Pain and pain generation in pancreatic diseases

The pathophysiology of pain in pancreatic diseases is complex and multifactorial. Human data are available only for chronic pancreatitis patients and sometimes for pancreatic cancer. For acute pancreatitis, only animal data are available to date. The various hypotheses attempting to explain the genesis of pain also reflect the different therapeutical approaches to pain in these patients. The “neurogenic inflammation” hypothesis is a theory supported by various studies of all pancreatic disorders. Immunohistological reports have shown that the amount of neurotransmitters, such as substance P and its receptor calcitonin gene–related peptide and other neurotransmitters, is increased in afferent pancreatic nerves, and a correlation between pain and immune cell infiltration of the nerves has been described mainly in chronic pancreatitis patients. The most interesting finding is the existence of a spatial relationship between peptidergic neurons and inflammatory cells. Furthermore, there is the intriguing possibility of functional interaction among neuropeptides, immune cells, cytokines, and nerve growth factors.