The pathogenesis of pain in chronic pancreatitis remains an enigma. The cause of pain is almost certainly multifactorial and may vary at different stages of the disease process. These factors may include the release of excessive oxygen-derived free radicals, tissue hypoxia and acidosis, inflammatory infiltration with influx of pain transmittent substances into damaged nerve ends, and the development of pancreatic ductal and tissue fluid hypertension due to morphological changes of the pancreas. Investigations into the causes of pain have been limited by changes in the dynamics with the progression of the disease process, limitations in studying functional and morphological changes of the pancreas in the clinical setting, and the psychosomatic profile of patients. Many of these patients are addicted to alcohol, and suffer from personality disorders. The difficulty in quantifying pain, which is at best subjective, further compounds the issue, especially when assessing the efficacy of treatment.
A possible mechanism for pain in alcohol-induced chronic pancreatitis is increased pancreatic duct pressure. A study has been done to compare sphincter of Oddi and pancreatic duct pressures in normal controls and patients with alcohol-induced chronic pancreatitis who had recently had pain or who were pain-free. Pressures were measured in the sphincter of Oddi in 10 controls and 33 patients, in the pancreatic duct in six controls and 15 patients, and in the common bile duct in four controls and five patients during station pull-through at the time of an endoscopic retrograde cholangiopancreatogram. There was no significant difference in the mean pressures in the pancreatic duct, sphincter of Oddi (basal and phasic), and frequency of papillary contraction when comparing patients with alcoholic pancreatitis and controls. There was also no difference between patients with or without pain and patients with or without strictures. This study has not confirmed the hypothesis that increased pancreatic duct pressures may be incriminated as a possible mechanism of pain in alcoholic-induced chronic pancreatitis.
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