Table 3.
Biomarkers of chronic fatigue syndrome/myalgic encephalomyelitis
| Biomarkers Studied | Reference |
|---|---|
| >IL-10, IFNγ, TNFα by PHA stimulated lymphocytes; >CD4+CD25+ T cells expressing FoxP3 and VPACR2; <cytotoxic activity of NK and CD8+T cells; <granzyme and >perforin by gene expression. | Brenu, et al., 2011 |
| >IL-4, IL-5, IL-12, LTα, IL-1α, IL-1β, IL-6; <IL-8, IL-13, IL-15; unchanged IL-2, IFNγ, IL-17, IL-23, TNFα in plasma IL Subjects at rest. | Fletcher, et al., 2009 |
| Cytokine co-expression networks distinct in CFS/ME compared to HC and suggested persistent inflammation and humoral immune activation. | Broderick, et al., 2010 |
| <Perforin in NK cells and CD8+T cells by quantitative flow cytometry. Subjects at rest. | Maher, et al., 2005 |
| <Perforin by gene expression in GWI compared to HC at VO2Max in exercise challenge | Whistler, et al, 2009 |
| <Natural killer cell cytotoxicity; < plasma dipeptidyl peptidase IV;>T-cell activation. Subjects at rest. | Fletcher, et al., 2010 |
| Effect of exercise challenge in CFS/ME compared to HC: absence of significant increase in IL-6, IL-10, IL-12, LTα in CFS/ME | Harvey, et al., 2011 |
| In CFS/ME compared to HC: absence of significant increase in IL-6 & TNFα following exercise challenge | Jammes, et al., 2009 |
| IL-1β, IL-12, IL-6, IL-8, IL-10, and IL-13 were elevated at 8 hours post exercise in subjects showing symptom flair at 48 hours. | White, et al, 2010 |
| >NPY in CFS/ME subjects at rest by RIA; no exercise related NPY change in CFS/ME but > in HC | Fletcher, et al., 2010; Harvey, et al., 2011 |
| <Plasma CoQ10 in CFS/ME compared to HC | Maes et al., 2009 |
| <Serum vitamin E, a marker for oxidative stress | Miwa and Fujita, 2010 |
| Exercise related <plasma F(2)-isoprostanes (marker of oxidative stress); No effect of exercise on plasma IL-6 or sIL-6R in CFS/ME or HC | Robinson, et al., 2010 |
| In 71% of CFS/ME, exercise increased transcription for most sensory and adrenergic receptors and one cytokine. These correlated with fatigue and pain. No exercise related changes in HC. | Light, et al, 2012 |
| Metabolic syndrome predictors elevated in CFS/ME | Maloney, et al, 2010 |
| Increased lactate levels in ventricular cerebrospinal fluid of CFS patients. | Murrough et al. 2010 |
| Significant deficiencies in mitochondrial function in CFS/ME compared to HC | Myhill et al., 2009 |
| Quantitative proteomics using high resolution mass spectrometry of CSF | Schutzer, et al., 2011 |
| Unique CFS/ME spinal fluid proteome of 60 proteins when compared to HC and GWI. The CFS/ME and GWI patients shared 20 unique proteins | Baraniuk et al 2005 |
| > CRP in CFS/ME; >8-iso-prostaglandin F(2 alpha) isoprostanes | Spence, et al, 2008 |
| > CRP in CF cases not meeting the CFS/ME definition; no difference between CFS/ME and HC | Raison et al, 2009 |
| <basal salivary cortisol levels and illness symptoms | Torres-Harding, et al 2009 |
| <cortisol levels and flattened diurnal release of cortisol) associated with a poorer response to CBT. | Roberts, et al., 2010 |
| variations in the 5' region of NR3C1 (glucocorticoid receptor gene) | Rajeevan et al., 2007 |
| HPA axis dysfunction | Papadopoulos & Cleare, 2011 |
| HPA axis dysfunction | Ben-Zvi, et al., 2009 |
| No evidence of a biomarker using gene expression in a twin study | Byrnes et al., 2009 |
| Significant evidence for a heritable contribution to predisposition to CFS/ME | Albright, et al, 2011 |
| Gene expression revealed ‘CFS signature genes’ | Kerr, et al., 2008 |
| Reassessment CFS signature genes’ failed to confirm predictive ablity | Frampton, et al., 2011 |