Oral Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2014

Serum Activin A, B and follistatin levels provide novel markers of Chronic Fatigue Syndrome (CFS) patients.  (#201)

David de Kretser 1 , Susan Hayward 1 , Adnan Sali 1 , Brett A Lidbury 2 , Don P Lewis 3 , Badia Kita 4 , Mark P Hedger 1
  1. Monash University, Clayton, Vic, Australia
  2. Genome Biology, The John Curtain School of Medical Research, Australian National University, Canberra, ACT, Australia
  3. CFS Discovery, Melbourne, Victoria, Australia
  4. Paranta Biosciences, Melbourne, Victoria

Patients with symptoms of Chronic Fatigue Syndrome (CFS) create a diagnostic dilemma as no definitive tests have established its pathophysiological basis. While progress in defining and measuring the degree of the fatigue are available, biochemical tests have been unhelpful determining their cause. In some patients, the onset of their symptoms may be linked to an earlier inflammatory illness, but supportive biochemical data are unavailable. Activin A and B, TGFβ family members, have been identified as proinflammatory cytokines and are regulated by Follistatin (Fst), a high affinity binding protein and all can be measured by specific assays. In mice, serum activin A, B and Fst increase following a lipopolysaccharide injection and are elevated in many patients in intensive care 1,2,3 . In contrast, in the CFS cohort diagnosed by accepted clinical measures (n=47), serum activin A was not increased (97.5 ±10.1pg/ml) but serum activin B was increased (117 ±13.4 pg/ml, p<0.05) and lower Fst levels (7.92 ± 0.85 ng/ml p<0.05) were found compared to normal subjects (serum activin A 107.9 ± 6.8pg/ml; activin B 70.4 ± 4.6 pg/ml & FST 10.1± 0.5 ng/ml). The higher activin B:Fst and the activin A:Fst ratios indicate an increase in activin bioactivity. While the actions of activin B require further definition, the increased activin A bioactivity can cause apoptosis of hepatocytes and B lymphocytes as well as cachexia and muscle wasting 4,5 . Longitudinal studies of CFS patients are required to confirm the pathophysiological consequences of these changes.  Elevated Activin B and decreased Fst may be a biological signature for the diagnosis of CFS. Further studies are required to define the actions of the elevated serum activin B levels. (95%CI=mean+/-2SE)