Helicobacter pylori

Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.

Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.

Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.

The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.

Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.

H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries.

Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.

Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.

Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.

The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.

Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.

H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries.

Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.

Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.

Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.

The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.

Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.

H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries.

Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.

Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.

Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.

The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.

Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.

H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries.