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Published on: December 15, 2011
HLA genotypes and the increased incidence of coeliac disease in Sweden
R Ploski1, H Ascher, L M Sollid
1Institute of Transplantation Immunology, National Hospital, University of Oslo, Norway.
Insights
The rise in childhood coeliac disease (CD) in Sweden is not linked to individuals with less predisposing HLA genotypes. Genetic susceptibility in Swedish CD patients appears similar to other populations.
Area of Science:
- Immunogenetics
- Pediatric Gastroenterology
Background:
- Childhood coeliac disease (CD) incidence has risen in Sweden.
- This increase coincided with changes in infant feeding practices.
Purpose of the Study:
- To investigate if the CD increase in Sweden is due to individuals with less predisposing Human Leukocyte Antigen (HLA) genotypes.
- To compare HLA class-II genotypes between Swedish CD patients and controls.
Main Methods:
- Genomic HLA-DRB1, -DQA1, and -DQB1 typing was conducted.
- 135 Swedish CD patients (low- and high-incidence cohorts) and 179 controls were analyzed.
- Distribution of HLA class-II genotypes was compared across cohorts.
Main Results:
- Specific HLA genotypes (DQA1*0501 and DQB1*02) were associated with increased CD risk.
- A gene dosage effect for DQB1*02 was observed.
- No significant difference in HLA genotype distribution was found between the cohorts.
Conclusions:
- Swedish coeliac disease patients exhibit similar genetic susceptibility to other populations.
- The observed increase in CD is unlikely due to a higher prevalence of less predisposing HLA genotypes.
Background:
A strong increase of childhood coeliac disease (CD) was found in Sweden concurrently with changes in the infant feeding pattern. We investigated whether this increase reflects a recruitment of individuals with less predisposing HLA genotypes.
Methods:
Genomic HLA-DRB1, -DQA1, and -DQB1 typing was performed in 135 Swedish patients (48 belonging to a low- and 81 to a high-incidence cohort) and 179 controls. The distribution of HLA class-II genotypes in the cohorts was compared.
Results:
DQA1*0501 and DQB1*02 conferred increased risk for CD, and a gene dosage effect of DQB1*02 was found. The distribution of HLA genotypes among the cohorts did not differ.
Conclusions:
The results suggest that Swedish CD patients do not differ in genetic susceptibility compared with other populations. No evidence was found suggesting that the increase would be a result of more frequent development of disease in individuals carrying less predisposing HLA genotypes.
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