Primary gastric lymphoma with spontaneous perforation is rare. We report herein the case of a 53-year-old-man who was admitted to our hospital with severe epigastralgia. Emergency endoscopic examination showed a perforated gastric tumor in the lower body of the greater curvature, and a distal subtotal gastrectomy with lymph node dissection was performed. The resected tumor measured 10.0 x 8.0 cm and was associated with an area of ulceration, 8.0 x 6.0 cm in size, and perforation, 1.0 x 0.5 cm in size. Pathological examination confirmed a diagnosis of B-cell malignant lymphoma of the diffuse, medium-sized cell type. According to the Ann Arbor and Naqvi classifications, the lymphoma was stage II and stage III, respectively. Postoperative adjuvant chemotherapy comprising cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) was given. The patient is currently well with no signs of recurrence, 2 years 4 months after his operation.

We report a 74-year-old man with triple synchronous cancers occurring in the gallbladder, common bile duct, and pancreas. The patient had consulted a nearby physician because of epigastralgia and icterus. On September 30, 1997, the patient was admitted to our department for further evaluation and treatment. Abdominal computed tomography (CT) showed dilatation of the common bile duct, cystic duct, and intrahepatic bile duct, and swelling of the gallbladder. On CT, the wall of the distal common bile duct was thick and a low-density mass was detected on the left side. Cholangiography, performed via percutaneous transhepatic cholangiodrainage (PTCD), revealed stenosis of the distal common bile duct. Endoscopic retrograde pancreatography (ERP) showed marked dilatation of the main pancreatic duct. On October 17, 1997, pancreatoduodenectomy was performed under the diagnosis of carcinoma of common bile duct and pancreas. Histopathological examination revealed poorly differentiated tubular adenocarcinoma of the common bile duct, well-differentiated tubular adenocarcinoma of the gallbladder, and mucinous cystadenocarcinoma of the pancreas. These three tumors were histopathologically different. Moreover, p53-positive nuclei were recognized only in the pancreas tumor. These findings suggested that the oncogenic mechanisms of multiple synchronous cancers were not the result of only abnormal DNA reparative mechanisms.

dence of an abdominal mass or ascites. Hematologic examinations revealed mild anemia. On blood chemical analysis, the alkaline phosphatase was 401 IU/L, g-glutamyl transferase (GTP) was 101 IU/L, amylase was 133 IU/L, blood urea nitrogen (BUN) was 40.5 mg/dL, and creatinine was 2.6 mg/dL. However, the total bilirubin was normal (0.6 mg/dL). As for tumor markers, the concentration of elastase I was mildly elevated (Table 1). Percutaneous transluminal gall-bladder drainage findingsA drainage tube was placed in the gall-bladder, and PTGBD revealed two radiolucent areas measuring 20 ¥ 20 mm each in the gall-bladder. The common bile duct was dilated (diameter, 15 mm), and compression and stenosis were present at the left side of the inferior portion of the common bile duct (Fig. 1). Endoscopic retrograde cholangiopancreatography findingsThe main pancreatic duct at the head of the pancreas showed irregular stenosis, extending to approximately 30 mm. The portion of the main pancreatic duct adjacent to the tail of the pancreas was sightly dilated. In addition, irregular compression and stenosis extended for approximately 26 mm at the left side of the common bile duct (Fig. 2). Brushing cytologic diagnosis of the pancreatic duct indicated a class II lesion. Abdominal angiography and cholangiographyImages obtained simultaneously by angiography and cholangiography revealed poor visualization of the intra-A 62-year-old man with precordial pain and fever consulted a local practitioner. Blood tests revealed jaundice. Acute cholecystitis was diagnosed on ultrasonographic examination, and percutaneous transluminal gall-bladder drainage was performed. The patient was referred to the Department of Surgery for operation. Imaging studies performed via a drain disclosed compression and stenosis of the lower portion of the common bile duct. A computed tomographic scan showed a multilocular nodule-like low-density area measuring 2.0 ¥ 2.0 cm in diameter at the head of the pancreas. Endoscopic retrograde cholangiopancreatography disclosed compression and stenosis of the main pancreatic duct at the head of the pancreas. Angiographic examination revealed encasement of the intrapancreatic branch of the posterior pancreatic arcade, located in the same area as the compression stenosis of the bile duct. The results of imaging studies suggested cancer of the head of the pancreas, and a pancreatoduodenectomy was performed. The resected specimen included a mass measuring 3.5 ¥ 2.7 ¥ 1.7 cm, which was located at the head of the pancreas. On examination of a cut section, the mass was found to consist of small multilocular cysts. The cysts invaded the intrapancreatic bile duct. The histopathological diagnosis was serous cystadenoma.

A 58‐year‐old man presented with a 2‐month history of nausea and vomiting. Blood levels of hepatic enzymes and pancreatitis markers were slightly elevated. Hypotonic duodenographic and endoscopic examinations revealed stenosis encircling the descending duodenum. A computed tomography (CT) scan showed inflammatory changes in the head of the pancreas and thickening of the duodenal wall. Magnetic resonance cholangiography demonstrated stenosis of the intrapancreatic segment of the common bile duct and diffuse dilatation of the main pancreatic duct, without irregularity. At laparotomy, microscopic examination of a needle biopsy specimen of the head of pancreas revealed no evidence of malignancy. Distal gastrectomy with Billroth II anastomosis was performed. Microscopically, fibrous thickening of the duodenal wall, serositis and hyperplasia of Brunner's glands were found. The presence of duodenal stenosis due to segmental pancreatitis, referred to as groove pancreatitis, was confirmed. The elevated blood levels of pancreatitis markers returned to the normal range 8 months after the operation. Ultrasonic echography and abdominal CT also revealed a marked reduction in dilatation of the extrahepatic bile duct and the main pancreatic duct. In patients suspected of having pancreatic carcinoma or regional pancreatitis, groove pancreatitis should be included in the differential diagnosis.

In massive hemorrhage from acute gastric mucosal lesions, it is occasionally difficult to control the bleeding with nonsurgical therapy. We used the somatostatin analog, octreotide, which suppresses gastric and pancreatic function, to treat severe hemorrhagic erosive gastritis in a patient with acute pancreatitis. A 22-year-old man presented with epigastralgia and melena. Blood levels of pancreatitis markers were elevated. Computed tomography revealed diffuse enlargement of the pancreas, without fluid collection around the organ. An endoscopic examination showed extensive hemorrhagic erosions over almost the whole gastric mucosa. We diagnosed extensive hemorrhagic erosive gastritis with acute pancreatitis. A protease inhibitor (nafamostat mesilate 50 mg/day) and an H(2) receptor antagonist (famotidine 40 mg/day) were administered by injection for 6 days; the patient's serum and urine amylase levels fell, but the gastric erosions with hemorrhage were not attenuated. Octreotide was given subcutaneously, at a daily dose of 100 microg for 5 days, without famotidine administration. His melena disappeared, and the gastric erosions were markedly decreased. Administration of the somatostatin analog, octreotide, proved to be effective treatment in a patient with severe hemorrhagic erosive gastritis associated with acute pancreatitis.