Barrett's esophagus

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Barrett's esophagus
Other namesBarrett's oesophagus, Allison-Johnstone anomaly, columnar epithelium lined lower oesophagus (CELLO)
Barretts esophagus.jpg
Endoscopic image of Barrett's esophagus, which is the area of dark reddish-brown mucosa at the base of the esophagus. (Biopsies showed intestinal metaplasia.)
Specialty Gastroenterology
General surgery
Symptoms Nausea

Barrett's esophagus is a condition in which there is an abnormal (metaplastic) change in the mucosal cells lining the lower portion of the esophagus, from stratified squamous epithelium to simple columnar epithelium with interspersed goblet cells that are normally present only in the small intestine and large intestine. This change is considered to be a premalignant condition because of its potential to further transition to esophageal adenocarcinoma, an often-deadly cancer. [1] [2]

Contents

The main cause of Barrett's esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis. [3] Barrett's esophagus is diagnosed by endoscopy: observing the characteristic appearance of this condition by direct inspection of the lower esophagus; followed by microscopic examination of tissue from the affected area obtained from biopsy. The cells of Barrett's esophagus are classified into four categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma. High-grade dysplasia and early stages of adenocarcinoma may be treated by endoscopic resection or radiofrequency ablation. [4] Later stages of adenocarcinoma may be treated with surgical resection or palliation. Those with nondysplastic or low-grade dysplasia are managed by annual observation with endoscopy, or treatment with radiofrequency ablation. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater. [1]

The incidence of esophageal adenocarcinoma has increased substantially in the Western world in recent years. [1] The condition is found in 5–15% of patients who seek medical care for heartburn (gastroesophageal reflux disease, or GERD), although a large subgroup of patients with Barrett's esophagus are asymptomatic. The condition is named after surgeon Norman Barrett (1903–1979) even though the condition was originally described by Philip Rowland Allison in 1946. [5] [6] [7]

Signs and symptoms

The change from normal to premalignant cells indicate Barrett's esophagus does not cause any particular symptoms. Barrett's esophagus, however, is associated with these symptoms:

The risk of developing Barrett's esophagus is increased by central obesity (vs. peripheral obesity). [8] The exact mechanism is unclear. The difference in distribution of fat among men (more central) and women (more peripheral) may explain the increased risk in males. [9]

Pathophysiology

Histopathology of Barrett's esophagus, showing intestinalized epithelium with goblet cells, as opposed to normal stratified squamous epithelium of the esophagus, and pseudostratified columnar epithelium of the fundus of the stomach. The submucosa displays an infiltrate including lymphocytes and plasma cells, constituting an underlying chronic inflammation. The area between the stratified and the intestinalized epithelium displays reactive changes, but there is no secondary dysplasia in this case. H&E stain. Histopathology of Barrett's esophagus, annotated.jpg
Histopathology of Barrett's esophagus, showing intestinalized epithelium with goblet cells, as opposed to normal stratified squamous epithelium of the esophagus, and pseudostratified columnar epithelium of the fundus of the stomach. The submucosa displays an infiltrate including lymphocytes and plasma cells, constituting an underlying chronic inflammation. The area between the stratified and the intestinalized epithelium displays reactive changes, but there is no secondary dysplasia in this case. H&E stain.

Barrett's esophagus occurs due to chronic inflammation. The principal cause of chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. In turn, this provokes an advantage for cells more resistant to these noxious stimuli in particular HOXA13-expressing stem cells that are characterised by distal (intestinal) characteristics and outcompete the normal squamous cells. [10]

This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction.

Researchers are unable to predict who with heartburn will develop Barrett's esophagus. While no relationship exists between the severity of heartburn and the development of Barrett's esophagus, a relationship does exist between chronic heartburn and the development of Barrett's esophagus. Sometimes, people with Barrett's esophagus have no heartburn symptoms at all.

Some anecdotal evidence indicates those with the eating disorder bulimia are more likely to develop Barrett's esophagus because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid. However, a link between bulimia and Barrett's esophagus remains unproven. [11] [12]

During episodes of reflux, bile acids enter the esophagus, and this may be an important factor in carcinogenesis. [13] Individuals with GERD and BE are exposed to high concentrations of deoxycholic acid that has cytotoxic effects and can cause DNA damage. [13] [14]

Diagnosis

In incomplete Barrett's esophagus, there are both foveolar cells and goblet cells, the latter (indicated by arrows) usually having a slightly bluish color compared to the apical cytoplasm of foveolar cells on H&E stain. An occasional but specific sign of goblet cells is crescent shaped nuclei (seen in middle one). Histopathology of goblet cells (annotated) and foveolar cells in incomplete Barrett's esophagus.jpg
In incomplete Barrett's esophagus, there are both foveolar cells and goblet cells, the latter (indicated by arrows) usually having a slightly bluish color compared to the apical cytoplasm of foveolar cells on H&E stain. An occasional but specific sign of goblet cells is crescent shaped nuclei (seen in middle one).
Micrograph showing Barrett's esophagus - columnar epithelia with goblet cells - on the left side of image; and normal stratified squamous epithelium on the right side of image Alcian blue stain Barretts alcian blue.jpg
Micrograph showing Barrett's esophagus - columnar epithelia with goblet cells - on the left side of image; and normal stratified squamous epithelium on the right side of image Alcian blue stain
High-magnification micrograph of Barrett's esophagus showing the characteristic goblet cells, Alcian blue stain Barretts esophagus alcian blue high mag.jpg
High-magnification micrograph of Barrett's esophagus showing the characteristic goblet cells, Alcian blue stain

Both macroscopic (from endoscopy) and microscopic positive findings are required to make a diagnosis. 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 secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma. [15]

Screening

Endoscopic view of Barrett's esophagus showing location of biopsies for screening using the Seattle protocol Seattle Protocol Biopsies.jpg
Endoscopic view of Barrett's esophagus showing location of biopsies for screening using the Seattle protocol

Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. [16] Among those not expected to live more than five years screening is not recommended. [16]

The Seattle protocol is used commonly in endoscopy to obtain endoscopic biopsies for screening, taken every 1 to 2 cm from the gastroesophageal junction.

Since the COVID-19 pandemic In Scotland, the local NHS started using a swallowable sponge (Cytosponge) in hospitals to collect cell samples for diagnosis. [17] Preliminary studies have shown this diagnostic test to be a useful tool for screening people with heartburn symptoms and improved diagnosis. [18] [19]

Intestinal metaplasia

The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of Barrett's esophagus. This frequently occurs in the presence of other metaplastic columnar cells, but only the presence of goblet cells is diagnostic. The metaplasia is grossly visible 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. [20] [ citation needed ]

Many histologic mimics of Barrett's esophagus are known (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). 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 used to identify true intestinal-type metaplastic cells. The protein AGR2 is elevated in Barrett's esophagus [21] and can be used as a biomarker for distinguishing Barrett epithelium from normal esophageal epithelium. [22]

The presence of intestinal metaplasia in Barrett's esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barrett's esophagus. [23] Also intestinal metaplastic cells can be positive for CK 7+/CK20-. [24]

Epithelial dysplasia

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 epithelial dysplasia (or "intraepithelial neoplasia"). [25] Among all metaplastic lesions, around 8% were associated with dysplasia. particularly a recent study demonstrated that dysplastic lesions were located mainly in the posterior wall of the esophagus. [26]

Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. [15] For more accuracy and reproducibility, it is also recommended to follow international classification systems, such as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000). [27]

Management

Many people with Barrett's esophagus do not have dysplasia. Medical societies recommend that if a patient has Barrett's esophagus, and if the past two endoscopy and biopsy examinations have confirmed the absence of dysplasia, then the patient should not have another endoscopy within three years. [28] [29] [30]

Endoscopic surveillance of people with Barrett's esophagus is often recommended, although little direct evidence supports this practice. [1] Treatment options for high-grade dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction). [1]

The risk of malignancy is highest in the United States in Caucasian men over fifty years of age with more than five years of symptoms. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). Although in the past physicians have taken a watchful waiting approach, newly published research supports consideration of intervention for Barrett's esophagus. Balloon-based radiofrequency ablation, invented by Ganz, Stern, and Zelickson in 1999, is a new treatment modality for the treatment of Barrett's esophagus and dysplasia and has been the subject of numerous published clinical trials. [31] [32] [33] [34] The findings demonstrate radiofrequency ablation is at least 90% effective to completely clear Barrett's esophagus and dysplasia, with durability of up to five years and a favorable safety profile. [31] [32] [33] [34]

Anti-reflux surgery has not been proven to prevent esophageal cancer. However, the indication is that proton pump inhibitors are effective in limiting the progression of esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. A recent five-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor. [35]

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 the detection of three different genetic abnormalities was associated with as much as a 79% chance of developing cancer in six years. [36]

Endoscopic mucosal resection has also been evaluated as a management technique. [37] Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus. [38]

In a variety of studies, nonsteroidal anti-inflammatory drugs (NSAIDS) such as low-dose aspirin (75–300 mg/day) have shown evidence of preventing esophageal cancer in people with Barrett's esophagus. [39] [40] [41] [42]

Prognosis

Barrett's cancer adenocarcinoma (poor; signet-ringcell) Esophageal cancer-2626-02.jpg
Barrettʼs cancer
adenocarcinoma (poor; signet-ringcell)

Barrett's esophagus is a pre-malignant condition, not a cancerous one.

A small subset of patients with Barrett's esophagus will eventually develop malignant esophagogastric junctional adenocarcinoma, which has a mortality rate of over 85%. [43]

The risk of developing esophageal adenocarcinoma increases based on how severe the Barrett's esophagus has become. [44] Longer length of the Barrett's esophagus region is also associated with increased risk of developing cancer. [44] [45]

Progression and severity of Barrett's esophagus is measured by amount of dysplasia the cells show. Dysplasia is scored on a five-tier system: [45]

  1. negative for dysplasia (non-dysplastic Barrett’s esophagus or NDBE)
  2. indefinite for dysplasia (IND)
  3. low-grade dysplasia (LGD)
  4. high-grade dysplasia (HGD)
  5. carcinoma

A 2016 study found that the rate of progression to esophageal adenocarcinoma in Barrett's esophagus patients with no dysplasia, low-grade dysplasia, and high-grade dysplasia are around 0.6%, 13.4%, and 25%, respectively. [46]

However, for low-grade dysplasia, the true yearly rate of progression to cancer remains difficult to estimate, as results are highly variable from study to study, from 13.4% down to 0.84%. [44] This is partly due to each study having a different mix of intermediate disease states being combined under the umbrella diagnosis of LGD. [45]

Epidemiology

The incidence in the United States among Caucasian men is eight times the rate among Caucasian women and five times greater than African American men. Overall, the male to female ratio of Barrett's esophagus is 10:1. [47] Several studies have estimated the prevalence of Barrett's esophagus in the general population to be 1.3% to 1.6% in two European populations (Italian [48] and Swedish [49] ), and 3.6% in a Korean population. [50]

History

The condition is named after Australian thoracic surgeon Norman Barrett (1903–1979), who in 1950 argued that "ulcers are found below the squamocolumnar junction ... represent gastric ulcers within 'a pouch of stomach ... drawn up by scar tissue into the mediastinum' ... representing an example of a 'congenital short esophagus'". [51] [52] In contrast, Philip Rowland Allison and Alan Johnstone argued that the condition related to the "esophagus lined with gastric mucous membrane and not intra-thoracic stomach as Barrett mistakenly believed." [53] [6] Philip Allison, cardiothoracic surgeon and Chair of Surgery at the University of Oxford, suggested "calling the chronic peptic ulcer crater of the esophagus a 'Barrett's ulcer'", but added this name did not imply agreement with "Barrett's description of an esophagus lined with gastric mucous membrane as stomach." [53] [6] Bani-Hani KE and Bani-Hani KR argue that the terminology and definition of Barrett's esophagus is surrounded by extraordinary confusion unlike most other medical conditions and that "[t]he use of the eponym 'Barrett's' to describe [the condition] is not justified from a historical point of view". [6] Bani-Hani KE and Bani-Hani KR investigated the historical aspects of the condition and found they could establish "how little Norman Barrett had contributed to the core concept of this condition in comparison to the contributions of other investigators, particularly the contribution of Philip Allison". [6]

A further association was made with adenocarcinoma in 1975. [54]

Related Research Articles

<span class="mw-page-title-main">Gastroenterology</span> Branch of medicine focused on the digestive system and its disorders

Gastroenterology is the branch of medicine focused on the digestive system and its disorders. The digestive system consists of the gastrointestinal tract, sometimes referred to as the GI tract, which includes the esophagus, stomach, small intestine and large intestine as well as the accessory organs of digestion which include the pancreas, gallbladder, and liver.

<span class="mw-page-title-main">Esophagus</span> Vertebrate organ through which food passes to the stomach

The esophagus or oesophagus, colloquially known also as the food pipe, food tube, or gullet, is an organ in vertebrates through which food passes, aided by peristaltic contractions, from the pharynx to the stomach. The esophagus is a fibromuscular tube, about 25 cm (10 in) long in adults, that travels behind the trachea and heart, passes through the diaphragm, and empties into the uppermost region of the stomach. During swallowing, the epiglottis tilts backwards to prevent food from going down the larynx and lungs. The word oesophagus is from Ancient Greek οἰσοφάγος (oisophágos), from οἴσω (oísō), future form of φέρω + ἔφαγον.

<span class="mw-page-title-main">Esophageal achalasia</span> Rare, incurable, progressive motility disorder due to failure of esophogeal motor neurons

Esophageal achalasia, often referred to simply as achalasia, is a failure of smooth muscle fibers to relax, which can cause the lower esophageal sphincter to remain closed. Without a modifier, "achalasia" usually refers to achalasia of the esophagus. Achalasia can happen at various points along the gastrointestinal tract; achalasia of the rectum, for instance, may occur in Hirschsprung's disease. The lower esophageal sphincter is a muscle between the esophagus and stomach that opens when food comes in. It closes to avoid stomach acids from coming back up. A fully understood cause to the disease is unknown, as are factors that increase the risk of its appearance. Suggestions of a genetically transmittable form of achalasia exist, but this is neither fully understood, nor agreed upon.

Heartburn, also known as pyrosis, cardialgia or acid indigestion, is a burning sensation in the central chest or upper central abdomen. Heartburn is usually due to regurgitation of gastric acid into the esophagus. It is the major symptom of gastroesophageal reflux disease (GERD).

<span class="mw-page-title-main">Gastroesophageal reflux disease</span> Medical condition

Gastroesophageal reflux disease (GERD) or gastro-oesophageal reflux disease (GORD) is a chronic upper gastrointestinal disease in which stomach content persistently and regularly flows up into the esophagus, resulting in symptoms and/or complications. Symptoms include dental corrosion, dysphagia, heartburn, odynophagia, regurgitation, non-cardiac chest pain, extraesophageal symptoms such as chronic cough, hoarseness, reflux-induced laryngitis, or asthma. In the long term, and when not treated, complications such as esophagitis, esophageal stricture, and Barrett's esophagus may arise.

<span class="mw-page-title-main">Hiatal hernia</span> Type of hernia

A hiatal hernia or hiatus hernia is a type of hernia in which abdominal organs slip through the diaphragm into the middle compartment of the chest. This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR) with symptoms such as a taste of acid in the back of the mouth or heartburn. Other symptoms may include trouble swallowing and chest pains. Complications may include iron deficiency anemia, volvulus, or bowel obstruction.

<span class="mw-page-title-main">Esophageal cancer</span> Gastrointestinal system cancer that is located in the esophagus

Esophageal cancer is cancer arising from the esophagus—the food pipe that runs between the throat and the stomach. Symptoms often include difficulty in swallowing and weight loss. Other symptoms may include pain when swallowing, a hoarse voice, enlarged lymph nodes ("glands") around the collarbone, a dry cough, and possibly coughing up or vomiting blood.

<span class="mw-page-title-main">Stomach cancer</span> Cancerous tumor originating in the stomach lining

Stomach cancer, also known as gastric cancer, is a cancer that develops from the lining of the stomach. Most cases of stomach cancers are gastric carcinomas, which can be divided into a number of subtypes, including gastric adenocarcinomas. Lymphomas and mesenchymal tumors may also develop in the stomach. Early symptoms may include heartburn, upper abdominal pain, nausea, and loss of appetite. Later signs and symptoms may include weight loss, yellowing of the skin and whites of the eyes, vomiting, difficulty swallowing, and blood in the stool, among others. The cancer may spread from the stomach to other parts of the body, particularly the liver, lungs, bones, lining of the abdomen, and lymph nodes.

<span class="mw-page-title-main">Metaplasia</span> Medical condition

Metaplasia is the transformation of a cell type to another cell type. The change from one type of cell to another may be part of a normal maturation process, or caused by some sort of abnormal stimulus. In simplistic terms, it is as if the original cells are not robust enough to withstand their environment, so they transform into another cell type better suited to their environment. If the stimulus causing metaplasia is removed or ceases, tissues return to their normal pattern of differentiation. Metaplasia is not synonymous with dysplasia, and is not considered to be an actual cancer. It is also contrasted with heteroplasia, which is the spontaneous abnormal growth of cytologic and histologic elements. Today, metaplastic changes are usually considered to be an early phase of carcinogenesis, specifically for those with a history of cancers or who are known to be susceptible to carcinogenic changes. Metaplastic change is thus often viewed as a premalignant condition that requires immediate intervention, either surgical or medical, lest it lead to cancer via malignant transformation.

Gastrointestinal cancer refers to malignant conditions of the gastrointestinal tract and accessory organs of digestion, including the esophagus, stomach, biliary system, pancreas, small intestine, large intestine, rectum and anus. The symptoms relate to the organ affected and can include obstruction, abnormal bleeding or other associated problems. The diagnosis often requires endoscopy, followed by biopsy of suspicious tissue. The treatment depends on the location of the tumor, as well as the type of cancer cell and whether it has invaded other tissues or spread elsewhere. These factors also determine the prognosis.

<span class="mw-page-title-main">Eosinophilic esophagitis</span> Allergic inflammatory condition of the esophagus

Eosinophilic esophagitis (EoE) is an allergic inflammatory condition of the esophagus that involves eosinophils, a type of white blood cell. In healthy individuals, the esophagus is typically devoid of eosinophils. In EoE, eosinophils migrate to the esophagus in large numbers. When a trigger food is eaten, the eosinophils contribute to tissue damage and inflammation. Symptoms include swallowing difficulty, food impaction, vomiting, and heartburn.

Esophageal dysphagia is a form of dysphagia where the underlying cause arises from the body of the esophagus, lower esophageal sphincter, or cardia of the stomach, usually due to mechanical causes or motility problems.

Stretta is a minimally invasive endoscopic procedure for the treatment of gastroesophageal reflux disease (GERD) that delivers radiofrequency energy in the form of electromagnetic waves through electrodes at the end of a catheter to the lower esophageal sphincter (LES) and the gastric cardia – the region of the stomach just below the LES. The energy heats the tissue, ultimately causing it to swell and stiffen; the way this works was not understood as of 2015, but it was thought that perhaps the heat causes local inflammation, collagen deposition and muscular thickening of the LES and that it may disrupt the nerves there.

Norman Rupert Barrett CBE FRSA was an Australian-born British thoracic surgeon who is widely yet mistakenly remembered for describing what became known as Barrett's oesophagus.

Therapeutic endoscopy is the medical term for an endoscopic procedure during which treatment is carried out via the endoscope. This contrasts with diagnostic endoscopy, where the aim of the procedure is purely to visualize a part of the gastrointestinal, respiratory or urinary tract in order to aid diagnosis. In practice, a procedure which starts as a diagnostic endoscopy may become a therapeutic endoscopy depending on the findings, such as in cases of upper gastrointestinal bleeding, or the finding of polyps during colonoscopy.

<span class="mw-page-title-main">Intestinal metaplasia</span> Medical condition

Intestinal metaplasia is the transformation (metaplasia) of epithelium into a type of epithelium resembling that found in the intestine. In the esophagus, this is called Barrett's esophagus. Chronic inflammation caused by H. pylori infection in the stomach and GERD in the esophagus are seen as the primary instigators of metaplasia and subsequent adenocarcinoma formation. Initially, the transformed epithelium resembles the small intestine lining; in the later stages it resembles the lining of the colon. It is characterized by the appearance of goblet cells and expression of intestinal cell markers such as the transcription factor, CDX2.

<span class="mw-page-title-main">Chromoendoscopy</span>

Chromoendoscopy is a medical procedure wherein dyes are instilled into the gastrointestinal tract at the time of visualization with fibre-optic endoscopy. The purposes of chromoendoscopy is chiefly enhance the characterization of tissues, although dyes may be used for other functional purposes. The detail achieved with chromoendoscopy can often allow for identification of the tissue type or pathology based upon the pattern uncovered.

<span class="mw-page-title-main">Oesophagogastric junctional adenocarcinoma</span>

Oesophagogastric junctional adenocarcinoma is a cancer of the lower part of the oesophagus with a rising incidence in Western countries. This disease is often linked to Barrett's oesophagus.

Gastrointestinal intraepithelial neoplasia is also known as gastrointestinal dysplasia. Gastrointestinal dysplasia refers to abnormal growth of the epithelial tissue lining the gastrointestinal tract including the esophagus, stomach, and colon. Pancreatic, biliary, and rectal Intraepithelial Neoplasia are discussed separately. The regions of abnormal growth are confined by the basement membrane adjacent to the epithelial tissue and are thought to represent pre-cancerous lesions. 

Prateek SharmaFACG, FACP, FASGE is an Indian American gastroenterologist that specializes in esophageal diseases and endoscopic treatments.

References

  1. 1 2 3 4 5 Shaheen NJ, Richter JE (March 2009). "Barrett's oesophagus". Lancet. 373 (9666): 850–61. doi:10.1016/S0140-6736(09)60487-6. PMID   19269522. S2CID   13141959.
  2. ↑ Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN (December 2005). "The molecular biology of esophageal adenocarcinoma". Journal of Surgical Oncology. 92 (3): 169–90. doi: 10.1002/jso.20359 . PMID   16299787. S2CID   42893278.
  3. ↑ Stein HJ, Siewert JR (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management". Dysphagia. 8 (3): 276–88. doi:10.1007/BF01354551. PMID   8359051. S2CID   6715044.
  4. ↑ Shaheen, Nicholas J.; Falk, Gary W.; Iyer, Prasad G.; Gerson, Lauren B.; American College of Gastroenterology (January 2016). "ACG Clinical Guideline: Diagnosis and Management of Barrett's Esophagus". The American Journal of Gastroenterology. 111 (1): 30–50, quiz 51. doi: 10.1038/ajg.2015.322 . ISSN   1572-0241. PMC   10245082 . PMID   26526079. S2CID   2274838.
  5. ↑ Allison PR (March 1948). "Peptic ulcer of the oesophagus". Thorax. 3 (1): 20–42. doi:10.1136/thx.3.1.20. PMC   1018255 . PMID   18904843.
  6. 1 2 3 4 5 Bani-Hani KE, Bani-Hani BK (May 2008). "Columnar-lined esophagus: time to drop the eponym of "Barrett": Historical review". Journal of Gastroenterology and Hepatology. 23 (5): 707–15. doi:10.1111/j.1440-1746.2008.05386.x. PMID   18410605. S2CID   21531132.
  7. ↑ Katz-Summercorn, Annalise C.; Frankell, Alexander M.; Fitzgerald, Rebecca C. (2016). "Chapter 4: Genetics and Biomarkers in Barrett's Esophagus and Esophageal Adenocarcinoma". In Pleskow, Douglas K.; Erim, Tolga (eds.). Barrett's Esophagus - Emerging Evidence for Improved Clinical Practice. pp. 37–60. doi:10.1016/B978-0-12-802511-6.00004-1. ISBN   9780128025116.
  8. ↑ Edelstein ZR, Farrow DC, Bronner MP, Rosen SN, Vaughan TL (August 2007). "Central adiposity and risk of Barrett's esophagus". Gastroenterology. 133 (2): 403–11. doi: 10.1053/j.gastro.2007.05.026 . PMID   17681161.
  9. ↑ Reid BJ, Li X, Galipeau PC, Vaughan TL (February 2010). "Barrett's oesophagus and oesophageal adenocarcinoma: time for a new synthesis". Nature Reviews. Cancer. 10 (2): 87–101. doi:10.1038/nrc2773. PMC   2879265 . PMID   20094044.
  10. ↑ Janmaat VT, Nesteruk K, Spaander MC, Verhaar AP, Yu B, Silva RA, Phillips WA, Magierowski M, van de Winkel A, Stadler HS, Sandoval-Guzmán T, van der Laan LJ, Kuipers EJ, Smits R, Bruno MJ, Fuhler GM, Clemons NJ, Peppelenbosch MP (Jun 2021). "HOXA13 in etiology and oncogenic potential of Barrett's esophagus". Nature Communications. 12 (1): 3354. Bibcode:2021NatCo..12.3354J. doi: 10.1038/s41467-021-23641-8 . PMC   8184780 . PMID   34099670.
  11. ↑ Navab, Farhad; Avunduk, Canan; Gang, David; Frankel, Kenneth (1996). "Bulimia nervosa complicated by Barrett's esophagus and esophageal cancer". Gastrointestinal Endoscopy. 44 (4): 492–494. doi:10.1016/S0016-5107(96)70110-4. PMID   8905379 . Retrieved 28 July 2018.
  12. ↑ "Bulimia and cancer - what you need to know - Bulimia Help". Bulimiahelp.org. Archived from the original on 23 July 2018. Retrieved 28 July 2018.
  13. 1 2 Jürgens, S.; Meyer, F.; Spechler, S. J.; Souza, R. (September 2012). "The role of bile acids in the neoplastic progression of Barrett's esophagus - a short representative overview". Zeitschrift für Gastroenterologie. 50 (9): 1028–1034. doi:10.1055/s-0032-1312922. PMID   22965634. S2CID   1099567.
  14. ↑ Bernstein, H.; Bernstein, C.; Payne, C. M.; Dvorakova, K.; Garewal, H. (January 2005). "Bile acids as carcinogens in human gastrointestinal cancers". Mutation Research. 589 (1): 47–65. doi:10.1016/j.mrrev.2004.08.001. PMID   15652226.
  15. 1 2 Fléjou JF (March 2005). "Barrett's oesophagus: from metaplasia to dysplasia and cancer". Gut. 54 (Suppl 1): i6–12. doi:10.1136/gut.2004.041525. PMC   1867794 . PMID   15711008.
  16. 1 2 Bennett C, Moayyedi P, Corley DA, DeCaestecker J, Falck-Ytter Y, Falk G, et al. (May 2015). "BOB CAT: A Large-Scale Review and Delphi Consensus for Management of Barrett's Esophagus With No Dysplasia, Indefinite for, or Low-Grade Dysplasia". The American Journal of Gastroenterology. 110 (5): 662–82, quiz 683. doi:10.1038/ajg.2015.55. PMC   4436697 . PMID   25869390.
  17. ↑ "Cytosponge". www.nhsinform.scot. Retrieved 2022-04-05.
  18. ↑ "An innovative swallowable sponge detects Barrett's oesophagus in people with heartburn, study shows". NIHR Evidence (Plain English summary). 2021-02-16. doi:10.3310/alert_44006. S2CID   242399505.
  19. ↑ Fitzgerald, Rebecca C; di Pietro, Massimiliano; O'Donovan, Maria; Maroni, Roberta; Muldrew, Beth; Debiram-Beecham, Irene; Gehrung, Marcel; Offman, Judith; Tripathi, Monika; Smith, Samuel G; Aigret, Benoit (1 August 2020). "Cytosponge-trefoil factor 3 versus usual care to identify Barrett's oesophagus in a primary care setting: a multicentre, pragmatic, randomised controlled trial". The Lancet. 396 (10247): 333–344. doi:10.1016/S0140-6736(20)31099-0. PMC   7408501 . PMID   32738955.
  20. ↑ "Barrett's Esophagus". The Lecturio Medical Concept Library. Retrieved 3 July 2021.
  21. ↑ Pohler E, Craig AL, Cotton J, Lawrie L, Dillon JF, Ross P, et al. (June 2004). "The Barrett's antigen anterior gradient-2 silences the p53 transcriptional response to DNA damage". Molecular & Cellular Proteomics. 3 (6): 534–47. doi: 10.1074/mcp.M300089-MCP200 . PMID   14967811.
  22. ↑ Murray E, McKenna EO, Burch LR, Dillon J, Langridge-Smith P, Kolch W, et al. (December 2007). "Microarray-formatted clinical biomarker assay development using peptide aptamers to anterior gradient-2". Biochemistry. 46 (48): 13742–51. doi:10.1021/bi7008739. PMID   17994709.
  23. ↑ Salemme M, Villanacci V, Cengia G, Cestari R, Missale G, Bassotti G (February 2016). "Intestinal metaplasia in Barrett's oesophagus: An essential factor to predict the risk of dysplasia and cancer development". Digestive and Liver Disease. 48 (2): 144–7. doi:10.1016/j.dld.2015.10.021. PMID   26614646.
  24. ↑ Çoban Ş, Örmeci N, Savaş B, Ekiz F, Ensari A, Kuzu I, Palabıyıkoğlu M (2013). "Evaluation of Barrett's esophagus with CK7, CK20, p53, Ki67, and COX2 expressions using chromoendoscopical examination". Diseases of the Esophagus. 26 (2): 189–96. doi: 10.1111/j.1442-2050.2012.01352.x . PMID   22591041.
  25. ↑ Odze RD (October 2006). "Diagnosis and grading of dysplasia in Barrett's oesophagus". Journal of Clinical Pathology. 59 (10): 1029–38. doi:10.1136/jcp.2005.035337. PMC   1861756 . PMID   17021130.
  26. ↑ Bibbò S, Ianiro G, Ricci R, Arciuolo D, Petruzziello L, Spada C, Larghi A, Riccioni ME, Gasbarrini A, Costamagna G, Cammarota G (Sep 2016). "Barrett's oesophagus and associated dysplasia are not equally distributed within the esophageal circumference". Dig Liver Dis. 48 (9): 1043–7. doi:10.1016/j.dld.2016.06.020. PMID   27436487.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ↑ Schlemper RJ, Riddell RH, Kato Y, Borchard F, Cooper HS, Dawsey SM, et al. (August 2000). "The Vienna classification of gastrointestinal epithelial neoplasia". Gut. 47 (2): 251–5. doi:10.1136/gut.47.2.251. PMC   1728018 . PMID   10896917.
  28. ↑ American Gastroenterological Association, "Five Things Physicians and Patients Should Question" (PDF), Choosing Wisely: an initiative of the ABIM Foundation , American Gastroenterological Association, archived from the original (PDF) on August 9, 2012, retrieved August 17, 2012
  29. ↑ Spechler SJ, Sharma P, Souza RF, Inadomi JM, Shaheen NJ (March 2011). "American Gastroenterological Association medical position statement on the management of Barrett's esophagus". Gastroenterology. 140 (3): 1084–91. doi: 10.1053/j.gastro.2011.01.030 . PMID   21376940.
  30. ↑ Wang KK, Sampliner RE (March 2008). "Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett's esophagus". The American Journal of Gastroenterology. 103 (3): 788–97. doi: 10.1111/j.1572-0241.2008.01835.x . PMID   18341497. S2CID   8443847.
  31. 1 2 Fleischer DE, Overholt BF, Sharma VK, Reymunde A, Kimmey MB, Chuttani R, et al. (October 2010). "Endoscopic radiofrequency ablation for Barrett's esophagus: 5-year outcomes from a prospective multicenter trial". Endoscopy. 42 (10): 781–9. doi:10.1055/s-0030-1255779. PMID   20857372. S2CID   24224546.
  32. 1 2 Shaheen NJ, Sharma P, Overholt BF, Wolfsen HC, Sampliner RE, Wang KK, et al. (May 2009). "Radiofrequency ablation in Barrett's esophagus with dysplasia". The New England Journal of Medicine. 360 (22): 2277–88. doi: 10.1056/NEJMoa0808145 . PMID   19474425.
  33. 1 2 Shaheen NJ, Overholt BF, Sampliner RE, Wolfsen HC, Wang KK, Fleischer DE, et al. (August 2011). "Durability of radiofrequency ablation in Barrett's esophagus with dysplasia". Gastroenterology. 141 (2): 460–8. doi:10.1053/j.gastro.2011.04.061. PMC   3152658 . PMID   21679712.
  34. 1 2 van Vilsteren FG, Pouw RE, Seewald S, Alvarez Herrero L, Sondermeijer CM, Visser M, Ten Kate FJ, Yu Kim Teng KC, Soehendra N, Rösch T, Weusten BL, Bergman JJ (June 2011). "Stepwise radical endoscopic resection versus radiofrequency ablation for Barrett's oesophagus with high-grade dysplasia or early cancer: a multicentre randomised trial". Gut. 60 (6): 765–73. doi:10.1136/gut.2010.229310. PMID   21209124. S2CID   38316532.
  35. ↑ Overholt BF, Wang KK, Burdick JS, Lightdale CJ, Kimmey M, Nava HR, et al. (September 2007). "Five-year efficacy and safety of photodynamic therapy with Photofrin in Barrett's high-grade dysplasia". Gastrointestinal Endoscopy. 66 (3): 460–8. doi:10.1016/j.gie.2006.12.037. PMID   17643436.
  36. ↑ Galipeau PC, Li X, Blount PL, Maley CC, Sanchez CA, Odze RD, et al. (February 2007). "NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma". PLOS Medicine. 4 (2): e67. doi: 10.1371/journal.pmed.0040067 . PMC   1808095 . PMID   17326708.
  37. ↑ Reshamwala PA, Darwin PE (September 2006). "Endoscopic management of early gastric cancer". Current Opinion in Gastroenterology. 22 (5): 541–5. doi:10.1097/01.mog.0000239870.04457.80. PMID   16891887. S2CID   12959801.
  38. ↑ Abbas AE, Deschamps C, Cassivi SD, Allen MS, Nichols FC, Miller DL, et al. (February 2004). "Barrett's esophagus: the role of laparoscopic fundoplication". The Annals of Thoracic Surgery. 77 (2): 393–6. doi: 10.1016/S0003-4975(03)01352-3 . PMID   14759403.
  39. ↑ Corley DA, Kerlikowske K, Verma R, Buffler P (January 2003). "Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis". Gastroenterology. 124 (1): 47–56. doi: 10.1053/gast.2003.50008 . PMID   12512029.
  40. ↑ Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, Sanchez CA, Rabinovitch PS, Reid BJ (December 2005). "Non-steroidal anti-inflammatory drugs and risk of neoplastic progression in Barrett's oesophagus: a prospective study". The Lancet. Oncology. 6 (12): 945–52. doi:10.1016/S1470-2045(05)70431-9. PMID   16321762.
  41. ↑ García Rodríguez, Luis A.; Soriano-Gabarró, Montse; Vora, Pareen; Cea Soriano, Lucía (7 May 2020). "Low-dose aspirin and risk of gastric and oesophageal cancer: A population-based study in the United Kingdom using The Health Improvement Network". International Journal of Cancer. 147 (9): 2394–2404. doi: 10.1002/ijc.33022 . ISSN   0020-7136. PMC   7540378 . PMID   32329063.
  42. ↑ Schieszer, John (29 September 2019). "Study Shows Association Between Low-Dose Aspirin Use and Risk for Gastric and Esophageal Cancers". Oncology Nurse Advisor.
  43. ↑ Holmes RS, Vaughan TL (January 2007). "Epidemiology and pathogenesis of esophageal cancer". Seminars in Radiation Oncology. 17 (1): 2–9. doi:10.1016/j.semradonc.2006.09.003. PMID   17185192.
  44. 1 2 3 Li S, Hoefnagel S, Krishnadath KK (November 2023). "Molecular Biology and Clinical Management of Esophageal Adenocarcinoma". Cancers (Basel). 15 (22): 5410. doi: 10.3390/cancers15225410 . PMC   10670638 . PMID   38001670.
  45. 1 2 3 Stawinski PM, Dziadkowiec KN, Kuo LA, Echavarria J, Saligram S (January 2023). "Barrett's Esophagus: An Updated Review". Diagnostics (Basel). 13 (2): 321. doi: 10.3390/diagnostics13020321 . PMC   9858189 . PMID   36673131.
  46. ↑ Greyson EM, Bornschein J, Fitzgerald RC (July 2016). "Genetic progression of Barrett's oesophagus to oesophageal adenocarcinoma". British Journal of Cancer. 115 (4): 403–410. doi:10.1038/bjc.2016.219. PMC   4985359 . PMID   27441494.
  47. ↑ Zajac, P; Holbrook, A; Super, ME; Vogt, M (March–April 2013). "An overview: Current clinical guidelines for the evaluation, diagnosis, treatment, and management of dyspepsia". Osteopathic Family Physician. 5 (2): 79–85. doi:10.1016/j.osfp.2012.10.005.
  48. ↑ Zagari RM, Fuccio L, Wallander MA, Johansson S, Fiocca R, Casanova S, et al. (October 2008). "Gastro-oesophageal reflux symptoms, oesophagitis and Barrett's oesophagus in the general population: the Loiano-Monghidoro study". Gut. 57 (10): 1354–9. doi:10.1136/gut.2007.145177. PMID   18424568. S2CID   206947077.
  49. ↑ Ronkainen J, Aro P, Storskrubb T, Johansson SE, Lind T, Bolling-Sternevald E, et al. (December 2005). "Prevalence of Barrett's esophagus in the general population: an endoscopic study". Gastroenterology. 129 (6): 1825–31. doi:10.1053/j.gastro.2005.08.053. PMID   16344051.
  50. ↑ Kim JY, Kim YS, Jung MK, Park JJ, Kang DH, Kim JS, et al. (April 2005). "Prevalence of Barrett's esophagus in Korea". Journal of Gastroenterology and Hepatology. 20 (4): 633–6. doi:10.1111/j.1440-1746.2005.03749.x. PMID   15836715. S2CID   46543142.
  51. ↑ Barrett NR (October 1950). "Chronic peptic ulcer of the oesophagus and 'oesophagitis'". The British Journal of Surgery. 38 (150): 175–82. doi:10.1002/bjs.18003815005. PMID   14791960. S2CID   72315839.
  52. ↑ DeMeester SR, DeMeester TR (March 2000). "Columnar mucosa and intestinal metaplasia of the esophagus: fifty years of controversy". Annals of Surgery. 231 (3): 303–21. doi:10.1097/00000658-200003000-00003. PMC   1421001 . PMID   10714623.
  53. 1 2 Allison PR, Johnstone AS (June 1953). "The oesophagus lined with gastric mucous membrane". Thorax. 8 (2): 87–101. doi:10.1136/thx.8.2.87. PMC   1019247 . PMID   13077502.
  54. ↑ Naef AP, Savary M, Ozzello L (November 1975). "Columnar-lined lower esophagus: an acquired lesion with malignant predisposition. Report on 140 cases of Barrett's esophagus with 12 adenocarcinomas". The Journal of Thoracic and Cardiovascular Surgery. 70 (5): 826–35. doi:10.1016/s0022-5223(19)39666-7. PMID   1186274.
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