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• Effect of Midazolam and Endoscopy on Lower Esophageal Sphincter (LES) Function.
  Johannes Lenglinger
  Published on: 1 July 2004
• Authors' Reply to Nandurkar: Short segment reflux and acid pocket
  Professor Kenneth E.L. McColl
  Published on: 5 May 2004
• Short segment reflux: Acid but no Pocket?
  Sanjay Nandurkar
  Published on: 7 April 2004

• Published on: 1 July 2004

  Effect of Midazolam and Endoscopy on Lower Esophageal Sphincter (LES) Function.

  • Johannes Lenglinger
  • Other Contributors:
    • Enrico P Cosentini and Franz M Riegler

  Dear Editors

  With interest we read the article by J Fletcher et al,[1] entitled "Studies of acid exposure immediately above the gastroesophageal squamocolumnar junction: evidence of short segment reflux" published in the recent issue of GUT. Demonstration of an increased acid exposure to the most distal esophagus vs. 5 cm above the lower esophageal importantly contributes to better understanding of the...

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  Dear Editors

  With interest we read the article by J Fletcher et al,[1] entitled "Studies of acid exposure immediately above the gastroesophageal squamocolumnar junction: evidence of short segment reflux" published in the recent issue of GUT. Demonstration of an increased acid exposure to the most distal esophagus vs. 5 cm above the lower esophageal importantly contributes to better understanding of the pathophysiology of gastroesophageal reflux disease including "carditis" and "short segment Barrett esophagus".[1,2] However, methodological issues should be considered for interpretation of the data presented: Placement of the pH catheter was conducted endoscopically following intravenous administration of midazolam.[1] Controversy exists, if midazolam would exert an effect on LES pressure and esophageal motility.[3,4] While Rubin J et al.[3] showed that midazolam did not change LES pressure, Marsh JK et al.[4] demonstrated that i.v. midazolam affects LES pressure and esophageal motility, and concluded that midazolam should not be administered prior to esophageal motility testing. In addition, endoscopic insufflation of air causes gastric distention, which in turn would impair LES function by shortening of LES length and by inducing transient lower esophageal sphincter relaxations.[2,5] Thus, effects of midazolam and endoscopy on LES function and esophageal acid exposure cannot be ruled out. Clarification of the issues would be helpful for the design and interpretation of future studies involving upper GI function tests.

  References

  1. Fletcher J, Wirz A, Henry E, McColl KE. Studies of acid exposure immediately above the gastroesophageal squamocolumnar junction: evidence of short segment reflux. Gut 2004; 53: 168-173.

  2. Wykypiel H, Gadenstätter M, Granderath FA, Klingler PJ, Wetscher GJ. Pathophysiology of gastroesophageal reflux disease (GERD) with respect to reflux induced carcinogenesis. Eur Surg 2002; 34/5: 296-302.

  3. Rubin J, Brock-Utne JG, Downing JW. Intravenous midazolam does not change lower esophageal sphincter pressure. S Afr Med J 1983; 64(26): 1024.

  4. Marsh JK, Hoffman SM, Dmuchowski CF. Effect of intravenous midazolam on esophageal motility testing in normal human volunteers. Am J Gastroenterol 1993; 88(6): 860-863.

  5. Scheffer RC, Akkermans LM, Bais JE, Roelofs JM, Smout AJ, Gooszen HG.Neurogastroenterol Motil 2002; 14(6): 647-655.

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  Conflict of Interest:
  None declared.

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• Published on: 5 May 2004

  Authors' Reply to Nandurkar: Short segment reflux and acid pocket

  • Professor Kenneth E.L. McColl, Professor of Gastroenterology

  Dear Editor

  We thank Dr Nandurkar for his interest[1] in our recent papers regarding luminal acidity at the gastro-oesophageal junction following meals.

  In our first study, we observed a postprandial region of high acidity in the cardia region and extending across the Z-line.[2] The presence of this postprandial acid pocket at the cardia has been confirmed by two other groups[3,4]

  In our more rec...

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  Dear Editor

  We thank Dr Nandurkar for his interest[1] in our recent papers regarding luminal acidity at the gastro-oesophageal junction following meals.

  In our first study, we observed a postprandial region of high acidity in the cardia region and extending across the Z-line.[2] The presence of this postprandial acid pocket at the cardia has been confirmed by two other groups[3,4]

  In our more recent study, we observed a high degree of acid exposure when a pH electrode was clipped to the squamous mucosa which is proximal to the Z-line.[4]

  Dr Nandurkar wondered why we did not observe more prolonged acid exposure in the second study if the postprandial acid pocket extends into the distal oesophagus. There are several reasons for the apparent differences in the two studies. The first is that the design and methodology of the two studies were different. The first study involved slowly withdrawing a pH probe at 1cm increments every minute from the distal stomach into the oesophagus and was performed after a large fatty meal with the patient in a semirecumbant position. In contrast, the second study employed a static probe fixed to the distal oesophagus and which recorded both fasting and postprandial pH over a 24h ambulatory period. The difference in the duration of the recording of pH in the distal oesophagus between the two studies and the differences in relationship to food intake and difference in posture and mobility make it difficult to directly compare the two studies. In our second study, we did observe that the acid exposure of the most distal oesophagus was more during the postprandial period, consistent with the observations of the first study. However, we acknowledge that the duration of acid exposure of the most distal oesophagus during the postprandial period with the fixed probe was not as great as that observed in our earlier study when the probe was slowly withdrawn from the stomach into the oesophagus.

  It is possible that the methodology employed in the first study could exaggerate the degree of proximal extension of the unbuffered acid pocket into the distal oesophagus. This might be due to the pH probe carrying over some acidic juice from the cardia acid pocket into the oesophagus and this taking time to be fully cleared/neutralized. It is always difficult to know the extent to which the technique used to measure physiology may be altering events.

  What is clear from both of our studies and the two other groups which have undertaken similar studies is that during the postprandial period, (a) there is a region of relatively unbuffered high acidity in the proximal cardia region of the stomach and (b) this acid frequently encroaches on the distal oesophageal mucosa.[1-4]

  References

  1. Nandurkar S. Short segment reflux: Acid but no Pocket? [electronic response to Fletcheret al. Studies of acid exposure immediately above the gastro-oesophageal squamocolumnar junction: evidence of short segment reflux] gutjnl.com 2004http://gut.bmjjournals.com/cgi/eletters/53/2/168#343

  2. Fletcher J, Wirz A, Young J, Vallance R, McColl K E L. Unbuffered highly acidic gastric juice exists at the gastroesophageal junction after a meal. Gastroenterology, 2001; 121: 775-783.

  3. Hila A, Xue S, Knuff D, Katz P O, Castetll D O. Post-prandial gastric acid layer is not only localised below the EG junction. Gastroenterology, 2003; 124: 4: suppl. 1: A410.

  4. Iwakiri K, Nind G, Wu Zou D, Sifrim D, Rigda R, Dent J, Holloway R H. Regional variations in postprandial gastric pH and their relationship to acid reflux in healthy volunteers. Gastroenterology, 2003; 124: 4: suppl.1: A412.

  4. Fletcher J, Wirz A, Henry E, McColl K E L. Studies of acid exposure immediately above the gastro-oesophageal squamocolumnar junction: evidence of short segment reflux. Gut, 2004; 53: 168-173.

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  Conflict of Interest:
  None declared.

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• Published on: 7 April 2004

  Short segment reflux: Acid but no Pocket?

  • Sanjay Nandurkar, Gastroenterologist

  Dear Editor

  I read the recent paper by Fletcher et al. with interest.[1]

  In your earlier study,[2] your group reported the existence of an unbuffered acid pocket in 60% of your study subjects which extended for approximately 2 cms (median length) in the postprandial period. Furthermore, when pre and post-prandial pH step up distances were measured and correlated with clips fixed to the oesophagus...

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  Dear Editor

  I read the recent paper by Fletcher et al. with interest.[1]

  In your earlier study,[2] your group reported the existence of an unbuffered acid pocket in 60% of your study subjects which extended for approximately 2 cms (median length) in the postprandial period. Furthermore, when pre and post-prandial pH step up distances were measured and correlated with clips fixed to the oesophagus, this acid pocket was localised to a region "just above" the squamo-columnar junction. It would be fair to infer then, that if a pH sensor was firmly implanted just above the squamo-columnar junction, it would record a prolonged acid reflux event in the post prandial state as the probe would be continuously bathed in acid from this reservoir. This is distinct to intermittent acid reflux events due to transient lower oesophageal sphincter relaxations or straining.

  In your recent paper,[3] you found greater acid exposure at the squamo- columnar junction compared with a site located 5 cms proximally (standardised recording point), which intuitively is not unexpected. This is especially so if DeMeesters hypothesis (which you alluded to in your manuscript) were to be accepted which proposed that the lower oesophageal sphincter, incorporating the squamo-columnar junction, opens up and becomes part of the stomach in the postprandial period. However, you have stated that there was no significant difference in the mean length of acid reflux episodes when both sites were compared. This appears to be at odds with the first study as one would have expected to observe a prolonged acid reflux event at the distal oesophageal recording site (i.e. just above the squamo-columnar junction). However, this was not the case. In addition, the presentation of data in the results section of the current study shows a distinct lack of emphasis regarding the "acid pocket theory" which would lead one to assume that this was not observed. How do the authors reconcile these observations from their two studies?

  References

  1. J Fletcher, A Wirz, E Henry, and K E L McColl. Studies of acid exposure immediately above the gastro-oesophageal squamocolumnar junction: evidence of short segment reflux. Gut 2004; 53: 168-173

  2. Fletcher J, Wirz A, Young J, Vallance R, McColl KEL. Unbuffered highly acidic gastric juice exists at the gastroesophageal junction after a meal. Gastroenterology 2001;121:775-83.

  3. Fletcher J, Wirz A, Henry E, McColl KEL. Studies of acid exposure immediately above the gastro-oesophageal junction: evidence of short segment reflux. Gut 2004;53:168-73.

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  Conflict of Interest:
  None declared.

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