Document Detail


Neonatal liver failure and Leigh syndrome possibly due to CoQ-responsive OXPHOS deficiency.
MedLine Citation:
PMID:  12948744     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CoQ transfers electrons from complexes I and II of the mitochondrial respiratory chain to complex III. There are very few reports on human CoQ deficiency. The clinical presentation is usually characterized by: epilepsy, muscle weakness, ataxia, cerebellar atrophy, migraine, myogloblinuria and developmental delay. We describe a patient who presented with neonatal liver and pancreatic insufficiency, tyrosinemia and hyperammonemia and later developed sensorineural hearing loss and Leigh syndrome. Liver biopsy revealed markedly reduced complex I+III and II+III. Addition of CoQ to the liver homogenate restored the activities, suggesting CoQ depletion. Histological staining showed prominent bridging; septal fibrosis and widening of portal spaces with prominent mixed inflammatory infiltrate, associated with interface hepatitis, bile duct proliferation with numerous bile plugs. Electron microscopy revealed a large number of mitochondria, which were altered in shape and size, widened and disordered intercristal spaces. This may be the first case of Leigh syndrome with liver and pancreas insufficiency, possibly caused by CoQ responsive oxphos deficiency.
Authors:
E Leshinsky-Silver; A Levine; A Nissenkorn; V Barash; M Perach; E Buzhaker; M Shahmurov; S Polak-Charcon; D Lev; T Lerman-Sagie
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Publication Detail:
Type:  Case Reports; Journal Article    
Journal Detail:
Title:  Molecular genetics and metabolism     Volume:  79     ISSN:  1096-7192     ISO Abbreviation:  Mol. Genet. Metab.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-09-01     Completed Date:  2004-06-01     Revised Date:  2005-09-10    
Medline Journal Info:
Nlm Unique ID:  9805456     Medline TA:  Mol Genet Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  288-93     Citation Subset:  IM    
Affiliation:
Molecular Genetics and Brunner Institute, and Metabolic-Neurogenetic Unit and Mitochondrial Disease Center, Wolfson Medical Center, Holon, Israel.
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MeSH Terms
Descriptor/Qualifier:
Biopsy
Electron Transport Complex I / deficiency
Electron Transport Complex II / deficiency
Electron Transport Complex III / deficiency
Hearing Loss, Sensorineural / enzymology,  physiopathology
Humans
Hyperammonemia / enzymology
Infant
Leigh Disease / enzymology*,  physiopathology
Liver / enzymology,  pathology*,  ultrastructure
Liver Failure, Acute / enzymology*,  pathology
Male
Metabolism, Inborn Errors / enzymology
Mitochondria, Liver / enzymology
Mitochondrial Diseases*
Oxidative Phosphorylation
Pancreas / enzymology,  pathology
Ubiquinone / deficiency,  metabolism*
Chemical
Reg. No./Substance:
1339-63-5/Ubiquinone; EC 1.10.2.2/Electron Transport Complex III; EC 1.3.5.1/Electron Transport Complex II; EC 1.6.5.3/Electron Transport Complex I; EC 1.6.5.3/respiratory complex II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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