Helicobacter pylori infection overview: Difference between revisions
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'''For patient information, click [[Helicobacter pylori infection (patient information)|here]]''' | |||
{{Helicobacter pylori infection}} | {{Helicobacter pylori infection}} | ||
{{CMG}}; {{AE}} {{YK}} | {{CMG}}; {{AE}} {{YK}} | ||
==Overview== | ==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 gastrointestinal 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== | ==Historical Perspective== | ||
The association between ''[[helicobacter pylori]]'' and [[peptic ulcers]] was made by Barry Marshall and | 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== | ==Pathophysiology== | ||
Helicobacter pylori | 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== | |||
''[[Helicobacter pylori]]'' is a [[gram-negative]], [[microaerophile|microaerophilic]], and [[acidophile|acidophilic]] [[bacterium]] that [[infection|infects]] various areas of the [[stomach]] and [[duodenum]]. Many cases of [[peptic ulcer]]s, [[gastritis]], [[duodenitis]], and perhaps some [[cancer bacteria|cancer]]s are caused by ''H. pylori'' infections. However, many who are infected do not show any symptoms of [[disease]]. ''Helicobacter'' spp. are the only known microorganisms that can thrive in the highly acidic environment of the stomach. ''[[H. pylori]]'''s helical shape (from which the [[genus]] name is derived) is thought to have evolved to penetrate and favor its [[motility]] in the [[mucus]] gel layer. | |||
==Differential Diagnosis== | |||
''[[Helicobacter pylori]]'' infection must be differentiated from other diseases that cause [[nausea]], [[vomiting]], [[abdominal pain]], [[epigastric pain]] and unexplained weight loss such as [[atrophic gastritis]], [[GERD]], [[gastrinoma]], [[peptic ulcer disease]], [[gastric adenocarcinoma]], stress-induced gastritis and [[non-Hodgkin's lymphoma]]. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
''[[H. pylori]]'' inhabits more than 50% of world's population, especially in developing countries. The [[prevalence]] of [[infection]] increases with age. The [[prevalence]] of ''[[H. pylori]]'' is higher in developing countries than that in developed countries. In the United States, ''[[H. pylori]]'' infection is a common disease that tends to affect African Americans, Hispanics, and the elderly compared to whites. | |||
==Risk Factors== | |||
Common risk factors in the development of ''[[H. pylori]]'' infection are contaminated food and water, poor [[hygiene]], overcrowding, 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. | |||
==Natural history, Complications, and Prognosis== | |||
If left untreated, ''[[H. pylori]]'' infection may progress to develop [[gastritis]] which can be [[acute]] or [[chronic]], [[peptic ulcer disease]], [[adenocarcinoma]] and [[MALT lymphoma]]. Comnmon complications of the [[infection]] include [[Gastric ulcer|gastric]], [[duodenal ulcer|duodenal ulcers]], [[gastric adenocarcinoma]], [[MALT lymphoma]], [[pseudomembranous colitis]] following ''[[H. pylori]]'' treatment, [[B12 deficiency|B12]] and [[iron deficiency anemia]]. Prognosis is generally regarded as good. It is associated with less than 1% risk of gastric [[MALT lymphoma]] and 1-2% lifetime risk of [[stomach cancer]]. | |||
==Diagnosis== | |||
===Guideline recommendations=== | |||
'''ACG Guidelines''' | |||
American collage of gastroenterology guidelines for the management of ''[[Helicobacter pylori]]''. | |||
'''ESPGHAN and NASPGHAN Guidelines''' | |||
Evidence-based guidelines for ''[[H. pylori]]'' infection in children and adolescents in North America and Europe. | |||
===History and Symptoms=== | |||
Specific areas of focus when obtaining a history from the patient include history of [[nausea]], [[vomiting]], [[epigastric|epigastric pain]] or [[abdominal pain]], [[bloating]], [[gastrointestinal bleeding]], [[anorexia]], [[weight loss]], [[pallor]], a positive history of GI diseases or ''[[H. pylori]]'' infection, history of medication use ([[NSAIDS]]) and food and drinking water hygiene. Majority of patients infected are asymptomatic. Symptoms of ''[[H. pylori]]'' infection include [[halitosis]], [[nausea]], [[vomiting]], [[epigastric pain|epigatric]] or [[abdominal pain]], [[bloating]], [[belching]], dark or tarry like stools ([[melena]]), [[fatigue]], [[diarrhea]] and unexplained weight loss. | |||
===Physical Examination=== | |||
Common physical examination findings associated with ''[[H. pylori]]'' infection include [[fatigue]], [[abdominal pain]], conjunctival pallor and abdominal tenderness. | |||
===Diagnostic Tests=== | |||
In developed countries, the use of test and treat strategy is declining for younger patients presenting with [[dyspepsia]]. In developing countries, as the rates of [[ulcer]] or [[gastric cancer]] are high, the more appropriate initial approach in the diagnosis of ''[[H. pylori]]'' infection in developing countries are an empirical test-and-treat approach or initial [[endoscopy]]. | |||
'''Endoscopic Tests''' | |||
Endoscopic diagnostic tests are biopsy-based diagnostic methods for ''[[H. pylori]]'' infection. These include [[histology]], [[rapid urease testing]], [[culture]] and [[polymerase chain reaction|polymnerase chain reaction (PCR)]]. | |||
'''Nonendoscopic Tests''' | |||
The nonendoscopic diagnostic testing methods for ''[[H. pylori]]'' include antibody tests, urea breath test, and fecal antigen test. | |||
===Electrocardiogram=== | |||
There are no [[ECG]] findings associated with ''[[H. pylori]]'' infection. | |||
===X Ray=== | |||
There are no [[X ray]] findings associated with ''[[H. pylori]]'' infection. | |||
===CT=== | |||
There are no [[CT]] findings associated with ''[[H. pylori]]'' infection. | |||
===MRI=== | |||
There are no [[MRI]] findings associated with ''[[H. pylori]]'' infection. | |||
===Ultrasound=== | |||
There are no [[ultrasound]] findings associated with ''[[H. pylori]]'' infection. | |||
===Other Diagnostic Tests=== | |||
There are no other diagnostic studies associated with ''[[H. pylori]]'' infection. | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
Indications for treatment of ''[[H. pylori]]'' infection include past or present [[duodenal ulcer|duodenal]] and/or [[gastric ulcer]], with or without complications, following resection of [[gastric cancer]], [[MALT lymphoma|gastric mucosa-associated lymphoid tissue (MALT) lymphoma]], atrophic gastritis, [[dyspepsia]], patients with first-degree relatives with gastric cancer and patient‘s wishes. Factors involved in choosing treatment regimens include [[prevalence]] of ''[[H. pylori]]'' infection, [[prevalence]] of [[gastric cancer]], resistance to [[antibiotics]], availability of [[bismuth]], availability of [[endoscopy]] and ''[[H. pylori]]'' tests, ethnicity, drug allergies and tolerance, previous treatments and outcome, adverse effects, effectiveness of local treatment and recommended dosages and treatment duration. | |||
===Surgery=== | |||
Surgical intervention is not recommended for the management of ''[[H. pylori]]'' infection. | |||
===Primary Prevention=== | ===Primary Prevention=== | ||
Effective measures for primary prevention of the ''[[H. pylori]]'' infection include hand washing (antibacterial soaps), avoid contaminated food and water, maintain proper [[hygiene]] (hand sanitizers, antiseptic washes) and avoid close contact with infected family members ( e.g., kissing, by sharing eating utensils and drinking glasses). | |||
===Secondary Prevention=== | |||
The secondary prevention strategies following ''[[H. pylori]]'' infection to prevent recurrence of [[peptic ulcer disease]] and [[gastric cancer]] include the use of [[antbiotics]] to prevent recurrence of [[infection]] and the post treatment confirmation of ''[[H. pylori]]'' eradication after treatment using diagnostic tests. | |||
==References== | ==References== | ||
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{{WS}} | {{WS}} | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
Latest revision as of 17:54, 18 September 2017
For patient information, click here
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Helicobacter pylori infection Microchapters |
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Differentiating Helicobacter pylori infection from other Diseases |
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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 gastrointestinal 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 is a gram-negative, microaerophilic, and acidophilic bacterium that infects various areas of the stomach and duodenum. Many cases of peptic ulcers, gastritis, duodenitis, and perhaps some cancers are caused by H. pylori infections. However, many who are infected do not show any symptoms of disease. Helicobacter spp. are the only known microorganisms that can thrive in the highly acidic environment of the stomach. H. pylori's helical shape (from which the genus name is derived) is thought to have evolved to penetrate and favor its motility in the mucus gel layer.
Differential Diagnosis
Helicobacter pylori infection must be differentiated from other diseases that cause nausea, vomiting, abdominal pain, epigastric pain and unexplained weight loss such as atrophic gastritis, GERD, gastrinoma, peptic ulcer disease, gastric adenocarcinoma, stress-induced gastritis and non-Hodgkin's lymphoma.
Epidemiology and Demographics
H. pylori inhabits more than 50% of world's population, especially in developing countries. The prevalence of infection increases with age. The prevalence of H. pylori is higher in developing countries than that in developed countries. In the United States, H. pylori infection is a common disease that tends to affect African Americans, Hispanics, and the elderly compared to whites.
Risk Factors
Common risk factors in the development of H. pylori infection are contaminated food and water, poor hygiene, overcrowding, 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.
Natural history, Complications, and Prognosis
If left untreated, H. pylori infection may progress to develop gastritis which can be acute or chronic, peptic ulcer disease, adenocarcinoma and MALT lymphoma. Comnmon complications of the infection include gastric, duodenal ulcers, gastric adenocarcinoma, MALT lymphoma, pseudomembranous colitis following H. pylori treatment, B12 and iron deficiency anemia. Prognosis is generally regarded as good. It is associated with less than 1% risk of gastric MALT lymphoma and 1-2% lifetime risk of stomach cancer.
Diagnosis
Guideline recommendations
ACG Guidelines
American collage of gastroenterology guidelines for the management of Helicobacter pylori.
ESPGHAN and NASPGHAN Guidelines
Evidence-based guidelines for H. pylori infection in children and adolescents in North America and Europe.
History and Symptoms
Specific areas of focus when obtaining a history from the patient include history of nausea, vomiting, epigastric pain or abdominal pain, bloating, gastrointestinal bleeding, anorexia, weight loss, pallor, a positive history of GI diseases or H. pylori infection, history of medication use (NSAIDS) and food and drinking water hygiene. Majority of patients infected are asymptomatic. Symptoms of H. pylori infection include halitosis, nausea, vomiting, epigatric or abdominal pain, bloating, belching, dark or tarry like stools (melena), fatigue, diarrhea and unexplained weight loss.
Physical Examination
Common physical examination findings associated with H. pylori infection include fatigue, abdominal pain, conjunctival pallor and abdominal tenderness.
Diagnostic Tests
In developed countries, the use of test and treat strategy is declining for younger patients presenting with dyspepsia. In developing countries, as the rates of ulcer or gastric cancer are high, the more appropriate initial approach in the diagnosis of H. pylori infection in developing countries are an empirical test-and-treat approach or initial endoscopy.
Endoscopic Tests
Endoscopic diagnostic tests are biopsy-based diagnostic methods for H. pylori infection. These include histology, rapid urease testing, culture and polymnerase chain reaction (PCR).
Nonendoscopic Tests
The nonendoscopic diagnostic testing methods for H. pylori include antibody tests, urea breath test, and fecal antigen test.
Electrocardiogram
There are no ECG findings associated with H. pylori infection.
X Ray
There are no X ray findings associated with H. pylori infection.
CT
There are no CT findings associated with H. pylori infection.
MRI
There are no MRI findings associated with H. pylori infection.
Ultrasound
There are no ultrasound findings associated with H. pylori infection.
Other Diagnostic Tests
There are no other diagnostic studies associated with H. pylori infection.
Treatment
Medical Therapy
Indications for treatment of H. pylori infection include past or present duodenal and/or gastric ulcer, with or without complications, following resection of gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, atrophic gastritis, dyspepsia, patients with first-degree relatives with gastric cancer and patient‘s wishes. Factors involved in choosing treatment regimens include prevalence of H. pylori infection, prevalence of gastric cancer, resistance to antibiotics, availability of bismuth, availability of endoscopy and H. pylori tests, ethnicity, drug allergies and tolerance, previous treatments and outcome, adverse effects, effectiveness of local treatment and recommended dosages and treatment duration.
Surgery
Surgical intervention is not recommended for the management of H. pylori infection.
Primary Prevention
Effective measures for primary prevention of the H. pylori infection include hand washing (antibacterial soaps), avoid contaminated food and water, maintain proper hygiene (hand sanitizers, antiseptic washes) and avoid close contact with infected family members ( e.g., kissing, by sharing eating utensils and drinking glasses).
Secondary Prevention
The secondary prevention strategies following H. pylori infection to prevent recurrence of peptic ulcer disease and gastric cancer include the use of antbiotics to prevent recurrence of infection and the post treatment confirmation of H. pylori eradication after treatment using diagnostic tests.