Antral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a
gastrin-producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp)
infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp
infection in pediatric AGCH patients, Hp status, G cell function,
acid secretion, and
antral G and D cell populations were investigated in six children presenting with gastrointestinal
bleeding of unknown origin, sideropenic
anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal
acid output (BAO), maximal
acid output (
MAO), and
pentagastrin-stimulated
acid output (PAO). Circulating
pepsinogen I was also significantly increased. Three children had Hp
infection, as assessed by
enzyme-linked
immunosorbent assay,
urease test, and histology. Endoscopy showed duodenal erosions in three children, with
ulcer in two Hp-positive cases. At histology, moderate
gastritis was observed only in the three Hp-positive cases. In all patients, quantitative assessment of
antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP
infection as an overlapping factor complicating the clinical picture in some cases.