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Mortality Rates in Patients With Barrett's Oesophagus

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Mortality Rates in Patients With Barrett's Oesophagus
Background: It has been shown that the presence on diagnosis of endoscopic macroscopic markers indicates a high-risk group for Barrett's oesophagus.
Aim: To determine whether proton pump inhibitor therapy prior to diagnosis of Barrett's oesophagus influences markers for risk development of subsequent high-grade dysplasia/adenocarcinoma.
Methods: A review of all patients with Barrett's oesophagus entering a surveillance programme was undertaken. Five hundred and two patients diagnosed with Barrett's oesophagus were assessed on diagnosis for endoscopic macroscopic markers or low-grade dysplasia. Subsequent development of high-grade dysplasia/adenocarcinoma was documented. The relationship between the initiation of proton pump inhibitor therapy prior to the diagnosis of BE and the presence of macroscopic markers or low-grade dysplasia at entry was determined.
Results: Fourteen patients developed high-grade dysplasia/adenocarcinoma during surveillance. Patients who entered without prior proton pump inhibitor therapy were 3.4 times (95% CI: 1.98-5.85) more likely to have a macroscopic marker or low-grade dysplasia than those patients already on a proton pump inhibitor.
Conclusions: Use of proton pump inhibitor therapy prior to diagnosis of Barrett's oesophagus significantly reduced the presence of markers used to stratify patient risk. Widespread use of proton pump inhibitors will confound surveillance strategies for patients with Barrett's oesophagus based on entry characteristics but is justified because of the lower risk of neoplastic progression.

Barrett's oesophagus (BO) is a premalignant condition and adenocarcinoma (CA) is usually preceded by the development of dysplasia. Regular endoscopic surveillance has been advocated for patients with BO, and practice guidelines have recommended intensive endoscopic biopsy protocols to assess the degree of dysplasia and appropriate management. The cost/effectiveness of this has been questioned particularly as most cases of CA are diagnosed at entry and the cancer incidence per patient follow-up year varies greatly in the literature. If a subset of BO patients with higher rates of development of high-grade dysplasia (HGD) and CA could be identified, the cost-effectiveness of surveillance would be improved. It was previously shown by our group that high risk is predicted by male sex and endoscopic macroscopic oesophageal markers, with patients entering with one macroscopic marker 4.4 times more likely to develop low-grade dysplasia (LGD) and 6.7 times more likely to develop HGD/CA than those with no macroscopic marker. To develop appropriate surveillance strategies, risk stratification is required and those patients with strictures, ulcers and nodularity have been shown to be at high risk. But use of proton pump inhibitors (PPIs) may affect these very markers. Accordingly, this study set out to examine whether use of full-dose PPI therapy affected macroscopic markers, negating the utilization of them to select a high-risk patient group for surveillance.

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