Helicobacter pylori infection overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Person to person [[transmission]] is considered to be the most likely route of transmission of ''[[Helicobacter pylori]]''. ''[[H. pylori]]'' is a | Person to person [[transmission]] is considered to be the most likely route of transmission of ''[[Helicobacter pylori]]''. ''[[H. pylori]]'' is a noninvasive organism. It is found over [[mucus]] secreting cells but not in deeper [[gastric glands]]. Hence it can only inhabit gastric-type mucus but cannot colonize the [[esophagus]] or [[duodenum]]. Pathogenesis of ''[[H. pylori]]'' infection depends on bacterial, host and environmental factors. | ||
'''Gastritis''' | |||
The ''[[H. pylori]]'' induced [[gastritis]] includes the following stages. They are [[acute gastritis]], active chronic gastritis, [[atrophy]] and [[metaplasia|intestinal metaplasia]]. | |||
'''Peptic ulcer disease''' | |||
''[[H. pylori]]'' is closely associated with both [[duodenal ulcer|duodenal]] and [[gastric ulcer|gastric ulcers]]. The estimated lifetime risk for the development of [[peptic ulcer disease]] is 10-20%, in patients with ''[[H. pylori]]'' infection. ''[[H. pylori]]'' causes up to 90% of [[duodenal ulcers]] and 60-80% of [[gastric ulcer|gastric ulcers]]. | |||
'''Gastric adenocarcinoma''' | |||
[[Gastric adenocarcinoma|Gastric cancer]] is the second leading cause of cancer-related deaths worldwide and ''[[H. pylori]]'' is the strongest known risk factor for gastric cancer. ''[[H. pylori]]'' is considered as [[carcinogen|type I carcinogen]]. Among infected individuals, 1 to 3% develop [[gastric adenocarcinoma]]. | |||
'''MALT lymphoma''' | |||
*[[MALT lymphoma|MALT lymphoma (MALToma)]] is a form of [[lymphoma]] involving the [[mucosa-associated lymphoid tissue]] (MALT), frequently of the [[stomach]], but virtually any mucosal site can be afflicted. It is a [[cancer]] originating from [[B cell]]s in the [[marginal zone]] of the MALT. The evolution of gastric MALT lymphoma is a multistage process starting with the infection of ''[[helicobacter|H. pylori]]'' resulting in the recruitment of [[B-cell]] and [[T-cells]] and other inflammatory cells to the [[gastric mucosa]]. | |||
==Causes== | ==Causes== | ||
Revision as of 03:39, 24 January 2017
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Helicobacter pylori infection Microchapters |
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Differentiating Helicobacter pylori infection from other Diseases |
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Diagnosis |
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Guideline Recommendation |
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Treatment |
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Helicobacter pylori infection overview On the Web |
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Risk calculators and risk factors for Helicobacter pylori infection overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Helicobacter pylori infection is caused by H. pylori which is a gram-negative, microaerophilic, and acidophilic bacterium that infects various areas of the stomach and duodenum. It is the most prevalent, worldwide and chronic infection. It is associated with many gastro intestinal diseases like gastritis, peptic ulcer disease, adenocarcinoma and MALT lymphoma. It is estimated that 30%-40% of the United States population is associated with H. pylori infection.
Historical Perspective
The association between helicobacter pylori and peptic ulcers was made by Barry Marshall and Robin Warren in the year 1984 for which they were awarded Nobel prize in 2005 in physiology or medicine.
Pathophysiology
Person to person transmission is considered to be the most likely route of transmission of Helicobacter pylori. H. pylori is a noninvasive organism. It is found over mucus secreting cells but not in deeper gastric glands. Hence it can only inhabit gastric-type mucus but cannot colonize the esophagus or duodenum. Pathogenesis of H. pylori infection depends on bacterial, host and environmental factors.
Gastritis The H. pylori induced gastritis includes the following stages. They are acute gastritis, active chronic gastritis, atrophy and intestinal metaplasia.
Peptic ulcer disease H. pylori is closely associated with both duodenal and gastric ulcers. The estimated lifetime risk for the development of peptic ulcer disease is 10-20%, in patients with H. pylori infection. H. pylori causes up to 90% of duodenal ulcers and 60-80% of gastric ulcers.
Gastric adenocarcinoma Gastric cancer is the second leading cause of cancer-related deaths worldwide and H. pylori is the strongest known risk factor for gastric cancer. H. pylori is considered as type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.
MALT lymphoma
- MALT lymphoma (MALToma) is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT. The evolution of gastric MALT lymphoma is a multistage process starting with the infection of H. pylori resulting in the recruitment of B-cell and T-cells and other inflammatory cells to the gastric mucosa.
Causes
Helicobacter pylori infection is caused by H.pylori bacterium.
Epidemiology and Demographics
Approximately two-thirds of the world's population is infected with H. pylori. In the United States, H. pylori is more prevalent among older adults, African Americans, Hispanics, and lower socioeconomic groups.
Approximately 25 million Americans suffer from peptic ulcer disease at some point in their lifetime. Each year there are 500,000 to 850,000 new cases of peptic ulcer disease and more than one million ulcer-related hospitalizations.
Risk Factors
Common risk factors in the development of H.pylori infection are contaminated food and water, poor hygiene, over crowding, lower socio-economic status, smoking, age and race.
Screening
According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for H.pylori infection.
Treatment
Medical Therapy
Persons with active gastric or duodenal ulcers or documented history of ulcers should be tested for H. pylori, and if found to be infected, they should be treated. To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted. Testing for and treatment of H. pylori infection are recommended following resection of early gastric cancer and for low-grade gastric MALT lymphoma. Retesting after treatment may be prudent for patients with bleeding or otherwise complicated peptic ulcer disease. Treatment recommendations for children have not been formulated. Pediatric patients who require extensive diagnostic work-ups for abdominal symptoms should be evaluated by a specialist.
Primary Prevention
Since the source of H. pylori is not yet known, recommendations for avoiding infection have not been made. In general, it is always wise for persons to wash hands thoroughly, to eat food that has been properly prepared, and to drink water from a safe, clean source.