HELICOBACTER-PYLORI INFECTION IN CHILDREN WITH ANTRAL GASTRIN CELL HYPERFUNCTION

Antral gastrin cell hyperfunction (AGCH) is a rare syndrome characteri zed by persistent hypergastrinemia and important peptic symptoms in th e absence of a gastrin-producing tumor. The pathogenesis of AGCH is st ill unknown and debated. Helicobacter pylori (Hp) infection has been r eported as a possible cause of sustained hypergastrinemia. To assess t he relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations wer e investigated in six children presenting with gastrointestinal bleedi ng of unknown origin, sideropenic anemia, and variable abdominal sympt oms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid ou tput (BAO), maximal acid output (MAO), and pentagastrin-stimulated aci d output (PAO). Circulating pepsinogen I was also significantly increa sed. Three children had Hp infection, as assessed by enzyme-linked imm unosorbent assay, urease test, and histology. Endoscopy showed duodena l erosions in three children, with ulcer in two Hp-positive cases. At histology, moderate gastritis was observed only in the three Hp-positi ve cases. In all patients, quantitative assessment of antral gastrin a nd somatostatin cells gave significantly elevated G cell counts; D cel ls were at the lower reference limit and the G/D cell ratio was signif icantly elevated. These data indicated a diagnosis of AGCH, possibly d ue to the elevated G/D cell ratio, and suggest HP infection as an over lapping factor complicating the clinical picture in some cases.