Eva Morava, Marije Hogeveen, Maaike De Vries, Wim Ruitenbeek, Willem-Pieter de Boode, Jan Smeitink
{"title":"正常血清丙氨酸浓度可区分短暂性新生儿乳酸血症和先天性能量代谢错误。","authors":"Eva Morava, Marije Hogeveen, Maaike De Vries, Wim Ruitenbeek, Willem-Pieter de Boode, Jan Smeitink","doi":"10.1159/000093590","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Elevated blood lactate levels are common in the critically ill neonate; however, sometimes they are difficult to interpret. Persistent or recurrent lactic acidemia might point to an inborn error of metabolism, like disturbances of the oxidative phosphorylation. Chronic lactic acidemia results in increased serum alanine levels. Serum alanine levels in newborns with transient lactic acidemia have not yet been studied.</p><p><strong>Objective: </strong>We designed a pilot study to evaluate the use of serum alanine levels as an additional metabolic marker to differentiate the transient effect of circulatory failure from a possible mitochondrial dysfunction.</p><p><strong>Methods: </strong>We prospectively evaluated 10 newborns with transient lactic acidemia after mild dysoxia, and 10 newborns with recurrent lactic acidemia consecutively diagnosed with a disorder in oxidative phosphorylation.</p><p><strong>Results: </strong>No significant serum alanine level elevation was found in transient lactic acidemia. Increased serum alanine was a sensitive marker in mitochondrial dysfunction.</p><p><strong>Conclusions: </strong>We propose to measure the serum alanine level in hypotonic newborns with lactic acidemia to facilitate the decision making in further diagnostics and management.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"90 3","pages":"207-9"},"PeriodicalIF":0.0000,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093590","citationCount":"9","resultStr":"{\"title\":\"Normal serum alanine concentration differentiates transient neonatal lactic acidemia from an inborn error of energy metabolism.\",\"authors\":\"Eva Morava, Marije Hogeveen, Maaike De Vries, Wim Ruitenbeek, Willem-Pieter de Boode, Jan Smeitink\",\"doi\":\"10.1159/000093590\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Elevated blood lactate levels are common in the critically ill neonate; however, sometimes they are difficult to interpret. Persistent or recurrent lactic acidemia might point to an inborn error of metabolism, like disturbances of the oxidative phosphorylation. Chronic lactic acidemia results in increased serum alanine levels. Serum alanine levels in newborns with transient lactic acidemia have not yet been studied.</p><p><strong>Objective: </strong>We designed a pilot study to evaluate the use of serum alanine levels as an additional metabolic marker to differentiate the transient effect of circulatory failure from a possible mitochondrial dysfunction.</p><p><strong>Methods: </strong>We prospectively evaluated 10 newborns with transient lactic acidemia after mild dysoxia, and 10 newborns with recurrent lactic acidemia consecutively diagnosed with a disorder in oxidative phosphorylation.</p><p><strong>Results: </strong>No significant serum alanine level elevation was found in transient lactic acidemia. Increased serum alanine was a sensitive marker in mitochondrial dysfunction.</p><p><strong>Conclusions: </strong>We propose to measure the serum alanine level in hypotonic newborns with lactic acidemia to facilitate the decision making in further diagnostics and management.</p>\",\"PeriodicalId\":9091,\"journal\":{\"name\":\"Biology of the neonate\",\"volume\":\"90 3\",\"pages\":\"207-9\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2006-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000093590\",\"citationCount\":\"9\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biology of the neonate\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000093590\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2006/5/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology of the neonate","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000093590","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2006/5/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Normal serum alanine concentration differentiates transient neonatal lactic acidemia from an inborn error of energy metabolism.
Background: Elevated blood lactate levels are common in the critically ill neonate; however, sometimes they are difficult to interpret. Persistent or recurrent lactic acidemia might point to an inborn error of metabolism, like disturbances of the oxidative phosphorylation. Chronic lactic acidemia results in increased serum alanine levels. Serum alanine levels in newborns with transient lactic acidemia have not yet been studied.
Objective: We designed a pilot study to evaluate the use of serum alanine levels as an additional metabolic marker to differentiate the transient effect of circulatory failure from a possible mitochondrial dysfunction.
Methods: We prospectively evaluated 10 newborns with transient lactic acidemia after mild dysoxia, and 10 newborns with recurrent lactic acidemia consecutively diagnosed with a disorder in oxidative phosphorylation.
Results: No significant serum alanine level elevation was found in transient lactic acidemia. Increased serum alanine was a sensitive marker in mitochondrial dysfunction.
Conclusions: We propose to measure the serum alanine level in hypotonic newborns with lactic acidemia to facilitate the decision making in further diagnostics and management.