Fibromyalgia syndrome (FS) is associated with a neuroendocrinal disorder characterized by abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis, including hyperactive adrenocorticotropic hormone (ACTH) release and adrenal hyporesponsiveness.
Fibromyalgia Impact Questionnaire (FIQ), widespread pain index (WPI), circulating IL-6, IL-8, and TNF-α level were evaluated before and after the intervention using enzyme-linked immunosorbent assay.
Arm 1 comprised 33 216 patients with FM and arm 2 consisted of 7420 patients with migraine; all of these patients were diagnosed between 2000 and 2010.
Arm 1 comprised 33 216 patients with FM and arm 2 consisted of 7420 patients with migraine; all of these patients were diagnosed between 2000 and 2010.
TNF and SP levels in patients with FMS were compared between weeks 1 and 12, as well as between patients with FMS and untreated controls, using the Mann-Whitney U test.
Ankylosing Spondylitis Disease Activity Score-C-Reaktif Protein, Ankylosing Spondylitis Disease Activity Score-Erythyrocyte Sedimentation Rate, Ankylosing Spondylitis Quality of Life Scale, Bath Ankylosing Spondylitis Functional Index, Pittsburgh Sleep Quality Index, and Visual Analog Scale pain scores were significantly higher in the group with FMS (P < .05).
A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein.
A polymerase chain reaction-restriction fragment-length polymorphism analysis of eNOS gene polymorphism was performed, and the results of the patients with FS and healthy controls were compared.
A possible mechanism for the effect of LLLT on fibromyalgia pain is via the antinociceptive signaling of substance P in muscle nociceptors, although the neuropeptide has been known as a neurotransmitter to facilitate pain signals in the spinal cord.