Abstract
In contrast to Western countries, reflux esophagitis is considered to be less common in the Orient, including Japan. Transient LES relaxation (TLESR) is a major mechanism of gastroesophageal reflux (GER); however, there are no data on the mechanisms of GER in Japanese people. In addition, it is unclear whether or not the rate of TLESRs, in the sitting position, is higher in reflux esophagitis patients than in healthy subjects. The aim of this study is to determine the mechanisms of acid reflux and the rate of TLESRs, and to compare the rate of acid reflux during TLESRs between healthy volunteers and patients with reflux esophagitis in Japan. Preprandial and postprandial esophageal manometry and pH monitoring were performed in the sitting position in ten healthy volunteers and ten patients with reflux esophagitis of Los Angeles grade C. The energy level of the meal was 692 kcal and consisted of 33% fat. In healthy volunteers, 100% (median) of the acid reflux episodes occurred during TLESRs compared with 55.0% in patients with esophagitis. The remaining reflux episodes in the esophagitis patients were related to straining (12.8%) and absent basal LES pressure (19.5%). The rate of TLESRs in patients with esophagitis was 4.7 h−1 (3.3–5.7) [median, (interquartile range)] and did not vary significantly from that in healthy volunteers [5.0 h−1 (4.3–6.3)] 3 h postprandially. The rate of acid reflux during TLESRs in patients with esophagitis (42.7%, median) 3 h postprandially was significantly higher than in healthy volunteers (9.2%). In Japan, the mechanisms of GER in both groups are similar to those reported in Western countries. The rate of acid reflux during TLESRs in patients with reflux esophagitis is significantly higher than in healthy volunteers; however, compared to rates reported in Western countries these rates are very low for both groups.
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Furukawa N, Iwakiri R, Koyama T, Okamoto K, Yoshida T, Kashiwagi Y, Ohyama T, Noda T, Sakata H, Fujimoto K (1999) Proportion of reflux esophagitis in 6010 Japanese adults: prospective evaluation by endoscopy. J Gastroenterol 34:441–444
Dodds WJ, Dent J, Hogan WJ, Helm JF, Hauser R, Patel GK, Egide MS (1982) Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. N Engl J Med 307:1547–1552
Mittal RK, McCallum RW (1988) Characteristics and frequency of transient relaxations of the lower esophageal sphincter in patients with reflux esophagitis. Gastroenterology 95:593–599
Holloway RH, Kocyan FP, Dent J (1991) Provocation of transient lower esophageal sphincter relaxations by meals in patients with symptomatic gastroesophageal reflux. Dig Dis Sci 36:1034–1039
Penagini R, Schoeman MN, Dent J, Tippett MD, Holloway RH (1996) Motor events underlying gastro-oesophageal reflux in ambulant patients with reflux oesophagitis. Neurogastroenterol Motil 8:131–141
Van Herwaarden MA, Samsom M, Smout AJPM (2000) Excess gastroesophageal reflux in patients with hiatus hernia is caused by mechanisms other than transient LES relaxations. Gastroenterology 119:1439–1446
Sifrim D, Holloway R (2001) Transient lower esophageal sphincter relaxations: How many or how harmful? Am J Gastroenterol 96:2529–2532
Trudgill NJ, Riley SA (2001) Transient lower esophageal sphincter relaxations are no more frequent in patients with gastroesophageal reflux disease than in asymptomatic volunteers. Am J Gastroenterol 96:2569–2574
Sifrim D, Holloway R, Silny J, Tack J, Lerut A, Janssens J (2001) Composition of the postprandial refluxate in patients with gastroesophageal reflux disease. Am J Gastroenterol 96:647–655
Lidums I, Lehmann A, Checklin H, Dent J, Holloway RH (2000) Control of transient lower esophageal sphincter relaxations and reflux by the GABAB agonist baclofen in normal subjects. Gastroenterology 118:7–13
Zhang Q, Lehmann A, Rigda R, Dent J, Holloway RH (2002) Control of transient lower oesophageal sphincter relaxations and reflux by the GABAB agonist baclofen in patients with gastro-oesophageal reflux disease. Gut 50:19–24
Holloway RH, Penagini R, Ireland AC (1995) Criteria for objective definition of transient lower esophageal sphincter relaxation. Am J Physiol 268:G128–G133
Sifrim D, Holloway RH, Missotten T, Zelter A, Janssens J (1998) Swallow-induced abnormally prolonged lower esophageal sphincter relaxations (SAPLESRs). Gastroenterology 114:A838–A839
Kawahara H, Dent J, Davidson G (1997) Mechanisms responsible for gastroesophageal reflux in children. Gastroenterology 113:399–408
Sifrim D, Tack J, Zhang X, Huysmans W, Janssens J (2002) Continuous monitoring of esophageal shortening in man during swallowing, transient LES relaxations and intraesophageal acid perfusion. Gastroenterology 122:A-188
Dent J, Chir B (1976) A new technique for continuous sphincter pressure measurement. Gastroenterology 71:263–267
Kahrilas PJ, Shi G, Manka M, Joehl RJ (2000) Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia. Gastroenterology 118:688–695
Dent J, Holloway RH, Toouli J, Dodds WJ (1988) Mechanisms of lower oesophageal sphincter incompetence in patients with symptomatic gastrooesophageal reflux. Gut 29:1020–1028
Sifrim D, Holloway R, Silny J, Xin Z, Tack J, Lerut A, Janssens J (2001) Acid, nonacid, and gas reflux in patients with gastroesophageal reflux disease during ambulatory 24-h pH-impedance recordings. Gastroenterology 120:1588–1598
Fletcher J, Wirz A, Young J, Vallance R, McColl KEL (2001) Unbuffered highly acidic gastric juice exists at the gastroesophageal junction after a meal. Gastroenterology 121:775–783
Iwakiri K, Nind G, Zou DW, Sifrim D, Rigda R, Dent J, Holloway RH (2003) Regional variations in postprandial gastric pH and their relationship to acid reflux in healthy volunteers. Gastroenterology 124:A-412
Pandolfino JE, Shi G, Trueworthy B, Kahrilas PJ (2003) Esophagogastric junction opening during relaxation distinguishes nonhernia reflux patients, hernia patients, and normal subjects. Gastroenterology 125:1018–1024
Gardner JD, Rodriguez-Stanley S, Robinson M (2001) Integrated acidity and the pathophysiology of gastroesophageal reflux disease. Am J Gastroenterol 96:1363–1370
Collen MJ, Johnson DA, Sheridan MJ (1994) Basal acid output and gastric acid hypersecretion in gastroesophsageal reflux disease. Dig Dis Sci 39:410–417
Hirschowitz BI (1991) A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis. Gastroenterology 101:1149–1158
Kinoshita Y, Kawanami C, Kishi K, Nakata H, Chiba T (1997) Helicobactor pylori independent chronological change in gastric acid secretion in the Japanese. Gut 41:452–458
Feldman M, Cryer B, McArthur KE, Huet BA, Lee E (1996) Effects of aging and gastritis on gastric acid and pepsin secretion in humans: a prospective study. Gastroenterology 110:1043–1052
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The authors gratefully acknowledge Dr Richard Holloway of The Royal Adelaide Hospital, Australia for his review of this manuscript.
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Hayashi, Y., Iwakiri, K., Kotoyori, M. et al. Mechanisms of Acid Gastroesophageal Reflux in the Japanese Population. Dig Dis Sci 53, 1–6 (2008). https://doi.org/10.1007/s10620-007-0038-4
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DOI: https://doi.org/10.1007/s10620-007-0038-4