ICNC2018 Abstracts & Symposia Proposals, ICNC 2014

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SERUM VITAMIN D AND SOME BONE MARKERS LEVELS IN
Marian Yousry Girgis

Last modified: 2014-04-03

Abstract


Objectives:The study was designed to estimate serum vitamin D level and some biochemical markers of bone turnover in a group of Egyptian children with epilepsy on antiepileptic drugs.Patients and Methods: This case control cross sectional study was conducted on thirty children with epilepsy (19 males, and 11 females)on anticonvulsant therapy. They were divided into two subgroups according to their mode of therapy; 15 patients under polytherapy in group I, and 15 patients under monotherapy in group II. Twenty apparently healthy children of matched age and sex were recruited as control group.Results:Epileptic patients on polytherapy had highly significant low serum 25- hydroxy vitamin D level compared to those on monotherapy (p<0.001) with highly significant differences between patients versus controls (p<0.001). Differences between the cut off categories were highly statistically significant for patients versus controls (p<0.001), and among the polytherapy versus monotherapy subgroups (p<0.001). The mean serum calcium levels were found to be statistically significant lower inepileptic patients compared to control (p<0.01) with no significant difference between the patients subgroups. The mean serum levels of alkaline phosphatase were statistically significant higher in the patients group compared to controls (p<0.001), with no statistically significant difference between patients subgroups.Conclusion:Our results revealed high risk of vitamin D deficiency in epileptic children on antiepileptic drugs especially those under long term polytherapy. Routine monitoring of serum 25- hydroxy vitamin D is recommended with vitamin D supplementation on an individual basis.

Keywords


epilepsy- children- vitamin D - bone markers - antiepileptic drugs

References


(1)  Kotsopoulos IA, van Merode T, Kessels F G,de Krom MC, Knottnerus JA (2002): Systematic reviewand meta-analysis of incidence studies of epilepsy and unprovoked seizures.Epilepsia 43:1402–1409. (2) Mintzer S, Boppana P, Toguri J, DeSantisA (2006): Vitamin D levels and bone turnover in epilepsy patients takingcarbamazepine or oxcarbazepine. Epilepsia 47:510–515 (3) Zhou C,Assem M, Tay JC, Watkins PB, Blumberg B,Schuetz EG, Thummel KE (2006) :Steroid and xenobiotic receptor and vitaminD receptor crosstalk mediates CYP24 expression and drug-induced osteomalacia. JClin Invest 116:1703–1712  (4) AttilakosA, Papakonstantinou E, Schulpis K, Voudris K, Katsarou E, Mastroyianni S,Garoufi A (2006): Early effect of sodium valproate and carbamazepinemonotherapy on homocysteine metabolism in children with epilepsy. Epilepsy Res71:229– 232 (5) Souverein PC, Webb DJ, Weil JG, Van StaaTP, Egberts ACG (2006): Use of antiepileptic drugs and risk of fractures:case-control study among patients with epilepsy. Neurology; 66:1318–1324. [PubMed] (6) Shellhaas RA,Barks AK,Joshi SM(2010): Prevalence and risk factorsfor vitamin D insufficiency among children with epilepsy. PediatrNeurol. 2010 Jun; 42(6):422-6.  (7) Chabolla DR (2002): Characteristics of the epilepsies.Mayo Clin Proc; 77(9):981-990. (8) HiernauxJ. and Tanner J.M (1969): Growth, and physical studies. In: HumanBiology: guide to field methods. Eds. Weiner J.S.,Lourie S.A., IBP. London, Blackwell ScientificPublications, Oxford.U.K.(9) Visser, M., Deeg, D.J., Puts, M.T., Seidell, J.C., Lips, P. (2006): Lowserum concentrations of 25- hydroxyvitamin D in older persons and the risk ofnursing home admission. Am. J. Clin.Nutr. 84(3), 616-622.(10) Saintonge S, Band H, Gerber LM (2009):Implications of a new definition of vitamin D deficiency in a multiracial USadolescent population: The National health and nutrition examination surveyIII. Pediatrics; 123:797–803. [PubMed]    (11) Endres D.B andRude R.K (2008): Disorders of Bone (eds) Burtis C.A., Ashwood E.R. and Bruns D.E.In: Teitz Fundamentals of Clinical Chemistry, sixth edition, vol.2, SaundersElsevier, Philadelphia PA, USA,p.715-719                (12) PanteghiniM and Bais R. (2008): Enzymes (eds) Burtis C.A., Ashwood E.R. and Bruns D.E.In: Teitz     Fundamentals of ClinicalChemistry, sixth edition, vol.1, Saunders Elsevier, Philadelphia PA, USA, p. 326(13) Sander JW (2003): The epidemiology ofepilepsy revisited. Curr Opin Neurol; 16: 165-70. (14) Kandil MR, Ahmed WM, Sayed A, HamedSA (2007): Pattern ofepilepsy in Childhood And Adolescence: A hospital-based study. Departments ofNeurology, Assiut University Hospital,Assiut, Egypt African Journal ofNeurological Sciences Vol. 26 (1): pp. 33-44 (15) Shinnar S, Pellock JM (2002): Update on theepidemiology and prognosis of pediatric epilepsy. J Child Neurol.; 17(suppl1):S4-17. (16) Holick MF (2009):  Vitamin D status, measurement,interpretation, and clinical application Ann Epidemiol; 19:73–78. [PMC freearticle] [PubMed] (17) Fong CY,Riney CJ.(2013): Vitamin D deficiency among Children withEpilepsy in South Queensland. J Child Neurol, Jan; 22.  (18) GisselT, Poulsen CS, Vestergaard P (2007): Adverse effects of antiepileptic drugson bone mineral density in children. Expert Opin Drug Saf 6:267–278. (19) FitzpatrickLA (2004): Pathophysiology of bone loss in patients receivinganticonvulsant therapy. Epilepsy Behav 5(Suppl 2):S3–S15. (20) Öner N,Kaya M, Karasalihoğlu S, Karaca H, Celtik C, Tütüncüler F (2004):Bone mineral metabolism changes in epileptic children receiving valproic acid.J Paediatr Child Health 40:470–473. (21) WeismanSM, Matkovic V (2005): Potential use of biochemical markers of boneturnover for assessing the effect of calcium supplementation and predictingfracture risk. Clin Ther 27: 299–308. (22) VoudrisK, Moustaki M, Zeis PM, Dimou S, Vagiakou E,Tsagris B, Skardoutsou A (2002): Alkalinephosphatase and its isoenzyme activity for the evaluation of bone metabolism inchildren receiving anticonvulsant monotherapy. Seizure 11:377–380.(23) Nettekoven S,Ströhle A,Trunz B,Wolters M,Hoffmann S,Horn R,Steinert M,Brabant G,LichtinghagenR, WelkoborskyHJ, Tuxhorn I,Hahn A(2008 ):   Effects of antiepileptic drug therapy on vitamin D status and biochemicalmarkers of bone turnover in children with epilepsy. Eur J Pediatr. Dec; 167(12):1369-77.(24)  Misra A,Aggarwal A,Singh O,Sharma S(2010):  Effectof carbamazepine therapy on vitamin D and parathormone in epileptic childrenPediatr Neurol. Nov;43(5):320-4.   (25) Bergqvist AG, Schall JI, Stallings VA(2007): Vitamin D status in children with intractable epilepsy, and impactof the ketogenic diet. Epilepsia 48:66–71. (26) Guo CY,Ronen GM,Atkinson SA(2001) : Long-term valproate and lamotrigine treatment may be a marker forreduced growth and bone mass in children with epilepsy. Department ofPediatrics, McMaster University, Hamilton, Ontario, Canada.Epilepsia.Sep; 42(9):1141-7.  (27) Misra A,Aggarwal A,Singh O,Sharma S(2010):  Effectof carbamazepine therapy on vitamin D and parathormone in epileptic childrenPediatr Neurol. Nov;43(5):320-4.  (28) ShellhaasRA, Joshi SM (2000):  VitaminD and bone health among children with epilepsy. Pediatr Neurol; 42:385-393.

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