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High cell surface CD26-associated activities and low plasma adenosine concentration in fibromyalgia
  1. Régis Guieu1,2,
  2. Eric Guedj3,
  3. Roch Giorgi4,
  4. Alix Dousset5,
  5. Veronique Tuzzolino5,
  6. Youlet By6,
  7. Jean Marc Leveque5,
  8. Jean Claude Peragut5,
  9. Jean Régis5,
  10. Jean Ruf6,
  11. Emmanuel Fenouillet7,
  12. Philippe Roussel5
  1. 1UMR MD2, Aix-Marseille University, Marseille, France
  2. 2Laboratoire de Biochimie, AP-HM, France
  3. 3Nuclear Medicine, AP-HM, Marseilles, France
  4. 4LERTIM, Aix Marseille University, Marseilles, France
  5. 5Pain Center, Timone Hospital, AP-HM, Marseilles, France
  6. 6UMRMD2, Aix Marseille University, Marseilles, France
  7. 7UMRMD2, CNRS, Marseilles, France
  1. Correspondence to Régis Guieu, Aix-Marseille University, UMR MD2, Faculté de Médecine Nord, Marseille 10105, France; guieu.regis{at}numericable.fr

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The fibromyalgia syndrome (FMS) affects 2%–10% of the population. Its diagnosis is only based on a history of widespread pain involving limbs and trunk and mild or greater tenderness to digital palpation of tender points.1 While the role of several neurotransmitters including serotonin, dopamine and SP has been suggested, the influence of endogenous adenosine has never been investigated. Adenosine exerts strong antinociceptive effects mostly via the activation of A1 adenosine receptors2 following its release by endothelial cells and myocytes3 into the extracellular space where it is degraded by the enzyme adenosine deaminase (ADA). Large amounts of ADA are found at the surface of mononuclear cells …

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