The current understanding of mechanisms of peripheral sensitization is largely derived from studies examining the effects of injury or inflammation on visceral afferents. Most patients with chronic visceral pain, such as irritable bowel syndrome, nonulcer dyspepsia or interstitial cystitis, do not have signs of inflammation, raising questions about the relevance of these findings. While the definition of such functional diseases excludes active inflammation, up to one-third of patients with such functional disorders mentioned a precipitating infection or other insult (31,143,144). Interestingly, pelvic afferents demonstrated increased excitability up to two months after complete resolution of colitis in rats (58). Rectal pain and urgency were associated with an increase in the density of TRPV1 immunoreactive nerve fibers within the mucosa (18). These initial results suggest that persistent changes in visceral afferents are involved in the pathogenesis of visceral hyperalgesia and may be important targets in the treatment of visceral pain syndromes.
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Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.