Barrett's esophagus pathophysiology: Difference between revisions
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* [[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 [[hind-gut]] [[intestinal]] [[derivation]]) [[has]] [[also]] [[been]] [[utilized]] [[to]] [[identify]] [[true]] [[intestinal-type metaplastic cells]]. | * [[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 [[hind-gut]] [[intestinal]] [[derivation]]) [[has]] [[also]] [[been]] [[utilized]] [[to]] [[identify]] [[true]] [[intestinal-type metaplastic cells]]. | ||
* In the [[United States]], it is estimated that 8 - 12% of [[patients]] who are diagnosed with Barrett's esophagus have been [[misdiagnosed]]. | * [[In]] [[the]] [[United States]], [[it]] [[is]] [[estimated]] [[that]] 8 - 12% [[of]] [[patients]] [[who]] [[are]] [[diagnosed]] [[with]] [[Barrett's esophagus]] [[have]] [[been]] [[misdiagnosed]]. [[This]] [[significant]] [[diagnostic]] [[error]] [[may]] [[result]] [[in]] [[higher]] [[rates]] [[of]] [[medical]] [[and]] [[life]] [[insurance]] [[rates]] [[for]] [[those]] [[misdiagnosed]]; [[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]]. | ||
* 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. | * 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. | ||
Revision as of 15:33, 3 November 2017
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Barrett's Esophagus Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Barrett's esophagus pathophysiology On the Web |
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American Roentgen Ray Society Images of Barrett's esophagus pathophysiology |
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Risk calculators and risk factors for Barrett's esophagus pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amresh Kumar MD [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
- Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium & mdash; 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.[1]
- 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 intestines). 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.
- 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 cells in the epithelium and is necessary for the true diagnosis of Barrett's.
- 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 hind-gut intestinal derivation) has also been utilized to identify true intestinal-type metaplastic cells.
- In the United States, it is estimated that 8 - 12% of patients who are diagnosed with Barrett's esophagus have been misdiagnosed. This significant diagnostic error may result in higher rates of medical and life insurance rates for those misdiagnosed; 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.
- 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.
- 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.
- 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.
- Patients with BE tend to have more severe GERD.
- 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.
- Paull et.al. described three types of columnar epithelium that can be seen in BE:
- Gastric junctional-type epithelium which has a pitted (foveolar) surface and mucus-secreting cells.
- 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.
- Specialized intestinal (columnar) metaplasia that has a villiform surface with mucus-secreting columnar cells and goblet cells.
Pathophysiology
Pathogenesis
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].