The Contribution of the DLG5 113A Variant in Early-Onset Inflammatory Bowel Disease
Objective To assess the contribution of the 113 G→A missense mutation within the discs, large homolog 5 (DLG5) gene in childhood-onset inflammatory bowel disease (IBD) in Scotland. Study design Two-hundred and ninety-six children with IBD were studied. Parental DNA was also collected for transmissio...
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| Veröffentlicht in: | The Journal of pediatrics 2007-03, Vol.150 (3), p.268-273 |
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| creator | Russell, R.K., MRCPCH Drummond, H.E., BSc Nimmo, E.R., BSc, MSc, PhD Anderson, N., BSc, PhD Wilson, D.C., MD, FRCPCH Gillett, P.M., MBChB, FRCPCH McGrogan, P., MBChB, MRCP Hassan, K., MBBS, FRCPCH Weaver, L.T., MD, FRCPCH Bisset, W.M., MD, FRCPCH Mahdi, G., FRCPCH Satsangi, J., DPhil, FRCP |
| description | Objective To assess the contribution of the 113 G→A missense mutation within the discs, large homolog 5 (DLG5) gene in childhood-onset inflammatory bowel disease (IBD) in Scotland. Study design Two-hundred and ninety-six children with IBD were studied. Parental DNA was also collected for transmission disequilibrium testing (TDT) analysis. Genotyping was performed by TaqMan®. Genotype-phenotype analysis was also undertaken. Socioeconomic status was assigned using a deprivation category (DepCat) score 1 through 7 (1 = most affluent). Results TDT analysis demonstrated a significant association with IBD ( P = .045). On unifactorial analysis, 113A carriage was associated with: (1) higher social class (DepCat 1 compared with 2-7, and 1-2 compared with 3-7) (66.7% vs 22.6%, P = .0005, OR 6.84 [1.99-23.55] and 37.2% vs 22.2%, P = .03, OR 2.08 [1.04-4.17], respectively); (2) higher height centile (>75th centile vs |
| doi_str_mv | 10.1016/j.jpeds.2006.12.010 |
| format | Article |
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Study design Two-hundred and ninety-six children with IBD were studied. Parental DNA was also collected for transmission disequilibrium testing (TDT) analysis. Genotyping was performed by TaqMan®. Genotype-phenotype analysis was also undertaken. Socioeconomic status was assigned using a deprivation category (DepCat) score 1 through 7 (1 = most affluent). Results TDT analysis demonstrated a significant association with IBD ( P = .045). On unifactorial analysis, 113A carriage was associated with: (1) higher social class (DepCat 1 compared with 2-7, and 1-2 compared with 3-7) (66.7% vs 22.6%, P = .0005, OR 6.84 [1.99-23.55] and 37.2% vs 22.2%, P = .03, OR 2.08 [1.04-4.17], respectively); (2) higher height centile (>75th centile vs <75th centile) (42.9% vs 23.1%, P = .01, OR 2.50 [1.18-5.28]); and (3) male sex in Crohn’s disease (CD) (29.3% vs 16.9%, P = .04, OR 2.04 [1.01-4.11]). Multifactorial analysis demonstrated that higher social class (DepCat 1) was independently associated with carriage of variants of 113A ( P = .001, OR=6.92 [2.24-21.33]). Conclusions DLG5 113A is associated with increased susceptibility to IBD in Scottish children. The effect may be most marked for those children living in relative affluence.</description><identifier>ISSN: 0022-3476</identifier><identifier>EISSN: 1097-6833</identifier><identifier>DOI: 10.1016/j.jpeds.2006.12.010</identifier><identifier>PMID: 17307543</identifier><identifier>CODEN: JOPDAB</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Adolescent ; Age of Onset ; Biological and medical sciences ; Child ; Child, Preschool ; Cohort Studies ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation ; General aspects ; Genetic Predisposition to Disease - epidemiology ; Heterozygote ; Humans ; Incidence ; Inflammatory Bowel Diseases - epidemiology ; Inflammatory Bowel Diseases - genetics ; Inflammatory Bowel Diseases - physiopathology ; Logistic Models ; Male ; Medical sciences ; Membrane Proteins - genetics ; Mutation, Missense ; Odds Ratio ; Other diseases. Semiology ; Pediatrics ; Pedigree ; Phenotype ; Probability ; Prognosis ; Scotland - epidemiology ; Severity of Illness Index ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumor Suppressor Proteins - genetics</subject><ispartof>The Journal of pediatrics, 2007-03, Vol.150 (3), p.268-273</ispartof><rights>Mosby, Inc.</rights><rights>2007 Mosby, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-7000314bc2a3ca88abdc6d2b01db1c63d1a4f4f9ecfc3de412805af865deaea63</citedby><cites>FETCH-LOGICAL-c487t-7000314bc2a3ca88abdc6d2b01db1c63d1a4f4f9ecfc3de412805af865deaea63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jpeds.2006.12.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19943249$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17307543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Russell, R.K., MRCPCH</creatorcontrib><creatorcontrib>Drummond, H.E., BSc</creatorcontrib><creatorcontrib>Nimmo, E.R., BSc, MSc, PhD</creatorcontrib><creatorcontrib>Anderson, N., BSc, PhD</creatorcontrib><creatorcontrib>Wilson, D.C., MD, FRCPCH</creatorcontrib><creatorcontrib>Gillett, P.M., MBChB, FRCPCH</creatorcontrib><creatorcontrib>McGrogan, P., MBChB, MRCP</creatorcontrib><creatorcontrib>Hassan, K., MBBS, FRCPCH</creatorcontrib><creatorcontrib>Weaver, L.T., MD, FRCPCH</creatorcontrib><creatorcontrib>Bisset, W.M., MD, FRCPCH</creatorcontrib><creatorcontrib>Mahdi, G., FRCPCH</creatorcontrib><creatorcontrib>Satsangi, J., DPhil, FRCP</creatorcontrib><title>The Contribution of the DLG5 113A Variant in Early-Onset Inflammatory Bowel Disease</title><title>The Journal of pediatrics</title><addtitle>J Pediatr</addtitle><description>Objective To assess the contribution of the 113 G→A missense mutation within the discs, large homolog 5 (DLG5) gene in childhood-onset inflammatory bowel disease (IBD) in Scotland. Study design Two-hundred and ninety-six children with IBD were studied. Parental DNA was also collected for transmission disequilibrium testing (TDT) analysis. Genotyping was performed by TaqMan®. Genotype-phenotype analysis was also undertaken. Socioeconomic status was assigned using a deprivation category (DepCat) score 1 through 7 (1 = most affluent). Results TDT analysis demonstrated a significant association with IBD ( P = .045). On unifactorial analysis, 113A carriage was associated with: (1) higher social class (DepCat 1 compared with 2-7, and 1-2 compared with 3-7) (66.7% vs 22.6%, P = .0005, OR 6.84 [1.99-23.55] and 37.2% vs 22.2%, P = .03, OR 2.08 [1.04-4.17], respectively); (2) higher height centile (>75th centile vs <75th centile) (42.9% vs 23.1%, P = .01, OR 2.50 [1.18-5.28]); and (3) male sex in Crohn’s disease (CD) (29.3% vs 16.9%, P = .04, OR 2.04 [1.01-4.11]). Multifactorial analysis demonstrated that higher social class (DepCat 1) was independently associated with carriage of variants of 113A ( P = .001, OR=6.92 [2.24-21.33]). Conclusions DLG5 113A is associated with increased susceptibility to IBD in Scottish children. The effect may be most marked for those children living in relative affluence.</description><subject>Adolescent</subject><subject>Age of Onset</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Cohort Studies</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation</subject><subject>General aspects</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Incidence</subject><subject>Inflammatory Bowel Diseases - epidemiology</subject><subject>Inflammatory Bowel Diseases - genetics</subject><subject>Inflammatory Bowel Diseases - physiopathology</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Mutation, Missense</subject><subject>Odds Ratio</subject><subject>Other diseases. Semiology</subject><subject>Pediatrics</subject><subject>Pedigree</subject><subject>Phenotype</subject><subject>Probability</subject><subject>Prognosis</subject><subject>Scotland - epidemiology</subject><subject>Severity of Illness Index</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumor Suppressor Proteins - genetics</subject><issn>0022-3476</issn><issn>1097-6833</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EotvCL0BCvsAtYfyRrwNIZVtKpZV6aOFqOc5EOCT2Yieg_fd12JUqceE00uh5Z0bPEPKGQc6AlR-GfNhjF3MOUOaM58DgGdkwaKqsrIV4TjYAnGdCVuUZOY9xAIBGArwkZ6wSUBVSbMj9ww-kW-_mYNtltt5R39M59a52NwVlTFzS7zpY7WZqHb3WYTxkdy7iTG9dP-pp0rMPB_rZ_8GRXtmIOuIr8qLXY8TXp3pBvn25fth-zXZ3N7fby11mZF3NWZXuEUy2hmthdF3rtjNlx1tgXctMKTqmZS_7Bk1vRIeS8RoK3ddl0aFGXYoL8v44dx_8rwXjrCYbDY6jduiXqMoGeFVAk0BxBE3wMQbs1T7YSYeDYqBWl2pQf12q1aViXCWXKfX2NH5pJ-yeMid5CXh3AnQ0euyDdsbGJ65ppOByXf_xyGGS8dtiUNFYdAY7G9DMqvP2P4d8-idvRutsWvkTDxgHvwSXPCumYgqo-_Xt69ehBMbqqhCPKQmnCg</recordid><startdate>20070301</startdate><enddate>20070301</enddate><creator>Russell, R.K., MRCPCH</creator><creator>Drummond, H.E., BSc</creator><creator>Nimmo, E.R., BSc, MSc, PhD</creator><creator>Anderson, N., BSc, PhD</creator><creator>Wilson, D.C., MD, FRCPCH</creator><creator>Gillett, P.M., MBChB, FRCPCH</creator><creator>McGrogan, P., MBChB, MRCP</creator><creator>Hassan, K., MBBS, FRCPCH</creator><creator>Weaver, L.T., MD, FRCPCH</creator><creator>Bisset, W.M., MD, FRCPCH</creator><creator>Mahdi, G., FRCPCH</creator><creator>Satsangi, J., DPhil, FRCP</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070301</creationdate><title>The Contribution of the DLG5 113A Variant in Early-Onset Inflammatory Bowel Disease</title><author>Russell, R.K., MRCPCH ; Drummond, H.E., BSc ; Nimmo, E.R., BSc, MSc, PhD ; Anderson, N., BSc, PhD ; Wilson, D.C., MD, FRCPCH ; Gillett, P.M., MBChB, FRCPCH ; McGrogan, P., MBChB, MRCP ; Hassan, K., MBBS, FRCPCH ; Weaver, L.T., MD, FRCPCH ; Bisset, W.M., MD, FRCPCH ; Mahdi, G., FRCPCH ; Satsangi, J., DPhil, FRCP</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-7000314bc2a3ca88abdc6d2b01db1c63d1a4f4f9ecfc3de412805af865deaea63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Age of Onset</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Cohort Studies</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation</topic><topic>General aspects</topic><topic>Genetic Predisposition to Disease - epidemiology</topic><topic>Heterozygote</topic><topic>Humans</topic><topic>Incidence</topic><topic>Inflammatory Bowel Diseases - epidemiology</topic><topic>Inflammatory Bowel Diseases - genetics</topic><topic>Inflammatory Bowel Diseases - physiopathology</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Mutation, Missense</topic><topic>Odds Ratio</topic><topic>Other diseases. Semiology</topic><topic>Pediatrics</topic><topic>Pedigree</topic><topic>Phenotype</topic><topic>Probability</topic><topic>Prognosis</topic><topic>Scotland - epidemiology</topic><topic>Severity of Illness Index</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumor Suppressor Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Russell, R.K., MRCPCH</creatorcontrib><creatorcontrib>Drummond, H.E., BSc</creatorcontrib><creatorcontrib>Nimmo, E.R., BSc, MSc, PhD</creatorcontrib><creatorcontrib>Anderson, N., BSc, PhD</creatorcontrib><creatorcontrib>Wilson, D.C., MD, FRCPCH</creatorcontrib><creatorcontrib>Gillett, P.M., MBChB, FRCPCH</creatorcontrib><creatorcontrib>McGrogan, P., MBChB, MRCP</creatorcontrib><creatorcontrib>Hassan, K., MBBS, FRCPCH</creatorcontrib><creatorcontrib>Weaver, L.T., MD, FRCPCH</creatorcontrib><creatorcontrib>Bisset, W.M., MD, FRCPCH</creatorcontrib><creatorcontrib>Mahdi, G., FRCPCH</creatorcontrib><creatorcontrib>Satsangi, J., DPhil, FRCP</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of pediatrics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Russell, R.K., MRCPCH</au><au>Drummond, H.E., BSc</au><au>Nimmo, E.R., BSc, MSc, PhD</au><au>Anderson, N., BSc, PhD</au><au>Wilson, D.C., MD, FRCPCH</au><au>Gillett, P.M., MBChB, FRCPCH</au><au>McGrogan, P., MBChB, MRCP</au><au>Hassan, K., MBBS, FRCPCH</au><au>Weaver, L.T., MD, FRCPCH</au><au>Bisset, W.M., MD, FRCPCH</au><au>Mahdi, G., FRCPCH</au><au>Satsangi, J., DPhil, FRCP</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Contribution of the DLG5 113A Variant in Early-Onset Inflammatory Bowel Disease</atitle><jtitle>The Journal of pediatrics</jtitle><addtitle>J Pediatr</addtitle><date>2007-03-01</date><risdate>2007</risdate><volume>150</volume><issue>3</issue><spage>268</spage><epage>273</epage><pages>268-273</pages><issn>0022-3476</issn><eissn>1097-6833</eissn><coden>JOPDAB</coden><abstract>Objective To assess the contribution of the 113 G→A missense mutation within the discs, large homolog 5 (DLG5) gene in childhood-onset inflammatory bowel disease (IBD) in Scotland. Study design Two-hundred and ninety-six children with IBD were studied. Parental DNA was also collected for transmission disequilibrium testing (TDT) analysis. Genotyping was performed by TaqMan®. Genotype-phenotype analysis was also undertaken. Socioeconomic status was assigned using a deprivation category (DepCat) score 1 through 7 (1 = most affluent). Results TDT analysis demonstrated a significant association with IBD ( P = .045). On unifactorial analysis, 113A carriage was associated with: (1) higher social class (DepCat 1 compared with 2-7, and 1-2 compared with 3-7) (66.7% vs 22.6%, P = .0005, OR 6.84 [1.99-23.55] and 37.2% vs 22.2%, P = .03, OR 2.08 [1.04-4.17], respectively); (2) higher height centile (>75th centile vs <75th centile) (42.9% vs 23.1%, P = .01, OR 2.50 [1.18-5.28]); and (3) male sex in Crohn’s disease (CD) (29.3% vs 16.9%, P = .04, OR 2.04 [1.01-4.11]). Multifactorial analysis demonstrated that higher social class (DepCat 1) was independently associated with carriage of variants of 113A ( P = .001, OR=6.92 [2.24-21.33]). Conclusions DLG5 113A is associated with increased susceptibility to IBD in Scottish children. The effect may be most marked for those children living in relative affluence.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>17307543</pmid><doi>10.1016/j.jpeds.2006.12.010</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Age of Onset Biological and medical sciences Child Child, Preschool Cohort Studies Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation General aspects Genetic Predisposition to Disease - epidemiology Heterozygote Humans Incidence Inflammatory Bowel Diseases - epidemiology Inflammatory Bowel Diseases - genetics Inflammatory Bowel Diseases - physiopathology Logistic Models Male Medical sciences Membrane Proteins - genetics Mutation, Missense Odds Ratio Other diseases. Semiology Pediatrics Pedigree Phenotype Probability Prognosis Scotland - epidemiology Severity of Illness Index Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumor Suppressor Proteins - genetics |
| title | The Contribution of the DLG5 113A Variant in Early-Onset Inflammatory Bowel Disease |
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