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http://scihub22266oqcxt.onion/ C5493831!5493831!28698729     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Iran+J+Child+Neurol 2017 ; 11 (2): 57-60 Nephropedia Template TP {{tp|p=28698729|t=2017. Neurological and Vascular Manifestations of Ethylmalonic Encephalopathy |pdf=|usr=}}{{28698729}} gab.com Text Neurological and Vascular Manifestations of Ethylmalonic Encephalopathy JO: Iran J Child Neurol http://www.kidney.de/pget.php?&tw=1&pmid=28698729 #FOAvip ObjectiveEthylmalonic encephalopathy (EE) is a severe mitochondrial disease of early infancy clinically characterized by a combination of developmental delay, progressive pyramidal signs, and vascular lesions including petechial purpura, orthostatic acrocyanosis, and chronic hemorrhagic diarrhea.Biochemical hallmarks of the disease are persistently high level of lactate, and C4?C5-acylcarnitines in blood, markedly elevated urinary excretion of methylsuccinic and ethylmalonic (EMA) acids. Here we report two patients with EE as a 16-months-old male infant and a 2-yr-old boy referred to Pediatric Neurology Clinic in Children?s Medical Center, Tehran-Iran that in one patient genetic analysis revealed a homozygous mutation of the ETHE1 gene in favor of ethylmalonic acidemia. Twit Text FOAVip Neurological and Vascular Manifestations of Ethylmalonic Encephalopathy ????Iran J Child Neurol http://www.kidney.de/pget.php?&tw=1&pmid=28698729 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28698729 #FOAvip English Wikipedia <ref>{{Cite pmid|28698729}}</ref> Neurological and Vascular Manifestations of Ethylmalonic Encephalopathy #MMPMID28698729 TAVASOLI AR; ROSTAMI P; ASHRAFI MR; KARIMZADEH P Iran J Child Neurol 2017[Spr]; 11 (2): 57-60 PMID28698729show ga ObjectiveEthylmalonic encephalopathy (EE) is a severe mitochondrial disease of early infancy clinically characterized by a combination of developmental delay, progressive pyramidal signs, and vascular lesions including petechial purpura, orthostatic acrocyanosis, and chronic hemorrhagic diarrhea.Biochemical hallmarks of the disease are persistently high level of lactate, and C4?C5-acylcarnitines in blood, markedly elevated urinary excretion of methylsuccinic and ethylmalonic (EMA) acids. Here we report two patients with EE as a 16-months-old male infant and a 2-yr-old boy referred to Pediatric Neurology Clinic in Children?s Medical Center, Tehran-Iran that in one patient genetic analysis revealed a homozygous mutation of the ETHE1 gene in favor of ethylmalonic acidemia. äNeurological and Vascular Manifestations of Ethylmalonic Encephalopath(epmc).pdf DeepDyve Pubget Overpricing