Abstract
In a prospective study of consecutive patientswith reflux esophagitis and/or hiatal hernia andBarrett's esophagus, the prevalence of Helicobacterpylori was assessed. Antral biopsy specimens werestudied and a serum sample for detection of IgGantibodies against Helicobacter pylori was taken. As areference group patients presenting with a normalesophagus, stomach, and duodenum were taken. Refluxesophagitis was diagnosed in 118 patients, hiatal herniawithout esophageal inflammation in 109, and Barrett'sesophagus in 13. Helicobacter pylori was present in 74(30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacterpylori was significantly lower in all groups comparedwith the reference group (P < 0.001). There was nodifference when patients with esophagitis, Barrett'sesophagus, or hiatal hernia were compared. Patients withesophagitis and Helicobacter pylori in their antrum aresignificantly older than esophagitis patients withoutconcomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). Itis concluded that the prevalence of Helicobacter pyloriinfection in patients with gastroesophageal refluxdisease is significantly lower than in the reference group, irrespective of the severity ofesophagitis. Helicobacter pylori infection has no rolein the pathogenesis of reflux esophagitis.
Similar content being viewed by others
REFERENCES
Loffeld RJLF, Ten Tije BJ, Arends JW: The prevalence and significance of Helicobacter pylori in patients with Barrett's esophagus. Am J Gastroenterology 87:1598–1600, 1992
Levi S, Beardshall K, Haddey G, Playford R, Gosh P, Calam J: Campylobacter pylori and duodenal ulcers: The gastrin link. Lancet 1:1167–1168, 1989
Moss SF, Calam J: Acid secretion and sensitivity to gastrin in patients with duodenal ulcer: Effect of eradication of Helicobacter pylori. Gut 34:888–892, 1993
El-Omar E, Penman I, Dorrian CA, Ardhill JS, McColl KEL: Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer. Gut 34:1060–1065, 1993
Wagner S, Gladziwa U, Haruma K, Varrentrapp M, Gebel M: Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer. Gut 33:1024–1028, 1992
Pena AS, Endtz HpH, Offerhaus GJ, Hoogenboom-Verdegaal A, van Duijn W, de Vargas N, Den Hartog G, Kreuning J, Van der Reyden J, Mouton RP, Lamers CBHW: Value of serology (ELISA and immunoblotting) for the diagnosis of Campylobacter pylori infection. Digestion 44:131–141, 1989
Walker SJ, Binch P, Stewart M, Stoddard CJ, Hart CA, Day DB: Disease association and origin of Campylobacter pylori in the oesophagus: Study by culture, histology and electron microscopy. In Gastroduodenal Pathology and Campylobacter pylori, F Megraud, H Lamouilatte (ed). Amsterdam, Excerpta Medica, Elsevier Science, 1989, pp 507–509
Hedenbro JL, Schalen C, Wadström T, Willen R: Oesophageal Campylobacter pylori colonisation in gastrooesophageal reflux disease. In Gastroduodenal Pathology and Campylobacter pylori, F Megraud, H Lamouilatte (ed). Amsterdam, Excerpta Medica, Elsevier Science, 1989, pp 503–506
Rosioru C, Glassman MS, Halata MS, Schwarz SM: Esophagitis and Helicobacter pylori in children: Incidence and therapeutic implications. Am J Gastroenterol 88:510–513, 1993
Loffeld RJLF, v/d Putten ABMM: Hiatal hernia, refluxoesophagitis and Barrett's oesophagus. A retrospective clinical and endoscopic study. Dis Esophagus 6:57–61, 1993
Kuipers EJ, Uyterlinde AM, Pena AS, Roosendaal R, Pals G, Nelis GF, Festen HPM, Meuwissen SGM: Long-term sequelae of Helicobacter pylori gastritis. Lancet 345:1525–1528, 1995
Rights and permissions
About this article
Cite this article
Werdmuller, B., Loffeld, R. Helicobacter pylori Infection Has No Role in the Pathogenesis of Reflux Esophagitis. Dig Dis Sci 42, 103–105 (1997). https://doi.org/10.1023/A:1018841222856
Issue Date:
DOI: https://doi.org/10.1023/A:1018841222856