Halling ML, Kjeldsen J, Knudsen T, Nielsen J, Hansen LK. Patients with inflammatory bowel disease have increased risk of autoimmune and inflammatory diseases. World J Gastroenterol 2017; 23(33): 6137-6146 [PMID: 28970729 DOI: 10.3748/wjg.v23.i33.6137]
Corresponding Author of This Article
Morten L Halling, MD, Department of Gastroenterology and Hepatology, Hospital of Southwest Jutland, Medicinsk Gastroenterologisk Afdeling, Sydvestjysk Sygehus, Finsensgade 35, 6700 Esbjerg, Denmark. mortenhalling@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Sep 7, 2017; 23(33): 6137-6146 Published online Sep 7, 2017. doi: 10.3748/wjg.v23.i33.6137
Patients with inflammatory bowel disease have increased risk of autoimmune and inflammatory diseases
Morten L Halling, Jens Kjeldsen, Torben Knudsen, Jan Nielsen, Lars Koch Hansen
Morten L Halling, Torben Knudsen, Department of Gastroenterology and Hepatology, Hospital of Southwest Jutland, 6700 Esbjerg, Denmark
Jens Kjeldsen, Lars Koch Hansen, Department of Medical Gastroenterology S, Odense University Hospital, 5000 Odense, Denmark
Jan Nielsen, Center for Clinical Epidemiology, Odense University Hospital, 5000 Odense, Denmark
Author contributions: Halling ML, Kjeldsen J, Knudsen T and Koch Hansen L designed the study; Koch Hansen L performed data collection; Nielsen J performed statistical analyses; Halling ML and Koch Hansen L drafted the manuscript and obtained funding; all authors revised and accepted the final manuscript.
Institutional review board statement: This study was approved by the Danish Data Protection Agency (approval # 2013-41-1596).
Conflict-of-interest statement: The authors report no conflict of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Morten L Halling, MD, Department of Gastroenterology and Hepatology, Hospital of Southwest Jutland, Medicinsk Gastroenterologisk Afdeling, Sydvestjysk Sygehus, Finsensgade 35, 6700 Esbjerg, Denmark. mortenhalling@gmail.com
Telephone: +45-79-183141 Fax: +45-79-183147
Received: March 2, 2017 Peer-review started: March 3, 2017 First decision: April 21, 2017 Revised: May 30, 2017 Accepted: July 12, 2017 Article in press: July 12, 2017 Published online: September 7, 2017 Processing time: 189 Days and 8 Hours
Core Tip
Core tip: Essential to inflammatory bowel disease (IBD) pathogenesis are environmental factors, altered gut microbiota and genetic susceptibility. The latter causing impairment of barrier function, autophagy, and Th1, 2 and 17 cell responses. Interestingly, these mechanisms are also thought important in other immune mediated diseases, as is the overlap of susceptibility genes. Besides the classic extraintestinal manifestations, we found a variety of immune mediated diseases to be more frequent in individuals with IBD. Physicians should be aware of this when treating these patients. Furthermore, these findings support the hypothesis that immune mediated diseases may have overlapping pathogeneses. Thus, understanding IBD might help us understand other immune mediated diseases and vice versa.
