Children With Stroke: Polymorphism of the MTHFR Gene, Mild Hyperhomocysteinemia, and Vitamin Status
The aim of this study was to investigate a possible association among the thermolabile polymorphism, nucleotide 677 cytosine to thymidine point mutation (677 C→T) of the methylenetetrahydrofolate reductase (MTHFR) gene, hyperhomocysteinemia, serum folate, vitamins B12 and B6, and stroke in children....
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| Veröffentlicht in: | Journal of child neurology 2000-05, Vol.15 (5), p.295-298 |
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| container_title | Journal of child neurology |
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| creator | Cardo, Esther Monrós, Eugènia Colomé, Catrina Artuch, Rafael Campistol, Jaume Pineda, Mercè Vilaseca, M. Antònia |
| description | The aim of this study was to investigate a possible association among the thermolabile polymorphism, nucleotide 677 cytosine to thymidine point mutation (677 C→T) of the methylenetetrahydrofolate reductase (MTHFR) gene, hyperhomocysteinemia, serum folate, vitamins B12 and B6, and stroke in children. Allele and genotype frequencies for the 677 C→T polymorphism in 21 children with stroke and 28 healthy children of the same age were studied. No differences in allelic frequency were detected between the two populations. However, the prevalence of homozygous 677 C→T was doubled in the stroke population (28.6%) compared to the healthy group (14.3%). Total plasma homocysteine (tHcy) levels were significantly increased in children aged 2 months to 15 years with stroke compared to reference values. No association was observed between the homozygous genotype (T/T) and hyperhomocysteinemia, nor between the T/T genotype and low folate levels (below the 95th percentile) in this group of patients. Vitamin concentrations in patients were not significantly different from reference values. Significant negative correlations were found between tHcy and folate and between tHcy and cobalamin, but not between tHcy and B6 concentrations. In summary, a higher prevalence of hyperhomocysteinemia and the 677 C→T polymorphism were observed in children with stroke, but were not always associated. The systematic study of both abnormalities in children with stroke is recommended, so that hyperhomocysteinemia of any genetic origin can be corrected with vitamin supplementation. Moreover, the 677 C→T genotype is a strong factor for predisposition to hyperhomocysteinemia and recurrent risk of stroke that might also be prevented with folate supplementation. (J Child Neurol 2000;15:295-298). |
| doi_str_mv | 10.1177/088307380001500505 |
| format | Article |
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Antònia</creator><creatorcontrib>Cardo, Esther ; Monrós, Eugènia ; Colomé, Catrina ; Artuch, Rafael ; Campistol, Jaume ; Pineda, Mercè ; Vilaseca, M. Antònia</creatorcontrib><description>The aim of this study was to investigate a possible association among the thermolabile polymorphism, nucleotide 677 cytosine to thymidine point mutation (677 C→T) of the methylenetetrahydrofolate reductase (MTHFR) gene, hyperhomocysteinemia, serum folate, vitamins B12 and B6, and stroke in children. Allele and genotype frequencies for the 677 C→T polymorphism in 21 children with stroke and 28 healthy children of the same age were studied. No differences in allelic frequency were detected between the two populations. However, the prevalence of homozygous 677 C→T was doubled in the stroke population (28.6%) compared to the healthy group (14.3%). Total plasma homocysteine (tHcy) levels were significantly increased in children aged 2 months to 15 years with stroke compared to reference values. No association was observed between the homozygous genotype (T/T) and hyperhomocysteinemia, nor between the T/T genotype and low folate levels (below the 95th percentile) in this group of patients. Vitamin concentrations in patients were not significantly different from reference values. Significant negative correlations were found between tHcy and folate and between tHcy and cobalamin, but not between tHcy and B6 concentrations. In summary, a higher prevalence of hyperhomocysteinemia and the 677 C→T polymorphism were observed in children with stroke, but were not always associated. The systematic study of both abnormalities in children with stroke is recommended, so that hyperhomocysteinemia of any genetic origin can be corrected with vitamin supplementation. Moreover, the 677 C→T genotype is a strong factor for predisposition to hyperhomocysteinemia and recurrent risk of stroke that might also be prevented with folate supplementation. (J Child Neurol 2000;15:295-298).</description><identifier>ISSN: 0883-0738</identifier><identifier>EISSN: 1708-8283</identifier><identifier>DOI: 10.1177/088307380001500505</identifier><identifier>PMID: 10830195</identifier><identifier>CODEN: JOCNEE</identifier><language>eng</language><publisher>Thousand Oaks, CA: Sage Publications</publisher><subject>Adolescent ; Case-Control Studies ; Child ; Child, Preschool ; Cytosine - metabolism ; Female ; Folic Acid - blood ; Genetic Predisposition to Disease ; Genotype ; Humans ; Hyperhomocysteinemia - genetics ; Hyperhomocysteinemia - metabolism ; Infant ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; Oxidoreductases Acting on CH-NH Group Donors - genetics ; Point Mutation ; Polymorphism, Genetic ; Pyridoxine - blood ; Secondary Prevention ; Stroke - blood ; Stroke - genetics ; Stroke - metabolism ; Stroke - prevention & control ; Thymidine - genetics ; Vitamin B 12 - blood ; Vitamins - blood</subject><ispartof>Journal of child neurology, 2000-05, Vol.15 (5), p.295-298</ispartof><rights>Copyright Decker Periodicals, Inc. May 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-1ee8c13276beaf6cb50352ed6d2f904e9f935aee500ea2a376151eaa811eaf3e3</citedby><cites>FETCH-LOGICAL-c397t-1ee8c13276beaf6cb50352ed6d2f904e9f935aee500ea2a376151eaa811eaf3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/088307380001500505$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/088307380001500505$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21798,27901,27902,43597,43598</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10830195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cardo, Esther</creatorcontrib><creatorcontrib>Monrós, Eugènia</creatorcontrib><creatorcontrib>Colomé, Catrina</creatorcontrib><creatorcontrib>Artuch, Rafael</creatorcontrib><creatorcontrib>Campistol, Jaume</creatorcontrib><creatorcontrib>Pineda, Mercè</creatorcontrib><creatorcontrib>Vilaseca, M. Antònia</creatorcontrib><title>Children With Stroke: Polymorphism of the MTHFR Gene, Mild Hyperhomocysteinemia, and Vitamin Status</title><title>Journal of child neurology</title><addtitle>J Child Neurol</addtitle><description>The aim of this study was to investigate a possible association among the thermolabile polymorphism, nucleotide 677 cytosine to thymidine point mutation (677 C→T) of the methylenetetrahydrofolate reductase (MTHFR) gene, hyperhomocysteinemia, serum folate, vitamins B12 and B6, and stroke in children. Allele and genotype frequencies for the 677 C→T polymorphism in 21 children with stroke and 28 healthy children of the same age were studied. No differences in allelic frequency were detected between the two populations. However, the prevalence of homozygous 677 C→T was doubled in the stroke population (28.6%) compared to the healthy group (14.3%). Total plasma homocysteine (tHcy) levels were significantly increased in children aged 2 months to 15 years with stroke compared to reference values. No association was observed between the homozygous genotype (T/T) and hyperhomocysteinemia, nor between the T/T genotype and low folate levels (below the 95th percentile) in this group of patients. Vitamin concentrations in patients were not significantly different from reference values. Significant negative correlations were found between tHcy and folate and between tHcy and cobalamin, but not between tHcy and B6 concentrations. In summary, a higher prevalence of hyperhomocysteinemia and the 677 C→T polymorphism were observed in children with stroke, but were not always associated. The systematic study of both abnormalities in children with stroke is recommended, so that hyperhomocysteinemia of any genetic origin can be corrected with vitamin supplementation. Moreover, the 677 C→T genotype is a strong factor for predisposition to hyperhomocysteinemia and recurrent risk of stroke that might also be prevented with folate supplementation. 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Antònia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Children With Stroke: Polymorphism of the MTHFR Gene, Mild Hyperhomocysteinemia, and Vitamin Status</atitle><jtitle>Journal of child neurology</jtitle><addtitle>J Child Neurol</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>15</volume><issue>5</issue><spage>295</spage><epage>298</epage><pages>295-298</pages><issn>0883-0738</issn><eissn>1708-8283</eissn><coden>JOCNEE</coden><abstract>The aim of this study was to investigate a possible association among the thermolabile polymorphism, nucleotide 677 cytosine to thymidine point mutation (677 C→T) of the methylenetetrahydrofolate reductase (MTHFR) gene, hyperhomocysteinemia, serum folate, vitamins B12 and B6, and stroke in children. Allele and genotype frequencies for the 677 C→T polymorphism in 21 children with stroke and 28 healthy children of the same age were studied. No differences in allelic frequency were detected between the two populations. However, the prevalence of homozygous 677 C→T was doubled in the stroke population (28.6%) compared to the healthy group (14.3%). Total plasma homocysteine (tHcy) levels were significantly increased in children aged 2 months to 15 years with stroke compared to reference values. No association was observed between the homozygous genotype (T/T) and hyperhomocysteinemia, nor between the T/T genotype and low folate levels (below the 95th percentile) in this group of patients. Vitamin concentrations in patients were not significantly different from reference values. Significant negative correlations were found between tHcy and folate and between tHcy and cobalamin, but not between tHcy and B6 concentrations. In summary, a higher prevalence of hyperhomocysteinemia and the 677 C→T polymorphism were observed in children with stroke, but were not always associated. The systematic study of both abnormalities in children with stroke is recommended, so that hyperhomocysteinemia of any genetic origin can be corrected with vitamin supplementation. Moreover, the 677 C→T genotype is a strong factor for predisposition to hyperhomocysteinemia and recurrent risk of stroke that might also be prevented with folate supplementation. (J Child Neurol 2000;15:295-298).</abstract><cop>Thousand Oaks, CA</cop><pub>Sage Publications</pub><pmid>10830195</pmid><doi>10.1177/088307380001500505</doi><tpages>4</tpages></addata></record> |
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| ispartof | Journal of child neurology, 2000-05, Vol.15 (5), p.295-298 |
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| source | MEDLINE; SAGE Complete |
| subjects | Adolescent Case-Control Studies Child Child, Preschool Cytosine - metabolism Female Folic Acid - blood Genetic Predisposition to Disease Genotype Humans Hyperhomocysteinemia - genetics Hyperhomocysteinemia - metabolism Infant Male Methylenetetrahydrofolate Reductase (NADPH2) Oxidoreductases Acting on CH-NH Group Donors - genetics Point Mutation Polymorphism, Genetic Pyridoxine - blood Secondary Prevention Stroke - blood Stroke - genetics Stroke - metabolism Stroke - prevention & control Thymidine - genetics Vitamin B 12 - blood Vitamins - blood |
| title | Children With Stroke: Polymorphism of the MTHFR Gene, Mild Hyperhomocysteinemia, and Vitamin Status |
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