[HTML][HTML] Integration of gene expression, clinical, and epidemiologic data to characterize Chronic Fatigue Syndrome

T Whistler, ER Unger, R Nisenbaum… - Journal of Translational …, 2003 - Springer
T Whistler, ER Unger, R Nisenbaum, SD Vernon
Journal of Translational Medicine, 2003Springer
Background Chronic fatigue syndrome (CFS) has no diagnostic clinical signs or diagnostic
laboratory abnormalities and it is unclear if it represents a single illness. The CFS research
case definition recommends stratifying subjects by co-morbid conditions, fatigue level and
duration, or functional impairment. But to date, this analysis approach has not yielded any
further insight into CFS pathogenesis. This study used the integration of peripheral blood
gene expression results with epidemiologic and clinical data to determine whether CFS is a …
Background
Chronic fatigue syndrome (CFS) has no diagnostic clinical signs or diagnostic laboratory abnormalities and it is unclear if it represents a single illness. The CFS research case definition recommends stratifying subjects by co-morbid conditions, fatigue level and duration, or functional impairment. But to date, this analysis approach has not yielded any further insight into CFS pathogenesis. This study used the integration of peripheral blood gene expression results with epidemiologic and clinical data to determine whether CFS is a single or heterogeneous illness.
Results
CFS subjects were grouped by several clinical and epidemiological variables thought to be important in defining the illness. Statistical tests and cluster analysis were used to distinguish CFS subjects and identify differentially expressed genes. These genes were identified only when CFS subjects were grouped according to illness onset and the majority of genes were involved in pathways of purine and pyrimidine metabolism, glycolysis, oxidative phosphorylation, and glucose metabolism.
Conclusion
These results provide a physiologic basis that suggests CFS is a heterogeneous illness. The differentially expressed genes imply fundamental metabolic perturbations that will be further investigated and illustrates the power of microarray technology for furthering our understanding CFS.
Springer