Helicobacter pylori in the pathogenesis of peptic ulcer
Over the years, it has been noted that some antibiotics can promote ulcer healing, so that certain bacteria might be one of the risk factors for ulcers. Australian scholar Warren and Matrshall in 1983 from human gastric mucosa after Helicobacter pylori isolated in culture and found that the bacteria and ulcer disease in a very close relationship. Duodenal ulcer patients with Helicobacter pylori detection rate as high as 70% ~ 100% detection rate in patients with gastric ulcer 60% 1 70%. Ulcer after healing by drug treatment was still positive for H. pylori in patients with ulcer recurrence rate was significantly higher than the negative patients. Helicobacter pylori duodenal ulcer precipitating mechanism is unclear, there are several hypotheses:
1, excessive gastric acid secretion, the duodenal bulb has been over-acidification, can lead to duodenal gastric metaplasia within the lesion, in order to Helicobacter pylori from the gastric mucosa in the duodenal bulb moved to create the conditions for the . The study confirmed that survival of Helicobacter pylori in duodenal gastric metaplasia is indeed limited to foci. Pathogen survival and reproduction in the bulb induced by chronic inflammation, other factors, the role of induced ulcers, the occurrence of duodenal ulcer.
2, some scholars report on H. pylori-positive persons is more than the amount of gastrin released no such infections in patients with hypergastrinemia stimulate gastric acid secretion of parietal cells increased and increased the duodenal acidification easily understood ulceration.
Background on the reasons for the increase in Helicobacter pylori led gastrin may be related to the bacteria containing the urease on the enzyme decomposition of urea produces ammonia, so that antrum partial alkaline (pH) increased, reduced stomach acid on the gastric antral mucosa G cells, feedback inhibition, leading to an increase in G cells to secrete gastrin.
Comments
Leave a Reply
WordPress ·