evidence of a current common viral infection. This observation was further substantiated by an absence of specific fatty acid anomalies which have been previously reported to be associated with single current acute or chronic viral infections such as by the herpes family of viruses (EBV, CMV) or retroviruses (HIV).

The subgroup of CFS patients reporting a sudden onset had a different lipid profile compared with the controls, with the trans-9-octadecenoate:octadecanoate ratio as the primary inter-group difference. Those CFS patients reporting a gradual-onset also had different lipid profiles compared with controls and the trans-9-octadecenoate:octadecanoate ratio was again the primary discriminant factor. Both sudden onset and gradual onset patients therefore had the same fatty acid anomaly differentiating them from controls.

The sudden-onset CFS group lipid profile could be differentiated from the gradual-onset group profile using the cis-9,12-octadecadienoate:cis-9-octadecanoate ratio. This ratio has been previously identified as a key post-viral (EBV) modification to lipid homeostasis.

Although the patient's viral infective history and subsequent post-viral modifications may play some role in determining the onset and progression of CFS, the primary lipid changes in CFS patients were related to other potentially non-virally-induced lipid changes. The differences in lipid homeostasis characterised for the sudden- and gradual-onset groups provides a molecular basis for the heterogeneity observed in the CFS patients which may have arisen from combinations of underlying genetic, dietary, immunological, environmental or pathogen altered responses.

 

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

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