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Muscle biopsies reveal ragged red bers which are strongly reactive to SDH but COX-negative64,65 However, there are also many COX-negative bers which do not colocalize to ragged red and SDH positive bers Biochemical assay have demonstrated decreased activity of respiratory chain enzymes containing mtDNAencoded subunits, sparing the entirely nuclear-encoded SDH and citrate synthetase
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Multiple mtDNA deletions may be found and the genetic defect is suspected to lie in nuclear genes involved in regulating the mitochondrial genome
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Surgery to correct ptosis may help As with other mitochondrial disorders, individuals with PEO can deMany patients will die from the severe cardiomyopathy within the rst two decades of life, unless they receive cardiac transplantation
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MITOCHONDRIAL DNA DEPLETION SYNDROMES Clinical Features
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The mtDNA depletion syndrome is an autosomal recessive disorder characterized by decreased mtDNA copy number in affected tissues Onset is usually in infancy or early childhood and the spectrum of severity can vary A severe fatal form presents during infancy with generalized hypotonia and weakness66 70 Some infants may appear normal during the rst year of life71,72 There is a predilection for proximal muscle involvement but ptosis and ophthalmoplegia are also common Some affected infants also have a superimposed polneuropathy Muscle stretch re exes are diminished or absent Besides the myopathy, affected infants can develop a cardiomyopathy, De Toni-Fanconi-Debr syndrome (a renal tubular e defect), seizures, or liver failure The muscle weakness is severe and progressive leading to feeding dif culties, respiratory failure, and death usually within the rst year of life There is also a more benign form that can resemble the fatal form of myopathy initially4,54,70,73,74 It can present shortly after birth or later in childhood Affected infants can have severe hypotonia, weakness, respiratory and feeding dif culties Although ventilatory assistance may be required for a period of time, muscle strength gradually improves Motor milestones may be delayed but are usually attained, and by age two or three years children appear to be normal Some children die in the rst two decades of life but other have normal life expectancy In contrast to the fatal infantile form, patients with the benign infantile myopathy usually do not have a renal tubular defect
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muscle tissue of affected patients is greatly diminished or absent
Molecular Genetics and Pathogenesis
At least half the cases are sporadic in nature but some are inherited in an autosomal recessive fashion A depletion of mtDNA was rst reported by Moraes et al in 199175 and subsequently con rmed by others67,73,74,76 79 The quantity of mtDNA indirectly correlates with the clinical severity of the disorder As much as a 99% reduction in mtDNA is present in the fatal infantile myopathy form of the disease, while the more benign myopathy has been demonstrated to have lesser depletions (36 88%) of mtDNA Nuclear genes important in regulating the mitochondrial genome are responsible for mitochondrial DNA depletion Mutations in thymidine kinase 2 (TK2) and deoxyguanosine kinase gene (DGK), both important in mitochondrial deoxynucleotide metabolism, have been associated with this syndrome71,72,80 82,83 Mitochondrial deoxyribonucleoside triphosphate (dNTP) pools measured in patients broblasts reveals an imbalance in dNTP pools80,81 Speci cally, deoxythymidine triphosphate (dTTP) content was markedly decreased, resulting in reduced dTTP:deoxycytidine triphosphate ratio Not all cases of fatal and benign infantile myopathy are associated with mtDNA depletion Some cases are related to mutations in one of the genes encoding for subunits of COX or assessory proteins necessary for complex IV assembly (eg, SURF1)3 However, most of these infants have other neurological de cits (Leigh syndrome)
Treatment Laboratory Features
Serum CK can be normal or elevated as can serum lactate levels The associated renal tubular defect results in glycosuria, proteinuria, and aminoaciduria Cerebral atrophy and patchy areas of hypomyelination of subcortical white matter may be apparent on MRI scans74 Unlike most other mitochondrial myopathies, EMG may demonstrate numerous brillation potentials and positive sharp waves in those myopathies with mtDNA depletion67 Motor units can have a mixed myopathic and neuropathic appearance67,74 NCS can be normal or reveal features of an axonal or demyelinating sensorimotor neuropathy74 No speci c medical therapy has been demonstrated to be effective
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