Patency of the accessory pancreatic duct in chronic pancreatitis.

I read the paper by Hernández Garces et al. [1] with interest and I have some questions. I have prospectively examined patency of the accessory pancreatic duct (APD) by dyeinjection endoscopic retrograde pancreatography in 410 cases (291 controls, 46 acute pancreatitis, 32 chronic pancreatitis, 27 pancreaticobiliary maljunction, and 14 intraductal papillary mucinous tumor of the pancreas) [2, 3, 4]. Egress of dye from the minor duodenal papilla observed endoscopically was taken as an indication of APD patency. Patency of the APD in the control group was 43% (125/291). APD patency was correlated to the course and shape of the APD: patency in the long type (75%) was significantly greater than in the intermediate (38%), short (34%), or ansa types (15%) (P<0.01). The shape of the terminal portion was also correlated with patency of the APD: patency in the spindle type (93%) and cudgel type (88%) was significantly greater than in the branch type (7%) and saccular type (14%) (P<0.01). Patency of the APD in patients with acute pancreatitis was 17% (8/46), significantly less than in the control group (P<0.01). I think that a patent APD may prevent acute pancreatitis by reducing pressure in the main pancreatic duct. Patency of the APD in 32 patients with chronic pancreatitis was 32%. The APD was not detected in 6 cases and obliteration of the APD near the duodenum was seen in 4 cases. Cudgel appearance of the APD was detected in 8 cases, wherein the main pancreatic duct was also dilated. I think the appearance of the APD in patients with chronic pancreatitis is sometimes changed by acquired factors due to stagnation of pancreatic juice. I wonder what the patency of APD is in patients with chronic pancreatitis in Hernández Garces series, and how many cases show no APD or halfway APD.