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| {{DiseaseDisorder infobox | | | __NOTOC__ |
| Name = Barrett's esophagus |
| | {{Barrett's esophagus}} |
| Image = Barretts esophagus.jpg |
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| Caption = Endoscopic image of '''Barrett's esophagus''', which is the area of red mucosa projecting like a tongue. Biopsies showed intestinal metaplasia. |
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| ICD10 = {{ICD10|K|22|7|k|20}} |
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| ICD9 = {{ICD9|530.85}} |
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| ICDO = |
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| OMIM = 109350 |
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| MedlinePlus = 001143 |
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| eMedicineSubj = radio |
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| eMedicineTopic = 73 |
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| DiseasesDB = 1246 |
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| }} | |
| {{SI}}
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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
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| {{CMG}} | | {{CMG}}; {{AE}} {{AMK}}, {{MKK}}, {{HQ}} |
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| '''Barrett's esophagus''' (sometimes called '''[[Barrett's syndrome]]''', '''[[CELLO]]''', columnar epithelium lined lower (o)esophagus or colloquially as '''[[Barrett's]]''') refers to an abnormal change ([[metaplasia]]) in the cells of the lower end of the [[esophagus]] thought to be caused by damage from chronic acid exposure, or [[reflux esophagitis]].<ref name=Stein_1993>{{cite journal |author=Stein H, Siewert J |title=Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management |journal=Dysphagia |volume=8 |issue=3 |pages=276-88 |year=1993 |pmid=8359051}}</ref> Barrett's esophagus is found in about 10% of patients who seek medical care for heartburn ([[gastroesophageal reflux]]). It is considered to be a [[premalignant condition]] and is associated with an increased risk of [[esophageal cancer]].<ref name=Koppert_2005>{{cite journal |author=Koppert L, Wijnhoven B, van Dekken H, Tilanus H, Dinjens W |title=The molecular biology of esophageal adenocarcinoma |journal=J Surg Oncol |volume=92 |issue=3 |pages=169-90 |year=2005 |pmid=16299787}}</ref>
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| == Definition == | | {{SK}} Barrett's syndrome; CELLO; gastric metaplasia of esophagus |
| | ==[[Barrett's esophagus overview|Overview]]== |
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| Barrett’s esophagus is a condition in which abnormal columnar epithelium replaces the normal squamous epithelium in the distal esophagus (metaplasia). The typical appearance is that of salmon pink segments of columnar epithelium extending above the GE (gastroenterology) junction, into the whitish squamous epithelium that is typically present in the distal esophagus. This can be seen on EGD (esophago-gastroduodenoscopy) in ~ 1 % of all patients, but in up to 20 % of those with symptoms of GERD (Gastroesophageal Reflux Disease). Although the diagnosis can be presumed during the EGD, it needs to be confirmed by biopsy.
| | ==[[Barrett's esophagus historical perspective|Historical Perspective]]== |
| * Unfortunately, there is a lot of debate as to where the esophagus ends. Anatomists, radiologists, physiologists and endoscopists can’t agree on the location of the GE junction, and this ‘line’ can vary by several centimeters depending on who defines it.
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| *:* Criteria differ from as little as 2 cm, to as much as 5 cm of abnormal epithelium needed to make the diagnosis.
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| * Paull et.al. described three types of columnar epithelium that can be seen in BE:
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| *:* Gastric junctional-type epithelium which has a pitted (foveolar) surface and mucus-secreting cells.
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| *:* Gastric fundus-type epithelium that also has a pitted surface lined by mucus-secreting cells, in addition to having a deeper glandular layer that contains chief and parietal cells.
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| *:* Specialized intestinal (columnar) metaplasia that has a villiform surface with mucus-secreting columnar cells and goblet cells.
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| *:*:* This is the most common type of epithelial change that is associated with BE, and is also the type associated with the development of adenocarcinoma.
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| * Additionally, although the risk of developing adeno carcinoma with ‘extensive’ BE is clear, the risk is not defined for ‘short segment’ BE (< 2 – 3 cm of metaplasia).
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| * It appears that chronic GE reflux is causes the injury – repair cycle that stimulates squamous metaplasia. The columnar cells are more resistant to acid injury than the squamous cells.
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| *:* Patients with BE tend to have more severe GERD.
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| * Although one would think that BE develops over years, with slow replacement of squamous cells by columnar cells, it appears that this is not the case. BE tends to develop all at once with little or no progression. The reason for this is unknown.
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| ==Etymology== | | ==[[Barrett's esophagus classification|Classification]]== |
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| The condition is named after Dr. Norman Barrett (1903–1979), Australian-born British surgeon at [[St Thomas' Hospital]], who described the condition in 1957.<ref name=Barrett_1957>{{cite journal |author=Barrett N |title=The lower esophagus lined by columnar epithelium |journal=Surgery |volume=41 |issue=6 |pages=881-94 |year=1957 |pmid=13442856}}</ref>
| | ==[[Barrett's esophagus pathophysiology|Pathophysiology]]== |
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| Norman Barrett, in 1950, defined the esophagus as, ‘that part of the foregut, distal to the cricopharyngeal sphincter, which is lined by squamous epithelium’. It is ironic, then, that columnar metaplasia of the esophagus is referred to as Barrett’s esophagus (BE). Tileston, however, was the first to describe columnar metaplasia of the esophagus in 1906, as ‘peptic ulcer of the esophagus’.
| | ==[[Barrett's esophagus causes|Causes]]== |
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| ==Causes and Symptoms== | | ==[[Barrett's esophagus differential diagnosis|Differentiating Barrett's Esophagus from other Diseases]]== |
| Barrett's esophagus is caused by [[gastroesophageal reflux disease]], which allows the stomach's contents to damage the cells lining the lower esophagus. However, not every person who has GERD will develop Barrett's esophagus. Researchers are unable to predict which heartburn sufferers will develop Barrett's esophagus. While there is no relationship between the severity of heartburn and the development of Barrett's esophagus, there is a relationship between chronic heartburn and the development of Barrett's esophagus. Sometimes people with Barrett's esophagus will have no heartburn symptoms at all. 25 % of patients are asymptomatic, and BE is picked up when EGD is performed for other, unrelated conditions. The radiographic appearance of BE is neither sensitive or specific, however certain findings are suggestive.
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| In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as [[lye]].
| | ==[[Barrett's esophagus epidemiology and demographics|Epidemiology and Demographics]]== |
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| The change from normal to premalignant cells that indicates Barrett's esophagus does not cause any particular symptoms. However, warning signs that should not be ignored include:
| | ==[[Barrett's esophagus risk factors|Risk Factors]]== |
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| * frequent and longstanding heartburn
| | ==[[Barrett's esophagus screening|Screening]]== |
| * trouble swallowing (dysphagia)
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| * vomiting blood
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| * pain under the breastbone where the esophagus meets the stomach
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| * unintentional weight loss because eating is painful
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| == Pathology == | | ==[[Barrett's esophagus natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| Barrett's esophagus is marked by the presence of [[columnar epithelia]] in the lower esophagus, replacing the normal [[squamous cell]] epithelium—an example of [[metaplasia]]. The columnar epithelium is better able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased cancer risk of the [[adenocarcinoma]] type.<ref name=Fléjou_2005>{{cite journal |author=Fléjou J |title=Barrett's oesophagus: from metaplasia to dysplasia and cancer |journal=Gut |volume=54 Suppl 1 |issue= |pages=i6-12 |year=2005 |pmid=15711008}}</ref> | | ==Diagnosis== |
| | [[Barrett's esophagus history and symptoms|History and Symptoms]] | [[Barrett's esophagus physical examination |Physical Examination]] | [[Barrett's esophagus laboratory findings|Laboratory Findings]] | [[Barrett's esophagus endoscopy|Endoscopy]] | [[Barrett's esophagus other imaging findings|Other Imaging Findings]] | [[Barrett's esophagus other diagnostic studies|Other Diagnostic Studies]] |
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| The metaplastic columnar cells may be of two types: gastric (similar to those in the [[stomach]], which is NOT technically Barrett's esophagus) or colonic (similar to cells in the [[intestine]]s). A biopsy of the affected area will often contain a mixture of the two. Colonic-type metaplasia is the type of metaplasia associated with risk of malignancy in genetically susceptible people.
| | ==Treatment== |
| | [[Barrett's esophagus medical therapy|Medical Therapy]] | [[Barrett's esophagus surgery|Surgery]] | [[Barrett's esophagus endoscopic therapy|Endoscopic Therapy]] | [[Barrett's esophagus primary prevention|Primary Prevention]] | [[Barrett's esophagus secondary prevention|Secondary Prevention]] | [[Barrett's esophagus cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Barrett's esophagus future or investigational therapies|Future or Investigational Therapies]] |
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| The metaplasia of Barrett's esophagus is visible grossly through a [[gastroscope]], but biopsy specimens must be examined under a [[microscope]] to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding [[goblet cell]]s in the epithelium and is necessary for the true diagnosis of Barrett's.
| | ==Case Studies== |
| | | [[Barrett's esophagus case study one|Case#1]] |
| There are many histologic mimics of Barrett's esophagus (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar (gastric) type mucin simulates the acid mucin true goblet cells). Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true Barrett's esophagus (specialized columnar metaplasia). Use of the histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been utilized to identify true intestinal-type metaplastic cells.
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| In the United States, it is estimated that 8 - 12% of patients who are diagnosed with Barrett's esophagus have been mis-diagnosed. This significant diagnostic error may result in higher rates of medical and life insurance rates for those mis-diagnosed; as well as enrollment of patients in unnecessary surveillance programs (i.e. annual endoscopic evaluation and biopsy to monitor for the development of Barrett's esophagus). Second (consulting) opinions on pathologic materials are easily available as slides and tissue blocks are retained for 10 and 20 years, respectively. To request a consultation opinion, patients may contact their gastroenterologist for referral to a GI pathology specialty center.
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| After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of dysplasia. There is considerable variability in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high grade dysplasia in Barrett's be confirmed by at least two fellowship trained GI pathologists prior to definitive treatment for patients.
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| Recent evidence has pointed to a similar condition developing in the distal gut epithelium. Barrett's Anus is a metaplastic change in the distal rectum whose cellularity is similar to that of the gastric mucosa. While the condition is stable for many years, there has been recent evidence to show that it is the predisposing lesion to both anal teratoma and squamous cell carcinoma of the anus. Frequent bouts of [[steatorrhea]] are commonly cited as the most likely cause of Barrett's Anus, but much more research needs to be done in order to rule out causes such as HPV 8,13.
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| == Treatment == | |
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| Current recommendations include routine [[endoscopy]] and [[biopsy]] (looking for [[dysplastic change]]s) every 12 months or so while the underlying reflux is controlled with [[proton pump inhibitor]] drugs in combination with measures to prevent reflux. Proton pump inhibitor drugs have not yet been proven to prevent esophageal cancer. [[Laser surgery#Medical|Laser treatment]] is used in severe dysplasia, while overt malignancy may require [[surgery]], [[radiation therapy]], or systemic [[chemotherapy]]. There is presently no reliable way to determine which patients with Barrett's esophagus will go on to develop esophageal cancer, although a recent study found that the detection of three different genetic abnormalities were associated with as much as a 79% chance of developing cancer in 6 years.<ref name=Galipeau_2007>{{cite journal |author=Galipeau P, Li X, Blount PL, Maley CC, Sanchez CA Odze RD, Ayub K, Rabinovitch PS, Vaughan TV, Reid BJ |title=NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma |joiurnal=PLoS Medicine |volume=4 |issue=2 |pages=e67 |year=2007 |pmid=17326708}}</ref> ''Endoscopic mucosal resection'' (EMR) has also been evaluated as a management technique.<ref name=Reshamwala_2006>{{cite journal |author=Reshamwala P, Darwin P |title=Endoscopic management of early gastric cancer |journal=Curr Opin Gastroenterol |volume=22 |issue=5 |pages=541-5 |year=2006 |pmid=16891887}}</ref>
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| Additionally an operation known as a ''[[Nissen fundoplication]]'' can reduce the reflux of acid from the stomach into the esophagus.<ref name=Abbas_2004>{{cite journal |author=Abbas A, Deschamps C, Cassivi SD, et al. |title=The role of laparoscopic fundoplication in Barrett’s esophagus |journal=Annals of Thoracic Surgery |volume=77 |issue=2 |pages=393-396 |year=2004 |pmid=14759403}}</ref>
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| In a variety of studies, non-steroidal anti-inflammatory drugs ([[NSAIDS]]), like [[Aspirin | aspirin]], have shown evidence of preventing esophageal cancer in Barrett's esophagus patients.<ref name=Corley_2003>{{cite journal |author=Corley DA, Kerlikowske K, Verma R, Buffler P |title=Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. |journal=Gastroenterology |volume=124 |pages=47-56 |year=2003 |pmid=12512029}}</ref><ref name=Vaughan_2005>{{cite journal |author=Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, Sanchez, CA, Rabinovitch PS, Reid BJ |title=Non-steroidal anti-inflammatory drugs and risk of neoplastic progression in Barrett's oesophagus: a prospective study |journal=Lancet Oncol |volume=6 |pages=945-52 |year=2005 |pmid=16321762}}</ref> However, none of these studies have been [[Randomized controlled trials | randomized, placebo controlled trials]], which are considered the gold standard for evaluating a medical intervention. In addition, the best dose of NSAIDs for cancer prevention is not yet known.
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| == Surgery and Device Based Therapy ==
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| * It seems that surgical therapy for BE / GERD may be superior to medical therapy (based on studies with 1 – 2 years of f/u in the medical arms).
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| * The next step is routine endoscopy to identify dysplasia. Patients with BE develop malignancy at a rate of 1 % / year. There are no studies, however, that correlate the presence of BE with a reduced survival. However, this may be due to the fact that the studies were carried out in an older population that died of disease other than esophageal CA, routine EGD is still recommended.
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| == Epidemiology and Demographics ==
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| * BE can be seen in younger patients, but is most commonly diagnosed in patients ~ 55 years old.
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| * It is more common in whites, than blacks or Asians, and males are more frequently affected than females.
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| == References ==
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| {{Reflist|2}}
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| == External links == | | == External links == |
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| * [http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/ Barrett's Esophagus] at [[National Institute of Diabetes and Digestive and Kidney Diseases]] (NIDDKD) | | * [http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/ Barrett's Esophagus] at [[National Institute of Diabetes and Digestive and Kidney Diseases]] (NIDDKD) |
| * [http://www.barrettsinfo.com/ Barrett's Info] a peer-reviewed web site of information on Barrett's esophagus and its clinical management.
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| * [http://pathology2.jhu.edu/beweb/ Barrett's Esophagus] at [[Johns Hopkins University]]
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| * [http://www.mayoclinic.org/barretts-esophagus/index.html Barrett's Esophagus Video Overview] and [http://www.mayoclinic.com/health/barretts-esophagus/HQ00312 Barrett's Esophagus Health Information] at [[Mayo Clinic]]
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| * [http://www.barrettsfoundation.org.uk The Barrett's Oesophagus Foundation] The UK charity committed to research into prevention of adenocarcinoma of the oesophagus
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| {{Gastroenterology}} | | {{Gastroenterology}} |
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| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| | [[Category:Disease]] |
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