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Omeprazole, a powerful and long-lasting gastric anti-secretory benziimidazole derivative has been used to treat a particularly severe case of Zollinger-Ellison syndrome with familial type I multiple endocrine involvement. Before treatment with omeprazole, the patient's basal acid secretion, ranging from 50 to 100 mmol/h, had been poorly controlled by cimetidine (doses of up to 2,400 mg/d), ranitidine (doses of up to 1,200 mg/d) and even by ranitidine (1,200 mg/d) combined with pirenzepine (150 mg/d). Upon oral administration of four 20-mg capsules of omeprazole twice daily, rapid healing of the diffuse mucosal ulcerations of the upper GI tract as well as control of diarrhea were achieved. Clinical benefit accompagnied dramatic and sustained reductions in gastric acid secretion as demonstrated by repeated basal output measurements and 24-hour intragastric pH recording. The biodisponibility of omeprazole improved as gastric intraluminal acidity was reduced. The effects of omeprazole on pepsin output appeared to be mainly related to the reduction of gastric secretory volume. After more than one year of treatment, neither clinical nor biological side-effects were noted. However, repeated ultrastructural studies of fundic gastric mucosa revealed two types of alterations: a) a pattern of hyper-stimulated parietal cells with turgescent intra-cellular micro-canalicus invested by numerous microvilli; b) in about a fourth of the parietal cells, cytoplasmic modifications resembling auto-phagosomia and mitochondrial reduction in number and morphological transformation. Poorly understood to date, these alterations call for regular histological control of the gastric mucosa in patients with Zollinger-Ellison syndrome submitted to long-term administration of large doses of omeprazole.

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The aim of this study was to determine the influence of 24 h of ranitidine treatment on gastric bacterial flora and N-nitroso compound formation. Nitrate, nitrite levels, N-nitroso compound concentration were measured and bacterial flora was studied in the fasting and postprandial gastric juice of four healthy men under placebo and ranitidine treatment (150 mg. bid). The pH of seventy-five per cent of the gastric juice samples was over 4 when the patients received their ranitidine treatment. While the mean intragastric concentrations of nitrate, nitrite, N-nitroso compounds and counts of nitrate-reducing organisms were not significantly altered by ranitidine, there was a statistically significant rise in the number of total bacteria. During ranitidine treatment, the nitrite/nitrate ratio was positively correlated with intragastric pH and with the nitrate-reducing organism count of the placebo period. These results suggest that the reduction of nitrate to nitrite required the combination of two factors: a high count of nitrate-reducing organisms before treatment and a high intragastric pH.

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Gastric acid secretion, whole blood histamine concentration and serum gastrin were measured in dogs, equipped with Heidenhain pouch, in response to feeding alone and in combination with antral histamine (AH)--Antramine--or with somatostatin. Feeding stimulated acid secretion, histamine and gastrin responses in a dose-related manner. Addition of antramine to feeding resulted in a potentiated acid and gastrin responses while histamine response corresponded to sum of individual responses to antramine and to feeding. Somatostatin reduced markedly acid and histamine responses, while gastrin response was unchanged. Serum gastrin and whole blood histamine appear to be agonistic factors responsible together for acid secretion. Somatostatin suppresses histamine response and would inhibit gastrin activity on acid secreting cells by this mean. Somatostatin and histamine might act antagonistically on gastrin which would be their common substrate, and thus they could intervene in a regulation process of acid secretion. In regard to synthetic histamine, native antral histamine--antramine--appears to be a better candidate for a physiological histamine regulation of acid secretion.

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The authors describe the case of a 16-year-old African woman presenting with a cystic dilatation of the common bile duct associated with a dilatation of the left intrahepatic bile duct, hepatic fibrosis and portal hypertension. The disease was revealed by a non-infectious cholestatic syndrome. The diagnosis was made before the intervention by abdominal ultrasonography and computed tomography. A choledococyst-jejunostomy was performed which led to progressive normalisation of liver function. This report emphasizes the possibility of simultaneous lesions at different levels of the biliary tree in patients with choledocal cysts. The prognosis depends upon the state of the liver. A liver biopsy is therefore mandatory when an operation is performed. In the present case, the follow-up is too short to assess the regression of the biliary cirrhosis as described in the literature.

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Two high-performance liquid chromatographic procedures were proposed to measure histamine. The first, with UV detection and a strong acid cation exchanger (Partisil 10, SCX Whatman), made it possible to isolate histamine and some methylated derivatives. The second, with a C18 sorbent (mu Bondapak, Waters, 10 microns particle size) eluted with ion-pairing phases, made it possible to isolate the histamine-o-phthaldialdehyde complexes. This last procedure allied with a chromatographic purification step gave lower or identical amounts of histamine than those described in human urine (16 +/- 7 micrograms per 24 h), canine whole blood (1.5 +/- 1 ng/ml) and human gastric juice (2.3 +/- 1.4 ng/ml). The two procedures gave the concentration of a histamine-like compound isolated from the antral mucosa.

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1 Ranitidine oral kinetics and plasma concentration-effect relationships upon meal-induced gastric secretion were investigated in normal subjects. Four oral doses of ranitidine (50, 100, 150 or 200 mg) and placebo were tested. 2 Oral ranitidine showed a terminal half-life of about 2 h 25 min. Maximal plasma level was about 240 ng/ml for a 100 mg dose, and occurred about 1 h after dose. From the range of 50 to 200 mg dose, no indication of non-linearity was observed in the drug kinetics. 3 Ranitidine administration resulted in a dose-related reduction in meal-stimulated acid secretion reaching, 46, 70, 82 and 92%, respectively. Mean ranitidine plasma concentrations producing 50 and 80% inhibition of acid secretion were 73 and 180 ng/ml, respectively, with great inter-individual variability. 150 and 200 mg ranitidine oral doses maintained IC50 for at least 4.5 and 5.5 h, respectively. Upon oral administration, ranitidine exerted no effect on gastric emptying of the meal but slightly decreased the gastrin response to the meal.

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The authors report on a 66-year-old man who presented with major undernutrition 3 1/2 years after total gastrectomy for gastric lymphosarcoma. This case shows that severe post-gastrectomy undernutrition can still be seen nowadays. It also provides an opportunity to discuss the complex pathophysiology of major deficiency syndromes and underlines the predominant role of inadequate food intake in the pathogenesis of the syndrome.

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