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Vitamin-Responsive Epileptic Encephalopathies in Children

DOI: 10.1155/2013/510529

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Abstract:

Untreated epileptic encephalopathies in children may potentially have disastrous outcomes. Treatment with antiepileptic drugs (AEDs) often may not control the seizures, and even if they do, this measure is only symptomatic and not specific. It is especially valuable to identify potential underlying conditions that have specific treatments. Only a few conditions have definitive treatments that can potentially modify the natural course of disease. In this paper, we discuss the few such conditions that are responsive to vitamin or vitamin derivatives. 1. Introduction Epileptic encephalopathies (EEs) are conditions in which progressive cognitive and neuropsychological regression occurs, attributable to excessive ictal and interictal epileptogenic activity during brain maturation [1]. The progression in such disorders is mostly relentless and leads to irreversible damage to the developing brain. Original classification of International League Against Epilepsy (ILAE) included only a few conditions under strict criteria of EE; however, in 2010, they extended the definition to any form of epilepsy that can cause encephalopathic effect [2]. Most of these conditions are managed symptomatically with AEDs; very rarely do these conditions have treatable underlying causes, including genetic, metabolic, autoimmune, and nutritional causes. Treatment with a specific vitamin or vitamin derivative in these specific cases may halt such inexorable progression. 2. Pyridoxine Dependent Epilepsy (PDE) Hunt and colleagues reported the first case of intractable epilepsy in an infant controlled by pyridoxine in 1954 [3]. Subsequently, many anecdotal case reports surfaced [4, 5]. For a while, it was speculated that a mutation affecting Glutamate decarboxylase (GAD) was the cause for PDE. However, Battaglioli and colleagues showed that GAD mutation is not linked to PDE [6]. In 2006, Mills et al. for the first time reported that alpha aminoadipic semialdehyde dehydrogenase (antiquitin) deficiency due to ALDH1A7 mutation is a cause for PDE [7]. It usually manifest in neonatal period. The affected neonates usually manifest within the first few hours after birth with seizures. The seizure evolves into status epilepticus despite adequate treatment with AEDs. An antenatal history of unusual fetal movements indicating intrauterine seizures may be present although this is not very common. The seizure semiology is quite variable with focal, generalized, myoclonic, epileptic spasms, and/or mixed seizure patterns. PDE can be easily confused with hypoxic ischemic encephalopathy or sepsis due

References

[1]  O. Dulac, “Epileptic encephalopathy,” Epilepsia, vol. 42, no. 3, pp. 23–26, 2001.
[2]  A. T. Berg, S. F. Berkovic, M. J. Brodie et al., “Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005–2009,” Epilepsia, vol. 51, no. 4, pp. 676–685, 2010.
[3]  A. D. Hunt Jr., J. Stokes Jr., W. W. McCrory, and H. H. Stroud, “Pyridoxine dependency: report of a case of intractable convulsions in an infant controlled by pyridoxine,” Pediatrics, vol. 13, no. 2, pp. 140–145, 1954.
[4]  R. Garty, Z. Yonis, J. Braham, and K. Steinitz, “Pyridoxine-dependent convulsions in an infant,” Archives of disease in childhood, vol. 37, no. 191, pp. 21–24, 1962.
[5]  M. Bejsovec, Z. Kulenda, and E. Ponca, “Familial intrauterine convulsions in pyridoxine dependency,” Archives of disease in childhood, vol. 42, no. 222, pp. 201–207, 1967.
[6]  G. Battaglioli, D. R. Rosen, S. M. Gospe Jr., and D. L. Martin, “Glutamate decarboxylase is not genetically linked to pyridoxine- dependent seizures,” Neurology, vol. 55, no. 2, pp. 309–311, 2000.
[7]  P. B. Mills, E. Struys, C. Jakobs et al., “Mutations in antiquitin in individuals with pyridoxine-dependent seizures,” Nature Medicine, vol. 12, no. 3, pp. 307–309, 2006.
[8]  C.-A. Haenggeli, E. Girardin, and L. Paunier, “Pyridoxine-dependent seizures, clinical and therapeutic aspects,” European Journal of Pediatrics, vol. 150, no. 7, pp. 452–455, 1991.
[9]  P. Baxter, P. Griffiths, T. Kelly, and D. Gardner-Medwin, “Pyridoxine-dependent seizures: demographic, clinical MRI and psychometric features, and effect of dose on intelligence quotient,” Developmental Medicine and Child Neurology, vol. 38, no. 11, pp. 998–1006, 1996.
[10]  P. Baxter, “Epidemiology of pyridoxine dependent and pyridoxine responsive seizures in the UK,” Archives of Disease in Childhood, vol. 81, no. 5, pp. 431–433, 1999.
[11]  S. B. Coker, “Postneonatal vitamin B6-dependent epilepsy,” Pediatrics, vol. 90, no. 2, pp. 221–223, 1992.
[12]  F. Goutières and J. Aicardi, “Atypical presentations of pyridoxine-dependent seizures: a treatable cause of intractable epilepsy in infants,” Annals of Neurology, vol. 17, no. 2, pp. 117–120, 1985.
[13]  A. Bankier, M. Turner, and I. J. Hopkins, “Pyridoxine dependent seizures: a wider clinical spectrum,” Archives of Disease in Childhood, vol. 58, no. 6, pp. 415–418, 1983.
[14]  B. Plecko, C. Hikel, G.-C. Korenke et al., “Pipecolic acid as a diagnostic marker of pyridoxine-dependent epilepsy,” Neuropediatrics, vol. 36, no. 3, pp. 200–205, 2005.
[15]  B. Plecko, K. Paul, E. Paschke et al., “Biochemical and molecular characterization of 18 patients with pyridoxine-dependent epilepsy and mutations of the antiquitin (ALDH7A1) gene,” Human Mutation, vol. 28, no. 1, pp. 19–26, 2007.
[16]  S. M. Gospe Jr. and S. T. Hecht, “Longitudinal MRI findings in pyridoxine-dependent seizures,” Neurology, vol. 51, no. 1, pp. 74–78, 1998.
[17]  P. B. Mills, E. J. Footitt, K. A. Mills et al., “Genotypic and phenotypic spectrum of pyridoxine-dependent epilepsy (ALDH7A1 deficiency),” Brain, vol. 133, no. 7, pp. 2148–2159, 2010.
[18]  J. J. Shih, H. Kornblum, and D. A. Shewmon, “Global brain dysfunction in an infant with pyridoxine dependency: evaluation with EEG, evoked potentials, MRI, and PET,” Neurology, vol. 47, no. 3, pp. 824–826, 1996.
[19]  H. Ulvi, B. Müngen, C. Yakinci, and T. Yolda?, “Pyridoxine-dependent seizures: long-term follow-up of two cases with clinical and MRI findings, and pyridoxine treatment,” Journal of Tropical Pediatrics, vol. 48, no. 5, pp. 303–306, 2002.
[20]  A. Alkan, R. Kutlu, M. Aslan, A. Sigirci, I. Orkan, and C. Yakinci, “Pyridoxine-dependent seizures: magnetic resonance spectroscopy findings,” Journal of Child Neurology, vol. 19, no. 1, pp. 75–78, 2004.
[21]  S. M. Gospe Jr., “Pyridoxine-dependent epilepsy and pyridoxine phosphate oxidase deficiency: unique clinical symptoms and non-specific EEG characteristics,” Developmental Medicine and Child Neurology, vol. 52, no. 7, pp. 602–603, 2010.
[22]  B. Schmitt, M. Baumgartner, P. B. Mills et al., “Seizures and paroxysmal events: symptoms pointing to the diagnosis of pyridoxine-dependent epilepsy and pyridoxine phosphate oxidase deficiency,” Developmental Medicine and Child Neurology, vol. 52, no. 7, pp. e133–e142, 2010.
[23]  G. Kluger, R. Blank, K. Paul et al., “Pyridoxine-dependent epilepsy: normal outcome in a patient with late diagnosis after prolonged status epilepticus causing cortical blindness,” Neuropediatrics, vol. 39, no. 5, pp. 276–279, 2008.
[24]  C. L. Bennett, Y. Chen, S. Hahn, I. A. Glass, and S. M. Gospe Jr., “Prevalence of ALDH7A1 mutations in 18 North American pyridoxine-dependent seizure (PDS) patients,” Epilepsia, vol. 50, no. 5, pp. 1167–1175, 2009.
[25]  J. Kanno, S. Kure, A. Narisawa et al., “Allelic and non-allelic heterogeneities in pyridoxine dependent seizures revealed by ALDH7A1 mutational analysis,” Molecular Genetics and Metabolism, vol. 91, no. 4, pp. 384–389, 2007.
[26]  G. S. Salomons, L. A. Bok, E. A. Struys et al., “An intriguing “silent” mutation and a founder effect in antiquitin (ALDH7A1),” Annals of Neurology, vol. 62, no. 4, pp. 414–418, 2007.
[27]  P. M. Rankin, S. Harrison, W. K. Chong, S. Boyd, and S. E. Aylett, “Pyridoxine-dependent seizures: a family phenotype that leads to severe cognitive deficits, regardless of treatment regime,” Developmental Medicine and Child Neurology, vol. 49, no. 4, pp. 300–305, 2007.
[28]  M. A. Mikati, E. Trevathan, K. Krishnamoorthy, and C. T. Lombroso, “Pyridoxine-dependent epilepsy: EEG investigations and long-term follow-up,” Electroencephalography and Clinical Neurophysiology, vol. 78, no. 3, pp. 215–221, 1991.
[29]  S. M. Gospe Jr., “Neonatal vitamin-responsive epileptic encephalopathies,” Chang Gung Medical Journal, vol. 33, no. 1, pp. 1–12, 2010.
[30]  L. A. Bok, N. M. Maurits, M. A. Willemsen et al., “The EEG response to pyridoxine-IV neither identifies nor excludes pyridoxine-dependent epilepsy,” Epilepsia, vol. 51, no. 12, pp. 2406–2411, 2010.
[31]  H.-J. Gdynia, T. Müller, A.-D. Sperfeld et al., “Severe sensorimotor neuropathy after intake of highest dosages of vitamin B6,” Neuromuscular Disorders, vol. 18, no. 2, pp. 156–158, 2008.
[32]  H. Schaumburg, J. Kaplan, and A. Windebank, “Sensory neuropathy from pyridoxine abuse. A new megavitamin syndrome,” The New England Journal of Medicine, vol. 309, no. 8, pp. 445–448, 1983.
[33]  C. D. van Karnebeek, H. Hartmann, S. Jaggumantri et al., “Lysine restricted diet for pyridoxine-dependent epilepsy: first evidence and future trials,” Molecular Genetics and Metabolism, vol. 107, no. 3, pp. 335–344, 2012.
[34]  K. Baynes, S. T. Farias, and S. M. Gospe Jr., “Pyridoxine-dependent seizures and cognition in adulthood,” Developmental Medicine and Child Neurology, vol. 45, no. 11, pp. 782–785, 2003.
[35]  Y. Ohtsuka, J. Hattori, T. Ishida, T. Ogino, and E. Oka, “Long-term follow-up of an individual with vitamin B6-dependent seizures,” Developmental Medicine & Child Neurology, vol. 41, no. 3, pp. 203–206, 1999.
[36]  L. A. Bok, F. J. Halbertsma, S. Houterman et al., “Long-term outcome in pyridoxine-dependent epilepsy,” Developmental Medicine & Child Neurology, vol. 54, no. 9, pp. 849–854, 2012.
[37]  S. Stockler, B. Plecko, S. M. Gospe et al., “Pyridoxine dependent epilepsy and antiquitin deficiency. Clinical and molecular characteristics and recommendations for diagnosis, treatment and follow-up,” Molecular Genetics and Metabolism, vol. 104, no. 1-2, pp. 48–60, 2011.
[38]  M.-F. Kuo and H.-S. Wang, “Pyridoxal phosphate-responsive epilepsy with resistance to pyridoxine,” Pediatric Neurology, vol. 26, no. 2, pp. 146–147, 2002.
[39]  P. B. Mills, R. A. H. Surtees, M. P. Champion et al., “Neonatal epileptic encephalopathy caused by mutations in the PNPO gene encoding pyridox(am)ine 5′-phosphate oxidase,” Human Molecular Genetics, vol. 14, no. 8, pp. 1077–1086, 2005.
[40]  G. F. Hoffmann, B. Schmitt, M. Windfuhr et al., “Pyridoxal 5′-phosphate may be curative in early-onset epileptic encephalopathy,” Journal of Inherited Metabolic Disease, vol. 30, no. 1, pp. 96–99, 2007.
[41]  S. Bagci, J. Zschocke, G. F. Hoffmann et al., “Pyridoxal phosphate-dependent neonatal epileptic encephalopathy,” Archives of Disease in Childhood: Fetal and Neonatal Edition, vol. 93, no. 2, pp. F151–F152, 2008.
[42]  A. Ruiz, J. García-Villoria, A. Ormazabal et al., “A new fatal case of pyridox(am)ine 5′-phosphate oxidase (PNPO) deficiency,” Molecular Genetics and Metabolism, vol. 93, no. 2, pp. 216–218, 2008.
[43]  A. Ormazabal, M. Oppenheim, M. Serrano et al., “Pyridoxal 5′-phosphate values in cerebrospinal fluid: reference values and diagnosis of PNPO deficiency in paediatric patients,” Molecular Genetics and Metabolism, vol. 94, no. 2, pp. 173–177, 2008.
[44]  E. J. Footitt, S. J. Heales, P. B. Mills, G. F. G. Allen, M. Oppenheim, and P. T. Clayton, “Pyridoxal 5′-phosphate in cerebrospinal fluid; Factors affecting concentration,” Journal of Inherited Metabolic Disease, vol. 34, no. 2, pp. 529–538, 2011.
[45]  R. A. Wevers, S. I. Hansen, J. L. M. van Hellenberg Hubar, J. Holm, M. Hoier-Madsen, and P. J. H. Jongen, “Folate deficiency in cerebrospinal fluid associated with a defect in folate binding protein in the central nervous system,” Journal of Neurology Neurosurgery and Psychiatry, vol. 57, no. 2, pp. 223–226, 1994.
[46]  V. T. Ramaekers and N. Blau, “Cerebral folate deficiency,” Developmental Medicine and Child Neurology, vol. 46, no. 12, pp. 843–851, 2004.
[47]  V. T. Ramaekers, S. P. Rothenberg, J. M. Sequeira et al., “Autoantibodies to folate receptors in the cerebral folate deficiency syndrome,” The New England Journal of Medicine, vol. 352, no. 19, pp. 1985–1991, 2005.
[48]  S. U. Steele, S. M. Cheah, A. Veerapandiyan, W. Gallentine, E. C. Smith, and M. A. Mikati, “Electroencephalographic and seizure manifestations in two patients with folate receptor autoimmune antibody-mediated primary cerebral folate deficiency,” Epilepsy & Behavior, vol. 24, no. 4, pp. 507–512, 2012.
[49]  M. Grapp, I. A. Just, T. Linnankivi et al., “Molecular characterization of folate receptor 1 mutations delineates cerebral folate transport deficiency,” Brain, vol. 135, no. 7, pp. 2022–2031, 2012.
[50]  F. Scaglia, “Cerebral Folate Deficiency and Epilepsy,” in Inherited Metabolic Epilepsies, pp. 261–266, Demos Publication, 2012.
[51]  K. Hyland, J. Shoffner, and S. J. Heales, “Cerebral folate deficiency,” Journal of Inherited Metabolic Disease, vol. 33, no. 5, pp. 563–570, 2010.
[52]  B. Wolf, “Worldwide survey of neonatal screening for biotinidase deficiency,” Journal of Inherited Metabolic Disease, vol. 14, no. 6, pp. 923–927, 1991.
[53]  B. Afroze and M. Wasay, “Biotinidase deficiency in Pakistani children; what needs to be known and done,” Journal of the Pakistan Medical Association, vol. 62, no. 4, pp. 312–313, 2012.
[54]  B. Wolf, G. S. Heard, and K. A. Weissbecker, “Biotinidase deficiency: initial clinical features and rapid diagnosis,” Annals of Neurology, vol. 18, no. 5, pp. 614–617, 1985.
[55]  B. Wolf, R. Pomponio, K. Norrgard et al., “Delayed-onset profound biotnidase deficiency,” Journal of Pediatrics, vol. 132, no. 2, pp. 362–365, 1998.
[56]  B. A. Salbert, J. M. Pellock, and B. Wolf, “Characterization of seizures associated with biotinidase deficiency,” Neurology, vol. 43, no. 7, pp. 1351–1355, 1993.
[57]  B. Wolf, “The neurology of biotinidase deficiency,” Molecular Genetics and Metabolism, vol. 104, no. 1-2, pp. 27–34, 2011.
[58]  P. C. Navarro, A. Guerra, J. G. Alvarez, and F. J. Ortiz, “Cutaneous and neurologic manifestations of biotinidase deficiency,” International Journal of Dermatology, vol. 39, no. 5, pp. 363–365, 2000.
[59]  S. N. Joshi, M. Fathalla, R. Koul, M. Al. Maney, and R. Bayoumi, “Biotin responsive seizures and encephalopathy due to biotinidase deficiency,” Neurology India, vol. 58, no. 2, pp. 323–324, 2010.
[60]  S. Desai, K. Ganesan, and A. Hegde, “Biotinidase deficiency: a reversible metabolic encephalopathy. Neuroimaging and MR spectroscopic findings in a series of four patients,” Pediatric Radiology, vol. 38, no. 8, pp. 848–856, 2008.
[61]  D. M. Mock, “Skin manifestations of biotin deficiency,” Seminars in Dermatology, vol. 10, no. 4, pp. 296–302, 1991.
[62]  B. Wolf, “Biotinidase deficiency: ‘if you have to have an inherited metabolic disease, this is the one to have’,” Genetics in Medicin, vol. 14, no. 6, pp. 565–575, 2012.
[63]  B. Wolf and G. S. Heard, “Biotinidase deficiency,” Advances in pediatrics, vol. 38, pp. 1–21, 1991.
[64]  B. Tabark, S. Al-Shafi, S. Al-Shahwan, et al., “Biotin-responsive basal ganglia disease revisited: clinical, radiologic, and genetic findings,” Neurology, vol. 80, no. 3, pp. 261–267, 2013.
[65]  B. Wolf, “Clinical issues and frequent questions about biotinidase deficiency,” Molecular Genetics and Metabolism, vol. 100, no. 1, pp. 6–13, 2010.
[66]  B. Wolf and G. S. Heard, “Screening for biotinidase deficiency in newborns: Worldwide experience,” Pediatrics, vol. 85, no. 4, pp. 512–517, 1990.
[67]  B. Wolf, R. Spencer, and T. Gleason, “Hearing loss is a common feature of symptomatic children with profound biotinidase deficiency,” Journal of Pediatrics, vol. 140, no. 2, pp. 242–246, 2002.
[68]  S. Grünewald, M. P. Champion, J. V. Leonard, J. Schaper, and A. A. M. Morris, “Biotinidase deficiency: a treatable leukoencephalopathy,” Neuropediatrics, vol. 35, no. 4, pp. 211–216, 2004.
[69]  O. Leichtenstern, “Progressive pernici?se an?mie bei tabeskranken,” Deutsche Medizinische Wochenschrift, vol. 10, pp. 849–850, 1884.
[70]  L. Lichtheim, “Zur kenntniss der pernici?sen an?mie,” Munchener Medizinische Wochenschrift, vol. 34, pp. 301–306, 1887.
[71]  M. Jadhav, J. K. G. Webb, S. Vaishnava, and S. J. Baker, “Vitamin-B12 deficiency in Indian infants,” The Lancet, vol. 280, no. 7262, pp. 903–907, 1962.
[72]  U. von Schenck, C. Bender-G?tze, and B. Koletzko, “Persistence of neurological damage induced by dietary vitamin B-12 deficiency in infancy,” Archives of Disease in Childhood, vol. 77, no. 2, pp. 137–139, 1997.
[73]  J. R. Russell, F. Batten, and J. Collier, “Subacute combined degeneration of the spinal cord,” Brain, vol. 23, no. 1, pp. 39–110, 1900.
[74]  S. D. Shorvon, M. W. P. Carney, I. Chanarin, and E. H. Reynolds, “The neuropsychiatry of megaloblastic anaemia,” British Medical Journal, vol. 281, no. 6247, pp. 1036–1038, 1980.
[75]  E. Reynolds, “Vitamin B12, folic acid, and the nervous system,” The Lancet Neurology, vol. 5, no. 11, pp. 949–960, 2006.
[76]  S. A. Rasmussen, P. M. Fernhoff, and K. S. Scanlon, “Vitamin B12 deficiency in children and adolescents,” Journal of Pediatrics, vol. 138, no. 1, pp. 10–17, 2001.
[77]  S. M. Graham, O. M. Arvela, and G. A. Wise, “Long-term neurologic consequences of nutritional vitamin B12 deficiency in infants,” Journal of Pediatrics, vol. 121, no. 5, pp. 710–714, 1992.
[78]  G. C. Korenke, D. H. Hunneman, S. Eber, and F. Hanefeld, “Severe encephalopathy with epilepsy in an infant caused by subclinical maternal pernicious anaemia: case report and review of the literature,” European Journal of Pediatrics, vol. 163, no. 4-5, pp. 196–201, 2004.
[79]  K.-O. L?vblad, G. Ramelli, L. Remonda, A. C. Nirkko, C. Ozdoba, and G. Schroth, “Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings,” Pediatric Radiology, vol. 27, no. 2, pp. 155–158, 1997.
[80]  P. T. Monagle and G. P. Tauro, “Infantile megaloblastosis secondary to maternal vitamin B12 deficiency,” Clinical and Laboratory Haematology, vol. 19, no. 1, pp. 23–25, 1997.
[81]  G.-A. Gutiérrez-Aguilar, P. Abenia-Usón, A. García-Cazorla, M. A. Vilaseca, and J. Campistol, “Encephalopathy with methylmalonic aciduria and homocystinuria secondary to a deficient exogenous supply of vitamin B12,” Revista de Neurologia, vol. 40, no. 10, pp. 605–608, 2005.
[82]  J. Lundgren and G. Blennow, “Vitamin B12 deficiency may cause benign familial infantile convulsions: a case report,” Acta Paediatrica, vol. 88, no. 10, pp. 1158–1160, 1999.
[83]  I. Erol, F. Alehan, and A. Gümüs, “West syndrome in an infant with vitamin B12 deficiency in the absence of macrocytic anaemia,” Developmental Medicine and Child Neurology, vol. 49, no. 10, pp. 774–776, 2007.
[84]  M. Lee, H.-S. Chang, H.-T. Wu, H.-H. Weng, and C.-M. Chen, “Intractable epilepsy as the presentation of vitamin B12 deficiency in the absence of macrocytic anemia,” Epilepsia, vol. 46, no. 7, pp. 1147–1148, 2005.
[85]  S. Kumar, “Recurrent seizures: an unusual manifestation of vitamin B12 deficiency,” Neurology India, vol. 52, no. 1, pp. 122–123, 2004.
[86]  E. P. Frenkel, “Abnormal fatty acid metabolism in peripheral nerves of patients with pernicious anemia,” Journal of Clinical Investigation, vol. 52, no. 5, pp. 1237–1245, 1973.
[87]  A. L. Bj?rke Monsen and P. M. Ueland, “Homocysteine and methylmalonic acid in diagnosis and risk assessment from infancy to adolescence,” American Journal of Clinical Nutrition, vol. 78, no. 1, pp. 7–21, 2003.
[88]  R. H. Allen, S. P. Stabler, D. G. Savage, and J. Lindenbaum, “Metabolic abnormalities in cobalamin (vitamin B12) and folate deficiency,” The FASEB Journal, vol. 7, no. 14, pp. 1344–1353, 1993.
[89]  K. Stollhoff and F. J. Schulte, “Vitamin B12 and brain development,” European Journal of Pediatrics, vol. 146, no. 2, pp. 201–205, 1987.
[90]  L. J. Wolansky, G. Goldstein, A. Gozo, H. J. Lee, L. Sills, and S. Chatkupt, “Subacute combined degeneration of the spinal cord: MRI detection of preferential involvement of the posterior columns in a child,” Pediatric Radiology, vol. 25, no. 2, pp. 140–141, 1995.
[91]  E. B. Healton, D. G. Savage, J. C. M. Brust, T. J. Garrett, and J. Lindenbaum, “Neurologic aspects of cobalamin deficiency,” Medicine, vol. 70, no. 4, pp. 229–245, 1991.

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