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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
Abstract

A possible role for Helicobacter pylori (H. pylori) infection in pancreatic diseases remains controversial. H. pylori infection with antral predomination leading to an increase in pancreatic bicarbonate output and inducing ductal epithelial cell proliferation could contribute to the development of pancreatic cancer via complex interactions with the ABO genotype, dietary and smoking habits and N-nitrosamine exposure of the host. Although the individual study data available so far is inconsistent, several meta-analyses have reported an increased risk for pancreatic cancer among H. pylori seropositive individuals. 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, enzymes that are highly expressed in the pancreatic ductal and acinar cells, respectively. Future studies involving large numbers of cases are needed in order to examine the role of H. pylori in autoimmune pancreatitis more fully. Considering the worldwide pancreatic cancer burden, as well as the association between autoimmune pancreatitis and other autoimmune conditions, a complete elucidation of the role played by H. pylori in the genesis of such conditions could have a substantial impact on healthcare.

Keywords: Helicobacter pylori; Pancreatic cancer; Pancreatitis; Autoimmune pancreatitis; Molecular mimicry

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.