Mechanisms and pathways of pain in chronic pancreatitis

Pain is the most common reason for hospitalization among chronic pancreatitis patients, and as many as 40% require three or more admissions during their lifetime for pain management. Improved treatments depend on a better understanding of the mechanisms of chronic visceral pain, a subject that has gained attention recently with the development of suitable animal models and reproducible experimental measures of sustained pancreatic pain. One of the best characterized pain receptors is transient receptor potential vanilloid 1 (TRPV1). Nociceptive pathways, inflammatory mediators, and sensitization of both central and peripheral pathways have been shown to play important roles in pancreatic pain. Trinitrobenzene sulfonic acid (TNBS) murine model can be used to examine both peripheral and central mechanisms of sustained pain and for comparison with models of somatic pain, such as peripheral or spinal nerve ligation, so that both shared and unique pathways can be identified.