The role of amino acid decarboxylase in the stimulation of gastrin release in man.

As amino acid-induced gastrin release is dependent on amino acid decarboxylase activity in rat, we examined the gastrin response to intragastric phenylalanine before and after treatment with carbidopa in 12 healthy male volunteers; carbidopa is an inhibitor of aromatic amino acid decarboxylation. Our results showed no significant difference between the pre- and postcarbidopa periods in the same subjects, suggesting that decarboxylation is not a necessary step for amino acids to stimulate G-cells in man. However, carbidopa seems to have an inhibitory effect on gastrin release, independently of its action on decarboxylase activity.

Treatment with cisapride of the gastrointestinal and urological sequelae of spinal cord transection: case report.

We describe the case of a paraplegic patient who suffered traumatic spinal cord injury at the level of the twelfth thoracic vertebra. Within a short period of time following the injury, urinary (neuropathic bladder) and gastrointestinal (atomic colon) sequelae arose. Treatment with Cisapride (R 51 619, Janssen Pharmaceutica) was undertaken in an attempt to increase colonic motility and to reduce urinary retention. These goals were reached rapidly with a dose of 10 mg q.i.d.; the effect has been maintained for at least 18 months since starting the therapy.

Inhibition of pentagastrin-stimulated gastric acid secretion and plasma levels of the new histamine H2-receptor antagonist ramixotidine dihydrochloride (CM 57755) in human volunteers.

The new competitive histamine H2-receptor antagonist, ramixotidine 2 HCl (CM 57755), has been tested in healthy male volunteers for its ability to inhibit pentagastrin-stimulated gastric acid secretion. In the first study, in 8 subjects, pentagastrin 6 micrograms.kg-1 was injected s.c., 90 min after the following 4 oral treatments given in random order at weekly intervals: placebo, 100, 200 and 400 mg CM 57755. Gastric contents were collected over 15-min periods during the 2 h after pentagastrin stimulation. In a second, similar study, 8 subjects received placebo, 0.5 and 1.0 g CM 57755 and 800 mg cimetidine, 120 min before a 2 h i.v. infusion of 6 micrograms.kg-1.h-1 pentagastrin. Cumulative gastric secretion in placebo-treated subjects was 46 +/- 14 and 62 +/- 11 mmol H+.2 h-1 (mean +/- SD), respectively, in the first and second studies. It was significantly reduced only after 400 mg CM 57755 in the first study. In the second study either dose of CM 57755 and cimetidine caused a significant reduction in gastric acid secretion. Average plasma levels of ramixotidine were dose-related after 0.2 and 1.0 g and ranged from 0.3 and 1.6 micrograms/ml, respectively, at 60 min to 0.5 and 3.7 micrograms/ml at 180 min. The peak cimetidine level averaged 3.6 micrograms/ml at 150 min. Individual CM 57755 plasma levels throughout the test period were fairly consistent with the inhibition of cumulative gastric acid secretion scored concurrently in each subject. No subjective side-effects attributable to the treatments were reported, and no abnormal findings were seen in the ECG or in laboratory tests.

[Assay of trace elements in the serum by the PIXE method in patients with Crohn's disease]. / Dosage des oligoéléments dans le sérum, par la méthode PIXE, chez des patients atteints de la maladie de Crohn.

Concentrations of trace elements were determined by the PIXE method (particle induced X-ray emission) in 43 serum samples from 29 Crohn's disease patients and compared with the results obtained from a control group of 100 healthy subjects. Most of the patients were outpatients whose disease was quiescent or moderately active. Half of them had a good nutritional state. Mean serum selenium level was significantly higher in the Crohn's disease group than in the control group. A negative correlation was found between serum selenium and C-reactive protein levels. Mean serum bromine was normal in the Crohn's disease group, but there was a positive correlation between serum bromine and fibrinogen and C-reactive protein levels and leucocytosis. Mean serum copper concentration was higher in women than in men in both groups. In Crohn's disease patients, copper serum concentration was increased and correlated positively to fibrinogen and C-reactive protein concentrations, erythrocyte sedimentation rate and thrombocytosis, and negatively to hematocrit. Copper serum level could be used as a marker of Crohn's disease activity. Mean serum zinc level was decreased in the Crohn's disease group. There was a positive correlation between serum zinc level and erythrocyte sedimentation rate and fibrinogen concentration.

[Effects of intragastric calcium on gastric acid secretion and release of gastrin in normal man and in various pathological cases]. / Effet du calcium intragastrique sur la sécrétion gastrique acide et la libération de gastrine chez l'homme normal et dans divers cas pathologiques.

Two hundred millilitres of an isotonic solution of CaCl2 (0,118 M) were injected and left 15 min in the stomach of normal subjects (SN1; n = 21), of patients with gastric ulcer (UG; n = 16), patients with duodenal ulcer (UD; n = 40), patients with normochlorhydric gastritis (G1; n = 13) and patients with hypo- or achlorhydric gastritis (G2; n = 7). Gastric acid secretion and gastrinemia were measured during 90 min. After intragastric calcium injection, the acid secretion was increased during 60 min in almost all subjects (87 to 100 p. 100 of subjects in the various groups) whereas gastrin release was increased in the majority (57 to 84 p. 100) of cases. The possible dissociation between the acid and gastrinic responses implies that the calcium-induced acid response is independent of the calcium-induced gastrin release. During control experiments in normal individuals, continuous intragastric perfusion (300 ml/h) of NaCl 0.15 M failed to alter gastric acid secretion or gastrin release, whereas continuous intragastric perfusion of CaCl2 0,118 M enhanced gastric acid secretion and gastrin release. The action of CaCl2 0,118 M is therefore not attributable to gastric distension but directly to calcium itself. The stimulation of acid secretion by intragastric calcium was more conspicuous in patients with gastric or duodenal ulcer than in normal subjects. The release of gastrin was higher in gastritis and duodenal ulcer than in the normal group. It is hypothesized that intragastric calcium increases the cholinergic tone of the parietal cell.