PMID- 23266348 OWN - NLM STAT- MEDLINE DCOM- 20131024 LR - 20181202 IS - 1532-2688 (Electronic) IS - 1059-1311 (Linking) VI - 22 IP - 2 DP - 2013 Mar TI - Assessment of atherosclerosis risk due to the homocysteine-asymmetric dimethylarginine-nitric oxide cascade in children taking antiepileptic drugs. PG - 124-7 LID - S1059-1311(12)00296-8 [pii] LID - 10.1016/j.seizure.2012.11.007 [doi] AB - PURPOSE: The aim of this study was to assess the atherogenicity risk of antiepileptics in children by investigating the cascade, "hyperhomocysteinemia (HHcy)-->asymmetric dimethylarginine (ADMA) increase-->nitric oxide (NO) decrease", which is thought to contribute to the developmental process of atherosclerosis. METHODS: The participants included 53 epilepsy patients who received either valproic acid (VPA, n=26) or oxcarbazepine (OXC, n=27). Twenty-four healthy sex- and age-matched children served as controls. Fasting plasma total homocysteine (tHcy), ADMA and NO levels were measured. RESULTS: The differences in Hcy, ADMA, NO, vitamin B(12) and folate levels between VPA, OXC and control groups were all insignificant (p>0.05 for all). In the patient group (VPA and OXC groups), 22.6% of the children (12/53) had tHcy levels above the normal cutoff (13.1mumol/l) for children and 17% of the children (9/53) had tHcy levels of greater than 15mumol/l which is accepted as the critical value for an increased atherosclerosis risk (p<0.05 for both). The difference in rate of HHcy between VPA and OXC groups was statistically insignificant (p>0.05, for both cut off levels of HHCy). There was a positive correlation of tHcy levels and antiepileptic drug treatment duration in the patient group (r=+0.276, p<0.05). CONCLUSION: HHcy may develop in patients using OXC. Contrary to some previous publications, our data do not suggest that OXC is safer than VPA in terms of HHcy risk. Further prospective, large scale and longer term studies investigating all suggested pathways responsible for development of atherosclerosis due to HHcy should be conducted to define the exact mechanism responsible for AEDs related atherosclerosis. CI - Copyright (c) 2012 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. FAU - Emeksiz, Hamdi Cihan AU - Emeksiz HC AD - Department of Pediatrics, Gazi University, TR-06450 Ankara, Turkey. hcemeksiz@gmail.com FAU - Serdaroglu, Ayse AU - Serdaroglu A FAU - Biberoglu, Gursel AU - Biberoglu G FAU - Gulbahar, Ozlem AU - Gulbahar O FAU - Arhan, Ebru AU - Arhan E FAU - Cansu, Ali AU - Cansu A FAU - Arga, Mustafa AU - Arga M FAU - Hasanoglu, Alev AU - Hasanoglu A LA - eng PT - Journal Article DEP - 20121221 PL - England TA - Seizure JT - Seizure JID - 9306979 RN - 0 (Anticonvulsants) RN - 0 (Biomarkers) RN - 0LVT1QZ0BA (Homocysteine) RN - 31C4KY9ESH (Nitric Oxide) RN - 33CM23913M (Carbamazepine) RN - 614OI1Z5WI (Valproic Acid) RN - 63CV1GEK3Y (N,N-dimethylarginine) RN - 94ZLA3W45F (Arginine) RN - VZI5B1W380 (Oxcarbazepine) SB - IM MH - Adolescent MH - Anticonvulsants/adverse effects/therapeutic use MH - Arginine/*analogs & derivatives/blood MH - Atherosclerosis/*blood/chemically induced/epidemiology MH - Biomarkers/blood MH - Carbamazepine/adverse effects/*analogs & derivatives/therapeutic use MH - Child MH - Epilepsy/blood/drug therapy/epidemiology MH - Female MH - Homocysteine/*blood MH - Humans MH - Male MH - Nitric Oxide/*blood MH - Oxcarbazepine MH - Prospective Studies MH - Risk Factors MH - Valproic Acid/adverse effects/*therapeutic use EDAT- 2012/12/26 06:00 MHDA- 2013/10/25 06:00 CRDT- 2012/12/26 06:00 PHST- 2012/04/11 00:00 [received] PHST- 2012/11/19 00:00 [revised] PHST- 2012/11/20 00:00 [accepted] PHST- 2012/12/26 06:00 [entrez] PHST- 2012/12/26 06:00 [pubmed] PHST- 2013/10/25 06:00 [medline] AID - S1059-1311(12)00296-8 [pii] AID - 10.1016/j.seizure.2012.11.007 [doi] PST - ppublish SO - Seizure. 2013 Mar;22(2):124-7. doi: 10.1016/j.seizure.2012.11.007. Epub 2012 Dec 21.