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{{Peptic ulcer}}
{{Peptic ulcer}}
{{CMG}} ;{{AE}} {{MKK}}
{{CMG}} ;{{AE}}:{{MKK}}
 
==Overview==
==Overviews==
Common risk factors in the development of [[peptic ulcer disease]] include [[infection]] from [[Helicobacter pylori]], chronic use of [[NSAID]]s, [[cigarette smoking]], alcolhol intake, family history of [[peptic ulcer]], and age >50 years. Less common risk factors in the development of [[peptic ulcer disease]] include  [[psychological stress]], nosocomial stress [[ulcers]], and [[coagulopathy]]. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, [[mastocytosis]], or a retained antrum following partial gastrectomy, [[gastrinoma]] or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias or [[short bowel syndrome]].
Common risk factors in the development of peptic ulcer disease include chronic use of [[NSAID]]s, cigarette smoking, alcohol intake, family history of peptic ulcer, and age >50 years.


==Risk Factors==
==Risk Factors==
Despite the finding that a [[bacterial infection]] is the cause of ulcers in 80% of cases, [[bacterial infection]] does not appear to explain all ulcers and researchers continue to look at stress as a possible cause, or at least a complication in the development of ulcers.
The most potent risk factor leading to the development of [[peptic ulcer disease]] is an infection of [[Helicobacter pylori|Helicobacter pylori.]] Other risk factors include chronic use of [[NSAIDs]], family history of [[peptic ulcer|peptic ulce]]<nowiki/>r, [[tobacco smoking]], and  psychological and nosocomial stress.<ref name="pmid11809181">{{cite journal |vauthors=Huang JQ, Sridhar S, Hunt RH |title=Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis |journal=Lancet |volume=359 |issue=9300 |pages=14–22 |year=2002 |pmid=11809181 |doi=10.1016/S0140-6736(02)07273-2 |url=}}</ref><ref name="pmid11336566">{{cite journal |vauthors=Ballinger A, Smith G |title=COX-2 inhibitors vs. NSAIDs in gastrointestinal damage and prevention |journal=Expert Opin Pharmacother |volume=2 |issue=1 |pages=31–40 |year=2001 |pmid=11336566 |doi=10.1517/14656566.2.1.31 |url=}}</ref><ref name="pmid1855677">{{cite journal |vauthors=Holvoet J, Terriere L, Van Hee W, Verbist L, Fierens E, Hautekeete ML |title=Relation of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study |journal=Gut |volume=32 |issue=7 |pages=730–4 |year=1991 |pmid=1855677 |pmc=1378985 |doi= |url=}}</ref><ref name="pmid1670734">{{cite journal |vauthors=Laporte JR, Carné X, Vidal X, Moreno V, Juan J |title=Upper gastrointestinal bleeding in relation to previous use of analgesics and non-steroidal anti-inflammatory drugs. Catalan Countries Study on Upper Gastrointestinal Bleeding |journal=Lancet |volume=337 |issue=8733 |pages=85–9 |year=1991 |pmid=1670734 |doi= |url=}}</ref><ref name="pmid12948263">{{cite journal |vauthors=Wachirawat W, Hanucharurnkul S, Suriyawongpaisal P, Boonyapisit S, Levenstein S, Jearanaisilavong J, Atisook K, Boontong T, Theerabutr C |title=Stress, but not Helicobacter pylori, is associated with peptic ulcer disease in a Thai population |journal=J Med Assoc Thai |volume=86 |issue=7 |pages=672–85 |year=2003 |pmid=12948263 |doi= |url=}}</ref><ref name="pmid12524398">{{cite journal |vauthors=Rosenstock S, Jørgensen T, Bonnevie O, Andersen L |title=Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults |journal=Gut |volume=52 |issue=2 |pages=186–93 |year=2003 |pmid=12524398 |pmc=1774958 |doi= |url=}}</ref><ref name="pmid11876703">{{cite journal |vauthors=Stack WA, Atherton JC, Hawkey GM, Logan RF, Hawkey CJ |title=Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding |journal=Aliment. Pharmacol. Ther. |volume=16 |issue=3 |pages=497–506 |year=2002 |pmid=11876703 |doi= |url=}}</ref><ref name="pmid9521179">{{cite journal |vauthors=Everhart JE, Byrd-Holt D, Sonnenberg A |title=Incidence and risk factors for self-reported peptic ulcer disease in the United States |journal=Am. J. Epidemiol. |volume=147 |issue=6 |pages=529–36 |year=1998 |pmid=9521179 |doi= |url=}}</ref>
 
An expert panel convened by the Academy of Behavioral Medicine research concluded that ulcers are not purely an [[infectious disease]] and that psychological factors do play a significant role. Researchers are examining how stress might promote ''H. pylori'' infection.  For example, ''Helicobacter pylori'' thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid.
 
The discovery that ''Helicobacter pylori'' is a cause of peptic ulcer has tempted many to conclude that psychological factors are unimportant. But this is dichotomised thinking. There is solid evidence that psychological stress triggers many ulcers and impairs response to treatment, while helicobacter is inadequate as a monocausal explanation as most infected people do not develop ulcers. Psychological stress probably functions most often as a cofactor with ''H pylori''. It may act by stimulating the production of [[gastric acid]] or by promoting behavior that causes a risk to health. Unravelling the aetiology of peptic ulcer will make an important contribution to the biopsychosocial model of disease.<ref name="bmj">{{cite web | url= http://bmj.bmjjournals.com/cgi/content/full/316/7130/538| title=Stress and peptic ulcer: life beyond helicobacter|accessdate=2007-08-26}}</ref>
 
A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor (PMID 12948263).
 
A study on mice showed that both long-term water-immersion-restraint stress and ''H. pylori'' infection were independently associated with the development of peptic ulcers (PMID 12465722).
 
The following factor raises the risk of peptic ulcer:
* Episode of [[H. pylori]] infection.
* Chronic use [[NSAID]]s.
* [[Cigarette]]s/[[Alcohol]] intake.
* Family history of peptic ulcer.
* Age 50 years or more.
There are no established risk factors for [disease name].
 
OR
 
The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
 
OR
 
Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
 
OR
 
Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
==Risk Factors==
*The most potent risk factor in the development of peptic ulcer disease is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
 
*Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
===Common Risk Factors===
*Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
*Common risk factors in the development of [disease name] include:
**[Risk factor 1]
**[Risk factor 2]
**[Risk factor 3]


=== Common risk factors ===
Common risk factors in the development of peptic ulcer disease include:
*[[Helicobacter pylori infection]]
*Chronic use of [[NSAIDs]]
*Family history of [[peptic ulcer]]
===Less Common Risk Factors===
===Less Common Risk Factors===
*Less common risk factors in the development of [disease name] include:
Less common risk factors in the development of [[peptic ulcer disease]] include:
**[Risk factor 1]
*[[Tobacco]]
**[Risk factor 2]
*[[Alcohol]]
**[Risk factor 3]
*[[Psychological stress]]
*Nosocomial stress [[ulcers]] due the to the use of [[mechanical ventilation]] for more than 48 hours, and [[coagulopathy]]
*Rare conditions associated with [[Gastric acid|gastric acid hypersecretion]] such as:
**[[Zollinger-Ellison syndrome]], [[mastocytosis]], or a retained antrum following partial [[gastrectomy]]
**[[gastrinoma]] or [[multiple endocrine neoplasia]] types I (MEN-I), antral G cell hyperplasia, [[basophilic]] [[leukemias]], [[short bowel syndrome]]


==References==
==References==
{{reflist|2}}
{{reflist|2}}
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Latest revision as of 23:38, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: :Manpreet Kaur, MD [2]

Overview

Common risk factors in the development of peptic ulcer disease include infection from Helicobacter pylori, chronic use of NSAIDs, cigarette smoking, alcolhol intake, family history of peptic ulcer, and age >50 years. Less common risk factors in the development of peptic ulcer disease include psychological stress, nosocomial stress ulcers, and coagulopathy. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy, gastrinoma or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias or short bowel syndrome.

Risk Factors

The most potent risk factor leading to the development of peptic ulcer disease is an infection of Helicobacter pylori. Other risk factors include chronic use of NSAIDs, family history of peptic ulcer, tobacco smoking, and psychological and nosocomial stress.[1][2][3][4][5][6][7][8]

Common risk factors

Common risk factors in the development of peptic ulcer disease include:

Less Common Risk Factors

Less common risk factors in the development of peptic ulcer disease include:

References

  1. 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.
  2. Ballinger A, Smith G (2001). "COX-2 inhibitors vs. NSAIDs in gastrointestinal damage and prevention". Expert Opin Pharmacother. 2 (1): 31–40. doi:10.1517/14656566.2.1.31. PMID 11336566.
  3. Holvoet J, Terriere L, Van Hee W, Verbist L, Fierens E, Hautekeete ML (1991). "Relation of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study". Gut. 32 (7): 730–4. PMC 1378985. PMID 1855677.
  4. Laporte JR, Carné X, Vidal X, Moreno V, Juan J (1991). "Upper gastrointestinal bleeding in relation to previous use of analgesics and non-steroidal anti-inflammatory drugs. Catalan Countries Study on Upper Gastrointestinal Bleeding". Lancet. 337 (8733): 85–9. PMID 1670734.
  5. Wachirawat W, Hanucharurnkul S, Suriyawongpaisal P, Boonyapisit S, Levenstein S, Jearanaisilavong J, Atisook K, Boontong T, Theerabutr C (2003). "Stress, but not Helicobacter pylori, is associated with peptic ulcer disease in a Thai population". J Med Assoc Thai. 86 (7): 672–85. PMID 12948263.
  6. Rosenstock S, Jørgensen T, Bonnevie O, Andersen L (2003). "Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults". Gut. 52 (2): 186–93. PMC 1774958. PMID 12524398.
  7. Stack WA, Atherton JC, Hawkey GM, Logan RF, Hawkey CJ (2002). "Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding". Aliment. Pharmacol. Ther. 16 (3): 497–506. PMID 11876703.
  8. Everhart JE, Byrd-Holt D, Sonnenberg A (1998). "Incidence and risk factors for self-reported peptic ulcer disease in the United States". Am. J. Epidemiol. 147 (6): 529–36. PMID 9521179.

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