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Adenocarcinoma arising in columnar lined oesophagus following treatment with argon plasma coagulation
  1. A SHAND,
  2. H DALLAL,
  3. K PALMER,
  4. S GHOSH
  1. Gastrointestinal Unit, Western General Hospital
  2. Edinburgh, EH4 2XU, UK
  3. Department of Pathology, Western General Hospital
  4. Edinburgh, EH4 2XU, UK
  1. Dr A Shand.ashand{at}
  1. Department of Gastroenterology
  2. Erasme University Hospital, Brussels, Belgium
  3. jvlaethe{at}

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Editor,—Following the recent report by Van Laethemet al (OpenUrlCrossRefPubMedWeb of Science) of adenocarcinoma developing in a patient whose columnar lined oesophagus had been treated by argon plasma coagulation, we wish to highlight a second case.

A 67 year old man presented with epigastric discomfort but no “alarm” symptoms of dysphagia or weight loss. Endoscopy revealed a 5 cm length of columnar lined oesophagus with no evidence of ulceration or stricture. Histology showed intestinal metaplasia with low grade dysplasia. He consented to enter a study of argon plasma coagulation treatment in Barrett's oesophagus.

One half of the affected oesophagus was treated with argon plasma coagulation (Erbe APC 300, Erbe Elektromedizin GmbH, Germany). He was commenced on omeprazole 40 mg. Repeat endoscopy at two months showed macroscopic regrowth of the squamous epithelium in the area treated by argon plasma coagulation. This was confirmed histologically and the previously noted dysplasia had disappeared. He did not attend for repeat endoscopy at four months but was admitted because of significant weight loss and dysphagia. Endoscopy showed a stricture at the gastro-oesophageal junction and biopsies confirmed poorly differentiated adenocarcinoma. CT scanning of the thorax and abdomen showed thickening of the oesophageal wall but no obvious metastases. However, at laparotomy, he was found to have an unresectable tumour with extensive local spread and distant metastases to the liver.

This case illustrates two key points. Firstly, carcinoma developed in spite of argon plasma coagulation treatment. Only half of the affected mucosa was treated in this study to allow the remaining half to serve as an internal control and so it is impossible to state whether this oesophageal carcinoma arose in the argon plasma coagulation treated or untreated segment. The central issue is whether squamous re-epithelialisation abolishes the malignant potential of the gastro-oesophageal junction. Destruction of columnar epithelium by argon plasma coagulation followed by restitution of squamous epitheliummay reverse dysplastic changes but could simply hide them.

Secondly, and perhaps more importantly, this carcinoma went undetected in spite of rigorous endoscopic follow up and a well defined biopsy protocol, raising further doubts over the effectiveness of conventional endoscopic surveillance of columnar lined oesophagus. The surveillance process is subject to several potential sampling errors. The dysplastic process may be patchy and changes may be missed at biopsy. The histological interpretation of dysplasia is subjective and observer dependent. Finally, carcinoma may arise from the submucosal layers of the oesophagus, with very little mucosal abnormality, and beyond the reach of conventional endoscopic biopsy forceps. Such carcinomas are likely to remain undetected until a very late stage.

No evidence of the phenomenon of “buried glands” was seen following argon plasma coagulation treatment in this case. Other authors have reported this appearance following thermal ablative treatment of columnar lined oesophagus.1-4 These islands of persistent metaplastic tissue may retain the potential for malignant transformation. Their significance is as yet unclear but, in this case at least, they cannot be implicated in the progression to carcinoma.

All patients with columnar lined oesophagus who have participated in clinical studies of argon plasma coagulation will require close follow up over many years to ensure that potentially malignant tissue has truly been ablated and not merely covered by a “whitewash” of squamous epithelium.



Editor,—Dr Shand and colleagues clearly underlined, as we did (), the major concerns about the eradication of Barrett's mucosa by thermocoagulation. Their case differs from ours in the followings ways: our patient did not show any dysplasia at baseline diagnosis, has completed full eradication of the Barrett's segment, and showed recurrence of neoplasic glands after a period of 18 months, clearly beneath the squamous; this last finding supports the fact that emergence of neoplastic glands was probably newly developed. The present case is interesting because it raises another concern with this type of management; as no buried glands were evidenced under the new squamous layer and the interval between endotherapy and occurrence of unresectable tumour was very short (approximately four months), this case clearly illustrates the need for a complete and optimal staging and mapping of the target areas before starting the destruction of Barrett's mucosa disclosing dysplasia.

As stated and discussed by the authors, the initial dysplastic process was probably patchy and changes may be missed or under staged at biopsy; in this situation, argon plasma coagulation treatment only hides the dysplastic areas.

Furthermore, submucosal origin of the carcinoma ideally should be excluded by performing endoscopic ultrasonography and profound biopsies with large forceps.

Reporting these cases clearly shows that:

Barrett's mucosa destruction remains experimental and surveillance has to be strictly maintained.
Selection of patients is paramount and should include accurate staging and mapping of the target areas before endotherapy.