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Anti-Saccharomyces cerevisiae antibodies in twins with inflammatory bowel disease
Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden.
Laboratoire de Mycologie Fondamentale and Appliquée, Inserm E360, Faculté de Médecine, CHU Lille, Lille, France .
Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden .
Laboratoire de Mycologie Fondamentale and Appliquée, Inserm E360, Faculté de Médecine, CHU Lille, Lille, France .
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2005 (English)In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 54, no 9, 1237-1243 p.Article in journal (Refereed) Published
Abstract [en]

Background and aims: An increased occurrence of anti-Saccharomyces cerevisiae antibodies (ASCA) is reported in unaffected members of families with Crohn’s disease. Whether ASCA is a familial trait due to genetic factors or is caused by exposure to environmental factors is unknown. To assess the genetic influence of ASCA we studied its occurrence in a twin population.

Patients and methods: ASCA were analysed in 98 twin pairs with inflammatory bowel disease and were related to clinical phenotype and CARD15/NOD2 genotype.

Results: ASCA were more common in Crohn’s disease than in ulcerative colitis (40/70 (57%) twins v 5/43 (12%) twins). Associations with ileal Crohn’s disease, stricturing/penetrating behaviour, and young age, but not CARD15/NOD2 were confirmed. ASCA were found in 1/20 (5%) healthy siblings in discordant monozygotic pairs with Crohn’s disease compared with 7/27 (26%) in discordant dizygotic pairs. Using the intraclass correlation coefficient (ICC), no agreement in ASCA titres was observed in discordant twin pairs with Crohn’s disease, in monozygotic (ICC = −0.02) or dizygotic (ICC = −0.26) pairs. In contrast, strong agreement was seen within concordant monozygotic twin pairs with Crohn’s disease (ICC = 0.76).

Conclusions: These findings question the concept of ASCA as a marker of genetic susceptibility for Crohn’s disease. The agreement in ASCA titres within concordant monozygotic twin pairs with Crohn’s disease, suggests that the level of increase is genetically determined. We propose that ASCA are a marker of a response to an environmental antigen and that a specific gene(s) other than CARD15/NOD2 determines the level of response and perhaps also specific phenotypic characteristics.

Place, publisher, year, edition, pages
2005. Vol. 54, no 9, 1237-1243 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-33369DOI: 10.1136/gut.2005.066860Local ID: 19384OAI: oai:DiVA.org:liu-33369DiVA: diva2:254192
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2012-10-03Bibliographically approved
In thesis
1. Inflammatory bowel disease in twins: studies of genetics and environmental factors
Open this publication in new window or tab >>Inflammatory bowel disease in twins: studies of genetics and environmental factors
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The aetiology of inflammatory bowel disease (IBD) is unknown but considered to be caused by interplay of genetic and environmental factors.

The aims of this thesis were to study the influence of genetics and environmental factors in aetiology, disease phenotype and levels of Anti-Saccharomyces cerevisiae antibodies (ASCA), as well as to assess whether CARD15/NOD2 polymorphisms explain the influence of genetics in these aspects.

Twin pairs, where at least one twin in each pair had been hospitalized for IBD, were identified using a combination of the Swedish twin registry and the Swedish Hospital Discharge Register. Twin pairs with confirmed IBD were invited to take part in a questionnaire-based study on environmental factors and studies on ASCA and CARD 15/NOD2 polymorphisms.

The follow-up of the old Swedish twin group showed fairly stable concordance rates. A high degree of concordance regarding age at diagnosis, disease location and behaviour was seen in concordant monozygotic twin pairs with Crohn's disease (CD).

The three "classical" CARD15/NOD2 polymorphisms were infrequent in Swedish CD twins and healthy controls, but seemed to be more common among concordant than discordant monozygotic twins with CD.

No increased occurrence of ASCA was observed in healthy twin siblings in discordant monozygotic twin pairs, but a high degree of concordance in ASCA titres was seen in concordant monozygotic twin pairs with CD. ASCA were not associated with CARD15/NOD2.

Including both Swedish and Danish twins, associations between recurrent gastrointestinal infections up to age 20 years and both ulcerative colitis (UC) and CD were observed, whereas coffee and egg consumption was associated with UC only. Swimming in lakes in contrast with swimming pools, sea and rivers was also associated with UC.

These results confirm a stronger genetic influence in CD than in UC and suggest that genetic factors are important not only in acquiring the disease but also in determining disease characteristics of CD. The CARD15/NOD2 variants contribute, but do not fully explain concordance of CD and support the hypothesis that concordant monozygotic twins are under an increased load of susceptibility genes. Furthermore, the results question the concept of ASCA as a marker of genetic susceptibility for CD and we propose that ASCA are a marker of a response to an environmental antigen and that specific gene(s) other than CARD15/NOD2 determine the level of response and perhaps also specific phenotypic characteristics. The results also indicate, that markers of possible infectious events during childhood/adolescence and dietary factors may influence the risk of IBD. In addition, previous reported associations between smoking and IBD were confirmed.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2005. 76 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 909
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-30042 (URN)15498 (Local ID)91-852-9919-7 (ISBN)15498 (Archive number)15498 (OAI)
Public defence
2005-09-30, Wilandersalen, Universitetssjukhuset i Örebro, Örebro, 09:00 (English)
Opponent
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2012-10-03Bibliographically approved

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