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Biomedical subjects

M G Korman

Publications and source records attributed to M G Korman.

121 records · Page 7Linked to original sources
PubMed1971

Serum gastrin in chronic gastritis.

Fasting gastrin levels in serum were measured in 49 patients with different types of chronic gastritis and in matched controls. In 15 patients with established pernicious anaemia the mean (+/- S.E. of mean) level of gastrin was greatly raised (699 +/- 99 pg/ml). In 17 patients with chronic atrophic gastritis, seropositive for parietal cell antibody but with adequate vitamin-B(12) absorption, the level was also raised (476 +/- 74 pg/ml). By contrast, in "simple" atrophic gastritis seronegative for parietal cell antibody the gastrin levels were significantly lower for both diffuse atrophic gastritis (129 +/- 31 pg/ml) and multifocal gastritis (14 +/- 4 pg/ml). These levels were similar to those in the controls (46 +/- 7 pg/ml).The mechanism of the raised gastrin levels remains uncertain, but neither achlorhydria nor in vivo action of the parietal cell antibody wholly accounted for the hypergastrinaemia.We conclude that hypergastrinaemia is characteristic of gastritis associated with autoimmune reactions to gastric antigens and pernicious anaemia and that a raised serum gastrin is a useful marker of the type of gastritis that tends to progress to the gastric lesion of pernicious anaemia. The findings suggest that this type of gastritis is an essentially different disease from "simple" atrophic gastritis, and the differences in gastrin levels may be due to sparing of the antral mucosa in the autoimmune type but not in "simple" gastritis.

Achlorhydria↗
PubMed1971

Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine.

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.

Adult↗
PubMed1971

Serum gastrin in duodenal ulcer. II. Effect of insulin hypoglycaemia.

Serum gastrin has been measured by radioimmunoassay in normal subjects and patients with proven duodenal ulcer in response to insulin hypoglycaemia in conjunction with manoeuvres to decrease the intragastric acidity. Insulin hypoglycaemia alone caused a rise in the serum gastrin level from 5 +/- 1.0 to 49 +/- 2.9 pg/ml in duodenal ulcer and from 17 +/- 5.6 to 42 +/- 7.7 pg/ml in normals. With complete intragastric neutralization of acid and the same stimulus, the rise in duodenal ulcer was from 5 +/- 1.3 to 128 +/- 13.6 pg/ml and in normals from 13 +/- 2.6 to 84 +/- 2.6 pg/ml. These studies suggest an increased production rate of gastrin in response to vagal stimulation in duodenal ulcer, and indicate the precise role of acid inhibition in the control of gastrin release and support the concept of both an increased ;G cell' mass and parietal cell mass in duodenal ulcer. They have also offered an explanation of the variable vagal stimulation of gastrin release in normal subjects.

Bicarbonates↗
PubMed1971

Radioimmunoassay of gastrin: studies in pernicious anaemia.

Serum gastrin levels in patients with pernicious anaemia were measured by immunoassay in the fasting state, following gastric perfusion with 0.9% saline, 0.1N hydrochloric acid, and solutions of increasing acidity, and after the intravenous injection or infusion of secretin. The fasting serum gastrin level was measured in 21 patients with pernicious anaemia and found to be elevated at 1,036 +/- 215 pg per ml. Gastric perfusion with saline (pH 4.7) caused a mean fall in serum gastrin of 30% in four patients; perfusion with hydrochloric acid caused a further slight fall. Perfusion with solutions of increasing acidity resulted in a sharp fall in serum gastrin levels when the acidity was changed from pH 6 to pH 4. A single intravenous injection of secretin produced a mean maximal fall of 44% in the serum gastrin level in four patients, whereas continuous infusion of secretin produced a fall of 35% in four other patients. These studies suggest that the gastrin-secreting cells of the stomach are not affected by the atrophic process in pernicious anaemia and remain subject to the regulating control of acid and secretin.

Adult↗
PubMedDate not supplied

Helicobacter pylori prevalence in endoscopy and medical staff.

The epidemiology and mode of transmission of Helicobacter pylori is currently unclear; it is postulated that the human stomach is the natural reservoir and that spread occurs by faecal-oral or oral-oral transmission. The aim of this study was to assess the prevalence of H. pylori in gastroenterologists and gastroenterology nurses compared with internists, general nurses and the normal population. An enzyme-linked immunosorbent assay technique (sensitivity 96%, specificity 88%) was used to detect circulating H. pylori immunoglobulin G antibodies in 39 gastroenterologists, 107 gastroenterology nurses, 25 internists and 42 general nurses. These subjects were compared to an age- and sex-matched Caucasian population obtained by random sampling of an urban population area. The overall prevalence of H. pylori in gastroenterologists was 69% compared to 40% of internists (P < 0.01), 17% of gastroenterology nurses (P < 0.001), 19% of general nurses (P < 0.01) and 32% of controls (P < 0.01). There was no significant difference in H. pylori prevalence between the gastroenterology nurses and controls, general nurses and controls. The prevalence in gastroenterologists increased with years of practice to levels greater than age-matched controls. The prevalence in gastroenterology nurses increased with age and years of working and was similar to age-matched control subjects. These findings of an increased prevalence of H. pylori infection in gastroenterologists performing endoscopy support human-to-human transmission possibly from patients to medical staff.

Adult↗
PubMedDate not supplied

Sucralfate: the Bangkok review.

Sucralfate is a site-protective ulcer healing drug with a remarkable range of mechanisms of action. Recent studies highlight the capacity of sucralfate to bind basic fibroblast growth factor (bFGF) and deliver it in high concentration to the ulcer. Basic fibroblast growth factor stimulates the production of granulation tissue, angiogenesis and re-epithelization, thus improving the quality of ulcer healing. The effect of sucralfate in reducing parietal cell sensitivity may be another factor important in the lower relapse rate demonstrated after duodenal ulcer healing. Sucralfate has been demonstrated to be efficacious in healing both duodenal and gastric ulcers together with mild oesophagitis, and it is safe for both short-term use and maintenance. In stress ulcer prophylaxis it is as effective as acid suppression or neutralization and has the advantage of lesser rates of nosocomial pneumonia than are demonstrated with antacids or H2 antagonists. The potential advantages of sucralfate lie in the better quality of ulcer healing associated with longer duration of remission.

Clinical Trials as Topic↗