Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin
Background Genome-wide association studies have identified a plethora of risk genes for both Crohn’s disease (CD) and ankylosing spondylitis (AS). A subset of genes found to be risk factors for CD have also been found to be risk factors for AS. The objective of our study was to assess whether CD ris...
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doaj-c42e3df590424d19a6dc945a8da954682020-11-24T23:07:49ZengPeerJ Inc.PeerJ2167-83592018-06-016e508810.7717/peerj.5088Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectinRebecca L. Roberts0Mary C. Wallace1Andrew A. Harrison2Douglas White3Nicola Dalbeth4Lisa K. Stamp5Daniel Ching6John Highton7Tony R. Merriman8Philip C. Robinson9Matthew A. Brown10Simon M. Stebbings11Department of Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New ZealandDepartment of Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New ZealandDepartment of Medicine, University of Otago Wellington, Wellington, New ZealandDepartment of Rheumatology, Waikato Clinical School, Waikato Hospital, Hamilton, New ZealandDepartment of Medicine, University of Auckland, Auckland, New ZealandDepartment of Medicine, University of Otago Christchurch, Christchurch, New ZealandDepartment of Rheumatology, Timaru Hospital, Timaru, New ZealandDepartment of Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New ZealandDepartment of Biochemistry, University of Otago, Dunedin, New ZealandSchool of Medicine, Faculty of Medicine and Biomedical Sciences, University of Queensland, Brisbane, QLD, AustraliaInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, Princess Alexandra Hospital, QLD, AustraliaDepartment of Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New ZealandBackground Genome-wide association studies have identified a plethora of risk genes for both Crohn’s disease (CD) and ankylosing spondylitis (AS). A subset of genes found to be risk factors for CD have also been found to be risk factors for AS. The objective of our study was to assess whether CD risk genes were associated with non-invasive clinical markers of gut inflammation in patients with AS, indicating a potential subset of patients with clinical as well as genetic overlap. Methods A total of 308 Caucasian patients who fulfilled the modified New York Criteria for AS, were assessed for bowel symptoms using the Dudley Inflammatory Bowel Symptom Questionnaire (DISQ). Of these patients, 157 also had faecal calprotectin measured. All AS patients and 568 healthy controls were genotyped for 10 CD risk loci using predesigned single nucleotide polymorphism (SNP) genotyping assays. Chi-square analysis was used to test for association between genotype and DISQ score and faecal calprotectin level. Results The minor allele of two SNPs, one in chromosome region 1q32 SNP (rs11584383), and one in the gene coding for IL23R (rs11209026) conferred protection against AS. Only the association of 1q32 remained significant after Bonferroni correction for multiple testing. Stratification by DISQ score and faecal calprotectin did not influence the association of 1q32 with AS. Conclusion In patients with AS, the association of the CD 1q32 SNP was independent of non-invasive markers of bowel inflammation. Other CD related SNPs were not found have a significant association with AS.https://peerj.com/articles/5088.pdfDudley Inflammatory Bowel Symptom QuestionnaireAxial inflammationCrohn’s diseaseKinesin Family Member 21BBowel inflammation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Rebecca L. Roberts Mary C. Wallace Andrew A. Harrison Douglas White Nicola Dalbeth Lisa K. Stamp Daniel Ching John Highton Tony R. Merriman Philip C. Robinson Matthew A. Brown Simon M. Stebbings |
spellingShingle |
Rebecca L. Roberts Mary C. Wallace Andrew A. Harrison Douglas White Nicola Dalbeth Lisa K. Stamp Daniel Ching John Highton Tony R. Merriman Philip C. Robinson Matthew A. Brown Simon M. Stebbings Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin PeerJ Dudley Inflammatory Bowel Symptom Questionnaire Axial inflammation Crohn’s disease Kinesin Family Member 21B Bowel inflammation |
author_facet |
Rebecca L. Roberts Mary C. Wallace Andrew A. Harrison Douglas White Nicola Dalbeth Lisa K. Stamp Daniel Ching John Highton Tony R. Merriman Philip C. Robinson Matthew A. Brown Simon M. Stebbings |
author_sort |
Rebecca L. Roberts |
title |
Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
title_short |
Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
title_full |
Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
title_fullStr |
Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
title_full_unstemmed |
Association of Crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
title_sort |
association of crohn’s disease-related chromosome 1q32 with ankylosing spondylitis is independent of bowel symptoms and faecal calprotectin |
publisher |
PeerJ Inc. |
series |
PeerJ |
issn |
2167-8359 |
publishDate |
2018-06-01 |
description |
Background Genome-wide association studies have identified a plethora of risk genes for both Crohn’s disease (CD) and ankylosing spondylitis (AS). A subset of genes found to be risk factors for CD have also been found to be risk factors for AS. The objective of our study was to assess whether CD risk genes were associated with non-invasive clinical markers of gut inflammation in patients with AS, indicating a potential subset of patients with clinical as well as genetic overlap. Methods A total of 308 Caucasian patients who fulfilled the modified New York Criteria for AS, were assessed for bowel symptoms using the Dudley Inflammatory Bowel Symptom Questionnaire (DISQ). Of these patients, 157 also had faecal calprotectin measured. All AS patients and 568 healthy controls were genotyped for 10 CD risk loci using predesigned single nucleotide polymorphism (SNP) genotyping assays. Chi-square analysis was used to test for association between genotype and DISQ score and faecal calprotectin level. Results The minor allele of two SNPs, one in chromosome region 1q32 SNP (rs11584383), and one in the gene coding for IL23R (rs11209026) conferred protection against AS. Only the association of 1q32 remained significant after Bonferroni correction for multiple testing. Stratification by DISQ score and faecal calprotectin did not influence the association of 1q32 with AS. Conclusion In patients with AS, the association of the CD 1q32 SNP was independent of non-invasive markers of bowel inflammation. Other CD related SNPs were not found have a significant association with AS. |
topic |
Dudley Inflammatory Bowel Symptom Questionnaire Axial inflammation Crohn’s disease Kinesin Family Member 21B Bowel inflammation |
url |
https://peerj.com/articles/5088.pdf |
work_keys_str_mv |
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