BACKGROUND/AIMS: To determine whether or not portal venous obstruction affects pancreatic duct size. MATERIAL AND METHODS: The ERCP findings of 43 of 51 subjects with cavernous transformation of the portal vein (CTPV) were studied prospectively. In three, the ERCP failed to demonstrate the pancreatic duct (PD) for technical reasons and in 8 of the original 51 subjects, the ERCP was not attempted because of a lack of indications and unwillingness of the subject to undergo the procedure. The ERCP findings of the remaining 40 subjects were compared with those of 23 normal concurrent controls and those of reference controls. RESULTS: In 21 of the 51 patients, an underlying disorder responsible for portal vein thrombosis and cavernous transformation was identified. Despite a full clinical, radiologic, hematologic and biochemical evaluation, no etiology for CTPV was found in the remaining 30 patients. The pancreatic duct diameter was measured at the widest portion of the duct where it traverses the head of the pancreas. In 34 of the 40 patients with CTPV and a successful ERCP, the pancreatic duct was smaller (less than 2.28 mm in diameter) than that of concurrent control subjects and a reference control group (p < 0.05). In only 6 subjects with CTPV was the pancreatic duct size within normal limits. In 3 of these 6, a confounding common bile duct stone was shown to be present and may have accounted for the pancreatic duct enlargement as compared to the other 34 subjects with CTPV. CONCLUSIONS: These results indicate that a smoothly narrowing pancreatic duct hypoplasia or atrophy can be demonstrated in 85% of cases with CTPV. It is speculated that this finding is a consequence of the obstructed pancreatic venous drainage that occurs with CTPV.
BACKGROUND/AIMS: To determine whether or not portal venous obstruction affects pancreatic duct size. MATERIAL AND METHODS: The ERCP findings of 43 of 51 subjects with cavernous transformation of the portal vein (CTPV) were studied prospectively. In three, the ERCP failed to demonstrate the pancreatic duct (PD) for technical reasons and in 8 of the original 51 subjects, the ERCP was not attempted because of a lack of indications and unwillingness of the subject to undergo the procedure. The ERCP findings of the remaining 40 subjects were compared with those of 23 normal concurrent controls and those of reference controls. RESULTS: In 21 of the 51 patients, an underlying disorder responsible for portal vein thrombosis and cavernous transformation was identified. Despite a full clinical, radiologic, hematologic and biochemical evaluation, no etiology for CTPV was found in the remaining 30 patients. The pancreatic duct diameter was measured at the widest portion of the duct where it traverses the head of the pancreas. In 34 of the 40 patients with CTPV and a successful ERCP, the pancreatic duct was smaller (less than 2.28 mm in diameter) than that of concurrent control subjects and a reference control group (p < 0.05). In only 6 subjects with CTPV was the pancreatic duct size within normal limits. In 3 of these 6, a confounding common bile duct stone was shown to be present and may have accounted for the pancreatic duct enlargement as compared to the other 34 subjects with CTPV. CONCLUSIONS: These results indicate that a smoothly narrowing pancreatic duct hypoplasia or atrophy can be demonstrated in 85% of cases with CTPV. It is speculated that this finding is a consequence of the obstructed pancreatic venous drainage that occurs with CTPV.