نتایج جستجو برای: coa dehydrogenase deficiency

تعداد نتایج: 214964  

2013
Catharina ML Touw G Peter A Smit Klary E Niezen-Koning Conny Bosgraaf-de Boer Albert Gerding Dirk-Jan Reijngoud Terry GJ Derks

BACKGROUND Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most common inherited disorder of the mitochondrial fatty acid oxidation, caused by mutations in the ACADM gene. Since the introduction of neonatal screening for MCAD deficiency, a subgroup of newborns have been identified with variant ACADM genotypes that had never been identified before in clinically ascertained patients....

Journal: :Pediatrics 2006
Lisa Feuchtbaum Fred Lorey Lisa Faulkner John Sherwin Robert Currier Ajit Bhandal George Cunningham

OBJECTIVE In response to a California legislative mandate, a pilot tandem mass spectrometry (MS/MS) screening program was undertaken by the Genetic Disease Branch of the California Department of Health Services between January 2002 and June 2003. This article outlines the Genetic Disease Branch approach to implementing the MS/MS pilot program and the program evaluation strategies used. METHOD...

2015
Sacha Ferdinandusse Marisa W. Friederich Alberto Burlina Jos P. N. Ruiter Curtis R. Coughlin Megan K. Dishop Renata C. Gallagher Jirair K. Bedoyan Frédéric M. Vaz Hans R. Waterham Katherine Gowan Kathryn Chatfield Kaitlyn Bloom Michael J. Bennett Orly Elpeleg Johan L. K. Van Hove Ronald J. A. Wanders

BACKGROUND Short-chain enoyl-CoA hydratase (SCEH, encoded by ECHS1) catalyzes hydration of 2-trans-enoyl-CoAs to 3(S)-hydroxy-acyl-CoAs. SCEH has a broad substrate specificity and is believed to play an important role in mitochondrial fatty acid oxidation and in the metabolism of branched-chain amino acids. Recently, the first patients with SCEH deficiency have been reported revealing only a de...

Journal: :international journal of pediatrics 0
zarin banikazemi biochemistry and nutrition research center, department of nutrition, faculty of medicine, mashhad university of medical sciences, mashhad, iran. mohsen mazidi biochemistry and nutrition research center, department of nutrition, faculty of medicine, mashhad university of medical sciences, mashhad, iran. mohsen nematy biochemistry and nutrition research center, department of nutrition, faculty of medicine, mashhad university of medical sciences, mashhad, iran.

introduction: glutaric academia type i is a metabolic disorder that is caused due to deficiency of glutaryl-coa dehydrogenase. macrocephaly is a common sign in ga1, although many infants usually appear healthy at birth.   case report a 5.5 year old boy with ga1was admitted to nicu. chief compliance of patient for hospitalization was pneumonia and sepsis and he was intubated and mechanically ven...

Journal: :The Journal of biological chemistry 1986
A C Lenich S I Goodman

Glutaryl-CoA dehydrogenase, a multifunctional enzyme responsible for dehydrogenation and decarboxylation of glutaryl-CoA to crotonyl-CoA, has been purified 1,680-fold from porcine liver mitochondria. The purified porcine enzyme has a subunit molecular weight of 47,800 and a native molecular weight of 190,500. Porcine glutaryl-CoA dehydrogenase catalyzed the conversion of [1,5-14C]glutaryl-CoA t...

Introduction: Glutaric academia type I is a metabolic disorder that is caused due to deficiency of glutaryl-CoA dehydrogenase. Macrocephaly is a common sign in GA1, although many infants usually appear healthy at birth.   Case Report A 5.5 year old boy with GA1was admitted to NICU. Chief compliance of patient for hospitalization was pneumonia and sepsis and he was intubated and mechanically ven...

Journal: :Genes 2023

Riboflavin transporter 1 (RFVT1) deficiency is an ultrarare metabolic disorder due to autosomal dominant pathogenic variants in SLC52A1. The RFVT1 protein mainly expressed the placenta and intestine. To our knowledge, only five cases of from three families have been reported so far. While newborns infants with SLC52A1 showed a multiple acyl-CoA dehydrogenase deficiency-like presentation, indivi...

2017
Steven F. Dobrowolski Lina Ghaloul-Gonzalez Jerry Vockley

Medium-chain acyl-CoA dehydrogenase deficiency (MCADD) is identified by newborn screening (NBS). The natural history of MCADD includes metabolic decompensation with hypoglycemia, hyperammonemia, seizures, coma, and death. NBS enables expectant management thus severe symptoms are rare in managed patients. We report premature birth of an MCADD affected infant and resultant management challenges. ...

Journal: :Lancet 2001
Bridget Wilcken Kevin Carpenter Veronica Wiley

Neonatal screening for medium-chain acyl-CoA dehydrogenase (MCAD) deficiency has not yet been introduced in the UK, primarily because of uncertainty about the natural history of the disorder and concerns about the specificity of the screening test. To obtain data on these issues, we did a retrospective study in which we analysed the concentrations of acylcarnitines in stored neonatal blood spot...

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