Chapter 19

Vulnerable Points of the Helicobacter pylori Story – Based on Animal and Human Observations (1975 – 2012)

Gyula Mózsik, Imre L. Szabo and Jozsef Czimmer

Abstract

The pathological and therapeutical aspects of the Helicobacter pylori infection in patients with peptic ulcer disease, chronic atrophic gastritis and gastric cancer have been widely studied. However, various observations have indicated controversial results and highlighted a few questionable aspects of the broadly accepted role of Helicobacter pylori in generating certain gastroduodenal disorders. These are the following: 1. The sonicated Helicobacter pylori culture did not cause any direct cellular-damaging effect (at the level of the cell membrane, mitochondrion, DNA) in an application of 10<sup>6</sup>-to 10<sup>8</sup> germ/mL given alone or in combination with indomethacin (10<sup>-8</sup> to 10<sup>-4</sup> M) on freshly isolated gastric mucosal cells. 2 Ethanol (EtOH) dose-dependently induced cellular damage (at the level of the cell membrane, mitochondrion and DNA), however, the sonicated Helicobacter pylori culture did not aggravate the damaging effect produced by EtOH. 3. The gastric acid secretory responses in patients with classical duodenal ulcer did not decrease depending on the patients’ age and on the period since the onset of complaints, however, the gastric basal acid output (BAO) increased significantly in correlation with these parameters. Meanwhile the maximal acid output (MAO) did not change. 4. Authors never observed gastric cancer in duodenal ulcer patients without gastric surgery (in time period from 1962 to 2012), however, the gastric (stump) cancer developed after a partial gastrectomy in patients with duodenal ulcer. 5. The capsaicin-sensitive afferentation of the vagal nerve is involved in the development of gastric mucosal damage and prevention, which seems to be an independent pathway from the Helicobacter pylori infection or eradication treatment. Conclusions: the results of our experimental and clinical observations might offer some details underlying a reconsideration of the widely accepted etiological role of Helicobacter pylori in the development of gastric mucosal damage, gastroduodenal ulcers, chronic atrophic gastritis, gastric cancer and the treatment of Helicobacter pylori positive gastritis.

Total Pages: 429-480 (52)

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