Argon plasma coagulation ablation of Barrett's oesophagus

The incidence of oesophageal adenocarcinoma continues its prolific rise within the Western world [1,2]. The steady increase in incidence is very different from that of squamous cell carcinoma of the oesophagus, which has remained relatively static in the last two decades. Oesophageal adenocarcinoma presents late, which is reflected in the poor survival statistics with only a 26% survival rate at 1 year and 5% at 5 years (Trent Cancer Registry, UK). Only lung and pancreatic cancer have worse survival statistics. In view of this, research has been directed to premalignant conditions of the oesophagus such as Barrett’s oesophagus. Barrett’s oesophagus is caused by gastro-oesophageal reflux disease [3 /5]. Duodenogastro-oesophageal reflux (DGOR) has also recently been implicated in the aetiology of Barrett’s oesophagus [6]. Dresner et al. have shown that in patients with an intrathoracic oesophagogastrostomy after a subtotal oesophagectomy, there is significant DGOR. This environment causes Barrett’s metaplasia to develop and thus it has been shown that these patients have both excessive acid and bile reflux [6]. Barrett’s oesophagus is a metaplastic columnar replacement of the normal squamous lower oesophageal mucosa. In 1950 Norman Barrett described a case of a chronic peptic ulcer, covered by columnar epithelium, in the lower oesophagus [7]. Barrett originally thought this represented an intrathoracic tubular portion of stomach in a patient with a congenitally short oesophagus. It was not until 1953 that Allison & Johnstone reported that the structure was the oesophagus, which was lined by gastric mucosa, as it had no serosa and also had squamous epithelium found in patchy islands within the mucosa [8]. The metaplastic epithelium can continue to undergo differentiation through dysplasia and on to malignancy. When high-grade dysplasia (HGD) is diagnosed, there is a 40% risk of a concomitant carcinoma in situ [9,10]. In patients who have had oesophagectomies following the diagnosis of HGD, the risk of adenocarcinoma is reported to be between 38% and 50% [11 /14]. The diagnosis of HGD requires the confirmation of a second expert histopathologist. Continual debate has arisen regarding the actual cancer risk to patients with Barrett’s oesophagus and the literature shows marked variations in incidence rates between different studies (Table I). It has been proposed that the incidence of Barrett’s oesophagus is approximately 4% in the general population but that this rises to 12% in patients with oesophagitis. The relative risk of Barrett’s oesophagus progressing to cancer is reported as anywhere between 1 cancer per 52 patient years followed-up to 1 cancer per 441 patient years (Table I). This can also be represented as an approximate annual rate of cancer development of 0.4% from a world-wide systematic review [15]. A review from the UK of 8 studies showed the annual risk to be 1.0% [16]. Barrett’s oesophagus presents a continued clinical dilemma [17,18]. At present, treatment involves regular endoscopic surveillance and medical treatment with a proton-pump inhibitor (PPI), which although giving good symptomatic relief only causes minimal regression of Barrett’s epithelium [19]. Another treatment modality, which is gaining recog-