The American journal of gastroenterology · 1996
Parietal cell hyperactivity is not due to Helicobacter pylori infection in patients with duodenal ulcer.
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Valenzuela M, Martín-Ruiz J L, Cahallero-Plasencia A M, Alvarez-Cienfuegos I, Nogales F F, Guilarte J, Peña J F
Аннотация
OBJECTIVE: To determine the relationship between Helicobacter pylori infection and parietal cell mass and functional status in 10 patients with duodenal ulcer and 22 patients with functional dyspepsia.
METHODS: We measured pentagastrin-stimulated acid secretion, determined the activity status of parietal cells on the basis of ultrastructural morphological features, and measured parietal cell mass and canalicular area with computerized densitometric morphometry. The number of antral G cells per square millimeter of mucosa was estimated inmunohistochemically, and basal serum gastrinemia was determined.
RESULTS: In patients with duodenal ulcer, acid secretion, the percentage of activated parietal cells, and canalicular area were increased, but there was no difference between patients and dyspeptic controls in parietal cell mass. Helicobacter pylori infection did not modify these parameters, although it was associated with basal hypergastrinemia.
CONCLUSION: In patients with duodenal ulcer, parietal cells display functional hyperactivity, which causes hypersecretion of acid; this effect is apparently unrelated to Helicobacter pylori infection.
METHODS: We measured pentagastrin-stimulated acid secretion, determined the activity status of parietal cells on the basis of ultrastructural morphological features, and measured parietal cell mass and canalicular area with computerized densitometric morphometry. The number of antral G cells per square millimeter of mucosa was estimated inmunohistochemically, and basal serum gastrinemia was determined.
RESULTS: In patients with duodenal ulcer, acid secretion, the percentage of activated parietal cells, and canalicular area were increased, but there was no difference between patients and dyspeptic controls in parietal cell mass. Helicobacter pylori infection did not modify these parameters, although it was associated with basal hypergastrinemia.
CONCLUSION: In patients with duodenal ulcer, parietal cells display functional hyperactivity, which causes hypersecretion of acid; this effect is apparently unrelated to Helicobacter pylori infection.