Journal of Gastroenterology

, Volume 45, Issue 3, pp 291–299 | Cite as

Pancreatic acinar metaplasia in the distal oesophagus and the gastric cardia: prevalence, predictors and relation to GORD

  • Johan Johansson
  • Hans-Olof Håkansson
  • Lennart Mellblom
  • Antti Kempas
  • Gerhard Kjellén
  • Lars Brudin
  • Fredrik Granath
  • Karl-Erik Johansson
  • Olof Nyrén
Original Article—Alimentary Tract



The nature of pancreatic acinar metaplasia (PAM) in the gastro-oesophageal junction (GOJ) remains obscure. We aimed to estimate its prevalence and investigate into its risk factors in a population-based series of first-time endoscopy patients.


We investigated consecutive patients, endoscoped for the first time, representing defined catchment area populations. Biopsies were taken immediately below the GOJ and from the distal oesophagus. Endoscopy room-based cross-sectional clinical data were supplemented with exposure data from 160 population controls. Associations, expressed as odds ratios (OR), were modelled with multivariable logistic regression. A subsample of 26 patients underwent oesophageal pH monitoring.


Among 644 patients (mean age 53 years, 43% men), PAM was found in 121 patients (19%), exclusively above the GOJ in 40 (6%), below GOJ in 67 (10%), and both above and below GOJ in 14 (2%). PAM exclusively above the GOJ and PAM exclusively below the GOJ were both borderline associated with age (2% increase in prevalence per year). PAM exclusively above the GOJ was significantly associated with female gender (OR 2.8, 95% CI 1.3–6.3) and presence of Helicobacter pylori immediately below the GOJ (OR 2.6, 95% CI 1.3–5.4). Out of 21 patients with Barrett’s oesophagus (BO), 8 (38%) had PAM above the GOJ. The mean value for percentage time with oesophageal pH < 4.0 was 7.3% (95% CI 4.3–10.2%) among patients who had PAM above the GOJ (reference value 3.4%).


Pancreatic acinar metaplasia might be an age-dependent lesion, associated with H. pylori, female gender and gastro-oesophageal reflux if located above the GOJ.


Barrett esophagus Esophagogastric junction Gastroesophageal reflux Helicobacter pylori Pancreatic acinar metaplasia 



This study was funded by a grant from the Swedish Cancer Society (4570-B01-01XAB), by the Health Research Council in the South-East of Sweden (F97-310 and F2001-334), by the Department of Surgery, Kalmar County Hospital and by Kalmar County Council Research and Development Committee, Sweden. We express our gratitude to Susanne Kjellin and Gun Olsén for coordination of the endoscopies, to Agneta Hansson for data input, to Joakim Vang for database design, and to Professor Anders Borgström and Dr. Erik Svartholm for valuable discussions during the planning and early phase of the study.


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Copyright information

© Springer 2009

Authors and Affiliations

  • Johan Johansson
    • 1
  • Hans-Olof Håkansson
    • 2
  • Lennart Mellblom
    • 3
  • Antti Kempas
    • 6
  • Gerhard Kjellén
    • 4
  • Lars Brudin
    • 5
  • Fredrik Granath
    • 8
  • Karl-Erik Johansson
    • 7
  • Olof Nyrén
    • 1
  1. 1.Department of Medical Epidemiology and Biostatistics, Karolinska InstitutetStockholmSweden
  2. 2.Department of SurgeryKalmar County HospitalKalmarSweden
  3. 3.Department of PathologyKalmar County HospitalKalmarSweden
  4. 4.Department of Oto-Rhino-LaryngologyKalmar County HospitalKalmarSweden
  5. 5.Department of PhysiologyKalmar County HospitalKalmarSweden
  6. 6.Department of SurgeryVäxjö County HospitalVäxjöSweden
  7. 7.Department of SurgeryLinköping University HospitalLinköpingSweden
  8. 8.Unit of Clinical Epidemiology, Department of MedicineKarolinska Institutet, University HospitalStockholmSweden

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