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IJCM2016070510165294Fibromyalgia is a condition of complex aetiology and up to 2% of the population with a higher frequency in females are currently diagnosed.

The symptom profile includes chronic, widespread pain, abnormal processing of pain and increased sensitivity to external stimuli, along with fatigue, gastrointestinal symptoms and changes in memory, mood and sleep.

The milieu and array of inflammatory cells and inflammatory mediators are crucially involved in the genesis, persistence and severity of pain following trauma, infection or nerve injury [1]. The mechanisms and pathways mediating pain and nociception (hyperalgesia) are transcriptionally regulated. The transcriptional mediator nuclear factor (NF)-κB plays a major role in regulating inflammatory responses, ostensibly via the control of gene expression/suppression. An association has recently emerged to establish a possible link between NF-kB and pain/nociception, purportedly through the regulation of the inflammatory loop and the secretion (biosynthesis) of pro-inflammatory mediators.

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