Yasutaka Kamiya

A case of pancreaticoduodenal artery aneurysm causing pancreatic pseudotumour and duodenal obstruction

This case report describes a ruptured pancreaticoduodenal artery aneurysm (PDAA) causing pancreatic pseudotumour and duodenal obstruction. A 59-year-old man was referred to our hospital with a chief complaint of frequent vomiting without abdominal pain. Because a mass lesion 10 cm in diameter was palpated in the right para-umbilical region and found in the head of the pancreas on computerized tomography (CT) and ultrasonography, malignant tumour of the pancreas or tumour-forming pancreatitis was strongly suspected, and further examination was performed.Magnetic resonance imaging (MRI) results suggested subacute haematoma inside the mass. On angiography, an aneurysm 8 mm in diameter was found in the posterior superior pancreaticoduodenal artery (PSPD). Since an ultrasound-guided percutaneous needle biopsy from the solid part of the mass indicated no malignancy, the lesion was considered an inflammatory pseudotumour in the head of pancreas due to ruptured aneurysm. Bypass surgery was planned, but the tumour shrank significantly with conservative treatment. Obstruction disappeared completely without surgery 4 weeks after the first symptom.

Effects of Dibutyryl Cyclic AMP and Papaverine on Intrahepatocytic Bile Acid Transport Role of Vesicle Transport

The secondary messenger cyclic AMP plays an important role in regulating biliary excretory function by stimulating the transcytotic vesicle transport system, whereas papaverine exerts an inhibitory effect on this system. We therefore investigated their effects on bile acid-induced cytotoxicity and intrahepatocytic content of bile acid in primary cultured rat hepatocytes. Simultaneous addition of 1 mM dibutyryl cyclic AMP (DBcAMP), an analogue of cAMP, with 1 mM taurochenodeoxycholic acid (TCDCA) significantly decreased the release of lactate dehydrogenase (LDH) as compared with the case with 1 mM TCDCA alone (7.1 +/- 0.13% of total versus 10.7 +/- 0.3%). In contrast, 0.1 mM papaverine approximately doubled the amount of LDH (22.0 +/- 0.6% of total versus 10.7 +/- 0.3%; P < 0.01). The intracellular content of TCDCA 180 min after the administration of 1 mM TCDCA alone was 20.8 +/- 0.7 nmol/mg protein, that after simultaneous administration of 1 mM DBcAMP, 16.2 +/- 1.0 nmol/mg protein, and that after the simultaneous administration of 0.1 mM papaverine, 38.5 +/- 1.9 nmol/mg protein. A clear correlation between the release of LDH from hepatocytes and the intracellular content of TCDCA was thus observed. When given together with 1 mM taurocholic acid (TCA) or 1 mM tauroursodeoxycholic acid (TUDCA), papaverine exerted little effect on cytotoxicity or intrahepatocytic bile acid content. When cells were bathed in a medium free of bile acid after pretreatment with 1 mM TCDCA and 1 mM DBcAMP, additional exposure to DBcAMP for 30 min significantly stimulated reduction of intracellular TCDCA content (30.2 +/- 0.4% of total versus 44.0 +/- 1.4%).(ABSTRACT TRUNCATED AT 250 WORDS)