Barrett Esophagus

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 9387 Experts worldwide ranked by ideXlab platform

George Shih - One of the best experts on this subject based on the ideXlab platform.

Wei-jen Shih - One of the best experts on this subject based on the ideXlab platform.

Primo P Milan - One of the best experts on this subject based on the ideXlab platform.

Glyn G Jamieson - One of the best experts on this subject based on the ideXlab platform.

  • antireflux surgery Barrett Esophagus and adenocarcinoma there is still room for doubt
    Annals of Surgery, 2007
    Co-Authors: Glyn G Jamieson
    Abstract:

    It is our responsibility as scientists......to teach how doubt is not to be feared, but welcomed and discussed.” This statement was made by Richard Feynman of the United States, one of the last century's most brilliant theoretical physicists and original thinkers. And the article by Chang et al in this issue of the journal passes the responsibility test because it challenges what we, as surgeons, would like to believe about the treatment of Barrett Esophagus. Even if a little simplistic, the current wisdom regarding Barrett Esophagus suggests that it is caused by gastroesophageal reflux, and with continuing reflux, a proportion of patients with the condition develop an adenocarcinoma because of the Barrett's mucosa that is present. That this is an important topic is underscored by the rapidly rising incidence in the Western world of adenocarcinoma affecting the Esophagus, and, a priori, it seems reasonable to believe that if we can stop the reflux, we can stop the development of cancer. As antireflux surgery is the only treatment available that stops reflux, it should therefore be the most effective way of stopping the development of cancer. Chang et al document a number of studies where the conclusions suggest just such a scenario. However, using epidemiologic methods, they demonstrate that such studies are almost certainly unconsciously biased; and if the studies used are limited to those where some attempt has been made to obtain comparability of groups, then there is no statistical difference in outcome between those patients with Barrett Esophagus who are treated medically and those who are treated surgically. Two important points arise from the paper. First, when uncontrolled data are used, it can lead easily to erroneous conclusions. This is particularly true when the conclusions are ones that accord with the beliefs of those conducting the study (which is why, as surgeons and scientists, we have to strive to keep doubting). Second, at the present time, the aim of antireflux surgery should be to cure reflux and its symptoms and not to be seen as a means of preventing cancer of the Esophagus. Nevertheless, despite the authors' findings from their review of the literature, is it still possible that surgery might prevent cancer, and do so more effectively, than any other therapy? Certainly, it remains possible. First, as patients undergoing surgery are usually regarded as being at the most severe end of the reflux spectrum, the fact that there were not more cancers in the surgical group compared with the medical group might be interpreted as being a positive outcome (a greater number of cancers were seen in patients treated surgically in the population-based study reported by Ye et al1 in 2001). Probably the only way to overcome this difficulty would be to undertake a large randomized controlled trial; and according to the estimations of Chang et al, this would have to be a very large trial indeed and, therefore, is unlikely ever to be carried out. Second, it may be that, in any study of the effectiveness of surgery, it will be necessary to control for whether the surgery is actually working. This is because, in many studies of patients who have a Barrett Esophagus and who have undergone antireflux surgery, a substantial minority of patients develop acid reflux again.2,3 Furthermore, this recurrence of reflux is not always symptomatic.4 It is therefore possible that providing surgery stops reflux over the long term; it may prevent progression of Barrett's mucosa to cancer. If this was found to be so, then 24-hour pH surveillance following antireflux surgery would be much more important than is currently regarded to be the case. However, the study by Chang et al contains a finding that raises another and rather more fundamental doubt regarding the problem of Barrett Esophagus. Is it possible that Barrett Esophagus has nothing particularly to do with esophageal cancer at all? The problem with Barrett Esophagus being seen as an independent factor in the development of cancer of the Esophagus is the near impossibility of separating it from the reflux that causes it in the first place. Best current evidence tells us that there is an association between reflux and adenocarcinoma, and this association is strong in patients with severe symptoms of reflux over a long period.5 It also tells us that patients who develop Barrett Esophagus are at the worst end of the reflux spectrum.6,7 Now consider the following: Barrett's mucosa alone clearly does not cause adenocarcinoma of the Esophagus, since the great majority of patients with the condition do not develop a carcinoma of the Esophagus. That is, even if the presence of Barrett's mucosa is important, other factors must exist for cancer to develop. In whites, the incidence/prevalence ratios, male to female, for reflux disease, are approximately 1:1,8 and for the development of Barrett's mucosa approximately 1:1,9 and yet the ratio for adenocarcinoma of the Esophagus is more like 10:1.10 In any surgical series of esophagectomy for adenocarcinoma, the incidence of demonstrated Barrett's mucosa is only of the order of half of the patients.11,12 This is usually dismissed as being because the metaplastic mucosa has been replaced by cancer. However, it is equally possible that there was no metaplastic mucosa in the Esophagus in the first place. It was once thought that the longer the segment of Barrett's mucosa, the greater the risk for the development of adenocarcinoma. Strong doubt was raised about this association, however.13 Now the paper by Chang et al shows that significant regression of columnar-lined Esophagus occurred in the surgical group compared with the medical group of patients, without significantly changing the incidence of cancer. It is possible that adenocarcinomas do not arise from columnar cells but from some form of stem cell, and so perhaps the true proximate cause of the cancer is not Barrett's mucosa at all, but chronic inflammation, a time-honored pathogenetic factor for cancer. Reflux is an important cause for such inflammation but may not explain the steep rise in incidence of cancer in the past 30 years. It is certainly easier to explain the 5 points above if there is some other factor at work that has yet to be identified. And so, in the spirit that I think Richard Feynman would approve, the question needs to be asked: “Is Barrett's mucosa really so important in the development of adenocarcinoma, other than as a marker of severe reflux disease?” and does our persistent concentration on it divert our attention from finding an as yet unidentified, but much more important, cause of adenocarcinoma involving the Esophagus?

  • laparoscopic antireflux surgery in the treatment of gastroesophageal reflux in patients with Barrett Esophagus
    Archives of Surgery, 2000
    Co-Authors: David I Watson, Peter G Devitt, P A Game, Glyn G Jamieson
    Abstract:

    Background Patients with gastroesophageal reflux and Barrett Esophagus may represent a group of patients with poorer postoperative outcomes. It has been suggested that such patients should undergo open rather than laparoscopic antireflux surgery. Hypothesis The laparoscopic approach to antireflux surgery is appropriate treatment for patients with Barrett Esophagus who have symptomatic gastroesophageal reflux disease. Methods The outcome of 757 patients undergoing laparoscopic surgery for gastroesophageal reflux disease from January 1, 1992, through December 31, 1998, was prospectively examined. Barrett Esophagus was present in 81 (10.7%) of these patients (58 men and 23 women). The outcome for this group of patients was compared with that of patients undergoing surgery who did not have Barrett Esophagus. Results The types of operation performed were similar for the 2 patient groups. The mean±SD length of columnar mucosa was 47.4±43.6 mm. The average±SD operation time was 79.0±33.4 minutes. Conversion to open surgery occurred in 6 patients. Postoperative outcomes were as follows. Esophageal manometry and 24-hour pH studies before and after laparoscopic fundoplication demonstrated a significant increase in lower esophageal sphincter resting and residual relaxation pressures and a significant decrease in distal esophageal acid exposure. Four patients have developed high-grade dysplasia or invasive cancer within 4 years of their antireflux surgery, and all of these have subsequently undergone esophageal resection. Conclusions The outcome of laparoscopic antireflux surgery is similar for patients with Barrett Esophagus compared with other patients with gastroesophageal reflux disease. This suggests that laparoscopic surgery is appropriate treatment for this patient group.

David A. Katzka - One of the best experts on this subject based on the ideXlab platform.

  • gastroesophageal reflux disease Barrett Esophagus and esophageal adenocarcinoma
    JAMA Internal Medicine, 2004
    Co-Authors: John T Chang, David A. Katzka
    Abstract:

    The incidence of esophageal adenocarcinoma has been rising rapidly over the past few decades. The major risk factors predisposing to the development of adenocarcinoma are long-standing gastroesophageal reflux disease and Barrett Esophagus, but other factors may be involved as cancer can occur in their absence. In patients with Barrett Esophagus, the extent and degree of dysplasia influence the risk of esophageal adenocarcinoma. As neither medical nor surgical therapies have been proven to prevent adenocarcinoma, endoscopic screening of patients with chronic reflux and endoscopic surveillance of patients diagnosed with Barrett Esophagus are usually performed in an effort to detect adenocarcinomas at earlier stages. The evidence supporting strategies in the management of patients with gastroesophageal reflux and Barrett Esophagus is presented.