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Biomedical subjects

M G Korman

Publications and source records attributed to M G Korman.

At least 109 records · Page 6Linked to original sources
PubMed1973

Progressive increase in the functional G cell mass with age in atrophic gastritis.

Patients with atrophic gastritis but normal antral mucosa and achlorhydria were divided into three groups according to age-under 40, 40 to 70, and over 70 years. Serum gastrin, both basal and following a standard protein meal, was estimated in all patients by radioimmunoassay. There was a significant correlation between the magnitude of the gastrin response and age, the older the patient the greater the response. These results suggest that with increasing duration of gastritis and continued stimulation of a normal antrum in the absence of inhibition by acid, the functional G (gastrin) cell mass increases. However the possibility exists that each cell may secrete more gastrin in response to the same stimulus with age. This may be resolved by counting the number of G cells in the stomachs of subjects with atrophic gastritis and different ages.

Achlorhydria↗
PubMed1972

Hypergastrinaemia in chronic renal failure.

Fasting serum gastrin was measured by radioimmunoassay in 89 patients with chronic renal failure. When the serum creatinine level was used as an index of the degree of renal impairment serum gastrin rose proportionately with the degree of renal failure. Haemodialysis did not significantly alter serum gastrin levels but renal transplantation tended to return them towards normal. This study indicates that the kidney has a role in the degradation of gastrin.

Adult↗
PubMed1972

Serum gastrin in duodenal ulcer. 3. Influence of vagotomy and pylorectomy.

Following truncal vagotomy and anterior pylorectomy for duodenal ulcer, fasting serum gastrin levels were higher at 84 +/- 7.9 pg per ml than in unoperated patients with duodenal ulcer (16 +/- 1.5 pg per ml). In response to a standard protein meal, the peak serum gastrin achieved in the vagotomized group was 259 +/- 37.8 pg per ml at 75 minutes after ingestion, a much higher response than that obtained with a standard meal plus prior atropinization in the unoperated duodenal ulcer patients.These results suggest that truncal vagotomy allows release of gastrin which was previously inhibited with the vagi intact and the temporal characteristics of the response indicate that some of this gastrin is derived from an extragastric source. The results also exemplify the dependence of gastrin estimations as measured by this immunoassay on the acidity of the contents bathing the gastric antrum.

Adult↗
PubMed1972

Serum gastrin in duodenal ulcer. IV. Effect of selective gastric vagotomy.

Serum gastrin has been measured in 30 patients following selective gastric vagotomy. Basal serum gastrin was 52+/-5.7 pg/ml which was significantly lower than the corresponding level in 50 patients following truncal vagotomy (84+/-7.9 pg/ml). After a standard protein meal serum gastrin rose to 136+/-8.3 pg/ml at 60 minutes after the meal. The peak rise above basal levels was significantly lower than that achieved in patients who had undergone truncal vagotomy. These results complement our previous hypothesis that section of extragastric vagal fibres permits the release of additional gastrin above that expected with the diminution of acid secretion, and hence the decrease in inhibition of gastrin release from the antrum.

Adult↗
PubMed1972

Gastrin studies in gastric ulcer.

Basal serum gastrin in 40 patients with benign gastric ulcer was 103 +/- 10.7 pg/ml, a level significantly higher than corresponding estimations in normal subjects and patients with duodenal ulcer. Following stimulation by a protein meal, a mean rise of 124 pg/ml was achieved at 75 minutes and prior atropinization induced a rise of 208 pg/ml at 90 minutes. Insulin hypoglycaemia produced a rise of 63 pg/ml which was not significantly changed with concomitant neutralization of gastric contents. These results suggest that patients with gastric ulcer have higher basal gastrin levels than normal and this is probably related to the lowered antral acidity. In addition, the protein meal and insulin hypoglycaemia responses suggest an increased antral G cell mass and the possibility of additional gastrin release from sites outside the antrum. It is doubtful whether the relative hypergastrinaemia has an aetiological role in gastric ulcer but it may have a role in the maintenance of gastric ulcer.

Adult↗
PubMed1972

Extragastric gastrin.

Gastrin release in the basal state and following a standard protein meal has been estimated in patients after partial gastrectomy, partial gastrectomy with truncal vagotomy, and total gastrectomy. Following partial gastrectomy, gastrin rose from 8 +/- 0.8 to 20 +/- 3.8 pg/ml with a protein meal. The rise in the partial gastrectomy with truncal vagotomy group was 27 +/- 0.8 to 92 +/- 1.5 pg/ml and after total gastrectomy was 13 +/- 1.5 to 58 +/- 4.6 pg/ml. These results provide evidence for the release of gastrin from extragastric sites.

Adult↗
PubMed1972

The functional 'G' cell mass in atrophic gastritis.

The serum gastrin response to a standard protein meal has been determined in achlorhydric patients with atrophic gastritis and contrasted with the response in normal subjects whose gastric contents were kept continuously neutral by intragastric bicarbonate instillation. Five normal subjects showed a significant increase in serum gastrin from a mean (+/- SEM) of 17 +/- 3 pg/ml to 119 +/- 10 pg/ml but their response did not approach that of four patients with atrophic gastritis and antral sparing (605 +/- 133 pg/ml to 1418 +/- 186 pg/ml). By contrast, in four patients with antral gastritis, there was no significant change in gastrin levels (24 +/- 13 pg/ml to 55 +/- 19 pg/ml). These studies indicate that the gastrin-secreting cell mass is increased in atrophic gastritis with antral sparing and decreased in atrophic gastritis with antral involvement, as compared to the normal state. They provide further evidence for the existence in man of two distinct forms of atrophic gastritis.

Achlorhydria↗
PubMed1971

Serum gastrin and the antral mucosa in atrophic gastritis.

The gastric antral mucosa was studied histologically in 22 patients with atrophic gastritis, of whom 11 had high levels and 11 had normal levels of serum gastrin. The antrum was graded histologically from normal to grade 3 gastritis. All patients with hypergastrinaemia (nine seropositive and two seronegative for parietal cell antibody) had either a normal antrum or minimal (grade 1) antral gastritis. In contrast all but one patient without raised serum gastrin (nine seronegative and two seropositive for parietal cell antibody) had severe (grades 2-3) antral gastritis. Thus circulating gastrin levels observed in patients with gastritis and achlorhydria can be directly related to the presence or absence of antral mucosal damage.Comparison of the histological appearances of the antral mucosa with serum gastrin and parietal cell antibody status has provided a basis for the separation of two distinctive forms of atrophic gastritis.

Achlorhydria↗