Panminerva medica · 2002
Helicobacter pylori influence on gastric acid secretion in duodenal ulcer patients diagnosed for the first time.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Testino G, Cornaggia M, De Iaco F
Аннотация
BACKGROUND: Many experiences have hypothesised that Helicobacter pylori induced hypergastrinemia could lead to an increase of the parietal cell mass and, consequently, of acid secretion.
METHODS: The parietal cell mass and maximal acid output have been studied in patients with duodenal ulcer diagnosed for the first time, not due to drugs assumption. In particular, it has been evaluated the parietal cell mass and the acid secretion subdividing duodenal ulcer patients in relation to gastrinemia values (hypergastrinemia and normogastrinemia).
RESULTS: The parietal cell mass and the maximal acid output remain high independently of Helicobacter pylori presence. About 60% of the subjects in the Helicobacter pylori positive group show gastrinemia values higher than the average: neither did the study reveal in this group any variations in the parietal cell mass and acid secretion.
CONCLUSIONS: It emerges from the results that the mild chronic hypergastrinemia in Helicobacter pylori positive duodenal ulcer is not important enough to induce an increase in parietal cell mass and acid secretion. Therefore, Helicobacter pylori eradication is important in relapse prevention of duodenal ulcer, but not for its repercussions on the gastric secretion.
METHODS: The parietal cell mass and maximal acid output have been studied in patients with duodenal ulcer diagnosed for the first time, not due to drugs assumption. In particular, it has been evaluated the parietal cell mass and the acid secretion subdividing duodenal ulcer patients in relation to gastrinemia values (hypergastrinemia and normogastrinemia).
RESULTS: The parietal cell mass and the maximal acid output remain high independently of Helicobacter pylori presence. About 60% of the subjects in the Helicobacter pylori positive group show gastrinemia values higher than the average: neither did the study reveal in this group any variations in the parietal cell mass and acid secretion.
CONCLUSIONS: It emerges from the results that the mild chronic hypergastrinemia in Helicobacter pylori positive duodenal ulcer is not important enough to induce an increase in parietal cell mass and acid secretion. Therefore, Helicobacter pylori eradication is important in relapse prevention of duodenal ulcer, but not for its repercussions on the gastric secretion.