Ablation Therapies for Barrett's Esophagus
Ablation Therapies for Barrett's Esophagus
Barrett's esophagus, an acquired lesion, is characterized by replacement of the normal squamous mucosa in the distal esophagus by columnar mucosa -- specifically, intestinal metaplasia. This occurs in the setting of chronic gastroesophageal reflux disease (GERD). Barrett's esophagus is the premalignant lesion for adenocarcinoma of the esophagus and the esophago-gastric junction. The precise incidence of adenocarcinoma in patients with Barrett's esophagus is unclear, but has been reported to vary between 0.5% and 1% per year. A rapidly rising incidence rate for esophageal adenocarcinoma was reported initially in the 1970 and '80s, and updated information (through 1994) has documented a continuing increase in the incidence of this malignancy in the United States.
The link between Barrett's esophagus and adenocarcinoma of the distal esophagus has prompted efforts to cause or induce reversal of this premalignant lesion, ultimately in an attempt to decrease progression to cancer. Barrett's esophagus progresses from no dysplasia to low-grade dysplasia (LGD) to high-grade dysplasia (HGD), and finally to esophageal adenocarcinoma.
Up to 40% to 45% of patients with HGD have been reported to have undetected coexistent cancer in the resected esophageal specimen after undergoing esophagectomy. Patients with HGD also have the highest progression rate to cancer.
The use of ablation therapies for the eradication of Barrett's esophagus, dysplasia, and early esophageal cancer has been reported in recent publications.
Barrett's esophagus, an acquired lesion, is characterized by replacement of the normal squamous mucosa in the distal esophagus by columnar mucosa -- specifically, intestinal metaplasia. This occurs in the setting of chronic gastroesophageal reflux disease (GERD). Barrett's esophagus is the premalignant lesion for adenocarcinoma of the esophagus and the esophago-gastric junction. The precise incidence of adenocarcinoma in patients with Barrett's esophagus is unclear, but has been reported to vary between 0.5% and 1% per year. A rapidly rising incidence rate for esophageal adenocarcinoma was reported initially in the 1970 and '80s, and updated information (through 1994) has documented a continuing increase in the incidence of this malignancy in the United States.
The link between Barrett's esophagus and adenocarcinoma of the distal esophagus has prompted efforts to cause or induce reversal of this premalignant lesion, ultimately in an attempt to decrease progression to cancer. Barrett's esophagus progresses from no dysplasia to low-grade dysplasia (LGD) to high-grade dysplasia (HGD), and finally to esophageal adenocarcinoma.
Up to 40% to 45% of patients with HGD have been reported to have undetected coexistent cancer in the resected esophageal specimen after undergoing esophagectomy. Patients with HGD also have the highest progression rate to cancer.
The use of ablation therapies for the eradication of Barrett's esophagus, dysplasia, and early esophageal cancer has been reported in recent publications.
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