58 research outputs found

    Comparison of Serum Zinc and Copper levels in Children and adolescents with Intractable and Controlled Epilepsy

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    How to Cite This Article: Kheradmand Z, Yarali B, Zare A, Pourpak Z, Shams S, Ashrafi MR. Comparison of Serum Zinc and Copper levels in Children and adolescents with Intractable and Controlled Epilepsy. Iran J Child Neurol. 2014; 8(3):49-54. AbstractObjectiveTrace elements such as zinc and copper have physiological effects on neuronal excitability that may play a role in the etiology of intractable epilepsy. This topic has been rarely discussed in Iranian epileptic patients.This study with the analysis of serum zinc and copper levels of children and adolescents with intractable and controlled epilepsy may identifies the potential role of these two trace elements in the development of epilepsy and intractabilityto antiepileptic drug treatment. Materials & MethodsSeventy patients between the ages of 6 months to 15 years that referred to Children’s Medical Center with the diagnosis of epilepsy, either controlled or intractable to treatment enrolled in the study. After informed parental consent the levels of serum zinc and copper were measured with atomic absorptionspectrophotometer and analyzed with SPSS version 11.Results35 patients were enrolled in each group of intractable (IE) and controlled epilepsy (CE). 71.45% of the IE and 25.72% of the CE group had zinc deficiency that was statistically significant. 48.58% of the IE and 45.72 of the CE group were copper deficient, which was not statistically significant.ConclusionOur findings showed significant low serum zinc levels of patients with intractable epilepsy in comparison with controlled epilepsy group. We recommend that serum zinc level may play a role in the etiology of epilepsy and intractable epilepsy therefore its measurement and prescription may be regarded in the treatment of intractable epilepsy.ReferencesMikati MA. Seizures in childhood. In: Kliegman RM, Stanton BF, Schor NF, Geme JWS, Behrman R (eds). Nelson textbook of pediatrics. 19th ed. Elsevier:Saunders; 2011. Pp.2013-2033.Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342: 314-9.Patrick Kwan, Alexis Arzimanoglou, Anne T. Berg, et al.  Definition of drug resistant epilepsy: Consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia 2010;51(6):1069-1077.Berg AT, Shinnar S, Levy SR, Testa F, Smith-Rapaport S, Beckerman B. Early development of intractableepilepsy in children: a prospective study. Neurology 2001;56:1445-1452.Haoa XT, Wong ISM, Kwan P. Interrater reliability of the international consensus definition of drug-resistant epilepsy: A pilot study. Epilepsy & Behavior 2011;22;388-390. Ashrafi MR, Mohseni M, Shams S, Shabanian R, Yekaninejad MS, et al. A Probable Causative Factor for an Old Problem: Selenium and Glutathione Peroxidase Appear to Play Important Roles in Epilepsy pathogenesis. Epilepsia 2007;48(9):1750-1755.Liochev SI, Fridovich, I. Copper- and zinc-containing superoxide dismutase can act as a superoxide reductase and a superoxide oxidase. J Biol Chem 2000; 275: 38482-38485.Jacob RA. Trace Elements in textbook of Clinical Chemistry. WB Saunders, 1986. pp. 965-985.Salwen MJ. Vitamis and Trace Elements. In: Pherson RA, Pincus MR (eds). Henry’s Clinical Diagnosis and Management By Laboratory Methods Tweny-First Edition. Saunders; 2007. Pp. 379-389.Rokgauerj M, Klein J Kruse-Jarres J. D. Reference Values for the Trace Elements Copper, Manganese, Selenium, and Zinc in the Serum/ Plasma of Children, Adolescents, and Adults. J Trace Element Med Biol. 1997;11: 92-98.Volpe SL, Schall JI, Gallagher PR, Stallings VA, Bergqvist AGC. Nutrient intake of children with intractable epilepsy compared with healthy children. Journal of the American Dietetic Association 2007;107(6):1014-8. Epub 2007/05/26.Wojciak RW, Mojs E, Stanislawska-Kubiak M, Samborski W. The serum zinc, copper, iron, and chromium concentrations in epileptic children. Epilepsy Research 2013;104:40-44.Hamed SA, Abdellah MM, El-Melegy N. Blood levels of trace elements, electrolytes, and oxidative stress/antioxidant systems in epileptic patients. J Pharmacol Sci 2004;96:465-473.Dudek FE. Zinc and epileptogenesis. Epilepsy Curr 2001; 1:66-70.Mathie A, Sutton GL, Clarke CE, Veale EL. Zinc and copper: pharmacological probes and endogenous  modulators of neuronal excitability. Pharmacol Ther. 2006;111(3):567-83. Epub 2006/01/18.Schrauzer GN. Selenomethionine and Selenium Yeast: Appropriate Forms of Selenium for Use in Infant Formulas and Nutritional Supplements. Journal of medicinal food 1998;1(3):201-6.Seven M, Basaran SY, Cengiz M, Unal S. Deficiency of selenium and zinc as a causative factor For idiopathic intractable epilepsy. Epilepsy Research 2013;104 :35-39

    Mast cell density in gastric biopsies of pediatric age group and its relation to inflammation and presence of Helicobacter pylori

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    <p>Abstract</p> <p>Background</p> <p>The aim of this study was to investigate the relationship between mast cell density, histological severity of gastritis, and presence of Helicobacter pylori (H. pylori) in the antral mucosa of pediatric patients.</p> <p>Methods</p> <p>The study included 352 (192 male and 160 female, < 14 years old) patients. All cases underwent endoscopy, and biopsies were obtained for histopathological examination and evaluation of Helicobacter pylori. All biopsies were evaluated according to the Sydney system and mast cell density in the antral mucosa was analyzed by Giemsa stain. Spearman's correlation test was used to determine the relationship between mast cell density and other histopathological parameters. The comparison of mast cell density between H. pylori positive and negative groups was analyzed by Mann Whitney U test.</p> <p>Results</p> <p>Mast cell density was 12.6 ± 0.87 in 0.25 mm<sup>2 </sup>(0–81). Means of severity of gastric inflammation in H. pylori-positive and negative patients were 1.7 ± 0.6 and 0.6 ± 0.7, respectively, which was statistically significant (p = 0.0001). Mast cell density was not correlated with presence and degree of inflammation, activity, presence and score of H. pylori in the antrum (p > 0.05). There was no significant correlation between mast cell density and allergy.</p> <p>Discussion</p> <p>We concluded that there may be some other ways for contribution of mast cells in pathologic processes involving gastrointestinal tract in children.</p

    Prenatal Diagnosis of Leukocyte Adhesion Deficiency Type-1 (Five Cases from Iran with Two New Mutations)

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    Leukocyte adhesion deficiency type-1(LAD-1) is one of the autosomal recessive immunodeficiency diseases that results from mutation in integrin beta 2 (ITGB2) gene. The aim of this study was to investigate molecular prenatal diagnosis of LAD-1. Four pregnant women with five fetuses (one twin fetus) with clinical and laboratory diagnosis of LAD-1 in their previous children were studied. The chorionic villus sampling (CVS) was obtained when mothers were in 10-12th weeks of gestation. Mutation analysis of ITGB2 gene for affected children revealed 3 misssense mutations (c.382G>A,   a   novel   mutation,   c.2146G>C,   and   c.715G>A)   and   one   splice  site novel mutation (c.1877+2T>C). All parents were heterozygous for these mutations. Consideration of affected gene regions for five CVS samples showed two homozygotes and one heterozygote for mutant allele and two homozygotes for normal allele. Interestingly, one  of  the  twin  fetuses  was  affected  and  another  was  normal.  Briefly, two  cases  of CVS samples were affected and three cases of remained CVS samples were unaffected. This is the first report of prenatal diagnosis of LAD-1 from Iran with two new mutations that can be used for genetic and prenatal diagnosis for all patients suspected to LAD1 and can be helpful to prevent the birth of affected children with LAD-1. This  abstract  was presented  in  the  Second  International  Congress  of  Immunology, Asthma and Allergy, Tehran, Iran 2013

    Antibody Production after COVID-19 Vaccination in Patients with Inborn Errors of Immunity

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    Background: Few studies have evaluated COVID-19 vaccine efficacy in patients with inborn errors of immunity (IEI).Objective: To evaluate the levels of antibody (Ab) production and function after COVID-19 vaccination in IEI patients with phagocytic, complement, and Ab deficiencies and their comparison with healthy controls.Methods: Serum samples were collected from 41 patients and 32 healthy controls at least one month after the second dose of vaccination, while clinical evaluations continued until the end of the third dose. Levels of specific anti-receptor-binding domain (RBD) IgG and anti-RBD neutralizing antibodies were measured using EUROIMMUN and ChemoBind kits, respectively. Conventional SARS-CoV-2 neutralization test (cVNT) was also performed. Cutoff values of ≤20, 20-80, and ≥80 (for cVNT and Chemobined) and 0.8-4.2, 4.2-8.5, and ≥8.5 (for EUROIMMUN) were defined as negative/weak, positive/moderate, and positive/significant, respectively.Results: A considerable distinction was observed between the Ab-deficient patients and the controls for Ab concentration (EUROIMMUN, p<0.01) and neutralization (ChemoBind, p<0.001). However, there was no significant difference compared with the other patient groups. A near-zero cVNT in Ab-deficient patients was found compared to the controls (p<0.01). A significant correlation between the two kits was found using the whole data (R2=0.82, p<0.0001).Conclusion: Despite varying degrees of Ab production, all Ab deficient patients, as well as almost half of those with complement and phagocytic defects, did not effectively neutralize the virus (cVNT). In light of the decreased production and efficiency of the vaccine, a revised immunization plan may be needed in IEI

    Altered Pattern of Naive and Memory B cells and B1 Cells in Patients with Chronic Granulomatous Disease

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    Chronic granulomatous disease (CGD) is a rare primary immunodeficiency disorder characterized by a greatly increased susceptibility to severe fungal and bacterial infections caused by defects in NADPH oxidase of phagocytic cells. We aimed to investigate immunophenotype alterations of naive and memory B cells and B1a cells in peripheral whole blood from Iranian patients with CGD. Flow cytometric analysis was performed on peripheral blood samples from 31 CGD patients and 23 healthy controls (HC) to study naive (IgD+/CD27-), memory (CD27+) B and B1a (CD5+) cells. Soluble CD27 (sCD27) and immunoglobulins were also measured by ELISA and the nephelometric method, respectively. We found significantly higher levels of naive B cells and B1a cells but lower levels of memory B cells in CGD patients compared to HC. There was no significant difference in soluble CD27 (sCD27) alteration between CGD patients and HC. Our findings suggested a role for NADPH oxidase in process of B cell differentiation and impairing conversion of naive B cells to memory B cells and altered B1a cells in CGD patients. Increased susceptibility of CGD patients to opportunistic infections and autoimmune disorders could be partly explained by the altered phenotype of B lymphocytes in these patients
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