In conclusion, the present work has provided definitive data on the major plasma and urinary amino acids and urinary organic acids. None of the previously reported abnormalities in urinary amino acids or of organic acids [5,6] could be confirmed and many of the abnormalities reported may be ascribed to artefacts introduced by their use of non-standard methods [12].
Comparison between the groups studied (patients with ME/CFS, patients with depression, patients with rheumatoid arthritis and healthy control subjects) has shown some evidence for underlying inflammatory disease in patients with ME/CFS (histidine) and although other manifestations of this seen in patients with rheumatoid arthritis (asparagine and glutamate) were not evident in these patients, the exact mechanisms involved may differ and warrant further investigation.
The highly significant reduction in urinary hydroxyproline in patients with ME/CFS suggests, by analogy to similar observations in patients with fibromyalgia, reduced intramuscular collagen that may lower the threshold for muscle micro-injury and result in non-specific signs of muscle pathology. The present observations may reflect a similar basis in patients with ME/CFS.
A reduced threshold for muscle micro-injury in combination with active inflammatory disease may provide a basis for the fatigue and muscle pain that are the major symptoms in patients with ME/CFS and this may also warrant further investigation.
