Siblings with Ethylmalonic Encephalopathy: Case Report

Deficiency of mitochondrial sulfur dioxygenase (ETHE1) causes a rare inborn error of metabolism, ethylmalonic encephalopathy, which is characterized by early-onset encephalopathy, chronic hemorrhagic diarrhea, recurrent petechiae, orthostatic acrocyanosis, defective cytochrome C oxidase because of h...

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Bibliographic Details
Main Authors: Çiğdem Seher Kasapkara, Ayşe Aksoy, Emine Polat, Mustafa Kılıç, Serdar Ceylaner
Format: Article
Language:English
Published: Galenos Publishing House 2018-03-01
Series:Journal of Pediatric Research
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Online Access: http://jpedres.org/archives/archive-detail/article-preview/siblings-with-ethylmalonic-encephalopathy-case-rep/18780
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Summary:Deficiency of mitochondrial sulfur dioxygenase (ETHE1) causes a rare inborn error of metabolism, ethylmalonic encephalopathy, which is characterized by early-onset encephalopathy, chronic hemorrhagic diarrhea, recurrent petechiae, orthostatic acrocyanosis, defective cytochrome C oxidase because of hydrogen sulfide accumulation and death in the first years of life. Biochemical hallmarks of the disease are high level of lactate, C4-C5-acylcarnitines in blood and markedly elevated urinary excretion of methylsuccinic and ethylmalonic acids. We report on two siblings who were admitted to a pediatric metabolic unit with acrocyanosis, chronic diarrhea and psychomotor retardation later diagnosed as ethylmalonic encephalopathy. Molecular analyses revealed a homozygous for p.R163Q (c.488 G>A) mutation in ETHE1 gene.
ISSN:2147-9445
2587-2478