Barrett's esophagus: A review

Sjogren, Robert W.; Johnson, Lawrence F.

doi:10.1016/0002-9343(83)90635-6

Cited by 163 publications

(34 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, epidemiologic data suggest that the majority of patients with BE-associated adenocarcinoma are older white males (1,20). There is also evidence to support the contention that only those patients with specialized columnar epithelium are at an increased risk of developing Barrett's-related adenocarcinoma (16,(21)(22)(23).…”

Section: Be: What Is the Risk Of Progression To Dysplasia And Adenocamentioning

confidence: 99%

Barrett's Esophagus and Barrett's-Related Dysplasia

Goldblum

2003

Modern Pathology

108

View full text Add to dashboard Cite

Barrett's esophagus is a complication of chronic gastroesophageal reflux disease and can be diagnosed when there is an endoscopic abnormality in which a biopsy shows evidence of specialized columnar epithelium, characterized by the presence of acid mucin-containing goblet cells. Much of the controversy in this body of literature relates to the complex anatomy of the esophagogastric junction and the difficulty in precisely identifying this landmark at endoscopy. By definition, in Barrett's esophagus, the squamocolumnar junction is proximal to the esophagogastric junction. Although fundic-type or cardiac-type (junctional) columnar epithelium may be present in Barrett's esophagus, it is only the presence of specialized columnar epithelium that is diagnostic of this condition. Patients with Barrett's esophagus are at risk of progressing to esophageal dysplasia and adenocarcinoma. There are several problems with using dysplasia as a marker for increased cancer risk in these patients, including problems with sampling error and intraand interobserver variation in the recognition of dysplasia. It may be difficult to distinguish regenerative epithelial changes from dysplasia, low-grade from high-grade dysplasia, and high-grade dysplasia from intramucosal adenocarcinoma. Finally, there are relatively few prospective data evaluating the natural history of high-grade dysplasia. The management of patients with Barrett's-related dysplasia is controversial and varies from institution to institution. Future emphasis should be on costeffective techniques for sampling as much of the esophageal mucosa as possible in patients who are at the highest risk of progressing to dysplasia and adenocarcinoma. Identification of biomarkers that identify such patients before the histologic recognition of dysplasia will be an area of intensive research.

show abstract

Section: Be: What Is the Risk Of Progression To Dysplasia And Adenocamentioning

confidence: 99%

Barrett's Esophagus and Barrett's-Related Dysplasia

Goldblum

2003

Modern Pathology

108

View full text Add to dashboard Cite

show abstract

“…Thus, most investigators no longer accept the theory that Barrett's esophagus is a congenital abnormality. Barrett's esophagus is currently thought to be an acquired condition with progressive columnar metaplasia of the distal esophagus due to long-standing gastroesophageal reflux and reflux esophagitis [2,3,[10][11][12][13]. It has been postulated that chronic gastroesophageal reflux causes repeated mucosal damage and ulceration, so that the normal squamous epithelium is eventually denuded and replaced by a metaplastic columnar epithelial lining.…”

Section: Epidemiology Of Barrett's Esophagusmentioning

confidence: 99%

Barrett's esophagus and esophageal adenocarcinoma: the scope of the problem

1995

View full text Add to dashboard Cite

“…4 In a proportion of cases this proceeds in a stepwise fashion through increasing degrees of dysplasia to malignancy. 4 The metaplastic epithelium confers a lifetime risk of developing adenocarcinoma of 10%, 5 which equates to one in 52 to one in 441 patient-years, or 30-125 times the risk of the general population. [6][7][8][9] Furthermore, this risk increases significantly with increasingly severe dysplasia.…”

Section: Introductionmentioning

confidence: 99%

Endoscopic ablation of Barrett's oesophagus: a randomized‐controlled trial of photodynamic therapy vs. argon plasma coagulation

Kelty

Ackroyd²,

Brown

et al. 2004

Aliment Pharmacol Ther

109

View full text Add to dashboard Cite

SUMMARYBackground: Barrett's oesophagus is the major risk factor for oesophageal adenocarcinoma. 5-Aminlevulinic acid-induced photodynamic therapy and argon plasma coagulation have been shown to be effective for ablating Barrett's oesophagus, but a comparative trial of these two modalities has not been reported. Aims: To compare photodynamic therapy and argon plasma coagulation for the ablation of Barrett's oesophagus. Methods: A total of 68 patients (54 male, 14 female; median age 61) with Barrett's oesophagus were randomized to photodynamic therapy (n ¼ 34) or argon plasma coagulation (n ¼ 34). Photodynamic therapy was performed using 5-aminlevulinic acid (30 mg/kg) and red light. Argon plasma coagulation was administered at a power setting of 65 W.

show abstract

Barrett's esophagus: A review

Cited by 163 publications

References 91 publications

Barrett's Esophagus and Barrett's-Related Dysplasia

Barrett's Esophagus and Barrett's-Related Dysplasia

Barrett's esophagus and esophageal adenocarcinoma: the scope of the problem

Endoscopic ablation of Barrett's oesophagus: a randomized‐controlled trial of photodynamic therapy vs. argon plasma coagulation

Contact Info

Product

Resources

About