Effect of a single oral dose of enprostil on gastric secretion and gastrin release. Studies in healthy volunteers and patients with pernicious anemia.

In healthy human volunteers, a single oral dose of enprostil (35 micrograms) inhibited basal gastric acid output by a mean of 71 percent, pentagastrin-stimulated output by 46 percent, sham-meal-stimulated output by 48 percent, and histamine-stimulated output by 16 percent. In each case, there was a reduction in both the volume and acidity of the gastric juice. Pepsin output was unchanged. Although enprostil increased the gastric pH, it did not induce basal or post-prandial hypergastrinemia. In patients with hypergastrinemia secondary to achlorhydria, enprostil lowered the basal gastrin level and reduced or abolished the post-prandial gastrin rise in a dose-related fashion. Enprostil reduces basal and stimulated gastric acid secretion and inhibits gastrin release.

Effect of low-dose omeprazole on gastric acid secretion in duodenal ulcer patients.

The effect of 7 days of oral dosing with 5 mg day-1 and 20 mg day-1 omeprazole on basal and pentagastrin-stimulated gastric acid output was studied in nine duodenal ulcer patients. Basal acid output measured 5-6 h post-dosing was decreased by a mean of 75% on 5 mg omeprazole and by 90% on 20 mg omeprazole (P less than 0.05 and P less than 0.01, respectively). Peak acid output measured 6-7 h post-dosing was decreased by a mean of 75% on 5 mg omeprazole and 97% on 20 mg omeprazole (P less than 0.01 for each). There was a wide interindividual variation in response to the 5 mg dose, with five of the nine patients having more than 90% inhibition of peak acid output, but two patients having less than 40% inhibition. This unpredictable response to daily low-dose omeprazole therapy makes it unsuitable for maintenance treatment.

A comparison of the effects of treatment with either famotidine 40 mg or cimetidine 800 mg nocte on gastric acid secretion and serum gastrin.

The effects on gastric acid secretion and serum gastrin of 4 weeks treatment with famotidine 40 mg nocte or cimetidine 800 mg nocte (at 2200 h) were studied in 16 patients with previous duodenal ulcer. Patients were studied before commencing therapy, on days 5, 12 and 26 of treatment, and on days 3, 10 and 24 after completion of therapy. In contrast to cimetidine, basal and pentagastrin-stimulated gastric acid secretion measured 12 h after dosing was significantly inhibited during treatment with famotidine. In addition, with famotidine there was inhibition of stimulated gastric acid secretion at 3 and 24 days after completion of treatment. Fasting serum gastrin measured 12 h after dosing was not significantly altered by either drug.

The effect of ranitidine hydrochloride, a new histamine H2-receptor antagonist, on intrinsic factor secretion.

The effect on intrinsic factor (IF) secretion of eight weeks' continuous treatment with a clinically relevant oral dose of ranitidine hydrochloride, a new histamine H2-receptor antagonist, has been studied in 11 patients with duodenal ulcer. There was no significant difference between the mean IF output during treatment of after drug withdrawal as compared with the control value, despite highly significant (p less than 0.001) reduction in acid output during treatment. In the short term this potent drug is unlikely to cause pernicious anemia from interference with IF secretion, although further study is necessary to exclude this possibility after long-term use.

The effect of trimipramine (Surmontil) on the gastric secretion of acid and pepsin in patients with duodenal ulceration.

Twenty-three patients with endoscopically proven, symptomatic duodenal ulceration were randomized to receive trimipramine 50 mg daily or placebo. Maximal acid output studies and estimations of pepsin levels were performed before treatment, for 4 weeks while on drug or placebo and for 4 weeks after cessation of treatment. Gastric acid secretion was significantly reduced after 3 weeks treatment with trimipramine and this reduction was maintained for the duration of the study. Gastric pepsin levels were unaffected by the administration of the drug.

An evaluation of the 14C-glycocholic acid breath test in the diagnosis of bacterial colonisation of the jejunum.

In order to assess the performance of the 14C-glycocholic acid breath test as an indicator of bacterial colonisation of the jejunum, 145 combined breath tests and jejunal aspirate cultures were carried out on a total of 50 subjects who had an increased probability of being colonised. Ninety-one of the 145 cultures were positive while only 31 of the breath tests were positive. This poor performance of the breath test relative to the aspirate culture can be predicted with reasonable accuracy from known bile deconjugating capabilities of bacteria found in the small intestine.

A case of eye disease due to dietary vitamin A deficiency in Glasgow.

A 22 year old Caucasian girl living in Glasgow presented with eye disease due to Vitamin A deficiency. There was no evidence of liver disease or malabsorption and the vitamin deficiency was found to be due to her bizarre dietary habit.

A comparison of symptoms between non-ulcer dyspepsia patients positive and negative for Helicobacter pylori.

The role of Helicobacter pylori infection in the symptom complex associated with non-ulcer dyspepsia is uncertain, despite the presence of the organism in a high proportion of these patients. In order to exclude physician bias in history taking, 18 patients (9 female) diagnosed as non-ulcer dyspepsia, after endoscopy and gallbladder ultrasonography, underwent computer interrogation using the Glasgow Diagnostic System for Dyspepsia (GLADYS). Five antral and 3 fundal endoscopic biopsies from these patients were also histologically examined for the presence of Helicobacter pylori and quantitatively analysed for polymorph and chronic inflammatory cell densities per mm2 of lamina propria using computer-linked image analysis. In the group of 9/18 patients who were positive for Helicobacter pylori, there were significantly higher antral and fundal inflammatory cell counts than in negative patients. However, analysis of the GLADYS interrogation data showed no significant positive relationships between Helicobacter pylori positivity and any gastrointestinal symptoms. These results confirm a significant association between Helicobacter pylori and superficial gastritis but suggest that non-ulcer dyspepsia in patients with Helicobacter pylori colonisation is probably not a clinically identifiable and distinct syndrome.

Taking a calculated risk: predictive scoring systems in dyspepsia.

The derivation of a predictive index is illustrated using 14 simple questions to assess the chance of the presence of an ulcer. The evaluation and use of such a 'calculated-risk' is briefly described.

Hyperplasia of the gastric mucosa during pregnancy and lactation in the rat.

1. The growth of the gastric mucosa during pregnancy and afterwards has been studied by comparing the stomachs of rats, killed at weekly intervals after impregnation, with the stomachs of virgin rats of the same age and starting weight. The rate of growth of the gastric mucosa in both groups was determined from the changes observed in the weight of the whole stomach, the weight and surface area of the fundus, the volume (mass) of the fundic mucosa and the total parietal and total peptic cell populations.2. Hyperplasia of the gastric mucosa occurred during pregnancy and lactation, the effect being characterized by increases in the surface area and volume (mass) of the gastric mucosa, and in the total parietal and total peptic cell populations.3. The data suggest that the effect developed shortly after conception. Hyperplasia of the gastric mucosa continued throughout pregnancy and reached maximal values after the second week of lactation and waned thereafter; the maximal changes obtained for individual observations such as surface area and the total parietal and total peptic cell populations represented increases of the order of 40% above corresponding control values.4. From the observations that were made on food intake it seemed unlikely that the hyperplasia of the gastric mucosa was due to hyperphagia. It also seemed unlikely that the effect could be accounted for by the increase that occurred in body weight during pregnancy.

Hepatocellular and gastric carcinoma associated with familial polyposis coli.

A case of familial polyposis coli in association with hepatocellular and gastric carcinoma is reported. No similar case has ever been documented in the world literature. This may be surprising as it is well known that familial polyposis has a potent oncogenicity not only in the colon but also in extracolonic organs.

Further observations concerning the effects of hypophysectomy on the gastric mucosa of the rat.

Hypophysectomy in rats markedly reduced the weight and surface area of the stomach as well as the volume (mass) of the gastric mucosa and the total parietal and total peptic cell populations. The parietal cell population was reduced by about 50%, and this effect was due entirely to the reduction that occurred in the total surface area of the stomach (50%); the average number of parietal cells per unit area, which reflects the number of parietal cells in the gastric glands, was not affected. The peptic cell population was reduced by about 90%, the factors responsible being a reduction in the average number of peptic cells per unit area (70%) as well as the reduction that occurred in the surface area of the stomach. The disproportionate effect of hypophysectomy on the cell populations was thus due to the reduction in the number of peptic cells per unit area; this effect implies that hypophysectomy had caused a reduction in the number of the peptic cells in the gastric glands.Whatever the mechanisms involved these results were due to a direct effect of pituitary deprivation on the stomach, since they could not be accounted for simply by the inhibition of somatic growth that follows hypophysectomy in rats. Thus the experiment included a group of sham hypophysectomized rats whose somatic growth was inhibited to the same extent as that of the hypophysectomized animals by deliberate underfeeding. While underfeeding reduced the surface area of the stomach (20%) and the total peptic cell population (25%), as well as exerting a marginal effect on the parietal cell population, these effects were much smaller in magnitude than those of hypophysectomy; moreover underfeeding did not affect the number of peptic cells in the gastric glands. The results confirm that the pituitary gland exerts a strong influence on the growth of the gastricmucosa.

The effect of the non-steroidal anti-inflammatory drug choline magnesium trisalicylate on gastric mucosal cell exfoliation.

Gastric mucosal cell exfoliation was measured in 10 normal subjects taking choline magnesium trisalicylate (CMT), aspirin and placebo. Both drugs resulted in significantly elevated rates of exfoliation although the serum salicylate levels achieved with aspirin were lower than those achieved by CMT. Side-effects of tinnitus, nausea and increased faecal blood loss were more common while subjects were taking CMT.