Introduction
Barrett Esophagus (BE) is a long-term complication of inadequately controlled gastroesophageal reflux (GERD) resulting in the metaplastic transformation of the esophageal epithelium. Current therapy involves proton pump inhibitors (PPIs), aiming at reducing gastric, and consequently esophageal acid exposure time (AET), thereby eliminating the main pathogenic drive to dysplasia/adenocarcinoma progression. However, current guidelines recommend a standard dose PPI therapy for BE chemoprevention, without taking into consideration the need for 24-hour pH-impedance monitoring (24h MII-pH), which is the only investigation able to objectively estimate the esophageal acid exposure time (AET) and evaluate the real effectiveness of PPI therapy.
Aims & Methods
This study included prospectively enrolled BE patients referred to our tertiary care center. We identified consecutive patients with histological diagnosis of non-dysplastic BE treated with a standard dose of PPI administered once or twice daily (either pantoprazole or esomeprazole 40mg OD or 20mg BID), according to guidelines. After at least 8 weeks of PPI therapy, all participants underwent a high-resolution manometry (HRM) and 24h MII-pH monitoring on therapy. A cohort of refractory GERD patients matched for age, sex and PPI regimen (dose and type) were used as controls. GERD symptoms were recorded in the whole population by using the standardized GERD-Q questionnaire. Results are expressed as mean±SD.
Results
A total of 33 BE (23M, 50±17 years) and 33 GERD patients (21M, 48±14 years) were enrolled. Typical GERD symptoms were significantly less severe in BE patients compared to controls (2.1±2.1 vs 3.1±2.3; p<0.05). Half of the population of BE patients did not achieve adequate esophageal acid suppression (AET<4%) under standard dose regimen. Despite matching PPI regimen, the risk of having a pathological 24h MII-pH was doubled in BE compared to refractory GERD patients (50% vs 25%; p<0.05). The mean AET was significantly higher in BE compared to GERD patients (6.6±10.2%vs 1.9±3%; p<0.05), particularly in the supine position (7.3±15.5% vs 2.3±5.6%; p<0.05), despite similar levels of gastric acid suppression (44.1± 25.7% vs 49.2±27%; p=NS). Although the average number of reflux events was comparable between BE and controls (49±29 vs 40±22), BE exhibited a notably prolonged reflux clearance time (mean duration of the longest reflux episode: 27.8±25.7 vs 12.7±27.3 min; p<0.05). Furthermore, Type IIIA esophagogastric junction (EGJ) morphology was more prevalent BE group compared to controls (45% vs 21%; p<0.05) as was the prevalence of ineffective esophageal motility (IEM) according to the Chicago Classification version 4.0 (42% vs 12%; p<0.05).
Conclusion
Despite the reduced severity of typical GERD symptoms, analogous therapeutic regimens and comparable gastric acid suppression, BE patients showed a significantly increased esophageal AET, especially in the supine position, compared to refractory GERD patients. Furthermore, at HRM, BE patients showed a higher prevalence of Type IIIA EGJ morphology and IEM that could justify these results. Our data show that half of the whole BE population failed to achieve an adequate esophageal acid suppression despite therapy, emphasizing the relevance of performing an HRM and a 24h MII-pH in all non-dysplastic BE patients, in order to tailor the therapeutic strategy and improve BE long-term outcomes.
