Editing Duodenum (section)

==Clinical significance==
===Ulceration===
{{Main|Peptic ulcer disease}}

Ulcers of the duodenum commonly occur because of infection by the bacteria ''[[Helicobacter pylori]]''. These bacteria, through a number of mechanisms, erode the protective mucosa of the duodenum, predisposing it to damage from gastric acids. The first part of the duodenum is the most common location of ulcers since it is where the acidic chyme meets the duodenal mucosa before mixing with the alkaline secretions of the duodenum.<ref>{{cite book|last=Smith|first=Margaret E|title=The Digestive System}}</ref> Duodenal ulcers may cause recurrent abdominal pain and [[dyspepsia]], and are often investigated using a [[urea breath test]] to test for the bacteria, and [[endoscopy]] to confirm ulceration and take a [[biopsy]]. If managed, these are often managed through [[antibiotic]]s that aim to eradicate the bacteria, and [[proton-pump inhibitors]] and [[antacid]]s to reduce the gastric acidity.<ref name="DAVIDSONS2010">{{cite book |editor1-first=Nicki R. |editor1-last=Colledge |editor2-first=Brian R. |editor2-last=Walker |editor3-first=Stuart H. |editor3-last=Ralston |title=Davidson's principles and practice of medicine.|year=2010|publisher=Churchill Livingstone/Elsevier|location=Edinburgh|isbn=978-0-7020-3085-7|pages=871–874|edition=21st}}</ref>

===Celiac disease===
The [[British Society of Gastroenterology]] guidelines specify that a duodenal biopsy is required for the diagnosis of adult [[celiac disease]]. The biopsy is ideally performed at a moment when the patient is on a gluten-containing diet.<ref>{{cite journal|last1=Ludvigsson|first1=J. F.|last2=Bai|first2=J. C.|last3=Biagi|first3=F.|last4=Card|first4=T. R.|last5=Ciacci|first5=C.|last6=Ciclitira|first6=P. J.|last7=Green|first7=P. H. R.|last8=Hadjivassiliou|first8=M.|last9=Holdoway|first9=A.|last10=van Heel|first10=D. A.|last11=Kaukinen|first11=K.|last12=Leffler|first12=D. A.|last13=Leonard|first13=J. N.|last14=Lundin|first14=K. E. A.|last15=McGough|first15=N.|last16=Davidson|first16=M.|last17=Murray|first17=J. A.|last18=Swift|first18=G. L.|last19=Walker|first19=M. M.|last20=Zingone|first20=F.|last21=Sanders|first21=D. S.|title=Diagnosis and management of adult coeliac disease: Guidelines from the British Society of Gastroenterology|journal=Gut|volume=63|issue=8|year=2014|pages=1210–1228|issn=0017-5749|doi=10.1136/gutjnl-2013-306578|pmid=24917550|pmc=4112432}}</ref>

===Cancer===
Duodenal cancer is a cancer in the first section of the small intestine. Cancer of the duodenum is relatively rare compared to [[stomach cancer]] and [[colorectal cancer]]; malignant tumors in the duodenum constitute only around 0.3% of all the gastrointestinal tract tumors but around half of cancerous tissues that develop in the small intestine.<ref>{{cite book |last1=Fagniez |first1=Pierre-Louis |last2=Rotman |first2=Nelly |title= Malignant tumors of the duodenum |year=2001 |publisher=Zuckschwerdt |url=https://www.ncbi.nlm.nih.gov/books/NBK6953/}}</ref> Its histology is often observed to be [[adenocarcinoma]], meaning that the cancerous tissue arises from glandular cells in the [[epithelial tissue]] lining the duodenum.<ref>{{cite web |title=Definition of adenocarcinoma - NCI Dictionnary of Cancer Terms |url=https://www.cancer.gov/publications/dictionaries/cancer-terms/def/adenocarcinoma |access-date=12 July 2024 |website=National Cancer Institute}}</ref>

=== Obesity and Diabetes ===
A [[western diet]] induces duodenal mucosal hyperplasia and dysfunction that underlie insulin resistance, type 2 diabetes and obesity.<ref name=":1">{{Cite journal |last1=Aliluev |first1=Alexandra |last2=Tritschler |first2=Sophie |last3=Sterr |first3=Michael |last4=Oppenländer |first4=Lena |last5=Hinterdobler |first5=Julia |last6=Greisle |first6=Tobias |last7=Irmler |first7=Martin |last8=Beckers |first8=Johannes |last9=Sun |first9=Na |last10=Walch |first10=Axel |last11=Stemmer |first11=Kerstin |last12=Kindt |first12=Alida |last13=Krumsiek |first13=Jan |last14=Tschöp |first14=Matthias H. |last15=Luecken |first15=Malte D. |date=2021-09-22 |title=Diet-induced alteration of intestinal stem cell function underlies obesity and prediabetes in mice |journal=Nature Metabolism |language=en |volume=3 |issue=9 |pages=1202–1216 |doi=10.1038/s42255-021-00458-9 |issn=2522-5812 |pmc=8458097 |pmid=34552271}}</ref><ref>{{Cite journal |last1=Clara |first1=Rosmarie |last2=Schumacher |first2=Manuel |last3=Ramachandran |first3=Deepti |last4=Fedele |first4=Shahana |last5=Krieger |first5=Jean-Philippe |last6=Langhans |first6=Wolfgang |last7=Mansouri |first7=Abdelhak |date=January 2017 |title=Metabolic Adaptation of the Small Intestine to Short- and Medium-Term High-Fat Diet Exposure: INTESTINAL METABOLIC ADAPTATION TO HFD |url=https://onlinelibrary.wiley.com/doi/10.1002/jcp.25402 |journal=Journal of Cellular Physiology |language=en |volume=232 |issue=1 |pages=167–175 |doi=10.1002/jcp.25402|pmid=27061934 |url-access=subscription }}</ref> Diet-induced duodenal mucosal hyperplasia consists of increased mucosal mass,<ref>{{Cite journal |last1=Hvid |first1=Henning |last2=Jensen |first2=Stina Rikke |last3=Witgen |first3=Brent M. |last4=Fledelius |first4=Christian |last5=Damgaard |first5=Jesper |last6=Pyke |first6=Charles |last7=Rasmussen |first7=Thomas Bovbjerg |date=2016 |title=Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats |url=https://karger.com/DIG/article/doi/10.1159/000453107 |journal=Digestion |language=en |volume=94 |issue=4 |pages=199–214 |doi=10.1159/000453107 |pmid=27931035 |issn=0012-2823|url-access=subscription }}</ref> increased villus length,<ref name=":1" /><ref name=":2">{{Cite journal |last1=Taylor |first1=Samuel R. |last2=Ramsamooj |first2=Shakti |last3=Liang |first3=Roger J. |last4=Katti |first4=Alyna |last5=Pozovskiy |first5=Rita |last6=Vasan |first6=Neil |last7=Hwang |first7=Seo-Kyoung |last8=Nahiyaan |first8=Navid |last9=Francoeur |first9=Nancy J. |last10=Schatoff |first10=Emma M. |last11=Johnson |first11=Jared L. |last12=Shah |first12=Manish A. |last13=Dannenberg |first13=Andrew J. |last14=Sebra |first14=Robert P. |last15=Dow |first15=Lukas E. |date=2021-09-09 |title=Dietary fructose improves intestinal cell survival and nutrient absorption |journal=Nature |language=en |volume=597 |issue=7875 |pages=263–267 |doi=10.1038/s41586-021-03827-2 |issn=0028-0836 |pmc=8686685 |pmid=34408323}}</ref><ref>{{Cite journal |last=Dailey |first=Megan J. |date=September 2014 |title=Nutrient-induced intestinal adaption and its effect in obesity |journal=Physiology & Behavior |language=en |volume=136 |pages=74–78 |doi=10.1016/j.physbeh.2014.03.026 |pmc=4182169 |pmid=24704111}}</ref><ref>{{Cite journal |last1=Sagher |first1=F. A. |last2=Dodge |first2=J. A. |last3=Johnston |first3=C. F. |last4=Shaw |first4=C. |last5=Buchanan |first5=K. D. |last6=Carr |first6=K. E. |year=1991 |title=Rat small intestinal morphology and tissue regulatory peptides: effects of high dietary fat |url=https://www.cambridge.org/core/product/identifier/S0007114591000077/type/journal_article |journal=British Journal of Nutrition |language=en |volume=65 |issue=1 |pages=21–28 |doi=10.1079/BJN19910062 |pmid=1705145 |issn=0007-1145}}</ref> decreased crypt density,<ref name=":1" /> proliferation of enteroendocrine cells,<ref name=":3">{{Cite journal |last1=Gniuli |first1=D. |last2=Calcagno |first2=A. |last3=Dalla Libera |first3=L. |last4=Calvani |first4=R. |last5=Leccesi |first5=L. |last6=Caristo |first6=M. E. |last7=Vettor |first7=R. |last8=Castagneto |first8=M. |last9=Ghirlanda |first9=G. |last10=Mingrone |first10=G. |date=October 2010 |title=High-fat feeding stimulates endocrine, glucose-dependent insulinotropic polypeptide (GIP)-expressing cell hyperplasia in the duodenum of Wistar rats |url=http://link.springer.com/10.1007/s00125-010-1830-9 |journal=Diabetologia |language=en |volume=53 |issue=10 |pages=2233–2240 |doi=10.1007/s00125-010-1830-9 |pmid=20585935 |issn=0012-186X}}</ref> increased enterocyte mass,<ref>{{Cite journal |last1=Verdam |first1=Froukje J. |last2=Greve |first2=Jan Willem M. |last3=Roosta |first3=Sedigheh |last4=van Eijk |first4=Hans |last5=Bouvy |first5=Nicole |last6=Buurman |first6=Wim A. |last7=Rensen |first7=Sander S. |date=2011-02-01 |title=Small Intestinal Alterations in Severely Obese Hyperglycemic Subjects |url=https://academic.oup.com/jcem/article/96/2/E379/2709569 |journal=The Journal of Clinical Endocrinology & Metabolism |language=en |volume=96 |issue=2 |pages=E379–E383 |doi=10.1210/jc.2010-1333 |pmid=21084402 |issn=0021-972X}}</ref> and an accumulation of lipid droplets in the mucosa.<ref>{{Cite journal |last1=Sferra |first1=Roberta |last2=Pompili |first2=Simona |last3=Cappariello |first3=Alfredo |last4=Gaudio |first4=Eugenio |last5=Latella |first5=Giovanni |last6=Vetuschi |first6=Antonella |date=2021-07-06 |title=Prolonged Chronic Consumption of a High Fat with Sucrose Diet Alters the Morphology of the Small Intestine |journal=International Journal of Molecular Sciences |language=en |volume=22 |issue=14 |pages=7280 |doi=10.3390/ijms22147280 |doi-access=free |issn=1422-0067 |pmc=8303301 |pmid=34298894}}</ref><ref>{{Cite journal |last1=D’Aquila |first1=Theresa |last2=Zembroski |first2=Alyssa S. |last3=Buhman |first3=Kimberly K. |date=2019-03-05 |title=Diet Induced Obesity Alters Intestinal Cytoplasmic Lipid Droplet Morphology and Proteome in the Postprandial Response to Dietary Fat |journal=Frontiers in Physiology |volume=10 |page=180 |doi=10.3389/fphys.2019.00180 |doi-access=free |issn=1664-042X |pmc=6413465 |pmid=30890954}}</ref> Diet induced duodenal dysfunction  includes increased duodenal nutrient absorption,<ref name=":2" /><ref>{{Cite journal |last=Dyer |first=J. |last2=Wood |first2=I. 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P. |date=2002-02-01 |title=Expression of monosaccharide transporters in intestine of diabetic humans |url=https://www.physiology.org/doi/10.1152/ajpgi.00310.2001 |journal=American Journal of Physiology-Gastrointestinal and Liver Physiology |language=en |volume=282 |issue=2 |pages=G241–G248 |doi=10.1152/ajpgi.00310.2001 |issn=0193-1857|url-access=subscription }}</ref><ref>{{Cite journal |last=Fiorentino |first=Teresa Vanessa |last2=Suraci |first2=Evelina |last3=Arcidiacono |first3=Gaetano Paride |last4=Cimellaro |first4=Antonio |last5=Mignogna |first5=Chiara |last6=Presta |first6=Ivan |last7=Andreozzi |first7=Francesco |last8=Hribal |first8=Marta Letizia |last9=Perticone |first9=Francesco |last10=Donato |first10=Giuseppe |last11=Luzza |first11=Francesco |last12=Sesti |first12=Giorgio |date=2017-11-01 |title=Duodenal Sodium/Glucose Cotransporter 1 Expression Under Fasting Conditions Is Associated With Postload Hyperglycemia |url=https://academic.oup.com/jcem/article/102/11/3979/4117420 |journal=The Journal of Clinical Endocrinology & Metabolism |language=en |volume=102 |issue=11 |pages=3979–3989 |doi=10.1210/jc.2017-00348 |issn=0021-972X}}</ref><ref>{{Cite journal |last=Fiorentino |first=Teresa Vanessa |last2=De Vito |first2=Francesca |last3=Suraci |first3=Evelina |last4=Marasco |first4=Raffaella |last5=Hribal |first5=Marta Letizia |last6=Luzza |first6=Francesco |last7=Sesti |first7=Giorgio |date=March 2023 |title=Obesity and overweight are linked to increased sodium‐glucose cotransporter 1 and glucose transporter 5 levels in duodenum |url=https://onlinelibrary.wiley.com/doi/10.1002/oby.23653 |journal=Obesity |language=en |volume=31 |issue=3 |pages=724–731 |doi=10.1002/oby.23653 |issn=1930-7381|url-access=subscription }}</ref> altered duodenal hormone secretion,<ref name=":1" /><ref name=":3" /> and altered intestinal vagal afferent neuronal function.<ref>{{Cite journal |last1=de Lartigue |first1=Guillaume |last2=Barbier de la Serre |first2=Claire |last3=Espero |first3=Elvis |last4=Lee |first4=Jennifer |last5=Raybould |first5=Helen E. |date=2012-03-07 |editor-last=Gaetani |editor-first=Silvana |title=Leptin Resistance in Vagal Afferent Neurons Inhibits Cholecystokinin Signaling and Satiation in Diet Induced Obese Rats |journal=PLOS ONE |language=en |volume=7 |issue=3 |pages=e32967 |doi=10.1371/journal.pone.0032967 |doi-access=free |issn=1932-6203 |pmc=3296757 |pmid=22412960}}</ref>

=== Inflammation ===
Inflammation of the duodenum is referred to as [[duodenitis]]. There are multiple known causes.<ref name="pmid16679353">{{cite journal |vauthors=Serra S, Jani PA |title=An approach to duodenal biopsies |journal=J. Clin. Pathol. |volume=59 |issue=11 |pages=1133–50 |year=2006 |pmid=16679353 |pmc=1860495 |doi=10.1136/jcp.2005.031260 }}</ref> Celiac disease and inflammatory bowel disease are two of the known causes.<ref>{{Cite journal |last1=Alper |first1=Arik |last2=Hardee |first2=Steven |last3=Rojas-velasquez |first3=Danilo |last4=Escalera |first4=Sandra |last5=Morotti |first5=Raffaella A |last6=Pashankar |first6=Dinesh S. |date=February 2016 |title=Prevalence, clinical, endoscopic and pathological features of duodenitis in children |journal=Journal of Pediatric Gastroenterology and Nutrition |volume=62 |issue=2 |pages=314–316 |doi=10.1097/MPG.0000000000000942 |issn=0277-2116 |pmc=4724230 |pmid=26252915}}</ref>