{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:50764"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:50764","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Methotrexat-induzierte Leukenzephalopathie bei Patienten mit akuter lymphatischer Leukämie oder lymphoblastischem Non-Hodgkin-Lymphom in Abhängigkeit vom MTHFR-C677T-Status","abstract":"The antifolate Methotrexate and folate metabolism is central in therapy of pediatric Acute Lymphatic Leukemia (ALL). Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme of folate metabolism, so that combination of MTX-therapy and mutation of the MTHFR gene (MTHFR C677T) might result in altered toxicity. We examined 31 children with ALL or NHL, that were treated according to GPOH ALL-BFM 95 or 98 protokoll at the pediatric department of Aachen University Hospital, regarding mucositis, leucocytes, bilirubin and transaminases. 23 of them were also examined by MRT or MRS. The relation between chronic cerebral MTX toxicity as seen on MRT and MRS and MTHFR mutation has not been examined systematically so far. 14 of our patients were wildtype, 16 heterozygous and only 1 homozygous mutated TT for MTHFR. There was no statistically significant association between MTHFR mutation and acute or chronic MTX toxicity. However such association was stated before, but only when no additional folate was given, and not if folate rescue after high-dose MTX was administered, like we did. This means a possible effect of the MTHFR mutation might be concealed by high folate doses. So, as far we know today, changing the MTX regimen is not necessary to prevent more severe MTX toxicity.","abstract_html":"The antifolate Methotrexate and folate metabolism is central in therapy of pediatric Acute Lymphatic Leukemia (ALL). Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme of folate metabolism, so that combination of MTX-therapy and mutation of the MTHFR gene (MTHFR C677T) might result in altered toxicity. We examined 31 children with ALL or NHL, that were treated according to GPOH ALL-BFM 95 or 98 protokoll at the pediatric department of Aachen University Hospital, regarding mucositis, leucocytes, bilirubin and transaminases. 23 of them were also examined by MRT or MRS. The relation between chronic cerebral MTX toxicity as seen on MRT and MRS and MTHFR mutation has not been examined systematically so far. 14 of our patients were wildtype, 16 heterozygous and only 1 homozygous mutated TT for MTHFR. There was no statistically significant association between MTHFR mutation and acute or chronic MTX toxicity. However such association was stated before, but only when no additional folate was given, and not if folate rescue after high-dose MTX was administered, like we did. This means a possible effect of the MTHFR mutation might be concealed by high folate doses. So, as far we know today, changing the MTX regimen is not necessary to prevent more severe MTX toxicity.","abstract_has_math":false,"creators":["Deutz, Peter"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Mertens, Rolf"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2009,"date_issued":"2009","date_published":"2009","updated_at":"2026-07-30T19:40:25Z","subjects":["info:eu-repo/classification/ddc/610","Methotrexat","Akute lymphatische Leukämie","Kind","Chemotherapie","Leukoenzephalopathie","Folsäure","Folsäureantagonist","Folsäurestoffwechsel","Methylentetrahydrofolat-Reductase <5,10-Methylentetrahydrofolat-Reductase (FADH2)>","Medizin","MTHFRC677T","methotrexate","akute lymphatic leukemia","leukoencephalopathy","folatemetabolism","methylenetetrahydrofolate"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-113293%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-113293%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-113293%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/50764","outbound_label":"Repository record","outbound_source":"dc:identifier"},"source_record":{"url":"https://publications.rwth-aachen.de/oai2d?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Apublications.rwth-aachen.de%3A50764","prefix":"oai_dc"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Mertens, Rolf"]},{"key":"dc:creator","label":"Author","values":["Deutz, Peter"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2009"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-27645"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Methotrexat","Akute lymphatische Leukämie","Kind","Chemotherapie","Leukoenzephalopathie","Folsäure","Folsäureantagonist","Folsäurestoffwechsel","Methylentetrahydrofolat-Reductase <5,10-Methylentetrahydrofolat-Reductase (FADH2)>","Medizin","MTHFRC677T","methotrexate","akute lymphatic leukemia","leukoencephalopathy","folatemetabolism","methylenetetrahydrofolate"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/50764","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-113293%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The antifolate Methotrexate and folate metabolism is central in therapy of pediatric Acute Lymphatic Leukemia (ALL). Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme of folate metabolism, so that combination of MTX-therapy and mutation of the MTHFR gene (MTHFR C677T) might result in altered toxicity. We examined 31 children with ALL or NHL, that were treated according to GPOH ALL-BFM 95 or 98 protokoll at the pediatric department of Aachen University Hospital, regarding mucositis, leucocytes, bilirubin and transaminases. 23 of them were also examined by MRT or MRS. The relation between chronic cerebral MTX toxicity as seen on MRT and MRS and MTHFR mutation has not been examined systematically so far. 14 of our patients were wildtype, 16 heterozygous and only 1 homozygous mutated TT for MTHFR. There was no statistically significant association between MTHFR mutation and acute or chronic MTX toxicity. However such association was stated before, but only when no additional folate was given, and not if folate rescue after high-dose MTX was administered, like we did. This means a possible effect of the MTHFR mutation might be concealed by high folate doses. So, as far we know today, changing the MTX regimen is not necessary to prevent more severe MTX toxicity."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 110 S. : Ill., graph. Darst. (2009). = Aachen, Techn. Hochsch., Diss., 2009"]},{"key":"dc:title","label":"Title","values":["Methotrexat-induzierte Leukenzephalopathie bei Patienten mit akuter lymphatischer Leukämie oder lymphoblastischem Non-Hodgkin-Lymphom in Abhängigkeit vom MTHFR-C677T-Status"]}]}],"canonical_facts":{"dc:contributor":["Mertens, Rolf"],"dc:coverage":["DE"],"dc:creator":["Deutz, Peter"],"dc:date":["2009"],"dc:description":["The antifolate Methotrexate and folate metabolism is central in therapy of pediatric Acute Lymphatic Leukemia (ALL). Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme of folate metabolism, so that combination of MTX-therapy and mutation of the MTHFR gene (MTHFR C677T) might result in altered toxicity. We examined 31 children with ALL or NHL, that were treated according to GPOH ALL-BFM 95 or 98 protokoll at the pediatric department of Aachen University Hospital, regarding mucositis, leucocytes, bilirubin and transaminases. 23 of them were also examined by MRT or MRS. The relation between chronic cerebral MTX toxicity as seen on MRT and MRS and MTHFR mutation has not been examined systematically so far. 14 of our patients were wildtype, 16 heterozygous and only 1 homozygous mutated TT for MTHFR. There was no statistically significant association between MTHFR mutation and acute or chronic MTX toxicity. However such association was stated before, but only when no additional folate was given, and not if folate rescue after high-dose MTX was administered, like we did. This means a possible effect of the MTHFR mutation might be concealed by high folate doses. So, as far we know today, changing the MTX regimen is not necessary to prevent more severe MTX toxicity."],"dc:identifier":["https://publications.rwth-aachen.de/record/50764","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-113293%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-27645"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 110 S. : Ill., graph. Darst. (2009). = Aachen, Techn. 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