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*It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM">{{cite web |url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307 |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</ref> and nonsteroidal anti-inflammatory drugs (NSAIDs)<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM"><nowiki>{{cite web </nowiki><nowiki><ref name="pmid16847081"></nowiki>{{cite journal |vauthors=Kusters JG, van Vliet AH, Kuipers EJ |title=Pathogenesis of Helicobacter pylori infection |journal=Clin. Microbiol. Rev. |volume=19 |issue=3 |pages=449–90 |year=2006 |pmid=16847081 |pmc=1539101 |doi=10.1128/CMR.00054-05 |url=}}</ref><ref>url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307<nowiki> |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</nowiki></ref>
*It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM">{{cite web |url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307 |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</ref> and nonsteroidal anti-inflammatory drugs (NSAIDs)<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM"><nowiki>{{cite web </nowiki><nowiki><ref name="pmid16847081"></nowiki>{{cite journal |vauthors=Kusters JG, van Vliet AH, Kuipers EJ |title=Pathogenesis of Helicobacter pylori infection |journal=Clin. Microbiol. Rev. |volume=19 |issue=3 |pages=449–90 |year=2006 |pmid=16847081 |pmc=1539101 |doi=10.1128/CMR.00054-05 |url=}}</ref><ref>url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307<nowiki> |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</nowiki></ref>
*Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motility toward the mucus layer . The spiral morphology and flagellar motility then assist in penetration into the viscous mucus layer, where the more pH-neutral conditions allow growth of the gastric Helicobacter species.<ref name="pmid16847081">{{cite journal |vauthors=Kusters JG, van Vliet AH, Kuipers EJ |title=Pathogenesis of Helicobacter pylori infection |journal=Clin. Microbiol. Rev. |volume=19 |issue=3 |pages=449–90 |year=2006 |pmid=16847081 |pmc=1539101 |doi=10.1128/CMR.00054-05 |url=}}</ref>  
*Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motility toward the mucus layer . The spiral morphology and flagellar motility then assist in penetration into the viscous mucus layer, where the more pH-neutral conditions allow growth of the gastric Helicobacter species.<ref name="pmid16847081">{{cite journal |vauthors=Kusters JG, van Vliet AH, Kuipers EJ |title=Pathogenesis of Helicobacter pylori infection |journal=Clin. Microbiol. Rev. |volume=19 |issue=3 |pages=449–90 |year=2006 |pmid=16847081 |pmc=1539101 |doi=10.1128/CMR.00054-05 |url=}}</ref>  
**It secrete cytotoxins and produce virulence factors like Cag A, VacA, and OipA.Cytotoxin-associated gene pathogenicity encodes protein CagA and vacuolating cytotoxin VacA aids in the colonization of gastric mucosa and it modulates host's immune system.It causes local production of a range of proinflammatory and immunoregulatory cytokines, neutrophil infiltration, specific T- and B- cell responses and the development of gastric lymphoid follicles.Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen metabolite.Following injury to astric mucosa it secretes interleukns and chemokines ,which further leads to neutrophilic migration to  the site of infection.Cag A and Vac A leads to activation of IL-8 which leads to inflammation of gastric mucosa <ref name="pmid8730255">{{cite journal |vauthors=Logan RP |title=Adherence of Helicobacter pylori |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=3–15 |year=1996 |pmid=8730255 |doi= |url=}}</ref><ref name="pmid8730257">{{cite journal |vauthors=Crabtree JE |title=Gastric mucosal inflammatory responses to Helicobacter pylori |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=29–37 |year=1996 |pmid=8730257 |doi= |url=}}</ref><ref name="pmid7863238">{{cite journal |vauthors=Ernst PB, Jin Y, Reyes VE, Crowe SE |title=The role of the local immune response in the pathogenesis of peptic ulcer formation |journal=Scand. J. Gastroenterol. Suppl. |volume=205 |issue= |pages=22–8 |year=1994 |pmid=7863238 |doi= |url=}}</ref>
**It secrete cytotoxins and produce virulence factors like Cag A, VacA, and OipA.Cytotoxin-associated gene pathogenicity encodes protein CagA and vacuolating cytotoxin VacA aids in the colonization of gastric mucosa and it modulates host's immune system.It causes local production of a range of proinflammatory and immunoregulatory cytokines, neutrophil infiltration, specific T- and B- cell responses and the development of gastric lymphoid follicles.Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen me*It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM">{{cite web |url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307 |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</ref> and nonsteroidal anti-inflammatory drugs (NSAIDs)<ref name="urlPathogenesis of Peptic Ulcer and Implications for Therapy — NEJM"><nowiki>{{cite web </nowiki><nowiki><ref name="pmid16847081"></nowiki>{{cite journal |vauthors=Kusters JG, van Vliet AH, Kuipers EJ |title=Pathogenesis of Helicobacter pylori infection |journal=Clin. Microbiol. Rev. |volume=19 |issue=3 |pages=449–90 |year=2006 |pmid=16847081 |pmc=1539101 |doi=10.1128/CMR.00054-05 |url=}}</ref><ref>url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307<nowiki> |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}</nowiki></ref>
*Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motabolite.Following injury to astric mucosa it secretes interleukns and chemokines ,which further leads to neutrophilic migration to  the site of infection.Cag A and Vac A leads to activation of IL-8 which leads to inflammation of gastric mucosa <ref name="pmid8730255">{{cite journal |vauthors=Logan RP |title=Adherence of Helicobacter pylori |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=3–15 |year=1996 |pmid=8730255 |doi= |url=}}</ref><ref name="pmid8730257">{{cite journal |vauthors=Crabtree JE |title=Gastric mucosal inflammatory responses to Helicobacter pylori |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=29–37 |year=1996 |pmid=8730257 |doi= |url=}}</ref><ref name="pmid7863238">{{cite journal |vauthors=Ernst PB, Jin Y, Reyes VE, Crowe SE |title=The role of the local immune response in the pathogenesis of peptic ulcer formation |journal=Scand. J. Gastroenterol. Suppl. |volume=205 |issue= |pages=22–8 |year=1994 |pmid=7863238 |doi= |url=}}</ref>
**It secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities<ref name="pmid8730260">{{cite journal |vauthors=Mobley HL |title=The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=57–64 |year=1996 |pmid=8730260 |doi= |url=}}</ref><ref name="pmid8730261">{{cite journal |vauthors=Nilius M, Malfertheiner P |title=Helicobacter pylori enzymes |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=65–71 |year=1996 |pmid=8730261 |doi= |url=}}</ref><ref name="pmid2801678">{{cite journal |vauthors=Slomiany BL, Kasinathan C, Slomiany A |title=Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol) |journal=Am. J. Gastroenterol. |volume=84 |issue=10 |pages=1273–7 |year=1989 |pmid=2801678 |doi= |url=}}</ref>
**It secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities<ref name="pmid8730260">{{cite journal |vauthors=Mobley HL |title=The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=57–64 |year=1996 |pmid=8730260 |doi= |url=}}</ref><ref name="pmid8730261">{{cite journal |vauthors=Nilius M, Malfertheiner P |title=Helicobacter pylori enzymes |journal=Aliment. Pharmacol. Ther. |volume=10 Suppl 1 |issue= |pages=65–71 |year=1996 |pmid=8730261 |doi= |url=}}</ref><ref name="pmid2801678">{{cite journal |vauthors=Slomiany BL, Kasinathan C, Slomiany A |title=Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol) |journal=Am. J. Gastroenterol. |volume=84 |issue=10 |pages=1273–7 |year=1989 |pmid=2801678 |doi= |url=}}</ref>
*NSAIDs-
*NSAIDs-
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* For an example of this section, click [[Pericarditis pathophysiology#Gross Pathology Images|here]]
* For an example of this section, click [[Pericarditis pathophysiology#Gross Pathology Images|here]]


<gallery>
 
[[File:Deep_gastric_ulcer.png|thumb|350px|left]]
[[File:Deep_gastric_ulcer.png|thumb|350px|center]]
<\gallery>
[[File:Benign_gastric_ulcer_1_(1).jpg|thumb|150px|left]]


==Microscopic Pathology==
==Microscopic Pathology==

Latest revision as of 23:38, 7 November 2017

Peptic ulcer diease pathophysiology

Overview

  • The overview section should include the disease name in the first sentence.
  • The goal is to summarize the pathophysiology page in several sentences. This section can be the same as the pathophysiology segment on the overview page.
  • To see an example of an overview section on a symptoms page, click here.

Template

  • The overview is highly dependent on the individual disease pathophysiology. There is no specific template preference for the first sentence.

Template Sentences:

Template Sentence 1: [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
Template Sentence 2: Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
Template Sentence 3: On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Template Sentence 4: On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Template Sentence 5: [Disease name] is transmitted in [mode of genetic transmission] pattern.
Template Sentence 6: [Disease/malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
Template Sentence 7: Development of [disease name] is the result from multiple genetic mutations.
Template Sentence 8: Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
Template Sentence 9: The progression to [disease name] usually involves the [molecular pathway].
Template Sentence 10: The pathophysiology of [disease name] depends on the histological subtype.

Examples:

Example 1: Spores of C. difficile are transmitted via the fecal-oral route to the human host.
Example 2: Following ingestion, the acid-resistant spores of C. difficile are able to survive the human gastric acidity.
Example 3: Following ingestion, Shigella spp. uses the M cells of the GI tract to invade the epithelial cells of the large intestine.
Example 4: Following transcytosis and macrophage apoptosis, Shigella avoids extracellular exposure and spreads intercellularly using actin polymerization processes (rocket propulsion).
Example 5: On gross pathology, hyperemia with development of ulcers and edema are characteristic findings of shigellosis.
Example 6: On microscopic histopathological analysis, infiltration of PMN and inflammatory pseudomembrane formation are characteristic findings of shigellosis.
Example 7: Duchenne muscular dystrophy is transmitted in an X-linked recessive pattern.
Example 8: Malignant melanoma arises from the epidermal melanocytes, which are neural crest cells normally involved in the synthesis of melanin (a brown pigment with photoprotective properties).
Example 9: Development of melanoma is the result of multiple genetic mutations.
Example 10: Genes involved in the pathogenesis of melanoma include p53, RB, ARF, and BRAF.
Example 11: The progression to melanoma usually involves the serine-threonine kinases of the MAPK/ERK pathway (mitogen-activated protein kinase) following mutation of either the N-RAS or BRAF oncogene.
Example 12: The pathophysiology of gallbladder cancer depends on the histological subtype.

Pathogenesis

Pathogenesis is the mechanism by which a certain factor causes disease (pathos = disease, genesis = development). The term can also be used to describe the development of the disease, whether it is acute, chronic, or recurrent. It can also be used to describe whether the disease causes inflammation, malignancy, necrosis etc.

Template Sentences

  • It is found that peptic ulcer disease is the result of self-digestion which occurs due to an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa and is mediated by two major factors which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases[1] and nonsteroidal anti-inflammatory drugs (NSAIDs)[1][2]
  • Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motility toward the mucus layer . The spiral morphology and flagellar motility then assist in penetration into the viscous mucus layer, where the more pH-neutral conditions allow growth of the gastric Helicobacter species.[3]
    • It secrete cytotoxins and produce virulence factors like Cag A, VacA, and OipA.Cytotoxin-associated gene pathogenicity encodes protein CagA and vacuolating cytotoxin VacA aids in the colonization of gastric mucosa and it modulates host's immune system.It causes local production of a range of proinflammatory and immunoregulatory cytokines, neutrophil infiltration, specific T- and B- cell responses and the development of gastric lymphoid follicles.Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen me*It is found that peptic ulcer disease is the result of self-digestion which occurs due to an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa and is mediated by two major factors which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases[1] and nonsteroidal anti-inflammatory drugs (NSAIDs)[1][4]
  • Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motabolite.Following injury to astric mucosa it secretes interleukns and chemokines ,which further leads to neutrophilic migration to the site of infection.Cag A and Vac A leads to activation of IL-8 which leads to inflammation of gastric mucosa [5][6][7]
    • It secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities[8][9][10]
  • NSAIDs-
    • it inhibits systemic prostaglandins production and cause ulcers[11]
    • more common in the stomach than the duodenum[12]
  • Other factors responsible for peptic ulcer disease:
    • Smoking
      • It decreases the production of prostaglandins in fundic and antral part of stomach[13]
      • It causes reflux of bile acids[14]
      • It causes alteration of blood flow and lead to ischaemia
  • Duodenal ulcer:
    • Abnormalities of acid secretion:
      • Increase in basal acid output.
      • Increase in acid response to GRP
      • Increased maximal acid response to exogenous gastrin
      • Increased ratio of basal acid output to maximal gastrin-stimulated output
      • Increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output.[15][16]
    • Decreased in bicarbonate secretion and low ph leads to gastric metaplasia induced duodenitis which further increases the risk of acid damage and leads to ulcer .[17]
  • Gastric ulcer

There is decrease in acid and decrease in parietal cell volume which further predisposes to development to ulcer formation.[18]

Genetics

  • Genes involved in the pathogenesis of peptic ulcer disease is CagA is a gene that codes for an immunodominant antigen, is present only in Helicobacter pylori strains that are associated with peptic ulcer disease[19]
  • Duodenal ulcer:HLA-DQA1 genotype related in Helicobacter pylori positive in Duodenal ulcer. Allele frequency DQA1*0301 more common in H. pylori-positive and DQA1*0102 allele are significantly more common in H. pylori-negative

[20]

Associated Conditions

  • The most important conditions associated with peptic ulcer disease include:
    • Gastric cancer-Helicobacter pylori infection in duodenal ulcer leads to gastric metaplasia and gastric atrophy which increases the risk of gastric cancer[21]
    • Gastric mucosa-associated lymphoid tissue (MALT) lymphoma-helicobacter pylori infection is associated with increased the risk of develeopment of MALT Lymphoma.[22]
    • Idiopathic thrombocytopenic purpura-The ASH also recommended that eradication therapy for Helicobacter pylori be administered to adults with ITP who were found to have H. pylori based on a test of active infection.the patient who has a peptic ulcer disease is increased the risk of developing idiopathic thrombocytopenic purpura.[23][24]

Gross Pathology

  • Gross pathology refers to macroscopic or larger scale manifestations of disease in organs, tissues and body cavities. The term is commonly used by pathologist to refer to diagnostically useful findings made during the gross examination portion of surgical specimen processing or an autopsy.
Template Sentences
  • Template Sentences 1: On gross pathology, Ulcers, , and [feature3] are characteristic findings of [disease name].
  • Template Sentence 2: The most important characteristics of [disease name] on gross pathology are:
    • Organ 1: List of characteristics +
    • Organ 2: List of characteristics + image
    • Organ 3: List of characteristics + image
  • This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki [1] and Ask Dr. Wiki [2].
  • For an example of this section, click here


File:Benign gastric ulcer 1 (1).jpg

Microscopic Pathology

  • Microscopic pathology is the disease process as it occurs at the microscopic level.
  • Template Sentence 1: On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
  • Template Sentence 2: The most important histopathological characteristics of [disease name] are summarized in the table below:
Organs Light microscope Electron microscope Images
Organ 1 Characteristic 1a Characterstic 1b Image 1
Organ 2 Characteristic 2a Characterstic 2b Image 2
Organ 3 Characterstic 3a Characterstic 3b Image 3
  • This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki [3] and Ask Dr. Wiki [4].
  • For an example of this section, click here.

References

  • References should be cited for the material that you have put on your page. Type in {{reflist|2}}.This will generate your references in small font, in two columns, with links to the original article and abstract.
  • For information on how to add references into your page, click here.


Template:WikiDoc Sources

  1. ↑ 1.0 1.1 1.2 1.3 "Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM".
  2. ↑ url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307 |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}
  3. ↑ Kusters JG, van Vliet AH, Kuipers EJ (2006). "Pathogenesis of Helicobacter pylori infection". Clin. Microbiol. Rev. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
  4. ↑ url=http://www.nejm.org/doi/full/10.1056/NEJM199003293221307 |title=Pathogenesis of Peptic Ulcer and Implications for Therapy — NEJM |format= |work= |accessdate=}}
  5. ↑ Logan RP (1996). "Adherence of Helicobacter pylori". Aliment. Pharmacol. Ther. 10 Suppl 1: 3–15. PMID 8730255.
  6. ↑ Crabtree JE (1996). "Gastric mucosal inflammatory responses to Helicobacter pylori". Aliment. Pharmacol. Ther. 10 Suppl 1: 29–37. PMID 8730257.
  7. ↑ Ernst PB, Jin Y, Reyes VE, Crowe SE (1994). "The role of the local immune response in the pathogenesis of peptic ulcer formation". Scand. J. Gastroenterol. Suppl. 205: 22–8. PMID 7863238.
  8. ↑ Mobley HL (1996). "The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration". Aliment. Pharmacol. Ther. 10 Suppl 1: 57–64. PMID 8730260.
  9. ↑ Nilius M, Malfertheiner P (1996). "Helicobacter pylori enzymes". Aliment. Pharmacol. Ther. 10 Suppl 1: 65–71. PMID 8730261.
  10. ↑ Slomiany BL, Kasinathan C, Slomiany A (1989). "Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol)". Am. J. Gastroenterol. 84 (10): 1273–7. PMID 2801678.
  11. ↑ Borody TJ, George LL, Brandl S, Andrews P, Ostapowicz N, Hyland L, Devine M (1991). "Helicobacter pylori-negative duodenal ulcer". Am. J. Gastroenterol. 86 (9): 1154–7. PMID 1882793.
  12. ↑ Huang JQ, Sridhar S, Hunt RH (2002). "Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis". Lancet. 359 (9300): 14–22. doi:10.1016/S0140-6736(02)07273-2. PMID 11809181.
  13. ↑ Quimby GF, Bonnice CA, Burstein SH, Eastwood GL (1986). "Active smoking depresses prostaglandin synthesis in human gastric mucosa". Ann. Intern. Med. 104 (5): 616–9. PMID 3457547.
  14. ↑ Müller-Lissner SA (1986). "Bile reflux is increased in cigarette smokers". Gastroenterology. 90 (5 Pt 1): 1205–9. PMID 3956939.
  15. ↑ el-Omar EM, Penman ID, Ardill JE, Chittajallu RS, Howie C, McColl KE (1995). "Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease". Gastroenterology. 109 (3): 681–91. PMID 7657096.
  16. ↑ el-Omar E, Penman I, Dorrian CA, Ardill JE, McColl KE (1993). "Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer". Gut. 34 (8): 1060–5. PMC 1374354. PMID 8174954.
  17. ↑ Wyatt JI, Rathbone BJ, Dixon MF, Heatley RV (1987). "Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis". J. Clin. Pathol. 40 (8): 841–8. PMC 1141122. PMID 3654985.
  18. ↑ Malaty HM, Graham DY, Isaksson I, Engstrand L, Pedersen NL (2000). "Are genetic influences on peptic ulcer dependent or independent of genetic influences for Helicobacter pylori infection?". Arch. Intern. Med. 160 (1): 105–9. PMID 10632311.
  19. ↑ Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, Borodovsky M, Rappuoli R, Covacci A (1996). "cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors". Proc. Natl. Acad. Sci. U.S.A. 93 (25): 14648–53. PMC 26189. PMID 8962108.
  20. ↑ Azuma T, Konishi J, Ito Y, Hirai M, Tanaka Y, Ito S, Kato T, Kohli Y (1995). "Genetic differences between duodenal ulcer patients who were positive or negative for Helicobacter pylori". J. Clin. Gastroenterol. 21 Suppl 1: S151–4. PMID 8775009.
  21. ↑ Jung DH, Kim JH, Chung HS, Park JC, Shin SK, Lee SK, Lee YC (2015). "Helicobacter pylori Eradication on the Prevention of Metachronous Lesions after Endoscopic Resection of Gastric Neoplasm: A Meta-Analysis". PLoS ONE. 10 (4): e0124725. doi:10.1371/journal.pone.0124725. PMC 4411104. PMID 25915048.
  22. ↑ Nakamura S, Sugiyama T, Matsumoto T, Iijima K, Ono S, Tajika M, Tari A, Kitadai Y, Matsumoto H, Nagaya T, Kamoshida T, Watanabe N, Chiba T, Origasa H, Asaka M (2012). "Long-term clinical outcome of gastric MALT lymphoma after eradication of Helicobacter pylori: a multicentre cohort follow-up study of 420 patients in Japan". Gut. 61 (4): 507–13. doi:10.1136/gutjnl-2011-300495. PMID 21890816.
  23. ↑ {{cite journal |vauthors=Neunert C, Lim W, Crowther M, Cohen A, Solberg L, Crowther MA |title=The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia |journal=Blood |volume=117 |issue=16 |pages=4190–207 |year=2011 |
  24. ↑ name="urlAmerican Journal of Gastroenterology - ACG Clinical Guideline: Treatment of Helicobacter pylori Infection">"American Journal of Gastroenterology - ACG Clinical Guideline: Treatment of Helicobacter pylori Infection".
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