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World J Gastrointest Pathophysiol. Nov 15, 2014; 5(4): 380-383
Published online Nov 15, 2014. doi: 10.4291/wjgp.v5.i4.380
Helicobacter pylori and pancreatic diseases
Milutin Bulajic, Nikola Panic, Johannes Matthias Löhr
Milutin Bulajic, University Clinical Hospital “Santa Maria della Misericordia”, Piazzale S Maria della Misericordia 15, 33100 Udine, Italy
Milutin Bulajic, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia
Milutin Bulajic, Nikola Panic, University Clinical-Hospital Center “Dr Dragisa Misovic-Dedinje”, 11000 Belgrade, Serbia
Johannes Matthias Löhr, Karolinska Institute, SE-171 77 Stockholm, Sweden
Johannes Matthias Löhr, Department of Medicine II, Molecular Gastroenterology Unit, Medical Faculty Mannheim, University of Heidelberg, D-68135 Mannheim, Germany
Author contributions: Bulajic M and Panic N drafted the manuscript; Löhr JM reviewed the manuscript.
Correspondence to: Nikola Panic, MD, University Clinical-Hospital Center “Dr Dragisa Misovic-Dedinje”, Milana Tepica 1, 11000 Belgrade, Serbia. nikola.panicmail@gmail.com
Telephone: +381-11-3672025 Fax: +381-11-3672025
Received: February 10, 2014
Revised: April 14, 2014
Accepted: July 17, 2014
Published online: November 15, 2014
Processing time: 281 Days and 12.5 Hours
Core Tip

Core tip:Helicobacter pylori (H. pylori) infection with antral predomination could contribute to the development of pancreatic cancer through complex interactions with ABO genotypes, dietary and smoking habits and N-nitrosamine exposure of the host. It has been suggested that H. pylori causes autoimmune pancreatitis due to molecular mimicry between H. pyloriα-carbonic anhydrase (α-CA) and human CA type II, and between H. pylori plasminogen-binding protein and human ubiquitin-protein ligase E3 component n-recognin 2. Considering the worldwide burden of pancreatic diseases, complete elucidation of H. pylori role in their genesis could have substantial healthcare impact.