Presentation and Epidemiology of Gastroesophageal Reflux Disease

Richter, Joel E.; Rubenstein, Joel H.

doi:10.1053/j.gastro.2017.07.045

Cited by 446 publications

(310 citation statements)

References 87 publications

(111 reference statements)

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“…Though the time trends seem consistent with the hypothesis that declining H. pylori prevalence has led to a rise in BE and increased prevalence of EAC, these trends could be coincidental and not causally related. The increased prevalence of BE and EAC could also be related to the higher prevalence of obesity and a decrease in lower esophageal sphincter pressure leading to GERD . It is also possible that both processes may be at work.…”

Section: The Role Of Helicobacter In Eacmentioning

confidence: 99%

Risk factors for esophageal cancer: emphasis on infectious agents

El‐Zimaity

Pilato

Ringressi

et al. 2018

Annals of the New York Academy of Sciences

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Risk factors for esophageal cancer include genetic factors (such as tylosis) and infectious agents. A variety of organisms have been implicated in esophageal carcinogenesis, either directly or indirectly. In this review, we explore the normal esophageal flora and how it may be controlled, and also the variety of organisms that may affect esophageal carcinogenesis, either directly or indirectly. The organisms with potential direct effects in squamous cell carcinoma include human papillomavirus (HPV), Epstein-Barr virus, and polyoma viruses. Interestingly, HPV is now implicated in esophageal adenocarcinoma (EAC), not in its initiation but in the development of dysplasia, in which HPV33 in particular has been associated. Indirectly, Helicobacter pylori has been associated with EAC by, initially, causing increased acid secretion that increases acid reflux, and by reducing lower esophageal sphincter pressure, which increases gastroesophageal reflux; the latter increases the risk of Barrett's esophagus, and hence EAC. Conversely, subsequent atrophic gastritis may normalize that risk.

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Section: The Role Of Helicobacter In Eacmentioning

confidence: 99%

Risk factors for esophageal cancer: emphasis on infectious agents

El‐Zimaity

Pilato

Ringressi

et al. 2018

Annals of the New York Academy of Sciences

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“…Gastroesophageal reflux disease (GERD) is the most prevalent gastrointestinal disorder in the US with as many as 20% of the population experiencing weekly GERD symptoms. [1] A serious consequence of chronic GERD and its associated inflammatory and cellular stress is development of Barrett's esophagus (BE), a condition in which a metaplastic columnar epithelium with gastric and intestinal features replaces the normal stratified squamous esophageal epithelium. [2][3][4][5][6][7] BE, estimated to affect 5.6% of American adults, is most alarming because it is a significant risk factor for esophageal adenocarcinoma (EAC), an aggressive and deadly cancer with a five-year survival rate of only 19% that has increased in incidence by more than 400% since 1975.…”

Section: Introductionmentioning

confidence: 99%

GATA4, expressed in Barrett’s esophagus and esophageal adenocarcinoma, can block squamous epithelial cell gene expression in human esophageal cells

Stavniichuk

DeLaForest

Thompson

et al. 2020

Preprint

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Metaplasia often involves a change from one cell type to another that was present during organogenesis. The embryonic esophagus is initially lined by columnar cells that are replaced by squamous cells, and metaplasia in Barrett's esophagus (BE) involves a change from squamous to columnar cells in the setting of gastroesophageal reflux.Here, we explored the effect of ectopic expression of the essential developmental transcription factor GATA4 on squamous epithelial cell gene expression using human esophageal squamous epithelial cells. We found that GATA4 protein, although absent in mature human esophageal squamous epithelium, was present in BE and esophageal adenocarcinoma (EAC). Moreover, acid and bile induced GATA4 mRNA in esophageal squamous epithelial cells. Ectopic GATA4 expression in esophageal squamous epithelial cells generally compromised squamous cell marker gene expression, although the extent varied between cell lines studied. We observed GATA4 occupancy in the p63, KRT5, and KRT15 gene promoters, suggesting that GATA4 can directly repress expression of typical squamous epithelial cell marker genes. Overall, our data suggest a mechanism whereby GATA4 expression in abnormal esophageal cells, possibly induced by reflux, supports a columnar metaplastic cell identity by repressing expression of key genes required to program stratified squamous epithelial cell identity.

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“…При этом имеют место существенные гео-графические различия. Результаты большинства исследований свидетельствуют о том, что максимальная распространенность ГЭРБ наблюдается в Южной Азии и Юго-Восточной Европе (> 25%), минимальная -в Юго-Восточной Азии, Канаде и Франции (< 10%) [4]. В странах Западной Европы этот показатель колеблется от 10% в Испании и Великобритании до 17% в Швеции, в США -от 13 до 29% [3].…”

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