Etiopathogenesis of pediatric Crohn’s disease. Biologic pathways based on interactions between genetic and environmental factors
The incidence and prevalence of Crohn’s disease (CD) among children in developed countries is extremely high. Although, dietary factors have long been implicated, to date no single causative element has been identified. Risks or benefits for CD from dietary elements would depend on their appropriate...
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Veröffentlicht in: | Medical hypotheses 2003-03, Vol.60 (3), p.344-350 |
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description | The incidence and prevalence of Crohn’s disease (CD) among children in developed countries is extremely high. Although, dietary factors have long been implicated, to date no single causative element has been identified. Risks or benefits for CD from dietary elements would depend on their appropriate metabolism within the gut by xenobiotic metabolising enzymes (XME). The metabolising capacity among individuals differs and is determined by the level and/or activity of the specific XME. As the latter is the function of the DNA variants that code them, we propose that certain individuals exposed to dietary elements are likely to be more or less susceptible for CD. We highlight this hypothesis by describing gene–environment interaction (G×E) mechanisms that could determine susceptibility for CD. We suggest that investigating these mechanisms will be paramount for the appropriate identification of susceptible populations, such that preventive and/or therapeutic interventions could be adequately targeted. |
doi_str_mv | 10.1016/S0306-9877(02)00401-2 |
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We suggest that investigating these mechanisms will be paramount for the appropriate identification of susceptible populations, such that preventive and/or therapeutic interventions could be adequately targeted.</description><subject>Crohn Disease - etiology</subject><subject>Crohn Disease - genetics</subject><subject>DNA - metabolism</subject><subject>Environment</subject><subject>Humans</subject><subject>Models, Theoretical</subject><subject>Polymorphism, Genetic</subject><issn>0306-9877</issn><issn>1532-2777</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1uEzEURi1ERULhEUBeoXYxxT8zY88KQVSgUqQugLVle64To4kdbKdVdxVv0dfjSeo0ESxZWbo-33d1D0JvKLmghPbvvxFO-maQQpwRdk5IS2jDnqE57ThrmBDiOZr_RWboZc4_CSFDy-ULNKOsk7SnZI5-XxYft7qs4woCZJ9xdHgLo9cleYsXKa7Dn_uHjEefQWe4wJ98nOKq_u1Tt_ouY1PnI44B-1AgaVsbQ51CuQUIeN9bKq7DiCHc-BTDBkLRE3YVjSm_QidOTxleH99T9OPz5ffF12Z5_eVq8XHZWN7T0nAtjRYcTN86TpjretFTJ6VtjTSdGwcnqO0EZ8PAiB6GDgzjnTFUilZrAH6K3h16tyn-2kEuauOzhWnSAeIuK1FbJeN9BbsDaFPMOYFT2-Q3Ot0pStRevnqSr_ZmFWHqSb5iNff2uGBnNjD-Sx1tV-DDAYB65o2HpLL1EGzVncAWNUb_nxWPtzWX2A</recordid><startdate>20030301</startdate><enddate>20030301</enddate><creator>K Amre, Devendra</creator><creator>G Seidman, Ernest</creator><general>Elsevier Ltd</general><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>20030301</creationdate><title>Etiopathogenesis of pediatric Crohn’s disease. 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As the latter is the function of the DNA variants that code them, we propose that certain individuals exposed to dietary elements are likely to be more or less susceptible for CD. We highlight this hypothesis by describing gene–environment interaction (G×E) mechanisms that could determine susceptibility for CD. We suggest that investigating these mechanisms will be paramount for the appropriate identification of susceptible populations, such that preventive and/or therapeutic interventions could be adequately targeted.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>12581610</pmid><doi>10.1016/S0306-9877(02)00401-2</doi><tpages>7</tpages></addata></record> |
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subjects | Crohn Disease - etiology Crohn Disease - genetics DNA - metabolism Environment Humans Models, Theoretical Polymorphism, Genetic |
title | Etiopathogenesis of pediatric Crohn’s disease. Biologic pathways based on interactions between genetic and environmental factors |
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