Aorto-oesophageal fistula after oesophageal stent placement in a patient with a Roux-en-Y gastric bypass.

A 43-year-old female patient suffered from persistent anastomotic leakage after Roux-en-Y gastric bypass for morbid obesity. Endoscopic stenting of the anastomotic leakage was performed. The patient presented with haematemesis 3 weeks later. An aorto-oesophageal fistula was diagnosed, most likely due to ulceration of the oesophageal stent. The fistula was closed with an endovascular covered aortic stent and a new gastrojejunostomy was created. One year after surgery, the patient is in good condition. Endoscopic stents are increasingly being used to treat anastomotic leakage in bariatric patients. An aorto-oesophageal fistula is a life-threatening complication of stent placement, early clinical recognition is essential. More data are needed on the complications of anastomotic stenting in bariatric patients.

[Obstructive jaundice caused by portal varicosis]. / Obstructie-icterus door portale varicosis.

In a 66-year-old woman with pruritus, jaundice, dark-brown urine and light-colored faeces obstructive jaundice was diagnosed. Despite extensive investigations, it was not possible to clearly distinguish if varicosis or cholangiocarcinoma was the cause of the obstruction. During laparotomy the right lobe of the liver was seen to be greatly underdeveloped. The portal system showed a varicose deformation with compression of the bile ducts and portal hypertension. The right lobe of the liver was removed and the portal hypertension was treated by creating a shunt between the hepatic portal vein and the right ovarian vein. The jaundice disappeared and the patient recovered. Histological investigation showed atrophy, secondary biliary fibrosis, cirrhosis and a biliary cystadenoma. There were no signs of malignancy. The varicose deformation can be considered to be a result of the portal hypertension caused by fibrosis and cirrhosis with possibly a history of thrombosis and insufficient recanalization.

Volatile N-nitrosamines in gastric juice of patients with various conditions of the gastrointestinal tract determined by gas chromatography-mass spectrometry and related to intragastric pH and nitrate and nitrite levels.

Gastric juice samples of 71 patients undergoing upper gastrointestinal endoscopy were collected as well as saliva samples from 40 of these patients. Age, sex, endoscopic diagnosis and medication were recorded. The gastric juice samples were analyzed for the presence and quantity of individual volatile N-nitrosamines, which were detected by gas chromatography-mass spectrometry, without prior derivatization. The samples were screened for eight nitrosamines, i.e. N-nitrosodimethylamine, N-nitrosoethylmethylamine, N-nitrosodiethylamine, N-nitrosodi-n-propylamine, N-nitrosodi-n-butylamine, N-nitrosopyrrolidine, N-nitrosopiperidine and N-nitrosomorpholine. The pH of the fresh gastric juice as well as nitrate and nitrite levels of gastric juice and saliva were determined. The mean total level of volatile N-nitrosamines in gastric juice was found to be 4.84 nmol/l (range 0-17.7 nmol/l). The main N-nitrosamines found were N-nitrosodiethylamine (mean concentration 3.1 nmol/l), N-nitrosodimethylamine (mean concentration 0.90 nmol/l) and N-nitrosopyrrolidine (mean concentration 0.38 nmol/l). Significant correlations between mean intragastric pH values and mean N-nitrosodi-n-butylamine level (P = 0.005) and total volatile N-nitrosamine contents (P = 0.009) were observed.

Twenty-four-hour intragastric acidity: 300 mg ranitidine b.d., 20 mg omeprazole o.m., 40 mg omeprazole o.m. vs. placebo.

BACKGROUND: There is considerable controversy about the degree of acid suppression that is optimal for the treatment of peptic disorders. AIM: To compare the effects of three different regimens that are reported to strongly inhibit acid secretion. METHODS: Intragastric 24-hour pH monitoring was performed in 11 healthy subjects in a randomized, multiple, cross-over, double-blind study. Each subject received four dose regimens, each for 2 weeks, in a random order. The regimens were: 300 mg ranitidine b.d., 20 mg omeprazole o.m., 40 mg omeprazole o.m., and placebo. RESULTS: The decrease in gastric acidity during the daytime and during the total 24-hour period by all three treatments was significantly greater than after placebo; a significant difference in acid inhibition was found between ranitidine and 40 mg omeprazole, but not between ranitidine and 20 mg omeprazole, nor between the two doses of omeprazole. During the night-time the decrease in gastric acidity by all three treatments was significantly greater than after placebo; no difference was seen between the two doses of omeprazole and ranitidine. For the time of pH greater than 3 we found no statistical difference between the various acid decreasing regimens. The pH remained significantly longer above 4 after ranitidine and the two doses of omeprazole compared with placebo, and also longer above 4 after 40 mg omeprazole compared with ranitidine, but not after 20 mg omeprazole compared with ranitidine, nor after the two different doses of omeprazole. CONCLUSIONS: Dosing with 300 mg ranitidine b.d., 20 mg omeprazole or 40 mg omeprazole is superior in gastric acid inhibition compared with placebo, when measured using 24-hour pH monitoring.

Exocrine pancreatic insufficiency and pancreatic fibrosis due to duodenal somatostatinoma in a patient with neurofibromatosis.

A case of duodenal somatostatinoma is described in a patient with Von Recklinghausen neurofibromatosis. The patient presented with exocrine pancreatic insufficiency, probably due to distal obstruction of the pancreatic duct by the tumor. Preoperative evaluation with calcium-pentagastrin and tolbutamide stimulation tests were nondiagnostic. At laparotomy, local excision of the tumor was performed. Pathological findings were compatible with duodenal somatostatinoma, causing pancreatic fibrosis. Somatostatin extracted from the tumor coeluted with the somatostatin-14 standard on high performance liquid chromatography (HPLC).

Bacteria in the aetio-pathogenesis of gastric cancer: a review.

Severe atrophic gastritis, a precursor lesion of gastric carcinoma, is connected, in two different ways, with intragastric bacterial colonization: (1) in advanced atrophic body gastritis (type A), achlorhydria or severe hypochlorhydria leads to bacterial overgrowth with aerobic and anaerobic flora enabling the conversion of nitrate to nitrite and further to N-nitroso compounds; (2) the newly re-discovered Helicobacter pylori is probably one of the major causes of chronic atrophic antral gastritis (type B). Both types of bacteria may be involved in the pathogenesis of multifocal gastritis (type AB). In the western world, achlorhydric atrophic gastritis is not only found in pernicious anaemia but is latent in about 2 to 6% of the general population. In one study from the Mayo Clinic, about one-third of consecutive gastric carcinomas were present in achlorhydric stomachs, the remainder in acid-secretors. Apart from the N-nitroso compounds, other carcinogenic mechanisms may be active in type A gastritis: elevated serum gastrin; altered cell turnover; immunologic and hereditary traits. The association of H. pylori with gastric carcinoma is mainly based on circumstantial evidence: (i) epidemiological studies indicate a moderately increased risk for gastric cancer in H. pylori-positive subjects compared with H. pylori-negative; (ii) in the presence of H. pylori intragastric levels of the anti-oxidant ascorbic acid are lowered; (iii) H. pylori seems to be linked to mucosal atrophy and intestinal metaplasia; (iv) recent follow-up studies show a significant development of atrophic gastritis in H. pylori-positive patients compared to H. pylori-negative.(ABSTRACT TRUNCATED AT 250 WORDS)