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Barrett's oesophagus, proton pump inhibitors and gastrin: the fog is clearing
  1. Ernst J Kuipers1,2
  1. 1Department of Gastroenterology & Hepatology, Erasmus Medical University Center, PO BOX 2040, 3000 CA Rotterdam, The Netherlands
  2. 2Department of Internal Medicine, Erasmus Medical University Center, 2040, 3000 CA Rotterdam, The Netherlands
  1. Correspondence to Dr Ernst J Kuipers, Erasmus MC University Medical Center, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands; e.j.kuipers{at}

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The incidence of Barrett's oesophagus is rising rapidly.1 The presence of metaplastic tissue in the lower oesophagus is by itself an asymptomatic condition, but predisposes to oesophageal adenocarcinoma. Long-term cohort studies reported that the incidence of oesophageal cancer among patients with Barrett's oesophagus approximates 4 per 1000 patient years follow-up, and that ultimately 5–7% of patients with Barrett's oesophagus die of this condition.2 The majority of patients with Barrett's oesophagus suffer from chronic gastro-oesophageal reflux, and therefore often receive proton pump inhibitor (PPI) treatment. The effect of such treatment on Barrett's mucosa and the risk for progression to cancer have been much studied and debated. Reduction of oesophageal acid exposure decreases inflammation and proliferation, increases cell differentiation within the Barrett's segment, and might in theory reverse metaplasia, in particular in areas of ulceration. On the other hand, PPI therapy interferes with oesophageal exposure to secondary bile acids, and increases gastrin, which may induce proliferation, COX-2 upregulation, and perhaps expansion of metaplasia.3 Along this line it has been suggested that PPIs may promote progression of Barrett's metaplasia and progression to cancer. We thus have a body of seemingly conflicting research data, which are difficult to align and provide clinicians with a foggy image of this clinically relevant topic. …

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