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Gastro-Esophageal Reflux
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Gastro-esophageal reflux disease (GERD) is a common medical condition in which the liquid content of the stomach regurgitates (backs up or reflexes) into the esophagus. This liquid can damage the esophageal lining but surprisingly, the symptoms of such damage are not always visible! The regurgitated liquid usually contains acid and pepsin that are produced by the stomach. Treatment options for GERD include antacids (e.g., magaldrate, magnesium hydroxide, aluminum hydroxide, calcium carbonate), Histamine H2 receptor blockers (ranitidine, cimetidine) and proton pump inhibitors (PPI, e.g. omeprazole, pantoprazole, lansoprazole).
Antacids have been available for many years. However, their importance has declined since the development of histamine H2 antagonists and more recently proton pump inhibitors. Unfortunately, numbers of patients with GERD not responding to PPIs are increasing. This can be explained by the fact that, symptoms of GERD arise when the gastric fluid, which is acidic in nature, comes in contact with esophageal mucosa. Proton pump inhibitors decrease the acid production leading to increase in the pH of gastric fluid. However, PPIs do not neutralize the acid which is already present in the stomach. H2 blocker work in the same line as PPI and they are even less potent than PPIs, hence they are not useful for the patients not responding to PPI.
Not only the decreased effectiveness but increasing adverse events is also a problem with PPI. Reports of adverse events with use of PPI are increasing; among which, increased risk of osteoporosis and hypomagnesaemia are more common. Recently in a short period of time the US-FDA has warned the patients and physicians about these adverse events of PPI. It will not be a surprising situation if the patients look back to antacids for such diseases. Hence, scope of antacid in the management of GERD should be re-evaluated.
Antacids are believed to act by neutralizing the gastric acid. However, Efficacy of antacids in patients with heartburn does not seem to be related to their neutralizing capacity, but to their ability to ‘stick’ within the esophagus and provide local intra-esophageal antacid effect. Antacids might raise the pH locally and so provide relief from the symptom. In patients with reflux esophagitis, 2-weeks treatment with low dose antacid has resulted in lower global symptomatic scores (p < 0.05), less acid regurgitation (p < 0.05), and fewer days (p < 0.01) and nights (p < 0.05) with heartburn than during placebo therapy. Not only placebo, but antacids have also been compared with H2 blockers. In a randomized clinical trial, antacid was found to be better than placebo and was nearly as effective as ranitidine (150mg bid) in the management of symptoms of reflux disease. Antacid shows similar efficacy to cimetidine (20mg/kg/day) in terms of improvement in clinical scores, pH and endoscopic variables in children with gastro-esophageal reflux and peptic esophagitis.
Antacids provide similar efficacy as that of H2 blockers without systemic side effects. Hence, antacids can be the preferred choice for patients with mild GERD. Whereas, for patients with sever GERD, antacids can be used as an add-on therapy to PPI in order to increase the compliance of the therapy. In a consensus opinion regarding GERD treatment, Tytgat et al. has suggested to use antacids as an additional option for patients presenting at primary care with symptoms of reflux, or for patients with ongoing symptoms incompletely controlled with acid suppressant. In a recently publish trial, it is reported that addition of an antacid in a regular therapy of GERD, improves its results and accelerates elimination of clinical symptoms. By the end of the study, all symptoms of GERD were eliminated in 100% of the patients in patients receiving antacid as compared to only 78.3% in patients not receiving antacid (Fig 1).
Fig 1: Impact of adding antacid in regular therapy on elimination of GERD symptoms.
Because of the immediacy of their effect antacids continue to be useful to patients with milder reflux disease, or for those with more severe disease who experience breakthrough symptoms on prescription drugs.
References
i. Tytgat GN; Mccoll K; Tack J; Holtmann G; Hunt RH; Malfertheiner P; et al. New Algorithm for the Treatment of Gastro-Oesophageal Reflux Disease. Alimentary Pharmacology & Therapeutics. 2008;27(3):249-256.
ii. Decktor DL, Malcolm R, Maton, PN, et al. Effects of aluminum/ magnesium hydroxide and calcium carbonate on esophageal and gastric pH in subjects with heartburn. Am J Ther 1995; 2: 546-52
iii. Weberg R, Berstad A. Symptomatic effect of a low-dose antacid regimen in reflux oesophagitis. Scand J Gastroenterol. 1989 May;24(4):401-6.
iv. Grove O, Bekker C, Jeppe-Hansen MG, Karstoft E, Sanchez G, Axelsson CK, Nielsen HO, Andersen B, Rask-Madsen J. Ranitidine and high-dose antacid in reflux oesophagitis. A randomized, placebo-controlled trial. Scand J Gastroenterol. 1985 May;20(4):457-61.
v. Cucchiara S, Staiano A, Romaniello G, Capobianco S, Auricchio S. Antacids and cimetidine treatment for gastro-oesophageal reflux and peptic oesophagitis. Arch Dis Child. 1984 Sep;59(9):842-7.
vi. Maev IV, Samsonov AA, Beliantseva EV, Golubev NN, Odintsova AN, Andreev NG. Combined therapy of acid-dependent gastrointestinal disorders with the use of antacidic drug RelcerKlin Med (Mosk). 2009;87(8):48-52.
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Chillibreeze's disclaimer: This is a contributed article and was published on Chillibreeze in October, 2011. The views and opinions expressed in this article are those of the author(s) and do not reflect the views of Chillibreeze as a company. Chillibreeze has a strict anti-plagiarism policy. Please contact us to report any copyright issues related to this article. The relevance of the facts and figures cited (if any) could change after a period of time.
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