http://www.tandfonline.com/doi/abs/10.1080/21641846.2016.1207400?journalCode=rftg20&
DOI:10.1080/21641846.2016.1207400
Neil R. McGregora*, Christopher W. Armstrongb, Donald P. Lewisc, Henry L. Buttd & Paul R. Gooleyb
Received: 24 Apr 2016
Accepted: 24 Jun 2016
Published online: 29 Jul 2016
DOI:10.1080/21641846.2016.1207400
Neil R. McGregora*, Christopher W. Armstrongb, Donald P. Lewisc, Henry L. Buttd & Paul R. Gooleyb
Received: 24 Apr 2016
Accepted: 24 Jun 2016
Published online: 29 Jul 2016
Background: Widespread pain is noted in many patients with chronic fatigue syndrome (ME/CFS), fibromyalgia and temporomandibular disorders. These conditions usually start as a localized condition and spread to a widespread pain condition with increasing illness duration.
Purpose: To aim was to assess the changes in biochemistry associated with pain expression and alterations in renal function.
Methods: Forty-seven ME/CFS patients and age/sex-matched controls had a clinical examination, completed questionnaires, standard serum biochemistry, glucose tolerance tests and serum and urine metabolomes in an observational study.
Results: Increases in pain distribution were associated with reductions in serum essential amino acids, urea, serum sodium and increases in serum glucose and the 24-hour urine volume; however the biochemistry was different for each pain area. Regression modelling revealed potential acetylation and methylation defects in the pain subjects.
Conclusions: These findings confirm and extend our earlier findings. These changes appear consistent with repeated minor inflammatory-mediated alterations in kidney function resulting in essential amino acid deprivation and inhibition of protein synthesis and genetic translation within tissues.