Summary
Background
Barrett’s esophagus (BE) is the morphological consequence of gastroesophageal reflux disease (GERD). Via low- and high-grade dysplasia, nondysplastic Barrett’s esophagus (NDBE) may progress to cancer (0.1–0.6 % annual risk). We aim to summarize the impact of radiofrequency ablation (RFA) for the elimination of BE and cancer prevention.
Methods
This PUB MED search included 136 papers on the pathophysiology, diagnosis, and therapy (RFA, antireflux surgery) of BE £ T1a.
Results
The reflux of gastric acid and bile mediate a complex neurohumoral response within the esophageal mucosa, which orchestrates the formation of NDBE, dysplasia, and cancer. RFA effectively eliminates NDBE, dysplasia, and flat T1a cancer. Following 1–6 treatment sessions and 1–3.5 years follow-up, RFA for dysplastic BE effectively eliminates dysplasia and NDBE in > 80 and > 60 % of the cases, respectively, and mediates the development of a mucosa without genetic abnormalities. After 1–3 treatments for NDBE and 5 years follow-up, RFA eradicates NDBE in 92 % of the cases. NDBE expresses the genetic abnormalities of dysplasia and cancer and shares the same cancer risk as colonic polyps. Therefore, within clinical trials, RFA for NDBE should be offered to persons with NDBE and a risk profile, which predisposes them for cancer development (family history, GERD > 10 years, etc.). Antireflux surgery increases the yield of RFA for NDBE.
Conclusions
RFA (± endoscopic resection) is recommended for the elimination of BE with dysplasia and early cancer (T1a). Larger tumors are treated by surgical resection. The biological and genetic properties of NDBE justify the examination of RFA for this indication within clinical trials. Future studies will have to elucidate the combination of RFA, antireflux surgery, and medical therapy (PPI, statins, nonsteroidal antiinflammatory drugs) for cancer prevention.
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Mesteri, I., Beller, L., Fischer-See, S. et al. Radiofrequency ablation of Barrett’s esophagus and early cancer within the background of the pathophysiology of the disease. Eur Surg 44, 366–382 (2012). https://doi.org/10.1007/s10353-012-0183-7
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DOI: https://doi.org/10.1007/s10353-012-0183-7