Search results for "Cytochrome-c Oxidase Deficiency"

showing 4 items of 4 documents

Mutations of mitochondrial DNA and human death.

1990

In the skeletal muscle of patients with mitochondrial myopathies (Kearns-Sayre syndrome and chronic progressive external ophthalmoplegia) and in the heart and skeletal muscle of healthy persons cells lacking cytochrome c oxidase are found. The respiratory-defective cells have the following features in common: onset of the defect at juvenile or adult age; progressive character of the defect with increasing age; and focal pattern of respiratory-deficient cells (fibers). A statistic mutation of mtDNA in affected cells is suggested to cause the defect of mitochondrial function. It is postulated that the continuous accumulation of respiratory-deficient cells, mainly in the human heart with incre…

Mitochondrial DNAmedicine.medical_specialtyCytochrome-c Oxidase DeficiencyMitochondrionBiologyHuman mitochondrial geneticsDNA MitochondrialMitochondria HeartKearns–Sayre syndromeElectron Transport Complex IVMitochondrial myopathyMuscular DiseasesReference ValuesInternal medicinemedicineAnimalsHumansEcology Evolution Behavior and SystematicsGeneticsMammalsHomoplasmySkeletal muscleGeneral Medicinemedicine.diseaseMitochondria MuscleDeathEndocrinologymedicine.anatomical_structureMutationChronic progressive external ophthalmoplegiaDie Naturwissenschaften
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Myo-, neuro-, gastrointestinal encephalopathy (MNGIE syndrome) due to partial deficiency of cytochrome-c-oxidase

1987

A 42-year-old woman had a 10-year history of external ophthalmoplegia, malabsorption resulting in chronic malnutrition, muscle atrophy and polyneuropathy. Computer tomography revealed hypodensity of her cerebral white matter. A metabolic disturbance consisted of lactic acidosis after moderate glucose loads with increased excretion of hydroxybutyric and fumaric acids. Post-mortem studies revealed gastrointestinal scleroderma as the morphological manifestation of her malabsorption syndrome, ocular and skeletal myopathy with ragged red fibers, peripheral neuropathy, vascular abnormalities of meningeal and peripheral nerve vessels. Biochemical examination of the liver and muscle tissues reveale…

AdultPathologymedicine.medical_specialtyMalabsorptionGastrointestinal DiseasesEncephalopathyRespiratory chainCytochrome-c Oxidase DeficiencyEyePathology and Forensic Medicine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMuscular DiseasesMitochondrial myopathymedicineHumansMuscular dystrophy030304 developmental biology2. Zero hungerBrain Diseases0303 health sciencesbusiness.industryPeripheral Nervous System DiseasesSyndromemedicine.diseaseMitochondria MusclePeripheral neuropathyLactic acidosisFemaleNeurology (clinical)businessPolyneuropathy030217 neurology & neurosurgeryActa Neuropathologica
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Identification of a novel compound heterozygote SCO2 mutation in cytochrome c oxidase deficient fatal infantile cardioencephalomyopathy

2006

UNLABELLED Fatal infantile cardioencephalomyopathy (OMIM No. 604377) is a disorder of the mitochondrial respiratory chain and is characterised by neonatal progressive muscular hypotonia and cardiomyopathy because of severe Cytochrome c oxidase deficiency. Here we report a novel mutation in the Cytochrome c oxidase assembly gene SCO2 in an infant with fatal infantile cardioencephalomyopathy despite normal initial metabolic screening. CONCLUSION In newborns with unexplained muscular hypotonia and cardiomyopathy genetic testing of mitochondrial respiratory chain disorders might be helpful to establish a final diagnosis and guide treatment decisions.

Heterozygotemedicine.medical_specialtyPathologyCardiomyopathyCytochrome-c Oxidase DeficiencyCompound heterozygositymedicine.disease_causeMitochondrial ProteinsFatal OutcomeMitochondrial EncephalomyopathiesInternal medicinemedicineHumansCytochrome c oxidaseGeneGenetic testingMutationMuscular hypotoniamedicine.diagnostic_testbiologybusiness.industryInfantGeneral Medicinemedicine.diseaseEndocrinologyMitochondrial respiratory chainMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleCardiomyopathiesCarrier ProteinsbusinessMolecular ChaperonesActa Paediatrica
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Novel LRPPRC compound heterozygous mutation in a child with early-onset Leigh syndrome French-Canadian type: Case report of an Italian patient

2020

Abstract Background Mitochondrial diseases, also known as oxidative phosphorylation (OXPHOS) disorders, with a prevalence rate of 1:5000, are the most frequent inherited metabolic diseases. Leigh Syndrome French Canadian type (LSFC), is caused by mutations in the nuclear gene (2p16) leucine-rich pentatricopeptide repeat-containing (LRPPRC). It is an autosomal recessive neurogenetic OXPHOS disorder, phenotypically distinct from other types of Leigh syndrome, with a carrier frequency up to 1:23 and an incidence of 1:2063 in the Saguenay-Lac-St Jean region of Quebec. Recently, LSFC has also been reported outside the French-Canadian population. Patient presentation We report a male Italian (Sic…

MaleHypotonia - developmental delayPediatricsmedicine.medical_specialtyPopulationEncephalopathyCytochrome-c Oxidase DeficiencyCase ReportHypotoniaCompound heterozygosityDiagnosis Differential03 medical and health sciences0302 clinical medicineWhole-genome-sequencingHypotonia; developmental delay; Mitochondrial disease; Whole-exome sequencing; CCT5030225 pediatricsmedicineMissense mutationHumansGlobal developmental delayeducationeducation.field_of_studyComparative Genomic Hybridizationbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseHypotoniaHypoplasiaMitochondrial diseaseNeoplasm Proteinsdevelopmental delayNeonatal hypotoniaPhenotypeItalyWhole-exome sequencingMutationLSFCmedicine.symptomLeigh DiseaseCCT5business030217 neurology & neurosurgeryInfant Premature
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