How did the ancient bacterium, Helicobacter pylori, cause an epidemic of chronic duodenal ulceration?

Abstract

The association of Helicobacter pylori with chronic duodenal ulceration was a seminal observation in the short history of gastroenterology. However, H. pylori is now known to be an ancient bacterium, whereas there is persuasive evidence that the epidemic of duodenal ulceration began in the second half of the 19th century and continued into the second half of the 20th century. Possible explanations for the epidemic include genomic changes in the organism and environmental or other influences on the human host. While genomic changes resulted in the appearance of virulence factors, these seem likely to have appeared thousands of years ago with minimal effects on gastritis because of coexisting suppression of gastric immunity. In contrast, the emergence of duodenal ulceration is best explained by a change in the pattern of gastritis from inflammation involving the antrum and body in most individuals to a significant minority (10-20%) with antral gastritis but with relative sparing of the body of the stomach. In the latter group, the increase in serum gastrin (particularly G17) associated with antral gastritis had trophic effects on gastric parietal cells with an increase in the parietal cell mass and hypersecretion of gastric acid. Hypersecretion of acid is seen as the major risk factor for duodenal ulceration with significant contributions from environmental factors including smoking and use of nonsteroidal, antiinflammatory drugs. Host factors favoring changes in the pattern of gastritis include delayed acquisition of infection and improved nutrition; both with enhancing effects on mucosal immunity.

Exhaled Hydrogen after Lactulose Hydrogen Breath Test in Patient with Duodenal Ulcer Disease—A Pilot Study for Helicobacter-pylori-Associated Gastroduodenal Disease

“…Strain-specific virulent factors have been linked to a more severe grade of mucosal inflammation that may promote the presence of duodenal ulcer disease [ 22 ]; however, studies from the East Asian strain have disclosed inconsistent results [ 23 , 24 , 25 , 26 ]. Conceivably, factors other than bacterial virulence [ 27 ], the adopted classification of gastritis or the activity of DU should be considered in the interpretation of these findings.…”

Isoindolin-1-ones Fused to Barbiturates: From Design and Molecular Docking to Synthesis and Urease Inhibitory Evaluation

“…pylori to breed and harm gastric lining cells. This harm can cause peptic and duodenal ulcers in the short term and chronic inflammation and gastric cancer in the long term …”

“…This harm can cause peptic and duodenal ulcers in the short term and chronic inflammation and gastric cancer in the long term. 8 Numerous attempts have been made to design new drugs with multiple mechanisms to eradicate this group of bacteria and prevent the progression of Helicobacter pylori-induced gastric cancer. One of these attempts is to inhibit the urease enzyme for the purpose of preventing the escape from acidic pH.…”

Helicobacter pylori: Have potential benefits been overlooked?

“…A separate but smaller group has an increase in acid secretion with H. pylori with minimal inflammation in the body of the stomach and is at higher risk for duodenal ulceration. In this group, eradication of infection results in a fall in acid secretion, largely because of a fall in serum gastrin 24 . As eradication of infection increases acid secretion in a substantial majority, the overall effect is an increase in the acid secretion that increases the risk of GERD.…”

“…In this group, eradication of infection results in a fall in acid secretion, largely because of a fall in serum gastrin. 24 As eradication of infection increases acid secretion in a substantial majority, the overall effect is an increase in the acid secretion that increases the risk of GERD. By extension, more prominent esophageal inflammation could increase the risk of Barrett's esophagus and the subsequent risk of adenocarcinoma.…”