Risk Factors of the First Febrile Seizures in Iranian Children

Objective. Febrile seizures are the most common type of convulsion in children. The identification of influencing factors on incidence of the first febrile seizures is of prime priority. The aim of this study was to identify the risk factors of the first febrile seizures in Iranian children. Methods. In this case-control study 80 children aged 9 month to 5 years with their first febrile seizures were compared with 80 children with fever without seizure based on different risk factors in 2007. Results. There was significant difference between two groups regarding the gender, family history of febrile seizures, breast-feeding duration, and the body temperature (P < .05). Conclusion. Our study showed that factors including the gender, family history of febrile seizures, breast-feeding duration, and the body temperature are among the risk factors in occurrence of the first febrile seizure. Preventive measures to remove such risk factors could lead to lower the incidence of febrile seizures

A Case-Control Study of the Association Between Serum Copper Level and Febrile Seizures in Children

How to Cite this Article: Mahyar A, Ayazi P, Dalirani R, Bakhtiyari H, Daneshi Khohan MM, Javadi A. A Case-Control Study of the Association Between SerumCopper Level and Febrile Seizures in Children. Iranian Journal of Child Neurology 2012;6(1):23-28.ObjectiveFebrile seizures are the most common cause of seizure in children. Identification of risk factors is very important. This study was conducted to determine the association between the serum copper level and simple febrile seizure in children.Materials &amp; MethodsIn this study, 30 children with simple febrile seizures (case group) were compared with 30 children with febrile illness without seizures (control group) regarding serum copper level. This study was conducted in Qazvin children’s hospital (Qazvin, Iran).ResultsThe mean serum copper levels in the case and control groups were 141.41±30.90 and 129.43±18.97 mcg/dl, respectively. This difference was not significant statistically.ConclusionThis study revealed that there is no association between serum copper levels and febrile seizures. It seems that copper deficiency is not a risk factor for febrile seizures in children.References1. Mikati MA. Febrile seizures in: Kliegman RM, Stanton BF, GemeIII JWS, Schor NF, Behrman RE. Nelson textbookof pediatrics.19th edition. Philadelphia: Saunders; 2011.p. 2017-19.2. Ferrie C, Newton R, Martland T. Febrile seizure in:Mclntosh N, Helms PJ, Smyth RL, Logan S. Forfar&amp; Arneils textbook of pediatrics, London: ChurchillLivingstone; 2008. p. 860-1.3. Mahyar A, Ayazi P, Fallahi M, Javadi A.Risk factors ofthe first febrile seizures in Iranian children. Int J Pediatr2010;2010:862897.[Epub 2010 Jun 24].4. Siqueira LF. Febrile seizures: update on diagnosisand management. Rev Assoc Med Bras 2010 Jul-Aug;56(4):489-92.5. Daoud A, Batieha A. Iron status a possible risk factor forthe first seizure. Epilepsy 2002;43(7):740-43.6. Hartfield DS, Tan J, Yager JY, Rosychuk RJ, SpadyD, Haines C, et al. The association between irondeficiency and febrile seizures in childhood. Clin Pediatr(Phila) 2009;48(4):420-6.7. Vaswani RK, Dharaskar PG, Kulkarni S, Ghosh K. Irondeficiency as a risk factor for first febrile seizure. IndianPediatr 2010;47(5):437-9.8. Amiri M, Farzin L, Moassesi ME, Sajadi F. Serum traceelement levels in febrile convulsion. Biol Trace Elem Res2010;135(1-3):38-44.9. Ganesh R, Janakiraman L, Meenakshi B. Serum zinclevels are low in children with simple febrile seizurescompared with those in children with epileptic seizuresand controls. Ann Trop Paediatr 2011;31(4):345-9.10. Mahyar A, Ayazi P, Fallahi M, Javadi A.Correlationbetween serum selenium level and febrile seizures. PediatrNeurol 2010;43(5):331-4.11. Anderson JB. Copper in: Mahan KL, Stump SE. Krause,sFood, Nutrition,&amp; Diet Therapy 9th ed, Phila, Saunders;2004:150-4.12. Gaggelli E, Kozlowski H, Valensin G. Copperhomeostasis and neurodegenerative disorders. Chem Rev2006;106:1995-2044.13. Lazarchick J. Update on anemia and neutropenia incopper deficiency. Curr Opin Hematol 2012 ;19(1):58-60.14. Zatta P, Frank A. Copper deficiency and neurologicaldisorders in man and animals, Brain Res Rev2006;54(1):19-23.15. Tapiero H, Townsend DM, Tew KD. Trace elementsin human physiology and pathology. Copper. BiomedPharmacother 2003;57(9):386-98.16. Prasad R, Singh A, Das BK, Upadhyay RS,Singh TB,Mishra OP. Cerebrospinal Fluid And Serum Zinc, Copper,Magnesium And Calcium Levels In Children WithIdiopathic Seizure. JCDR 2009;3(6):1841-6.17. Sholomo S. Febrile seizures In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice.4th ed. Philadelphia: Mosby; 2006. p. 1079-86.18. Ashrafi MR, Shabanian R, Abbaskhanian A, NasirianA, Ghofrani M, Mohammadi M, et al. Selenium andintractable epilepsy: is there any correlation? PediatrNeurol 2007;36(1):25-9.19. Shenkin A, Baines M, Fell GS, Lyon TDG. Vitaminsand Trace Elements In: Burtis CA, Ashwood ER, BrunsDE. Tietz textbook of clinical chemistry and moleculardiagnostics. 4th ed. Phila: WB Saunders, 2006:1126-30.20. Mishra OP, Singhal D, Upadhyay RS, Prasad R, etal. Cerebrospinal fluid zinc, magnesium, copper andgamma-aminobutyric acid levels in febrile seizures. JPN2007;5(1):39-44.21. Wu J, Ricker M, Muench J. Copper deficiency as causeof unexplained hematologic and neurologic deficits inpatient with prior gastrointestinal surgery.J Am BoardFam Med 2006;19(2):191-4.22. Ilhan A, Özerol E, Güleç M, Bünyamin Isik B, IlhanN, Ilhan N, et al. The comparison of nail and serumtrace elements in patients with epilepsy and healthysubjects . Prog Neuropsychopharmacol Biol Psychiatry2004;289(1):99-104

Feasible Relation between Glutathione Peroxidase and Febrile Seizure

How to Cite This Article: Mahyar A, Ayazi P, Dalirani R, Mohammad Hoseini B, Sarookhani MR, Javadi A, Esmaeily Sh. Feasible Relation between Glutathione Peroxidase and Febrile Seizure. Iran J Child Neurol. Winter 2017; 11(1):65-69.AbstractObjectiveWe aimed to determine the relationship between serum glutathione peroxidase and febrile seizure.Materials &amp; MethodsIn this case-control study, 43 children with simple febrile seizure (case group) were compared with 43 febrile children without seizure (control group) in terms of serum glutathione peroxidase level, measured by ELISA method. This study was conducted in Qazvin Children Hospital, Qazvin University of Medical Sciences in Qazvin, Iran in 2012-2013. The results were analyzed and compared in two groups.ResultsFrom 43 children 24 (53%) were male and 19 (47%) were female in children with simple febrile seizure, and 26 (60%) were male and 17 (40%) were female in febrile children without seizure (control group) (P=0.827). Serum glutathione peroxidase level was 166 U/ml (SD=107) in the case group and 141 U/ml (SD=90.5) in the control group of no significant difference.ConclusionThere was no significant relationship between serum glutathione peroxidase and simple febrile seizure. Thus, it seems that glutathione peroxidase, an essential component of antioxidant system, does not play any role in the pathogenesis of simple febrile seizure.References1. Duffner PK, Baumann RJ, Berman P, Green JL, Schneider S, Hodgson ES, etal. Febrile seizures: clinical practice guideline for the long-term management of the child with simple febrile seizures. Pediatrics 2008 ;121:1281-6.Midline doi: 10.1542/peds.2008-0939.2.Shinnar S. Febrile seizures. In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice. 4th ed. Philadelphia: Mosby, 2006:1079-86.3. Mikati M A. Febrile seizures.In: Kliegman RM, Stanton B F, GemeIII J WS, Schor NF , Behrman RE. Nelson textbook of pediatrics.19th ed. Philadelphia: Saunders, 2011:2017-19. 4. Hara K, Tanabe T, Aomatsu T, Inoue N, Tamaki H, Okamoto N ,etal. Febrile seizures associated with influenza A. Brain and Development 2007;29: 30-38.5. Sugai K.Current management of febrile seizures in Japan: An overview . Brain and Development 2010; 32: 64-7. Midline doi: 10.1016/j.braindev.2009.09.019.6. Camfield P, Camfield C, Kurlemann G. Febrile seizures, epileptic syndromes in infancy, childhood, and adolescence. 3th ed. London: John Libbey &amp; Co Ltd,2002:145–52.7. Sapir D, Leitner Y, Harel S, Kraumer U. Unprovoked seizures after complex febrile convulsions. Brain Dev 2000; 22:484–6.8. Kumari PL, Nair MK, Nair SM, Kailas L, Geetha S. Iron deficiency as a risk factor for simple febrile seizures--a case control study. Indian Pediatr 2012; 49:17-9.9. Tutuncuoglu S, Kutukculer N, Kepe L, Coker C, Berdeli A, Tekgul H. Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions. Pediatr Int 2001;43:235-9.10. Ashrafi MR, Shams S, Nouri M, Mohseni M, Shabanian R, Yekaninejad MS, etal. A probable causative factor for an old problem: selenium and glutathione peroxidase appear to play important roles in epilepsy pathogenesis. Epilepsia 2007 ;48:1750-5.11. Willmore IJ, Rubin JJ. Antiperoxidant pretreatment and iron-induced epileptiform discharges in the rat: EEG and histopathologic studies. Neurology1981; 31:63–69. 12.Irshad M, Chaudhuri PS. Oxidant-antioxidant system: role and significance in human body. Indian J Exp Biol 2002 ;40:1233-9.13.Rayman MP.The importance of selenium to human health. Lancet 2000;356:233-41.14.Patel M. Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures. Free Radical Biology &amp; Medicine 2004;37:1951–1962.15.Li-Ping L, Patel M. Seizure induced changes in mitochondrial redox status. Free Radical Biology &amp; Medicine 2006;40:316–322.16. Weber GF, Maertens P, Meng XZ, Pippenger CE. Glutathione peroxidase deficiency and childhood seizures. Lancet 1991 15; 337:1443-4.17. Sudha K, Rao AV, Rao A. Oxidative stress and antioxidants in epilepsy. Clin Chim Acta 2001; 303:19-24.18. Verrotti A, Basciani F, Trotta D, Pomilio MP, Morgese G, Chiarelli F.Serum Copper, Zinc, Selenium, Glutathione peroxidase and Superoxide dismutase levels in epileptic children before and after 1 year of sodium valproate and carbamazepine therapy. Epilepsy Res 2002;48:71-5.19. Ben-Menachem E. Kyllerman M, Marklund S. Superoxide dismutase and glutathione peroxidase function in progressive myoclonus epilepsies. Epilepsy Res 2000;40:33-9.20. Turkdogan D, Toplan S, Karakoc Y. Lipid peroxidation and antioxidative enzyme activities in childhood epilepsy. J Child Neurol 2002; 17:673-6. 21.Naziroglu M, Kutluhan S, Yilmaz M. Selenium and topiramate modulates brain microsomal oxidative stress values, Ca2+-ATPase activity, and EEG records in pentylenetetrazol-induced seizures in rats. J Membr Biol 2008;225:39-49.22.Naziroglu M. Role of selenium on calcium signaling and oxidative stress-induced molecular pathways in epilepsy. Neurochem Res 2009; 34:2181-91.Medline doi: 10.1007/s11064-009-0015-8.23.Brigelius-Flohé R, Maiorino M.Glutathione peroxidases. Biochim Biophys Acta 2013 ;1830:3289-303. 24. Harapin I, Bauer M, Bedrica L, Potoanjak D. Correlation between gluthathione peroxidase activity and the quantity of selenium in the whole blood of beef calves. Acta Vet Brno 2000; 69: 87–92.Medline. doi: 10.1016/j.bbagen.2012.11.020.25.Koller LD, South PJ, Exon JH, Whitbeck GA, Maas J. Comparison of selenium levels and glutathione peroxidase activity in bovine whole blood. Can J Comp Med 1984 ;48:431-3

The Effect of Clofibrate on Hyperbilirubinemia of Term Neonates

Clofibrate is a glucuronosyl transferase inducer that has been proposed to increase the elimination of bilirubin in neonates with hyperbilirubinemia. This study was conducted to determine the therapeutic effect of clofibrate in term neonates with non-hemolytic jaundice. This study was conducted on 52 newborns with pathologic unconjugated jaundice in Qazvin children hospital. Newborns divided randomly in two groups. Case group treated with clofibrate and intensive phototherapy, while control group treated only with intensive phototherapy. Serum bilirubin level was measured before and 6, 12, 24 and 48 hours after treatment. Results were compared and analyzed. The mean serum level of bilirubin before treatment in the case and control groups were 20.78&plusmn;2.38 and 20.52 &plusmn;2.44 mg/dl, respectively (P=0.69). The mean serum level of bilirubin in 6, 12, 24 and 48 hours after treatment in the case group were 18.20&plusmn;2.20, 14.70&plusmn;2.06, 10.72&plusmn;2.40 and 8.90&plusmn;0.83 mg/dl , respectively. These values in control group were 18.26&plusmn;2.42, 15.36&plusmn;2.59, 12.29&plusmn;2.28 and 10.23&plusmn;1.50 mg/dl, respectively. There was significant difference between two groups regarding mean serum level of bilirubin 24 hours (P=0.019) and 48 hours after treatment (P=0.005). In conclusion, clofibrate was effective in reducing neonatal jaundice and its effect appeared 24 hours after treatment

Zinc and Copper Status in Children with Beta-Thalassemia Major

Objective: There are some reports in which a condition of zinc deficiency and its associated outcomes with a change in concentration of serum copper among the thalassemic patients has been highlighted. The aim of this prospective study was to determine the serum zinc and copper levels in children with beta-thalassemia major. Methods: In this cross sectional study all children under 12 years affected by beta thalassemia major (40 patients) were evaluated for serum zinc and copper levels in Qazvin thalassemia center (Qazvin, Iran) in 2007. Serum measurements for zinc and copper were performed by atomic absorption spectrophotometer. Findings: The mean concentrations of serum zinc and copper levels were 67.35±20.38 and 152.42±24.17 μg/dl respectively. Twenty-six (65%) of thalassemic patients had zinc concentration under 70 μg/dl (hypozincemia). None of the thalassemic children had copper deficiency. No significant correlation between serum zinc level with age, weight, height, body mass index, duration of blood transfusion, desferrioxamine dose and ferritin level was observed in thalassemic patients (P=0.3). Conclusion: This study revealed that hypozincemia is common in thalassemic patients, but in contrast, there is no copper deficiency. Further evaluation in this regard is recommended

Lack of Correlation between Plasma Neuropeptide Y and Typical and Atypical Febrile Seizures

It is known that neuropeptide Y which is widely distributed throughout the central nervous system is able to prevent seizures in animals. There are limited studies about the role of neuropeptide Y in febrile seizures. This study was conducted to evaluate the association between plasma neuropeptide Y level and febrile seizures in children. Seventy six patients with typical and atypical febrile seizures (each group 38 patients) and 38 sex and age matched control subjects were enrolled. The mean plasma levels of neuropeptide Y in typical and atypical febrile seizures were 90.60±28.01 and 97.34±41.27 pmol/l respectively. This value in control group was 88.94±32.66 pmol/l. There was no significant differences between groups regarding plasma neuropeptide Y level (P=0.532). Also, there was no significant difference in comparison with case groups (P=0.40). This study revealed that there is no association between plasma neuropeptide Y and febrile seizures