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Helicobacter heilmannii s.s. (H. heilmannii s.s.) is a species within the Helicobacter genus of Gram negative bacteria. [1] Helicobacter pylori (H. pylori) is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the non-lymphoma type, and ...
[10] [11] Infection with H. pylori is responsible for an estimated 89% of all gastric cancers and is linked to the development of 5.5% of all cases cancers worldwide. [13] [14] H. pylori is the only bacterium known to cause cancer. [15]
World Congress of Gastroenterology recommends eradicating H. pylori to cure duodenal ulcers. [51] First report of resistance of H. pylori to the antibiotic metronidazole. [52] Resistance of H. pylori to treatment will lead to the development of many different antibiotic and proton pump inhibitor regimens for eradication. [53] 1992
Helicobacter heilmannii sensu lato (i.e. H. heilmanni s.l.) is a grouping of non-H. pylori Helicobacter species that take as part of their definition a similarity to H. pylori in being associated with the development of stomach inflammation, stomach ulcers, [11] duodenum ulcers, [12] stomach cancers that are not lymphomas, and extranodal ...
Gastritis caused by H. pylori infection is termed Helicobacter pylori induced gastritis, and listed as a disease in ICD11. [6] [7] More than 80% of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology. [17]
Mucosal disruption in acid peptic disease patients can be caused by infection, barrier disruption, or gastric acid hypersecretion.Acid peptic diseases can arise due to various risk factors such as Helicobacter pylori infection, alcoholism, tobacco use, cocaine and amphetamine use, nonsteroidal anti-inflammatory drug use (NSAIDs), fasting, Zollinger-Ellison syndrome, angiogenesis inhibitor ...
Atrophic gastritis is a process of chronic inflammation of the gastric mucosa of the stomach, leading to a loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues.
In 1999, a review of existing studies found that, on average, 40% of GERD patients also had H. pylori infection. [39] The eradication of H. pylori can lead to an increase in acid secretion, [ 40 ] leading to the question of whether H. pylori -infected GERD patients are any different from non-infected GERD patients.