Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB102-DQA105 and TNF -308A
The overlap between genetic susceptibility to celiac disease (CD) and to type 1 diabetes is incomplete; therefore, some genetic polymorphisms may significantly modify the risk of CD in subjects with type 1 diabetes. This study aimed to investigate whether the susceptibility to CD in diabetic childre...
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| Veröffentlicht in: | Diabetes care 2006-04, Vol.29 (4), p.858-863 |
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| creator | Sumnik, Zdenek Cinek, Ondrej Bratanic, Nina Kordonouri, Olga Kulich, Michal Roszai, Barnabas Arato, Andras Lebl, Jan Soltesz, Gyula Danne, Thomas Battelino, Tadej Schober, Edit |
| description | The overlap between genetic susceptibility to celiac disease (CD) and to type 1 diabetes is incomplete; therefore, some genetic polymorphisms may significantly modify the risk of CD in subjects with type 1 diabetes. This study aimed to investigate whether the susceptibility to CD in diabetic children is modified by positivity for HLA-DQB1*02-DQA1*05 and DQB1*0302-DQA1*03 and by alleles of single nucleotide polymorphisms within the genes encoding CTLA4, transforming growth factor (TGF)-beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-2, IL-6, and IL-10.
Genotypic data were compared between 130 case subjects (children with type 1 diabetes and CD diagnosed using endomysium antibodies) and 245 control subjects (children with type 1 diabetes only, optimally two per case, matched for center, age at type 1 diabetes onset, and type 1 diabetes duration). The subjects were recruited from 10 major European pediatric diabetes centers performing regular screening for CD. The polymorphisms were determined using PCR with sequence-specific primers, and the risk was assessed by building a step-up conditional logistic regression model using variables that were significantly associated with CD in the univariate analysis.
The best-fitted model showed that risk of CD is increased by presence of HLA-DQB1*02-DQA1*05 (odds ratio 4.5 [95% CI 1.8-11], for homozygosity, and 2.0 [1.1-3.7], for a single dose) and also independently by TNF -308A (1.9 [1.1-3.2], for phenotypic positivity), whereas IL1-alpha -889T showed a weak negative association (0.6 [0.4-0.9]).
The results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A. |
| doi_str_mv | 10.2337/diacare.29.04.06.dc05-1923 |
| format | Article |
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Genotypic data were compared between 130 case subjects (children with type 1 diabetes and CD diagnosed using endomysium antibodies) and 245 control subjects (children with type 1 diabetes only, optimally two per case, matched for center, age at type 1 diabetes onset, and type 1 diabetes duration). The subjects were recruited from 10 major European pediatric diabetes centers performing regular screening for CD. The polymorphisms were determined using PCR with sequence-specific primers, and the risk was assessed by building a step-up conditional logistic regression model using variables that were significantly associated with CD in the univariate analysis.
The best-fitted model showed that risk of CD is increased by presence of HLA-DQB1*02-DQA1*05 (odds ratio 4.5 [95% CI 1.8-11], for homozygosity, and 2.0 [1.1-3.7], for a single dose) and also independently by TNF -308A (1.9 [1.1-3.2], for phenotypic positivity), whereas IL1-alpha -889T showed a weak negative association (0.6 [0.4-0.9]).
The results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A.</description><identifier>ISSN: 0149-5992</identifier><identifier>EISSN: 1935-5548</identifier><identifier>DOI: 10.2337/diacare.29.04.06.dc05-1923</identifier><identifier>PMID: 16567828</identifier><identifier>CODEN: DICAD2</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adolescent ; Case-Control Studies ; Celiac disease ; Celiac Disease - complications ; Celiac Disease - genetics ; Celiac Disease - immunology ; Child ; Children & youth ; Diabetes ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Female ; Genetic Predisposition to Disease ; Genetic research ; Genotype ; Genotype & phenotype ; HLA-DQ alpha-Chains ; HLA-DQ Antigens - genetics ; HLA-DQ beta-Chains ; Humans ; Male ; Phenotype ; Regression Analysis ; Risk Factors ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Diabetes care, 2006-04, Vol.29 (4), p.858-863</ispartof><rights>Copyright American Diabetes Association Apr 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-c2e9d85d2479afec0318e156b0fabe0b14f92c5f3a1081ad62375df5b4e094943</citedby><cites>FETCH-LOGICAL-c344t-c2e9d85d2479afec0318e156b0fabe0b14f92c5f3a1081ad62375df5b4e094943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16567828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sumnik, Zdenek</creatorcontrib><creatorcontrib>Cinek, Ondrej</creatorcontrib><creatorcontrib>Bratanic, Nina</creatorcontrib><creatorcontrib>Kordonouri, Olga</creatorcontrib><creatorcontrib>Kulich, Michal</creatorcontrib><creatorcontrib>Roszai, Barnabas</creatorcontrib><creatorcontrib>Arato, Andras</creatorcontrib><creatorcontrib>Lebl, Jan</creatorcontrib><creatorcontrib>Soltesz, Gyula</creatorcontrib><creatorcontrib>Danne, Thomas</creatorcontrib><creatorcontrib>Battelino, Tadej</creatorcontrib><creatorcontrib>Schober, Edit</creatorcontrib><title>Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB102-DQA105 and TNF -308A</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>The overlap between genetic susceptibility to celiac disease (CD) and to type 1 diabetes is incomplete; therefore, some genetic polymorphisms may significantly modify the risk of CD in subjects with type 1 diabetes. This study aimed to investigate whether the susceptibility to CD in diabetic children is modified by positivity for HLA-DQB1*02-DQA1*05 and DQB1*0302-DQA1*03 and by alleles of single nucleotide polymorphisms within the genes encoding CTLA4, transforming growth factor (TGF)-beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-2, IL-6, and IL-10.
Genotypic data were compared between 130 case subjects (children with type 1 diabetes and CD diagnosed using endomysium antibodies) and 245 control subjects (children with type 1 diabetes only, optimally two per case, matched for center, age at type 1 diabetes onset, and type 1 diabetes duration). The subjects were recruited from 10 major European pediatric diabetes centers performing regular screening for CD. The polymorphisms were determined using PCR with sequence-specific primers, and the risk was assessed by building a step-up conditional logistic regression model using variables that were significantly associated with CD in the univariate analysis.
The best-fitted model showed that risk of CD is increased by presence of HLA-DQB1*02-DQA1*05 (odds ratio 4.5 [95% CI 1.8-11], for homozygosity, and 2.0 [1.1-3.7], for a single dose) and also independently by TNF -308A (1.9 [1.1-3.2], for phenotypic positivity), whereas IL1-alpha -889T showed a weak negative association (0.6 [0.4-0.9]).
The results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A.</description><subject>Adolescent</subject><subject>Case-Control Studies</subject><subject>Celiac disease</subject><subject>Celiac Disease - complications</subject><subject>Celiac Disease - genetics</subject><subject>Celiac Disease - immunology</subject><subject>Child</subject><subject>Children & youth</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic research</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>HLA-DQ alpha-Chains</subject><subject>HLA-DQ Antigens - genetics</subject><subject>HLA-DQ beta-Chains</subject><subject>Humans</subject><subject>Male</subject><subject>Phenotype</subject><subject>Regression Analysis</subject><subject>Risk Factors</subject><subject>Tumor Necrosis Factor-alpha - 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complications</topic><topic>Celiac Disease - genetics</topic><topic>Celiac Disease - immunology</topic><topic>Child</topic><topic>Children & youth</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic research</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>HLA-DQ alpha-Chains</topic><topic>HLA-DQ Antigens - genetics</topic><topic>HLA-DQ beta-Chains</topic><topic>Humans</topic><topic>Male</topic><topic>Phenotype</topic><topic>Regression Analysis</topic><topic>Risk Factors</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sumnik, Zdenek</creatorcontrib><creatorcontrib>Cinek, Ondrej</creatorcontrib><creatorcontrib>Bratanic, Nina</creatorcontrib><creatorcontrib>Kordonouri, Olga</creatorcontrib><creatorcontrib>Kulich, Michal</creatorcontrib><creatorcontrib>Roszai, Barnabas</creatorcontrib><creatorcontrib>Arato, Andras</creatorcontrib><creatorcontrib>Lebl, Jan</creatorcontrib><creatorcontrib>Soltesz, Gyula</creatorcontrib><creatorcontrib>Danne, Thomas</creatorcontrib><creatorcontrib>Battelino, Tadej</creatorcontrib><creatorcontrib>Schober, Edit</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sumnik, Zdenek</au><au>Cinek, Ondrej</au><au>Bratanic, Nina</au><au>Kordonouri, Olga</au><au>Kulich, Michal</au><au>Roszai, Barnabas</au><au>Arato, Andras</au><au>Lebl, Jan</au><au>Soltesz, Gyula</au><au>Danne, Thomas</au><au>Battelino, Tadej</au><au>Schober, Edit</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB102-DQA105 and TNF -308A</atitle><jtitle>Diabetes care</jtitle><addtitle>Diabetes Care</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>29</volume><issue>4</issue><spage>858</spage><epage>863</epage><pages>858-863</pages><issn>0149-5992</issn><eissn>1935-5548</eissn><coden>DICAD2</coden><abstract>The overlap between genetic susceptibility to celiac disease (CD) and to type 1 diabetes is incomplete; therefore, some genetic polymorphisms may significantly modify the risk of CD in subjects with type 1 diabetes. This study aimed to investigate whether the susceptibility to CD in diabetic children is modified by positivity for HLA-DQB1*02-DQA1*05 and DQB1*0302-DQA1*03 and by alleles of single nucleotide polymorphisms within the genes encoding CTLA4, transforming growth factor (TGF)-beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-2, IL-6, and IL-10.
Genotypic data were compared between 130 case subjects (children with type 1 diabetes and CD diagnosed using endomysium antibodies) and 245 control subjects (children with type 1 diabetes only, optimally two per case, matched for center, age at type 1 diabetes onset, and type 1 diabetes duration). The subjects were recruited from 10 major European pediatric diabetes centers performing regular screening for CD. The polymorphisms were determined using PCR with sequence-specific primers, and the risk was assessed by building a step-up conditional logistic regression model using variables that were significantly associated with CD in the univariate analysis.
The best-fitted model showed that risk of CD is increased by presence of HLA-DQB1*02-DQA1*05 (odds ratio 4.5 [95% CI 1.8-11], for homozygosity, and 2.0 [1.1-3.7], for a single dose) and also independently by TNF -308A (1.9 [1.1-3.2], for phenotypic positivity), whereas IL1-alpha -889T showed a weak negative association (0.6 [0.4-0.9]).
The results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>16567828</pmid><doi>10.2337/diacare.29.04.06.dc05-1923</doi><tpages>6</tpages></addata></record> |
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| ispartof | Diabetes care, 2006-04, Vol.29 (4), p.858-863 |
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| subjects | Adolescent Case-Control Studies Celiac disease Celiac Disease - complications Celiac Disease - genetics Celiac Disease - immunology Child Children & youth Diabetes Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Female Genetic Predisposition to Disease Genetic research Genotype Genotype & phenotype HLA-DQ alpha-Chains HLA-DQ Antigens - genetics HLA-DQ beta-Chains Humans Male Phenotype Regression Analysis Risk Factors Tumor Necrosis Factor-alpha - genetics |
| title | Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB102-DQA105 and TNF -308A |
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