OBJECTIVES: It is widely believed that sphincter of Oddi dysfunction (SOD) induces pancreatitis through an increase in intrapancreatic ductal pressure. Animal models have demonstrated that increased intrapancreatic ductal pressure plays a role in the development of pancreatitis. The role of intrapancreatic ductal pressure in SOD-induced pancreatitis has not been investigated in humans. The present study sought to (1) investigate the effect of SOD on intrapancreatic ductal pressure and (2) identify the correlation between elevated intrapancreatic ductal pressure and the presence of pancreatitis. METHODS: A total of 263 patients presenting with abdominal pain, acute recurrent pancreatitis, or chronic pancreatitis were studied. Intrapancreatic ductal pressure was measured blindly. Subsequently complete SOM was performed in standard fashion. RESULTS: Intrapancreatic ductal pressure correlated significantly with sphincter of Oddi (SO) basal pressure (correlation coefficient: 0.39, P < 0.01). Individuals with SOD had a significantly higher pressure (19.6 +/- 15.9 mm Hg) as compared with those with normal SO motility (11.1 +/- 7.9 mm Hg) (P < 0.001). This significant difference was observed in all subgroups (recurrent abdominal pain, acute recurrent pancreatitis, and chronic pancreatitis) (P < 0.01). Patients with acute recurrent pancreatitis or chronic pancreatitis did not show a significant elevation in their intrapancreatic ductal pressures when compared with those with recurrent abdominal pain alone. CONCLUSIONS: SOD leads to an increase in intrapancreatic ductal pressure. Increased PD pressure is not the sole determinant for the development of pancreatitis.
OBJECTIVES: It is widely believed that sphincter of Oddi dysfunction (SOD) induces pancreatitis through an increase in intrapancreatic ductal pressure. Animal models have demonstrated that increased intrapancreatic ductal pressure plays a role in the development of pancreatitis. The role of intrapancreatic ductal pressure in SOD-induced pancreatitis has not been investigated in humans. The present study sought to (1) investigate the effect of SOD on intrapancreatic ductal pressure and (2) identify the correlation between elevated intrapancreatic ductal pressure and the presence of pancreatitis. METHODS: A total of 263 patients presenting with abdominal pain, acute recurrent pancreatitis, or chronic pancreatitis were studied. Intrapancreatic ductal pressure was measured blindly. Subsequently complete SOM was performed in standard fashion. RESULTS: Intrapancreatic ductal pressure correlated significantly with sphincter of Oddi (SO) basal pressure (correlation coefficient: 0.39, P < 0.01). Individuals with SOD had a significantly higher pressure (19.6 +/- 15.9 mm Hg) as compared with those with normal SO motility (11.1 +/- 7.9 mm Hg) (P < 0.001). This significant difference was observed in all subgroups (recurrent abdominal pain, acute recurrent pancreatitis, and chronic pancreatitis) (P < 0.01). Patients with acute recurrent pancreatitis or chronic pancreatitis did not show a significant elevation in their intrapancreatic ductal pressures when compared with those with recurrent abdominal pain alone. CONCLUSIONS: SOD leads to an increase in intrapancreatic ductal pressure. Increased PD pressure is not the sole determinant for the development of pancreatitis.