Prevalence of Barrett’s Esophagus and Esophageal Adenocarcinoma With and Without Gastroesophageal Reflux: A Systematic Review and Meta-analysis

Saha, Bibek; Vantanasiri, Kornpong; Mohan, Babu P.; Goyal, Rohit; Garg, Nikita; Gerberi, Danielle; Kisiel, John B.; Singh, Siddharth; Iyer, Prasad G.

doi:10.1016/j.cgh.2023.10.006

Cited by 5 publications

(1 citation statement)

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“…In the case of Barrett's esophagus (BE), the emergence of esophageal adenocarcinoma (EAC) is the most significant and relevant outcome. In Western countries, BE-the only recognized precursor of EACaffects 2-7% of adults [1,2], and over the last decade, there have been significant advances in the comprehension of biology and pathology of the esophagus and GEJ in response to injury sustained as a result of chronic gastresophageal reflux disease (GERD) [3], even if some studies revealed that BE prevalence is also substantial in patients without GERD [4] It is believed that BE progresses to EAC in stages, with dysplasia (low-grade-LGD and high-grade-HGD) occurring before the development of EAC. It is crucial to monitor patients with recognized and established BE to prevent the development of EAC.…”

Section: Introductionmentioning

confidence: 99%

Gastro-Esophageal Junction Precancerosis: Histological Diagnostic Approach and Pathogenetic Insights

Giacometti,

Gusella,

Cassaro

2023

Cancers

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Barrett’s esophagus (BE) was initially defined in the 1950s as the visualization of gastric-like mucosa in the esophagus. Over time, the definition has evolved to include the identification of goblet cells, which confirm the presence of intestinal metaplasia within the esophagus. Chronic gastro-esophageal reflux disease (GERD) is a significant risk factor for adenocarcinoma of the esophagus, as intestinal metaplasia can develop due to GERD. The development of adenocarcinomas related to BE progresses in sequence from inflammation to metaplasia, dysplasia, and ultimately carcinoma. In the presence of GERD, the squamous epithelium changes to columnar epithelium, which initially lacks goblet cells, but later develops goblet cell metaplasia and eventually dysplasia. The accumulation of multiple genetic and epigenetic alterations leads to the development and progression of dysplasia. The diagnosis of BE requires the identification of intestinal metaplasia on histologic examination, which has thus become an essential tool both in the diagnosis and in the assessment of dysplasia’s presence and degree. The histologic diagnosis of BE dysplasia can be challenging due to sampling error, pathologists’ experience, interobserver variation, and difficulty in histologic interpretation: all these problems complicate patient management. The development and progression of Barrett’s esophagus (BE) depend on various molecular events that involve changes in cell-cycle regulatory genes, apoptosis, cell signaling, and adhesion pathways. In advanced stages, there are widespread genomic abnormalities with losses and gains in chromosome function, and DNA instability. This review aims to provide an updated and comprehensible diagnostic approach to BE based on the most recent guidelines available in the literature, and an overview of the pathogenetic and molecular mechanisms of its development.

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