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©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2018; 24(1): 96-103
Published online Jan 7, 2018. doi: 10.3748/wjg.v24.i1.96
HLA-DQ: Celiac disease vs inflammatory bowel disease
Marta Maia Bosca-Watts, Miguel Minguez, Dolores Planelles, Samuel Navarro, Alejandro Rodriguez, Jesus Santiago, Joan Tosca, Francisco Mora
Marta Maia Bosca-Watts, Miguel Minguez, Joan Tosca, IBD Unit, Digestive Disease Department of the University Clinic Hospital of Valencia, University of Valencia, Valencia 46017, Spain
Dolores Planelles, Histocompatibility Department of the Transfusion Center of the Valencian Community, Valencia 46014, Spain
Samuel Navarro, Pathology Department of the University Clinic Hospital of Valencia, University of Valencia, Valencia 46017, Spain
Alejandro Rodriguez, Digestive Disease Department of the Hospital Virgen del Castillo of Yecla, Yecla 30510, Spain
Jesus Santiago, Digestive Disease Department of the Hospital de Manises, Valencia 46940, Spain
Francisco Mora, Digestive Disease Department of the University Clinic Hospital of Valencia, University of Valencia, Valencia 46017, Spain
Author contributions: The first four authors designed the study, and corrected the results and article; Bosca-Watts MM was responsible of carrying out the study and coordinating the parts; Rodriguez A and Santiago J did part of the technical interventions; Tosca J helped doing it and reviewing the statistical analysis; and Mora F supervised and corrected the article.
Supported by the Carlos III Institute and the University Clinic Hospital Research Institute, with a Rio Hortega specialised healthcare post-training contract granted to Bosca-Watts MM (No. CM07/00240).
Informed consent statement: All involved persons (subjects or legally authorized representative) gave their informed consent (written or verbal, as appropriate) prior to study inclusion.
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Data sharing statement: Participants gave informed consent for data sharing, although the presented data are anonymized and risk of identification is low.
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: Marta Maia Bosca-Watts, PhD, MD, Attending Doctor, Research Scientist, Staff Physician, IBD Unit, Digestive Disease Department of the University Clinic Hospital of Valencia, University of Valencia, C/ Blasco Ibañez 17, Valencia 46010, Spain. inflamatoriahcuv@gmail.com
Telephone: +34-9-61973500- 436449
Received: October 28, 2017
Peer-review started: October 29, 2017
First decision: November 14, 2017
Revised: November 22, 2017
Accepted: November 27, 2017
Article in press: November 27, 2017
Published online: January 7, 2018
AIM
To determine the genetic predisposition to celiac disease (CeD) in inflammatory bowel disease (IBD) patients by quantifying the frequency of CeD-related human leucocyte antigen (HLA) (HLA-CeD: HLA-DQ2 and -DQ8) in IBD patients globally, by type of IBD and gender, and by calculating the protective/risk contribution of these haplotypes in the development of the IBD disease.
METHODS
We conducted a prospective study with IBD patients from our Unit. Clinical information was gathered and blood was tested for HLA-CeD. The control group was made up of unrelated Valencian organ donors.
RESULTS
1034 subjects were analyzed: 457 IBD [207 ulcerative coliti (UC) and 250 Crohn’s disease (CD)] patients and 577 healthy controls. 39% of the controls and 34% of the patients had HLA-CeD (P = 0.0852). HLA-DQ2 was less frequent in UC patients (P = 0.0287), and HLA-DQ8 in CD (P = 0.0217). In women with UC, the frequency of DQ2.5cis (DQB1*02:01-DQA1*05:01) was reduced ≥ 50% [P = 0.0344; preventive fraction (PF) = 13%]. PFs (7%-14%) were obtained with all HLA-CeD haplotypes. HLA DQB1*02:02-DQA1*02:01 (HLA-DQ2.2) was more frequent in CD patients with respect to controls (P = 0.001) and UC patients (etiological fraction = 15%).
CONCLUSION
HLA-CeD is not more frequent in IBD patients, with an even lower frequency of HLA-DQ2 and -DQ8 in UC and CD respectively. HLA-DQ2.5 confers protection from the development of UC, especially in women, and HLA-DQ8 does so for the appearance of CD. HLA-DQ2.2 is present in 34% of the CD patients and may constitute a genetic risk factor for CD development.
Core tip: The higher risk for celiac disease (CeD) in inflammatory bowel disease (IBD) is controversial. Since the involvement of human leucocyte antigen (HLA)-DQ2 and -DQ8 antigens (HLA-CeD) in the susceptibility to CeD is clearly established and it has been accepted as a useful test to exclude CeD, we determined the frequency of HLA-CeD in IBD patients. We observed that HLA-CeD is not more frequent in IBD patients, with an even lower frequency of HLA-DQ2 and -DQ8 in ulcerative colitis and Crohn’s disease respectively. On the other hand, HLA-DQ2.2 was present in 34% of the Crohn’s disease patients and may constitute a genetic risk factor.
