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PAPERS:
Liam Murray, Peter Watson, Brian Johnston, James Sloan, Inder Mohan Lal Mainie, and Anna Gavin
Risk of adenocarcinoma in Barrett's oesophagus: population based study
BMJ 2003; 327: 534-535 [Full text]
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[Read Rapid Response] Cancer Risk in Barrett's oesophagus
Clive J Kelty, Martin D. Gough   (15 September 2003)
[Read Rapid Response] Without Oncological Terrain, oncogenesis does not occur.
Sergio Stagnaro   (15 September 2003)

Cancer Risk in Barrett's oesophagus 15 September 2003
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Clive J Kelty,
Specialist Registrar in General Surgery
Rotherham District General Hospital, Moorgate Road, Rotherham, S60 2UD,
Martin D. Gough

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Re: Cancer Risk in Barrett's oesophagus

Dear Sir,

We were interested to read the report by Murray and colleagues of the cancer risk in patients with Barrett’s oesophagus (1). This raises issues in the continuing debate over the risks associated with Barrett’s oesophagus, and how it should be managed (2). It is widely reported that the metaplastic epithelium confers a lifetime risk of developing adenocarcinoma of around 10%, which equates to 1 in 52 to 1 in 441 patient years, or 30-125 times the risk of the general population (2-5). However, many of these studies are retrospective, with short follow up, and include a mixture of patients with metaplastic and dysplastic epithelium in the analysis.

However, the most significant point of interest is that these studies have a very ‘loose’ definition of Barrett’s, namely columnar lined oesophagus on pathological examination. Indeed, in this paper by Murray et al, Barrett’s epithelium is defined as “the presence of columnar metaplasia”. It is now recognised that without histological evidence of specialised intestinal metaplasia, this carries no increase in risk for carcinoma (4).

In this study, the risk of adenocarcinoma in the subgroup of patients with specialised intestinal metaplasia equated to 1 in 250 years of patient follow up. This is consistent with other published studies, which still advocate surveillance. The authors also state that biopsies from the oesophago-gastric junction were excluded. This raises the issue of potentially excluding patients with short segment Barrett’s oesophagus (SSBO). It is now recognised that this does carry a risk of progression to adenocarcinoma, albeit presently this is difficult to quantify (5).

The risk associated with Barrett’s oesophagus remains a controversial topic. Further studies are required to ascertain the risk in patients who have histological confirmation of specialised intestinal metaplasia, and it may be that in these patients this risk is much higher (when compared to historical data), and that these groups of patients are the ones who merit endoscopic surveillance, or ablation techniques. This is an issue that requires to be addressed in large prospective clinical studies, and will allow present guidelines to be revised accordingly.

Clive J. Kelty, Specialist Registrar in General Surgery, Department of Surgery, Rotherham District General Hospital

Martin D. Gough, Specialist Registrar in General Surgery, Department of Surgery, Chesterfield and North Derbyshire Royal Hospital

References

1) Murray L, Watson P, Johnston B, Sloan J, Mainie IM, Gavin A. Risk of adenocarcinoma in Barrett’s oesophagus: population based study. BMJ 2003; 327:534-5

2) Shaheen NJ, Crosby MA, Bozymski EM, Sandler RS. Is there publication bias in the reporting of cancer risk in Barrett's esophagus? Gastroenterology 2000; 119:333-8

3) Hameeteman W, Tytgat GN, Houthoff HJ, van den Tweel JG. Barrett's esophagus: development of dysplasia and adenocarcinoma. Gastroenterology 1989; 96:1249-56

4) Haggitt RC. Barrett’s esophagus, dysplasia, and adenocarcinoma. Hum Pathol 1994; 25:982-93

5) Sharma P. Short segment Barrett esophagus and specialized columnar mucosa at the gastroesophageal junction. Mayo Clin Proc 2001; 76:331-4

Competing interests:   None declared

Without Oncological Terrain, oncogenesis does not occur. 15 September 2003
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Sergio Stagnaro,
Specialist in Blood, Gastrointestinal, and Metabolic Diseases.
Via Erasmo Piaggio 23/8. 16037 Riva Trigoso (Genoa) Italy

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Re: Without Oncological Terrain, oncogenesis does not occur.

I think that because congenital functional mitochondrial cytopathology is overlooked--a "conditio sine qua non" of the most frequent and dangerous human disorders, including malignancies (See Oncological Terrain in webb-site, HONCode 233736, http://digilander.libero.it/semeioticabiofisica, URL http://digilander.libero.it/semeioticabiofisica/oncologico.htm--all current clinical research is fundamentally biased. That is, it does not consider the existence or assess the seriousness as well as the location of Congenital Acidosic Enzyme-Metabolic Histangiopathy (1, 2).

In fact, both environmental risk factors including Barrett's oesophagus, suggested as a risk factor for cancer, "could" influence some human biological functions and/or bring about different disorders, such as cancers, exclusively in relation to both the presence and intensity of CAEMH in a well-defined biological system of individuals affected by an oncological constitution (in my town, about 33% of population!). Even in presence of Oncological Terrain, of course, in case of oesophagus cancer, the local "real" risk of malignancy is analogous to what happens in breast cancer (1). In conclusion, Oncological Terrain and the regional "real" risk" precede, for years or decades, any oncogenesis that occurs.

1) Stagnaro-Neri M., Stagnaro S., Cancro della mammella: prevenzione primaria e diagnosi precoce con la percussione ascoltata. Gazz. Med. It. – Arch. Sc. Med. 152, 447 1993

Competing interests:   None declared