Serum IgG, and IgM Levels in Children with Febrile Convulsions

At the Dr. Sami Ulus Children's Hospital Ankara, Turkiye, 20 patients, twelve being between 6 months-2 year old and eight being between 2-4 years, with their first febrile convulsions (FC) were examined for serum IgG, IgA, IgM levels during the period of March 1989-]uly 1989. Twenty healthy children were used as controls, seven being between 6 months-2 years old and thirteen being between 2-6 years. The serum IgG, IgA and IgM levels of the patients between 6 months-2 years were 805.000 + 307.8984 mg/ dl, 49.7167 + 27.9807 mg/dl and i55.1833 + 62.9696 mg/dl respecttvelly. The serum IgG, IgA and IgM levels of the patients between 2-4 years were : 989.1250 ± 314.5359 mg/dl, 92.6125 ± 34.5663 mg/dl and 159.8750 ± 45.6647 mg.ldl respectivelly. The mean IgA levels of the 12 FC patients between 6 months-2years were 49.7167 ± 27.9807 mg/dl and the mean level of IgA in the age matched control group was 81.0427± 31.3551 mg/dl and the difference between them was statistically significant (p <0. 005). We conclude that FC under 2 years of age is associated with low serum IgA levels

Effects of levetiracetam and valproic acid treatment on liver function tests, plasma free carnitine and lipid peroxidation in childhood epilepsies

Background and aims: The relationship between anti-epileptic usage and oxidative damage has not yet been clearly understood. In our study, we investigated oxidative stress parameters, carnitine levels, liver function tests (LFT) and their relationship in epileptic children treated with valproic acid or levetiracetam. Method. LFTs, serum free carnitine and oxidative damage markers and their relations with each other were determined in patients who are on valproic acid or levetiracetam treatment at least for 6 months. 25 patients on therapeutic doses of valproic acid, 26 patients on therapeutic doses of levetiracetam and 26 healthy volunteers as controls were included. LFTs, ammonia, carnitine, lipid peroxidation biomarker malondialdehyde (MDA) and a sensitive marker of DNA damage, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were measured. Results of patients are compared to healthy controls. The data is evaluated with IBM SPSS Statistics 22.0. Results: Ammonia and MDA levels were elevated in patients using levetiracetam; 8-OHdG levels were elevated in both patient groups. Carnitine levels were significantly low in patients under valproic acid therapy, however they were not found to be correlated with MDA, 8-OHdG or LFTs. MDA showed positive correlation with ammonia and 8-OHdG in the levetiracetam group. Conclusion: We did not observe hepatotoxicity in patients under therapeutic doses of valproic acid. However, epileptic children under therapeutic doses of levetiracetam showed significantly elevated levels of MDA and 8-OHdG, which is supportive for oxidative damage under levetiracetam therapy. This result was observed for the first time in childhood epilepsies and further studies are needed to understand its mechanism

Novel plasminogen gene mutations in Turkish patients with type I plasminogen deficiency

The plasminogen (Plg) protein is the inactive proenzyme form of plasmin that dissolves fibrin thrombi by a process called fibrinolysis. It has been shown that homozygous or compound-heterozygous deficiency of this protein is a major cause of a rare inflammatory disease affecting mainly mucous membranes found in different body sites. In this study, five individual Turkish patients and nine Turkish families with type 1 Plg deficiency were investigated for PLG gene mutations. All of the coding regions of the PLG gene mutations were screened for mutations using denaturing high-pressure liquid chromatography (DHPLC). Samples showing a different DHPLC profile were subjected to DNA sequencing analysis. Here, we described five novel mutations namely, Cys49Ter, +1 IVS6 G>A, Gly218Val, Tyr283Cys, and Gly703Asp. Previously identified five nonsynonymous (Lys38Glu, Glu180Lys, Gly420Asp, Asp453Asn, Pro763Ser), five synonymous (330 C>T, 582 C>T, 771 T>C, 1083 A>G, 2286 T>G), and a 3' untranslated region (3' UTR) mutation (c.*45 A>G) were also reported in this present study. In this study, we have identified a total of eight mutations, five of which are novel. The mutations/polymorphisms identified in eight of the patients do not explain the disease phenotype. These cases probably carry other pathological mutations (homozygous or compound heterozygous) that cannot be detected by DHPLC. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved