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Abolishment of Alkaline Tide by a Proton Pump Inhibitor (PPI) - An Indication for Successful Therapy in Barrett's Esophagus Patients – A Prospective Study
Maria Raskin and Yaron Niv*Department of Gastroenterology, Rabin Medical Center, Tel Aviv University, Israel
- *Corresponding Author:
- Prof. Yaron Niv
Department of Gastroenterology, Rabin Medical Center
49 Jabotinski Street, Petach Tikva 49100, Israel
Tel: 972-3-9377237
Fax: 972-3-9210313
E-mail: yniv@clalit.org.il
Received date: March 05, 2015; Accepted date: March 23, 2015; Published date: March 28, 2015
Citation: Raskin M, Niv Y (2015) Abolishment of Alkaline Tide by a Proton Pump Inhibitor (PPI) - An Indication for Successful Therapy in Barrett's Esophagus Patients – A Prospective Study. J Gastrointest Dig Syst 5:267. doi:10.4172/2161-069X.1000267
Copyright: © 2015 Raskin M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Abstract
Introduction: Gastro-esophageal-reflux disease (GERD) and its complication, Barrett's esophagus, are highly prevalent and request medical attention all over the world. Proton pump inhibitors (PPI) are the treatment of choice, acting as gastric acid secretion inhibitors. The transient increase in blood pH following gastric secretion has been termed alkaline tide (AT) phenomenon, and its measurement provides a non-invasive and inexpensive test for evaluation of hypo- and hyper secretory states. Till today it has never been shown that PPI is able to prevent AT, and to optimize treatment for GERD.
Aim: To investigate PPI effect on the AT phenomenon and to ascertain the power of 80 mg pantoprazole to abolish gastric acid secretion.
Methods: The study group comprised of 7 consecutive patients with endoscopically and histologically diagnosed Barrett's Esophagus. Alkaline tide was measured after a test meal, and then the test repeated after a bolus intravenous injection of 80 mg pantoprazole. Base Excess was measured, and AT calculated according to body weight and bicarbonate circulation distribution factor.
Results: Six patients had AT ≥5 mEQ/45min, and included in the study. In all the participants AT was abolished after pantoprazole injection, and a test meal of 400 kcal became ineffective as a stimulus for gastric acid secretion.
Conclusion: In this paper we demonstrate the efficiency of PPI in lowering acid secretion, established the association between gastric acid secretion and AT, and described a way to measure PPI successes in preventing secretion in Barrett's esophagus patients.
