Biological markers of fibromyalgia

Fibromyalgia is a chronic condition characterized by widespread musculoskeletal pain and pressure hyperalgesia at characteristic sites, i.e., soft tissue tender points. The biophysiology of fibromyalgia, however, has remained elusive. This paper reviews recent biological research on the role of the neuroendocrine and immune systems in the biophysiology of fibromyalgia. It is suggested that fibromyalgia is determined by a combination of different pathophysiological mechanisms, which reside in the catecholaminergic and immune systems and in peptidase activities. Subsensitive platelet alpha 2-adrenoceptors suggest a lowered affinity of presynaptic receptors and thus could indicate a lower autoinhibitory activity on the catecholaminergic neuron. The results do not corroborate the hypotheses that fibromyalgia is accompanied by a deficiency in serotonergic metabolism or in disturbances in the hypothalamic-pituitary-adrenal axis. It is hypothesized that aberrant pain perception and depressive symptoms in fibromyalgia may result from decreases in prolyl endopeptidase (PEP, EC 3.4.21.26), a cytosolic endopeptidase which inactivates algesic (e.g., bradykinin, substance P) and depression-related peptides. Most results show no significant signs of inflammation in fibromyalgia, but show indications of immunosuppression.