• Barrett’s oesophagus
• argon plasma coagulation
• proton pump inhibitors

Barrett’s oesophagus (BO) is undoubtedly associated with an increased risk of adenocarcinoma of the oesophagus.¹ Now that therapeutic endoscopy techniques have improved, it is therefore tempting to ablate Barrett’s intestinal metaplasia in order to decrease the risk of tumour development. However, ablation therapy is still controversial, especially for patients having no dysplasia, due to: (1) their low risk of cancer; (2) the risk associated with the technique of ablation; and (3) the fact that we do not know if Barrett’s ablation will really decrease the risk of cancer in the long term in an individual patient.

The rationale for current ablative therapy began with the observation that destruction or ablation of intestinal metaplasia associated with acid suppression results in its rapid replacement by a squamous epithelium.² Several groups of investigators have performed clinical studies evaluating the effectiveness of BO ablation associated with proton pump inhibitor (PPI) treatment. For patient having non-dysplastic BO without dysplasia, argon plasma coagulation (APC) has been the most popular technique.^3–8 After 1–6 sessions, a success rate of BO eradication ranging from 42% to 98% was achieved. Chest pain was very frequent after treatment and other complications were unusual, although not negligible since they included strictures,^3,7,8 fever,⁸ bleeding,³ or even perforation and death.^4,8 More importantly for the long term usefulness of this therapy was the observation of persisting buried intestinal metaplasia under the squamous re-epithelialisation, which was observed in the first clinical trials^3–5 with a frequency of 8–30%. Also, at least two cases of adenocarcinoma arising under the squamous re-epithelialisation have been observed after APC,^9,10 suggesting that even surveillance (and biopsy targeting) could become more difficult after this therapy. More recent trials^7,8 have observed a very low incidence of buried glands, probably because of the use of higher PPI doses and of higher power settings of the APC resulting in a deeper injury, but also at the cost of a higher incidence of strictures. In the current issue of Gut, Basu and colleagues¹¹ report on a series of 50 patients with BO treated by APC and followed for one year [see page 776]. They used a 30 watt power setting of APC (which corresponds to the low rage of energy) and cleared the BO macroscopically in 68% of cases, but 44% of those successful cases had buried glands at histology. As reported in other studies,^3,4 they found that the length of BO was a predictive factor for persistence after treatment. There was a slight trend for persistent acid reflux in cases where eradication was not achieved but this was difficult to evaluate as PPI doses were adjusted to reach effective acid suppression. At one year, they observed a higher rate of BO recurrence in patients who had reduced their PPI use, suggesting that, if eradication is obtained, it should be followed by lifelong high dose PPI therapy to avoid recurrence.

An interesting finding of this paper was the trend towards more severe biliary reflux among patients with persistent BO at the end of treatment, suggesting that acid reflux is not the only factor to be considered when examining the mechanisms affecting outcome of such therapy. Unfortunately, the authors did not perform bilimetry in all patients and may have compromised their chance of reaching a significant difference in this evaluation of biliary reflux and characterising the “factors determining persistence and recurrence of BO”.

Another major concern of such ablative therapy is cost effectiveness. Even if it was successful in every patient, the cost of a median of three endoscopic therapy sessions is not negligible. To that the cost of potential complication management has to be added, and may be significant, especially when higher power APC is used. Moreover, as suggested in this paper, if high doses of PPI have to be taken for life, this will further enhance the total cost. This might be justified if no further follow up is needed. However, taking into account that in this study after one year less than 50% of patients were clear of BO and that there was no evidence that surveillance could be avoided in some of the treated patients, endoscopic ablation therapy for non-dysplastic Barrett’s increased the cost of patient management without evidence of benefit.

Other ablative therapies (PDT, mucosectomy) have been shown recently to be useful in patients with BO and severe dysplasia or early carcinoma^12–15 and are currently the most interesting area of therapeutic endoscopy application in BO, especially in patients at higher risk of surgery (who are numerous among BO cases). These techniques are however associated with a higher rate of complications and not applicable for non-dysplastic BO. The study of Basu et al stresses that ablation of non-dysplastic BO is far from being proved useful for patients and should strictly remain in the area of experimental clinical studies.