Clinical implications of accessory pancreatic duct.

The accessory pancreatic duct (APD) is the main drainage duct of the dorsal pancreatic bud in the embryo, entering the duodenum at the minor duodenal papilla (MIP). With the growth, the duct of the dorsal bud undergoes varying degrees of atrophy at the duodenal end. Patency of the APD in 291 control cases was 43% as determined by dye-injection endoscopic retrograde pancreatography. Patency of the APD in 46 patients with acute pancreatitis was only 17%, which was significantly lower than in control cases (P < 0.01). The terminal shape of the APD was correlated with APD patency. Based on the data about correlation between the terminal shape of the APD and its patency, the estimated APD patency in 167 patients with acute pancreatitis was 21%, which was significantly lower than in control cases (P < 0.01). A patent APD may function as a second drainage system for the main pancreatic duct to reduce the pressure in the main pancreatic duct and prevent acute pancreatitis. Pancreatographic findings of 91 patients with pancreaticobiliary maljunction (PBM) were divided into a normal duct group (80 patients) and a dorsal pancreatic duct (DPD) dominant group (11 patients). While 48 patients (60%) with biliary carcinoma (gallbladder carcinoma, n = 42; bile duct carcinoma, n = 6) were identified in PBM with a normal pancreatic duct system, only two cases of gallbladder carcinoma (18%) occurred in DPD-dominant patients (P < 0.05). Concentration of amylase in the bile of DPD dominance was significantly lower than that of normal pancreatic duct system (75 403.5 ± 82 015.4 IU/L vs 278 157.0 ± 207 395.0 IU/L, P < 0.05). In PBM with DPD dominance, most pancreatic juice in the upper DPD is drained into the duodenum via the MIP, and reflux of pancreatic juice to the biliary tract might be reduced, resulting in less frequency of associated biliary carcinoma.