[Helicobacter pylori, endocrine cells of the gastric mucosa, and their function in duodenal ulcer].
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.
Zverkov
I V
IV
Isakov
V A
VA
Aruin
L I
LI
D001078:APUD Cells / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D002452:Cell Count; D004381:Duodenal Ulcer / Q000097:blood / Q000382:microbiology / Q000473:pathology*; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology*; D005755:Gastrins / Q000096:biosynthesis / Q000097:blood*; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D006965:Hyperplasia; D013004:Somatostatin / Q000097:blood
D005755:Gastrins; D013004:Somatostatin