Editing Enteritis (section)

== Causes ==

=== Immune mediated ===
[[Crohn's disease]] – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. The most common location for Crohn's disease to manifest, with or without the involvement of the [[Large intestine|colon]] or other parts of the GI tract, is in the terminal [[ileum]] (the final segment of the small intestine).<ref name=":7">{{Cite book |last1=Friedman |first1=Sonia |title=Harrison's Principles of Internal Medicine |last2=Blumberg |first2=Richard S. |publisher=McGraw Hill |year=2022 |isbn=978-1264268504 |edition=21st |location=New York |language=English |chapter=Chapter 326: Inflammatory Bowel Disease}}</ref> In 40% of cases, it is limited to the small intestine.<ref name=":1" />

=== Autoimmune ===
[[Coeliac disease]] – caused by an [[autoimmune]] reaction to gluten by genetically predisposed individuals.<ref name=":1" />

[[Eosinophilic gastroenteritis]], also known as eosinophilic enteropathy or eosinophilic enteritis<ref name=":8">{{Cite journal |last1=Pineton de Chambrun |first1=Guillaume |last2=Dufour |first2=Gaspard |last3=Tassy |first3=Barbara |last4=Rivière |first4=Benjamin |last5=Bouta |first5=Najima |last6=Bismuth |first6=Michael |last7=Panaro |first7=Fabrizio |last8=Funakoshi |first8=Natalie |last9=Ramos |first9=Jeanne |last10=Valats |first10=Jean-Christophe |last11=Blanc |first11=Pierre |date=2018-07-02 |title=Diagnosis, Natural History and Treatment of Eosinophilic Enteritis: a Review |url=https://doi.org/10.1007/s11894-018-0645-6 |journal=Current Gastroenterology Reports |language=en |volume=20 |issue=8 |pages=37 |doi=10.1007/s11894-018-0645-6 |pmid=29968127 |s2cid=49648502 |issn=1534-312X|url-access=subscription }}</ref> – a rare and [[heterogeneous condition]] where [[eosinophil]]s build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers.<ref>{{Cite journal|last1=Fleischer|first1=David M.|last2=Atkins|first2=Dan|date=2009-02-01|title=Evaluation of the patient with suspected eosinophilic gastrointestinal disease|pmid=19141341|journal=Immunology and Allergy Clinics of North America|volume=29|issue=1|pages=53–63, ix|doi=10.1016/j.iac.2008.09.002|issn=1557-8607}}</ref> It is most commonly seen in patients with a history of [[atopy]], however is overall relatively uncommon.<ref name=":2">{{Cite journal|last1=Mori|first1=Amit|last2=Enweluzo|first2=Chijioke|last3=Grier|first3=David|last4=Badireddy|first4=Madhu|date=2013-05-01|title=Eosinophilic gastroenteritis: review of a rare and treatable disease of the gastrointestinal tract|pmid=23904840|journal=Case Reports in Gastroenterology|volume=7|issue=2|pages=293–298|doi=10.1159/000354147|issn=1662-0631|pmc=3728613}}</ref>

=== Infectious enteritis ===
In Germany, 90% of cases of infectious enteritis are caused by four pathogens, [[Norovirus]], ''[[Rotavirus]]'', ''[[Campylobacter]]'', and ''[[Salmonella]]''.<ref>{{Cite journal|last1=Epple|first1=H.-J.|last2=Zeitz|first2=M.|s2cid=24574799|date=2011-09-01|title=[Infectious enteritis]|journal=Der Internist|volume=52|issue=9|pages=1038, 1040–1044, 1046|doi=10.1007/s00108-011-2862-z|issn=1432-1289|pmid=21847579}}</ref> Other common causes of infectious enteritis include bacteria such as ''[[Shigella]]'' and ''[[Escherichia coli|E. coli]],'' as well as viruses such as adenovirus, astrovirus, and calicivirus. Other less common pathogens include ''[[Bacillus cereus]]'', ''[[Clostridium perfringens]]'', ''[[Clostridioides difficile]]'', and ''[[Staphylococcus aureus]]''.<ref name=":3">{{Cite book|url=https://books.google.com/books?id=aVmRWrknaWgC|title=Textbook of Therapeutics: Drug and Disease Management|last1=Helms|first1=Richard A.|last2=Quan|first2=David J.|date=2006-01-01|publisher=Lippincott Williams & Wilkins|isbn=9780781757348}}</ref>

''[[Campylobacter jejuni]]''  is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in two-year-old and smaller children with diarrhoea.<ref name=":4">{{Cite journal|last1=Coker|first1=Akitoye O.|last2=Isokpehi|first2=Raphael D.|last3=Thomas|first3=Bolaji N.|last4=Amisu|first4=Kehinde O.|last5=Obi|first5=C. Larry|date=2016-10-14|title=Human Campylobacteriosis in Developing Countries1|pmc=2732465|journal=Emerging Infectious Diseases|volume=8|issue=3|pages=237–243|doi=10.3201/eid0803.010233|issn=1080-6040|pmid=11927019}}</ref> It has been linked to consumption of contaminated water and food, most commonly poultry and milk.<ref>{{Cite journal|last1=Colles|first1=F. M.|last2=McCarthy|first2=N. D.|last3=Howe|first3=J. C.|last4=Devereux|first4=C. L.|last5=Gosler|first5=A. G.|last6=Maiden|first6=M. C. J.|date=2009-01-01|title=Dynamics of Campylobacter colonization of a natural host, Sturnus vulgaris (European Starling)|journal=Environmental Microbiology|volume=11|issue=1|pages=258–267|doi=10.1111/j.1462-2920.2008.01773.x|issn=1462-2920|pmid=18826435|pmc=2702492|bibcode=2009EnvMi..11..258C }}</ref><ref>{{Cite journal|last=Peterson|first=Michael C.|date=2003-05-01|title=Campylobacter jejuni enteritis associated with consumption of raw milk|pmid=12762121|journal=Journal of Environmental Health|volume=65|issue=9|pages=20–21, 24, 26|issn=0022-0892}}</ref> The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.<ref name=":4" />

Rotavirus is responsible for infecting 140&nbsp;million people and causing 1&nbsp;million deaths each year, mostly in children younger than five years.<ref name=":1" /><ref name=":5">{{Cite journal|last=Ramig|first=Robert F.|date=2004-10-01|title=Pathogenesis of intestinal and systemic rotavirus infection|pmid=15367586|journal=Journal of Virology|volume=78|issue=19|pages=10213–10220|doi=10.1128/JVI.78.19.10213-10220.2004|issn=0022-538X|pmc=516399}}</ref> This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world.<ref name=":1" /> It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility.<ref name=":5" /> The net result of these changes is induced diarrhoea.<ref name=":5" />

[[Clostridial necrotizing enteritis|Enteritis necroticans]] is an often fatal illness, caused by [[β-toxin]] of ''Clostridium perfringens''.<ref name=":6">{{Cite journal|last1=Petrillo|first1=T. M.|last2=Beck-Sagué|first2=C. M.|last3=Songer|first3=J. G.|last4=Abramowsky|first4=C.|last5=Fortenberry|first5=J. D.|last6=Meacham|first6=L.|last7=Dean|first7=A. G.|last8=Lee|first8=H.|last9=Bueschel|first9=D. M.|date=2000-04-27|title=Enteritis necroticans (pigbel) in a diabetic child|pmid=10781621|journal=The New England Journal of Medicine|volume=342|issue=17|pages=1250–1253|doi=10.1056/NEJM200004273421704|issn=0028-4793|doi-access=free}}</ref> This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in [[Developing country|developing countries]]; however, it has also been documented in [[Aftermath of World War II|post-World War II]] [[Germany]].<ref name=":6" /> Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.<ref name=":6" />

=== Vascular disease ===
Ischemic enteritis is uncommon compared to ischemic colitis due to the highly vascularised nature of the small intestine,<ref name=":0">{{Cite journal|last1=Koshikawa|first1=Yorimitsu|last2=Nakase|first2=Hiroshi|last3=Matsuura|first3=Minoru|last4=Yoshino|first4=Takuya|last5=Honzawa|first5=Yusuke|last6=Minami|first6=Naoki|last7=Yamada|first7=Satoshi|last8=Yasuhara|first8=Yumiko|last9=Fujii|first9=Shigehiko|date=2016-10-12|title=Ischemic enteritis with intestinal stenosis|pmc=4754528|journal=Intestinal Research|volume=14|issue=1|pages=89–95|doi=10.5217/ir.2016.14.1.89|issn=1598-9100|pmid=26884740}}</ref> allowing for sufficient blood flow in most situations. It develops due to [[Shock (circulatory)|circulatory shock]] of mesenteric vessels in the absence of major vessel occlusion, often associated with an underlying condition such as hypertension, arrhythmia, or diabetes.<ref name=":0" /> Thus, it has been considered to be associated with atherosclerosis.<ref>{{Cite journal|last1=Takeuchi|first1=Nobuhiro|last2=Naba|first2=Kazuyoshi|date=2013-01-01|title=Small intestinal obstruction resulting from ischemic enteritis: a case report|pmc=3751282|journal=Clinical Journal of Gastroenterology|volume=6|issue=4|pages=281–286|doi=10.1007/s12328-013-0393-y|issn=1865-7257|pmid=23990850}}</ref> Surgical treatment is usually required due to the likelihood of stenosis or complete occlusion of the small intestine.<ref name=":0" /> Ischemic damage can range from [[Mucous membrane|mucosal]] [[infarction]], which is limited only to the mucosa; mural infarction of the mucosa and underlying [[submucosa]]; to transmural infarction of the full thickness of the gastrointestinal wall. Mucosal and mural infarcts in and of themselves may not be fatal, however may progress further to a transmural infarct.<ref name=":1">{{Cite book|title=Robbins Basic Pathology|last1=Kumar|first1=Vinay|last2=Abbas|first2=Abul K.|last3=Aster|first3=Jon C.|last4=Robbins|first4=Stanley L.|publisher=Elsevier/Saunders|year=2012|isbn=9781437717815|location=Philadelphia, PA|edition=9th}}</ref> This has the potential for perforation of the wall, leading to [[peritonitis]].{{citation needed|date=June 2022}}

=== Radiation enteritis ===
{{Main|Radiation enteropathy}}

Inflammation of the gastrointestinal tract is common after treatment with radiation therapy to the abdomen or pelvis.<ref name = radiation>{{Cite journal|last1=Hauer-Jensen|first1=Martin|last2=Denham|first2=James W.|last3=Andreyev|first3=H. Jervoise N.|date=2016-10-14 |title= Radiation Enteropathy – Pathogenesis, Treatment, and Prevention|pmc=4346191|journal=Nature Reviews. Gastroenterology & Hepatology|volume=11 |issue= 8|pages=470–479|doi=10.1038/nrgastro.2014.46|issn=1759-5045|pmid=24686268}}</ref> It is classified as early if it manifests within the first three months, and delayed if it manifests three months after treatment. Early radiation enteritis is caused by cell death of the [[Intestinal gland|crypt epithelium]] and subsequent mucosal inflammation, however usually subsides after the course of radiation therapy is completed. Delayed radiation enteritis is a chronic disease which has a complex pathogenesis involving changes in the majority of the intestinal wall.<ref name = radiation/><ref>{{cite journal |vauthors=Stacey R, Green JT |title=Radiation-induced small bowel disease: latest developments and clinical guidance |journal=Ther Adv Chronic Dis |volume=5 |issue=1 |pages=15–29 |year=2014 |pmid=24381725 |pmc=3871275 |doi=10.1177/2040622313510730 }}</ref>