To study the effects of ethanol on disulfiram-treated rats, we administered ethanol orally at a does of 2000 mg/kg, twice daily for 5 days. The administration of ethanol or disulfiram alone produced no recognizable changes in pancreatic acinar cells. Ethanol administration, in disulfiram-treated rats resulted in a decrease in the content of zymogen granules in acinar cells, and the appearance of intraplasmic vacuolization. Electron microscopically, these vacuoles appeared on the basal side of nuclei. In addition, similar vacuoles appeared in liver cells, and these vacuolizations seemed to show lipid inclusions. However, ethanol administration to disulfiram-treated rats did not cause inflammatory changes or edema in the pancreas. A comparison of blood ethanol levels in rats receiving ethanol alone and disulfiram plus ethanol showed no significant difference, but acetaldehyde levels in rats receiving ethanol plus disulfiram rats were significantly higher than those in rats receiving ethanol alone. These findings suggested that acetaldehyde caused a decrease of zymogen granules and the presence of lipid inclusions in pancreatic acinar cells.

The pathogenic role played by Helicobacter pylori in gastric mucosal defense was investigated in Japanese monkeys infected with H. pylori. Serum gastrin levels and ammonia concentrations in gastric juice were compared in H. pylori-infected (n = 6) and control (n = 7) groups. The gastritis score, the intracellular content of periodic acid-Schiff (PAS)-positive substance and hexosamine, and the bromodeoxyuridine (BrdU) labeling index in the gastric mucosa were compared in the two groups in the antrum and the corpus. The ammonia concentration in the gastric juice was significantly higher in the infected group (P < 0.01). The gastritis scores were significantly higher in the antrum and corpus in the infected group (P < 0.01, and P < 0.05, respectively). The content of PAS-positive substance and hexosamine was significantly decreased in the antrum of the infected group compared with that in the controls (P < 0.01, and P < 0.05, respectively), but there was no significant difference between the two groups in the corpus. The BrdU labeling indices were significantly higher in the antrum and corpus of the infected group (P < 0.01, and P < 0.01, respectively). Colonization by H. pylori injures the gastric mucosa by depressing the gastric mucosal defense factors, and, consequently, the cell kinetics are accelerated.

A 62-year old female was admitted for a detailed study of a pancreatic abnormality detected by abdominal ultrasonography. A CT and MRI revealed a fat deposition in the body and tail of the pancreas. An ERCP demonstrated the distal main pancreatic duct as 2 fine branches in the head, and accessory pancreatic ducts were visualized. An endoscopic ultrasonography revealed a swelling of the body. In the tail, a membrane-like hyDerechoic stmtcture was noted, and probably represented the pancreatic capsule. A angiography demonstrated branches of the dorsal and transverse pancreatic artery, and the diagnosis of acquired fatty replacement of the body and tail of the pancreas was confimned. Endoscopic ultrasonography appears to be a useful method to confimn fatty replacement of the body and tail of the pancreas.Key words : acquired f a t t y replacement of the pancreas, endoscopic ultrasonography, endoscopic retrograde cholangiopancreatography