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[Helicobacter pylori, endocrine cells of the gastric mucosa, and their function in duodenal ulcer].

Zverkov, Isakov Va, Aruin Li

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Abstract

Antral biopsies of 33 duodenal ulcer patients (15 with hypergastrinemia, group 1 and 18 with normal fasting serum gastrin, group 2) and also 13 healthy volunteers were studied for D- and G-cell density and HP-status. Basal acid output (BAO), maximal acid output (MAO) and serum somatostatin were also evaluated. G- and D-cell density was measured by PAP-immunostaining technique. Serum gastrin and somatostatin levels were studied by radioimmunoassay. HP-status was evaluated histologically with the use of semiquantitative enhanced method. Both groups of patients had decreased D-cell density compared with control (p < 0.05). Patients from group 1 had significantly increased BAO, MAO, G-cell density, index of infective load of HP, index of adherence of HP, comparing with group 2 (p < 0.05), and decreased serum somatostatin level and D-cell density compared with group 2. There were no significant differences found in serum somatostatin level, BAO, G-cell density, serum gastrin level between group 2 and control (p > 0.05). Hyperfunction of G-cells arose from impaired paracrine secretion of somatostatin, that strongly associated with increased index of infective load and increased index of adherence of HP to epitheliocytes of gastric antrum.

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What this paper is about

Antral biopsies of 33 duodenal ulcer patients (15 with hypergastrinemia, group 1 and 18 with normal fasting serum gastrin, group 2) and also 13 healthy volunteers were studied for D- and G-cell density and HP-status. Basal acid output (BAO), maximal acid output (MAO) and serum somatostatin were also evaluated. G- and D-cell density was measured by PAP-immunostaining technique. Serum gastrin and somatostatin levels were studied by radioimmunoassay. HP-status was evaluated histologically with the use of semiquantitative enhanced method. Both groups of patients had decreased D-cell density compared with control (p < 0.05). Patients from group 1 had significantly increased BAO, MAO, G-cell density, index of infective load of HP, index of adherence of HP, comparing with group 2 (p < 0.05), and decreased serum somatostatin level and D-cell density compared with group 2. There were no significant differences found in serum somatostatin level, BAO, G-cell density, serum gastrin level between group 2 and control (p > 0.05). Hyperfunction of G-cells arose from impaired paracrine secretion of somatostatin, that strongly associated with increased index of infective load and increased index of adherence of HP to epitheliocytes of gastric antrum.

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Available abstract

Antral biopsies of 33 duodenal ulcer patients (15 with hypergastrinemia, group 1 and 18 with normal fasting serum gastrin, group 2) and also 13 healthy volunteers were studied for D- and G-cell density and HP-status. Basal acid output (BAO), maximal acid output (MAO) and serum somatostatin were also evaluated. G- and D-cell density was measured by PAP-immunostaining technique. Serum gastrin and somatostatin levels were studied by radioimmunoassay. HP-status was evaluated histologically with the use of semiquantitative enhanced method. Both groups of patients had decreased D-cell density compared with control (p < 0.05). Patients from group 1 had significantly increased BAO, MAO, G-cell density, index of infective load of HP, index of adherence of HP, comparing with group 2 (p < 0.05), and decreased serum somatostatin level and D-cell density compared with group 2. There were no significant differences found in serum somatostatin level, BAO, G-cell density, serum gastrin level between group 2 and control (p > 0.05). Hyperfunction of G-cells arose from impaired paracrine secretion of somatostatin, that strongly associated with increased index of infective load and increased index of adherence of HP to epitheliocytes of gastric antrum.

Key concepts: Internal medicine, Somatostatin, Gastrin, Endocrinology, Radioimmunoassay, Antrum, G cell, Helicobacter pylori

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[Helicobacter pylori, endocrine cells of the gastric mucosa, and their function in duodenal ulcer]. — Research Paper | ScholarLens