Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: Prevalence and clinical data

Hirota, William K.; Loughney, Thomas M.; Lazas, Donald J.; Maydonovitch, Corinne; Rholl, Vicky; Wong, Roy K.H.

doi:10.1016/s0016-5085(99)70123-x

Cited by 476 publications

(319 citation statements)

References 31 publications

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“…While several previous studies stated that patients with SSBE may develop dysplasia (Sharma et al, 1997) and EAC (Rudolph et al, 2000), some prospective studies have shown an increased risk of EAC development only in patients with LSBE (Weston et al, 1997;Hirota et al, 1999;Hage et al, 2004). Rudolph et al (2000) demonstrated that segment length was not related to cancer risk in a prospective cohort study of 309 Barrett's patients followed in the Seattle Barrett's Esophagus Project (P>0.2); however, when patients with HGD at entrance were excluded, a strong trend was observed, with a 5 cm difference in length associated with a 1.7-fold increase in cancer risk (95% confidence interval, 0.8-to 3.8-fold).…”

Section: Discussionmentioning

confidence: 97%

“…Weston et al (1997) reported significant differences between SSBE and LSBE in the frequency of both dysplasia and EAC, at 8.1 vs 24.4% for dysplasia (Po0.0001) and 0 vs 15.4% for EAC (Po0.0005). Hirota et al (1999) reported that the prevalence of dysplasia and cancer differed significantly in patients with SSBE vs patients with LSBE in a comprehensive prospective study of 889 consecutive patients. More recently, Hage et al (2004) reported a significantly increased risk of progression to HGD or EAC with LSBE after a mean follow-up of 12.7 years.…”

Section: Discussionmentioning

confidence: 99%

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Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma

et al. 2007

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The nel-like1 (NELL1) gene maps to chromosome 11p15, which frequently undergoes loss of heterozygosity in esophageal adenocarcinoma (EAC). NELL1 promoter hypermethylation was examined by real-time methylationspecific polymerase chain reaction in 259 human esophageal tissues. Hypermethylation of this promoter showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinoma (ESCC) and EAC from normal esophagus (NE) (Po0.001). NELL1 normalized methylation values were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's (D) and EAC than in NE (Po0.0000001). NELL1 hypermethylation frequency was zero in NE but increased early during neoplastic progression, to 41.7% in BE from patients with Barrett's alone, 52.5% in D and 47.8% in EAC. There was a significant correlation between NELL1 hypermethylation and BE segment length. Three (11.5%) of 26 ESCCs exhibited NELL1 hypermethylation. Survival correlated inversely with NELL1 hypermethylation in patients with stages I-II (P ¼ 0.0264) but not in stages III-IV (P ¼ 0.68) EAC. Treatment of KYSE220 ESCC and BIC EAC cells with 5-aza-2 0 -deoxycytidine reduced NELL1 methylation and increased NELL1 mRNA expression. NELL1 mRNA levels in EACs with an unmethylated NELL1 promoter were significantly higher than those in EACs with a methylated promoter (P ¼ 0.02). Promoter hypermethylation of NELL1 is a common, tissue-specific event in human EAC, occurs early during Barrett's-associated esophageal neoplastic progression, and is a potential biomarker of poor prognosis in early-stage EAC.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma

et al. 2007

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“…Intrasphincteric acid exposure may explain how metaplasia of the distal esophagus is most prevalent at, and immediately proximal to, the SCJ and can occur in subjects without conventional evidence of refl ux disease. It could also account for short-segment Barrett ' s esophagus being several times more prevalent than long-segment Barrett ' s esophagus ( 30 ). It is provocative to note that, as bile acids have been detected within the acid pocket of healthy volunteers ( 31,32 ), this may explain why short-segment Barrett ' s esophagus has no association with GERD symptoms ( 33 ).…”

Section: The Acid Pocket In Health and Diseasementioning

confidence: 99%

The Acid Pocket: A Target for Treatment in Reflux Disease?

Kahrilas

McColl

Fox³

et al. 2013

American Journal of Gastroenterology

133

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The nadir esophageal pH of refl ux observed during pH monitoring in the postprandial period is often more acidic than the concomitant intragastric pH. This paradox prompted the discovery of the " acid pocket " , an area of unbuffered gastric acid that accumulates in the proximal stomach after meals and serves as the reservoir for acid refl ux in healthy individuals and gastroesophageal refl ux disease (GERD) patients. However, there are differentiating features between these populations in the size and position of the acid pocket, with GERD patients predisposed to upward migration of the proximal margin onto the esophageal mucosa, particularly when supine. This upward migration of acid, sometimes referred to as an " acid fi lm " , likely contributes to mucosal pathology in the region of the squamocolumnar junction. Furthermore, movement of the acid pocket itself to a supradiaphragmatic location with hiatus hernia increases the propensity for acid refl ux by all conventional mechanisms. Consequently, the acid pocket is an attractive target for GERD therapy. It may be targeted in a global way with proton pump inhibitors that attenuate acid pocket development, or with alginate / antacid combinations that colocalize with the acid pocket and displace it distally, thereby demonstrating the potential for selective targeting of the acid pocket in GERD.

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“…30 According to recent reports from Western countries, the prevalence of BE (histologically confirmed by the presence of goblet cell metaplasia/specialized columnar epithelium), LSBE, and SSBE is 1.6-25.0%, 0.5-7.2%, and 1.1-17.2%, respectively. 8,[40][41][42][43][44] In these reports, most of the patients included were Caucasian and had reflux symptoms like heartburn. A multicenter prospective study recently done in Japan showed that an overall prevalence of endoscopically suspected BE was 24.1%, of which 99.2% were SSBE.…”

Section: Significance and Prevalence Of Barrett's Esophagusmentioning

confidence: 99%

Endoscopic Definition of Esophagogastric Junction for Diagnosis of Barrett's Esophagus: Importance of Systematic Education and Training

Ishimura

Amano

Kinoshita

2009

Digestive Endoscopy

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The diagnosis of Barrett's esophagus (BE) requires an accurate recognition of the columnar-lined esophagus at endoscopy. However, a universally accepted standardized endoscopic grading system of BE was lacking prior to the development of the Prague 'circumferential and maximal' criteria. In this system, the landmark for the esophagogastric junction (EGJ) is the proximal end of the gastric folds, not the distal end of the palisade vessels, which are used to endoscopically identify the EGJ in Japan. Although the circumferential and maximal criteria are clinically relevant, an important shortcoming of this system may be failure to identify short-segment BE, a lesion that is found frequently in the Japanese. To compare the diagnostic yield for BE when using the palisade vessels versus gastric folds as a landmark for the EGJ, we evaluated interobserver diagnostic concordance. The endoscopic identification of the EGJ using both landmarks resulted in unacceptably low kappa coefficients of reliability. However, there was a statistically significant improvement after the participants were thoroughly trained in identification of the EGJ during the endoscopic study. Although it remains controversial which landmark is better for the endoscopic diagnosis of BE, it is important to systematically educate and train endoscopists in order to improve diagnostic consistency in patients with BE.

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Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: Prevalence and clinical data

Cited by 476 publications

References 31 publications

Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma

Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma

The Acid Pocket: A Target for Treatment in Reflux Disease?

Endoscopic Definition of Esophagogastric Junction for Diagnosis of Barrett's Esophagus: Importance of Systematic Education and Training

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