Successful reversal of Barrett's esophagus with multipolar electrocoagulation despite inadequate acid suppression

Kovacs, Brent J; Chen, Yang K.; Lewis, T. A.; DeGuzman, Lino J.; Thompson, Kevin

doi:10.1016/s0016-5107(99)70380-9

Cited by 74 publications

(36 citation statements)

References 20 publications

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“…9,10 Different endoscopic ablation techniques with variable success rates have been reported for the treatment of HGD. [11][12][13][14][15][16] Photodynamic therapy (PDT) uses the combination of a photosensitizer and light. Exposure to light of a specific wavelength leads to activation of the photosensitizer followed by creation of singlet oxygen, which causes tissue injury and is thought to be mediated by apoptosis, vascular injury, and the induction of immune and inflammatory responses.…”

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confidence: 99%

Utility of Biomarkers in Prediction of Response to Ablative Therapy in Barrett's Esophagus

et al. 2008

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Background & Aims-Photodynamic therapy (PDT) has been shown to be effective in the treatment of high-grade dysplasia (HGD)/mucosal carcinoma in Barrett's esophagus (BE). Substantial proportions of patients do not respond to PDT or progress to carcinoma despite PDT. The role of biomarkers in predicting response to PDT is unknown. We aimed to determine if biomarkers known to be associated with neoplasia in BE can predict loss of dysplasia in patients treated with ablative therapy for HGD/intramucosal cancer.

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confidence: 99%

Utility of Biomarkers in Prediction of Response to Ablative Therapy in Barrett's Esophagus

et al. 2008

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“…This has been reported in 0-44 % of cases, and the long-term follow-up of successfully treated patients showed recurrence of SIM ranging from 0-68 % [149]. This is not specific for the type of ablative therapy, and a number of investigators using various modes of ablative therapy have reported this finding [150][151][152][153][154][155][156]. Residual SIM carries with it the potential to progress to dysplasia/EAC, but the magnitude of this risk is not well characterized [155,156].…”

Section: Ablation Therapy For Dysplasia and Eacmentioning

confidence: 91%

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Watari

Oshima

Fukui

et al. 2013

Clin J Gastroenterol

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Barrett's esophagus (BE) is a premalignant condition of esophageal adenocarcinoma (EAC). Although the incidence of BE has risen rapidly in the West, it is rare in Asia despite a recent increase in the prevalence of gastroesophageal reflux disease. Controversies over the definition of BE are presented because most cases show shortsegment BE, especially ultra-short BE, in Asia. Here we review possible risk factors for the development of EAC, particularly possible roles of ethnicity, specialized intestinal metaplasia (SIM), BE length, and environmental factors, such as Helicobacter pylori infection and obesity. Additionally, we summarize recent studies on the effect of chemoprevention including proton pump inhibitors, nonsteroidal anti-inflammatory drugs or aspirin in order to reduce the risk of neoplastic progression in BE patients. Although substantial knowledge of risk factors of dysplasia/EAC in BE is shown, the risk for neoplastic development may be influenced by geographic variation, study population, the presence or absence of SIM or dysplasia at baseline, and the small number of BE patients investigated. Recently, the efficiency of surveillance for BE patients has been discussed from the standpoint of cost-effectiveness. It may be too difficult to draw conclusions because no randomized clinical trials of BE surveillance have been performed.

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“…Kovacs et al [39] reported on a group of 27 patients with BE who were treated with MPEC and lansoprazole 60 mg daily. At 9 weeks, pH studies were normal in only 15 of 26 patients.…”

Section: Ablation Plus Acid Suppression In Barrett's Epitheliummentioning

confidence: 99%

Acid Suppression and Reepithelialization after Ablation of Barrett’s Esophagus

Overholt

2000

Dig Dis

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The role of acid reflux in the development of esophageal columnar epithelium was first described in the early 1970s in the canine esophageal reflux model. In the presence of acid reflux, columnar epithelium developed at the site of induced esophageal mucosal injury. When reflux was suppressed, most epithelium reverted back to squamous mucosa. Similar findings in human patients with Barrett’s esophagus (BE) who were treated with laser ablation were first described in 1993. While acid suppression with antireflux surgery or proton pump inhibitors (PPIs) has proven insufficient to completely reverse BE, ablation of the lesion followed by acid suppression may be a promising option. Although at least one report disputes the importance of complete acid suppression following mucosal ablation of BE, most investigators use full-dose PPI therapy following ablation, in the belief that full acid suppression provides an environment that allows the esophageal progenitor cell to develop squamous mucosa. This article provides a review of the literature to date regarding ablative therapies and acid suppression for patients with BE.

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Successful reversal of Barrett's esophagus with multipolar electrocoagulation despite inadequate acid suppression

Cited by 74 publications

References 20 publications

Utility of Biomarkers in Prediction of Response to Ablative Therapy in Barrett's Esophagus

Utility of Biomarkers in Prediction of Response to Ablative Therapy in Barrett's Esophagus

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Acid Suppression and Reepithelialization after Ablation of Barrett’s Esophagus

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