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Helicobacter pylori and gastro-oesophageal reflux disease
- Giovanni Cammarota, Giovanni B. Gasbarrini, senior lecturer (12 June 2004)
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Does the study tell us about gastro-oesophageal reflux disease?
- Ian L. P. Beales (19 June 2004)
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Giovanni Cammarota, assistant professor Unit of Gastroenterology; Catholic University Hospital, largo A. Gemelli, 8 - 00168, Roma, Italy, Giovanni B. Gasbarrini, senior lecturer
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EDITOR-I read with interest the R.F. Harvey and co-Authors’ article on the effects of H. pylori infection on heartburn and gastro-oesophageal reflux (1). However, as the Authors recognize, the mechanism by which Helicobacter (H.) pylori infection might affect reflux symptoms is by affecting secretion of gastric acid, due to the H. pylori-related antral gastritis which results in an net increase in acid secretion (2). Nevertheless, an amount of recent studies, by combining old and new diagnostic tools (such as pH monitoring, bilimetry and intraluminal oesophageal impedance) are providing a new and more detailed characterisation of the factors contributing to the “so-called” gastro- oesophageal reflux disease (3-5). In other terms, as Harvey and co-Authors recognize, their study has some weaknesses, due to the missing of direct information on the pathology underlying the symptoms of the patients, and one of these is that a subset of the enrolled patients might have reflux symptoms due to the occurrence of non-acid or non-liquid reflux events. This fact may possibly lead to an underestimation of the real role of H. pylori in the pathogenesis of acid-related heartburn and gastro- oesophageal acid reflux. References: 1) Harvey RF, Lane A, Murray LJ, Harvey IM, Donovan JL, Nair P. Randomised controlled trial of effects of Helicobacter pylori infection and its eradication on heartburn and gastro-oesophageal reflux: Bristol helicobacter project. BMJ, 2004;328:1417, dol:10.1136/bmj.38082.626725.EE (published 4 May 2004). 2) El Omar EM, Penman ID, Ardill JE, Chittajallu RS, Howie C, McColl KE. Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. Gastroenterology 1995;109:681-91. 3) Tack J, Koek G, Demedts I, Sifrim D, Janssens J. Gastroesophageal reflux disease poorly responsive to single-dose proton pump inhibitors in patients without Barrett's esophagus: acid reflux, bile reflux, or both? Am J Gastroenterol 2004;99:981-8. 4) Kawamura O, Aslam M, Rittmann T, Hofmann C, Shaker R. Physical and pH properties of gastroesophagopharyngeal refluxate: a 24-hour simultaneous ambulatory impedance and pH monitoring study. Am J Gastroenterol 2004;99:1000-10. 5) Shay S, Tutian R, Sifrim D, Vela M, Wise J, Balaji N, et al. Twenty-four hour ambulatory simultaneous impedance and pH monitoring: a multicenter report of normal values from 60 healthy volunteers. Am J Gastroenterol 2004;99:1037-43. Competing interests: None declared |
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Ian L. P. Beales, Senior Lecturer Gastroenterology Department, Norfolk and Norwich University Hospital, Norwich, NR4 7UZ
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Editor – The relationships between H. pylori infection and gastro- oesophagal reflux disease (GORD) are controversial. The recent paper by Harvey at al (1) contributes to these questions but many inconsistencies in the paper need to be discussed before these data can be taken to usefully extend the debate. The very first line contains an error: patients with H. pylori do not usually have “antral gastritis with increased acid secretion and risk of duodenal ulcer,” most patients have a mild pangastritis with normal intragastric acidity, the antral inflammation stimulates hypergastrinaemia which is balanced by a relative suppression of acid-secretion in the oxyntic body.(2) These changes resolve with eradication.(2, 3) Duodenal ulcer only occurs in 10% of infected patients.(4) The authors seem confused as to whether they are assessing gastro- oesophageal reflux disease as they claim, or occasional symptoms. Heartburn is a relatively specific marker of GORD but is not sensitive, and acid regurgitation is even less sensitive.(5) The prevalence of reflux symptoms once a month, the authors’ definition, is very high, many people would not call this pathological and detecting effects of H pylori eradication against this background might be difficult. Most authorities suggest heartburn twice a week is a more reasonable definition of GORD (5) and of note the landmark paper linking symptomatic gastro-oesophageal reflux to oesophageal adenocarcinoma (6) used reflux symptoms once a week as the minimal criteria. These issues are important when comparing this paper to the others cited that have used much more objective diagnoses of GORD. If the study was genuinely intended specifically to address the H. pylori-reflux question, as opposed to a post hoc analysis of available data, the design is poor. Reflux is more troublesome and symptomatic in the elderly (7, 8) and by excluding those over 60, the authors may have failed to study those most at risk. The authors used a questionnaire but there is no evidence that this has been validated against reliable measures of gastro-oesophgeal reflux disease such as Los Angeles scoring at endoscopy (5) or preferably ambulatory oesophageal pH monitoring. Well- validated questionnaires designed for specifically for reflux symptoms are available (8) and it is unfortunate the authors did not use one of these. The data analysis in relation to the papers title is also confusing. The results are presented as the intention to treat analysis for the anti- H pylori dual therapy, but the authors’ discussion centres on the physiological changes of infection and surely the more important patholphysiological question is whether actual clearance of H pylori, as opposed to intending eradication treatment, actually exacerbates reflux? The authors have not presented this data. All these issues should be reviewed when considering if this paper tells us much more about the relationship between H. pylori and oesophageal acid exposure. References 1 Harvey RF, Lane JA, Murray LJ, Harvey IM, Donovan JL, Nair P. Randomised controlled trial of effects of Helicobacter pylori infection and its eradication on heartburn and gastro-oesophageal reflux: Bristol helicobacter project. BMJ 2004;328:1417-1419. 2 Beales, I. The H. pylori-Gastrin link. In: Merchant JL, Buchan AM, Wang TC, eds. Gastrin in the New Millennium. Los Angeles: CURE Foundation, 2004;253-263. 3 Prewett EJ, Smith JT, Nwokolo CU, Hudson M, Sawyerr AM, Pounder RE. Eradication of Helicobacter pylori abolishes 24-hour hypergastrinaemia: a prospective study in healthy subjects. Aliment Pharmacol Ther 1991;5:283- 290. 4 Vaira D, Vakil N, Rugge M, et al. Effect of Helicobacter pylori eradication on development of dyspeptic and reflux disease in healthy asymptomatic subjects. Gut 2003;52:1543-7. 5 Dent J, Brun J, Fendrick A, M., et al. An evidence-based appraisal of reflux disease managment - The Genval Workshop Report. Gut 1999;44:S1- S16. 6 Lagergren J, Bergstrom R, Lindgren A, Nyren O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999;340:825-31. 7 Collen MJ, Abdulian JD, Chen YR. Gastroesophageal reflux disease in the elderly: more severe disease that requires aggressive therapy. Am J Gastroenterol 1995;90:1053-7. 8 Diaz-Rubio M, Moreno-Elola-Olaso C, Rey E, Locke GR, Rodriguez- Artalejo F. Symptoms of gastro-oesophageal reflux: prevalence, severity, duration and associated factors in a Spanish population. Aliment Pharmacol Ther 2004;19:95-105. Competing interests: None declared |
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