Impact of the -174G/C interleukin-6 (IL-6) gene polymorphism on the risk of paediatric ischemic stroke, its symptoms and outcome
Ischemic stroke remains one of the top ten causes of death in children. There is evidence for the role of pro-inflammatory cytokines, such as IL-6 and the -174G>C promoter polymorphism of the IL-6 gene, in the occurrence and outcome of stroke in adults. The aim of the present study was to determi...
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Veröffentlicht in: | Folia neuropathologica 2012, Vol.50 (2), p.147-151 |
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creator | Balcerzyk, Anna Nowak, Marta Kopyta, Ilona Emich-Widera, Ewa Pilarska, Ewa Pienczk-Ręcławowicz, Karolina Kaciński, Marek Wendorff, Janusz Zak, Iwona |
description | Ischemic stroke remains one of the top ten causes of death in children. There is evidence for the role of pro-inflammatory cytokines, such as IL-6 and the -174G>C promoter polymorphism of the IL-6 gene, in the occurrence and outcome of stroke in adults. The aim of the present study was to determine a possible association between the -174G>C IL-6 polymorphism and occurrence of paediatric stroke, its symptoms and outcome.
The study group consisted of 340 individuals: 80 stroke children, 122 parents of patients and 138 controls. The -174G/C polymorphism was genotyped using the RFLP method. For the analysis of the relationship between genotypes and stroke we used two alternative methods: the case-control model and the transmission test for linkage disequilibrium using data from families.
We observed no differences in the transmission of alleles from parents to children. We also did not find any statistical differences in distribution of genotypes and alleles between patients and controls. However, the analysis showed that post-stroke epilepsy was genotype-dependent. All children with epilepsy were G allele carriers and none of them was a CC homozygote whereas about 25% of children without epilepsy had the CC genotype.
Our study did not show any associations between the IL-6 -174 G>C polymorphism and the occurrence of stroke but we observed a relation between post-stroke epilepsy and the G allele carrier-state. |
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The study group consisted of 340 individuals: 80 stroke children, 122 parents of patients and 138 controls. The -174G/C polymorphism was genotyped using the RFLP method. For the analysis of the relationship between genotypes and stroke we used two alternative methods: the case-control model and the transmission test for linkage disequilibrium using data from families.
We observed no differences in the transmission of alleles from parents to children. We also did not find any statistical differences in distribution of genotypes and alleles between patients and controls. However, the analysis showed that post-stroke epilepsy was genotype-dependent. All children with epilepsy were G allele carriers and none of them was a CC homozygote whereas about 25% of children without epilepsy had the CC genotype.
Our study did not show any associations between the IL-6 -174 G>C polymorphism and the occurrence of stroke but we observed a relation between post-stroke epilepsy and the G allele carrier-state.</description><identifier>ISSN: 1641-4640</identifier><identifier>EISSN: 1509-572X</identifier><identifier>PMID: 22773460</identifier><language>eng</language><publisher>Poland</publisher><subject>Adolescent ; Brain Ischemia - genetics ; Child ; Child, Preschool ; Children ; Data processing ; Epilepsy ; Female ; Gene polymorphism ; Genetic Predisposition to Disease - genetics ; Genotype ; Guanylate cyclase ; Homozygotes ; Humans ; Infant ; Inflammation ; Interleukin 6 ; Interleukin-6 - genetics ; Ischemia ; Linkage disequilibrium ; Male ; Neurotransmission ; Pediatrics ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Risk Factors ; Statistics ; Stroke ; Stroke - genetics</subject><ispartof>Folia neuropathologica, 2012, Vol.50 (2), p.147-151</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22773460$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Balcerzyk, Anna</creatorcontrib><creatorcontrib>Nowak, Marta</creatorcontrib><creatorcontrib>Kopyta, Ilona</creatorcontrib><creatorcontrib>Emich-Widera, Ewa</creatorcontrib><creatorcontrib>Pilarska, Ewa</creatorcontrib><creatorcontrib>Pienczk-Ręcławowicz, Karolina</creatorcontrib><creatorcontrib>Kaciński, Marek</creatorcontrib><creatorcontrib>Wendorff, Janusz</creatorcontrib><creatorcontrib>Zak, Iwona</creatorcontrib><title>Impact of the -174G/C interleukin-6 (IL-6) gene polymorphism on the risk of paediatric ischemic stroke, its symptoms and outcome</title><title>Folia neuropathologica</title><addtitle>Folia Neuropathol</addtitle><description>Ischemic stroke remains one of the top ten causes of death in children. There is evidence for the role of pro-inflammatory cytokines, such as IL-6 and the -174G>C promoter polymorphism of the IL-6 gene, in the occurrence and outcome of stroke in adults. The aim of the present study was to determine a possible association between the -174G>C IL-6 polymorphism and occurrence of paediatric stroke, its symptoms and outcome.
The study group consisted of 340 individuals: 80 stroke children, 122 parents of patients and 138 controls. The -174G/C polymorphism was genotyped using the RFLP method. For the analysis of the relationship between genotypes and stroke we used two alternative methods: the case-control model and the transmission test for linkage disequilibrium using data from families.
We observed no differences in the transmission of alleles from parents to children. We also did not find any statistical differences in distribution of genotypes and alleles between patients and controls. However, the analysis showed that post-stroke epilepsy was genotype-dependent. All children with epilepsy were G allele carriers and none of them was a CC homozygote whereas about 25% of children without epilepsy had the CC genotype.
Our study did not show any associations between the IL-6 -174 G>C polymorphism and the occurrence of stroke but we observed a relation between post-stroke epilepsy and the G allele carrier-state.</description><subject>Adolescent</subject><subject>Brain Ischemia - genetics</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Children</subject><subject>Data processing</subject><subject>Epilepsy</subject><subject>Female</subject><subject>Gene polymorphism</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Guanylate cyclase</subject><subject>Homozygotes</subject><subject>Humans</subject><subject>Infant</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - genetics</subject><subject>Ischemia</subject><subject>Linkage disequilibrium</subject><subject>Male</subject><subject>Neurotransmission</subject><subject>Pediatrics</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>Statistics</subject><subject>Stroke</subject><subject>Stroke - genetics</subject><issn>1641-4640</issn><issn>1509-572X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UF9LwzAcDKK4Of0KkscJFpM0f9pHGToHA18UfCtp-6uLa5qYpA9786NbdT7dcdwdx52gORWkzIRib6cTl5xmXHIyQxcxfhDCBS_ZOZoxplTOJZmjr431uknYdTjtAGdU8fXdCpshQehh3Jshk3i52WbyBr_DANi7_mBd8DsTLXbDbyqYuP9p8Bpao1MwDTax2YGdSEzB7eEWmxRxPFifnI1YDy12Y2qchUt01uk-wtURF-j18eFl9ZRtn9eb1f0285TTlHVEKCUKpllZT9B1INqai4KUTUu5FG1et5zposgVFBS6ohBsUutGSlW3SucLtPzr9cF9jhBTZaeN0Pd6ADfGihJZ0lKR6ZgFuj5ax9pCW_lgrA6H6v-1_BuJPWlA</recordid><startdate>2012</startdate><enddate>2012</enddate><creator>Balcerzyk, Anna</creator><creator>Nowak, Marta</creator><creator>Kopyta, Ilona</creator><creator>Emich-Widera, Ewa</creator><creator>Pilarska, Ewa</creator><creator>Pienczk-Ręcławowicz, Karolina</creator><creator>Kaciński, Marek</creator><creator>Wendorff, Janusz</creator><creator>Zak, Iwona</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>2012</creationdate><title>Impact of the -174G/C interleukin-6 (IL-6) gene polymorphism on the risk of paediatric ischemic stroke, its symptoms and outcome</title><author>Balcerzyk, Anna ; Nowak, Marta ; Kopyta, Ilona ; Emich-Widera, Ewa ; Pilarska, Ewa ; Pienczk-Ręcławowicz, Karolina ; Kaciński, Marek ; Wendorff, Janusz ; Zak, Iwona</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p141t-f0577582a29b582ffe5db45809cd1465d3bd42a8837e81ef885265dbc667bd7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adolescent</topic><topic>Brain Ischemia - genetics</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Children</topic><topic>Data processing</topic><topic>Epilepsy</topic><topic>Female</topic><topic>Gene polymorphism</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genotype</topic><topic>Guanylate cyclase</topic><topic>Homozygotes</topic><topic>Humans</topic><topic>Infant</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - genetics</topic><topic>Ischemia</topic><topic>Linkage disequilibrium</topic><topic>Male</topic><topic>Neurotransmission</topic><topic>Pediatrics</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><topic>Statistics</topic><topic>Stroke</topic><topic>Stroke - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Balcerzyk, Anna</creatorcontrib><creatorcontrib>Nowak, Marta</creatorcontrib><creatorcontrib>Kopyta, Ilona</creatorcontrib><creatorcontrib>Emich-Widera, Ewa</creatorcontrib><creatorcontrib>Pilarska, Ewa</creatorcontrib><creatorcontrib>Pienczk-Ręcławowicz, Karolina</creatorcontrib><creatorcontrib>Kaciński, Marek</creatorcontrib><creatorcontrib>Wendorff, Janusz</creatorcontrib><creatorcontrib>Zak, Iwona</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Folia neuropathologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Balcerzyk, Anna</au><au>Nowak, Marta</au><au>Kopyta, Ilona</au><au>Emich-Widera, Ewa</au><au>Pilarska, Ewa</au><au>Pienczk-Ręcławowicz, Karolina</au><au>Kaciński, Marek</au><au>Wendorff, Janusz</au><au>Zak, Iwona</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of the -174G/C interleukin-6 (IL-6) gene polymorphism on the risk of paediatric ischemic stroke, its symptoms and outcome</atitle><jtitle>Folia neuropathologica</jtitle><addtitle>Folia Neuropathol</addtitle><date>2012</date><risdate>2012</risdate><volume>50</volume><issue>2</issue><spage>147</spage><epage>151</epage><pages>147-151</pages><issn>1641-4640</issn><eissn>1509-572X</eissn><abstract>Ischemic stroke remains one of the top ten causes of death in children. There is evidence for the role of pro-inflammatory cytokines, such as IL-6 and the -174G>C promoter polymorphism of the IL-6 gene, in the occurrence and outcome of stroke in adults. The aim of the present study was to determine a possible association between the -174G>C IL-6 polymorphism and occurrence of paediatric stroke, its symptoms and outcome.
The study group consisted of 340 individuals: 80 stroke children, 122 parents of patients and 138 controls. The -174G/C polymorphism was genotyped using the RFLP method. For the analysis of the relationship between genotypes and stroke we used two alternative methods: the case-control model and the transmission test for linkage disequilibrium using data from families.
We observed no differences in the transmission of alleles from parents to children. We also did not find any statistical differences in distribution of genotypes and alleles between patients and controls. However, the analysis showed that post-stroke epilepsy was genotype-dependent. All children with epilepsy were G allele carriers and none of them was a CC homozygote whereas about 25% of children without epilepsy had the CC genotype.
Our study did not show any associations between the IL-6 -174 G>C polymorphism and the occurrence of stroke but we observed a relation between post-stroke epilepsy and the G allele carrier-state.</abstract><cop>Poland</cop><pmid>22773460</pmid><tpages>5</tpages></addata></record> |
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subjects | Adolescent Brain Ischemia - genetics Child Child, Preschool Children Data processing Epilepsy Female Gene polymorphism Genetic Predisposition to Disease - genetics Genotype Guanylate cyclase Homozygotes Humans Infant Inflammation Interleukin 6 Interleukin-6 - genetics Ischemia Linkage disequilibrium Male Neurotransmission Pediatrics Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Risk Factors Statistics Stroke Stroke - genetics |
title | Impact of the -174G/C interleukin-6 (IL-6) gene polymorphism on the risk of paediatric ischemic stroke, its symptoms and outcome |
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