Barrett's esophagus pathophysiology

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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

  • 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].

References

  1. Fléjou J (2005). "Barrett's oesophagus: from metaplasia to dysplasia and cancer". Gut. 54 Suppl 1: i6–12. PMID 15711008.

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