SYDNEY, Dec. 17 (Xinhua) -- New Australian research has identified simultaneous abnormalities across multiple biological systems in people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), supporting the idea that ME/CFS is a medical condition and not a psychological disorder.
The study, led by researchers from Macquarie University, compared whole blood samples from 61 people meeting clinical diagnostic criteria for ME/CFS, with samples from healthy age- and sex-matched volunteers, a university media release said Wednesday.
Key findings of this multimodal study, published in Cell Reports Medicine, include changes in markers of cellular energy metabolism, in the proportions and maturity of circulating immune cells, and in plasma proteins associated with blood vessel dysfunction in people with ME/CFS, it said.
White blood cells from ME/CFS patients showed evidence of "energy stress" in the form of higher levels of adenosine monophosphate and adenosine diphosphate, indicating reduced generation of adenosine triphosphate, the key energy source within cells, it added.
Profiling of immune cell populations revealed a trend toward less mature subsets of T-lymphocyte subsets, dendritic cells and natural killer cells in people with ME/CFS, researchers said, adding that plasma analysis showed these people had higher levels of proteins associated with activation of the endothelium and remodelling of vessel walls and lower levels of circulating immunoglobulin-related proteins.
"Our findings provide further insights into the clinical and biological complexity of ME/CFS," said study senior author Richard Schloeffel, clinical senior lecturer in the Macquarie Medical School and an experienced general practitioner.
"A model like this, if clinically validated, has the potential to reduce diagnostic delays and improve patient quality of life, alleviating the prolonged suffering and economic burden faced by patients with ME/CFS," Schloeffel said.
The study team identified seven biological variables strongly associated with ME/CFS, highlighting potential interactions between areas of dysfunction that contribute to the clinical manifestations of ME/CFS. ■
