Medical management of acid/bile reflux before, during and after endoscopic therapy for Barrett’s esophagus: a narrative review

Abstract

: Persistent injury from reflux to the distal esophagus is a known cause of Barrett’s esophagus (BE). Gastric acid can cause inflammation of the distal esophagus through inflammatory mediators such as cyclo-oxygenase-2, c-myc and mitogen-activated protein kinase signaling. Bile acid exposure to the esophageal mucosa can also exert damage by becoming non- ionized at acidic pH, entering cells and exerting mucosal injury through inflammation cytotoxic pathways. Bile acids also upregulate proto-oncogenes and c-myc. Inadequate acid suppression defined by impedance-pH monitoring is a modifiable risk factor and if left uncontrolled, will increase the risk of recurrence of intestinal metaplasia (IM). It has been shown that a rigorous acid control protocol in combination with endoscopic eradication therapy (EET) can reduce the recurrence of IM. We suggest the following medical treatment regimen for patients undergoing EET: to continue twice daily proton pump inhibitor (PPI), take liquid preparation sucralfate, a GI lidocaine cocktail mixture preparation for topical use as needed with meals and snacks, and a liquid diet for 1–2 days followed by a soft diet for up to a week after EET. Analgesia may be provided with acetaminophen and/or other non NSAIDS products if needed. Diet and lifestyle modifications should also be discussed alongside these recommendations. Both before and after EET, we recommend antireflux protocols including twice daily PPI and optimization of diet, lifestyle and adjunctive medications. By combining successful eradication of Barrett’s with a vigilant surveillance monitoring and optimal antireflux control, this can ultimately lead to improved patient outcomes and decrease recurrence of dysplasia and IM.