This work aimed to evaluate the metabolic and atherogenic effects of long-term antiepileptic drugs in a group of Egyptian epileptic patients. Sixty-nine epileptic patients on antiepileptic drug monotherapy for at least 2 years and 34 control subjects were recruited in this study. Patients were divided into 5 subgroups according to antiepileptic drugs used (valproate, carbamazepine, lamotrigine, topiramate, and levetiracetam). Fasting lipid profile (total cholesterol, triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol), lipoprotein(a), homocysteine, free thyroxine, thyroid-stimulating hormone, and common carotid artery intima-media thickness were measured for all subjects. Significant higher mean values of low-density lipoprotein cholesterol, low-density lipoprotein / high-density lipoprotein ratio, lipoprotein(a), homocysteine, significantly lower mean value of high-density lipoprotein cholesterol, and significantly larger diameter of common carotid artery intima-media thickness were observed in each drug-treated group versus control group. Our study supports that long-term monotherapy treatment with valproate, carbamazepine, lamotrigine, and topiramate had altered markers of vascular risk that might enhance atherosclerosis, whereas levetiracetam exerted minimal effect.

Cryptogenic epilepsy is a group of epilepsy syndromes where aetiology is unknown but an underlying brain disease is suspected. Increased seropositivity for Toxocara and Toxoplasma gondii have been observed in epileptic patients with sparse data about their seropositivity in cryptogenic epileptic patients. Therefore, we investigated the probable relationship between seropositivity against T. gondii and Toxocara with cryptogenic epilepsy. We examined patients who had cryptogenic epilepsy and healthy non epileptic controls for seropositivity for Toxocara and T. gondii antibodies by ELISA. Out of 132 cryptogenic epileptic patients, 80 (60.6 %) and 64 (48.5%) were seropositive for T. gondii and Toxocara immunoglobulin G (IgG) antibodies respectively. The seropositivity in the control group was 26 (43.3%) and 28 (46.7%) for T. gondii and Toxocara IgG respectively. We found a significant association between chronic T. gondii infection and cryptogenic epilepsy while the association between Toxocara infection and cryptogenic epilepsy was insignificant. Our findings indicate that toxoplasmosis may be a cause of cryptogenic epilepsy. We recommended both promoting health education to prevent such infection and screening children for toxoplasmosis which would help early treatment and so decreasing the incidence of epilepsy.

Objective: To assess growth hormone (GH)/insulin like growth factor-1 (IGF-1) axis as a possible non-nutritional factor for growth retardation in children with cerebral palsy (CP). Methods:A case-control study was conducted at a tertiary university hospital. Thirty children with CP (seven children with normal growth [CP-N] and 23 with retarded growth [CP-R]), 30 children with protein energy malnutrition (PEM), and 30 healthy children (REF group) underwent an assessment of growth parameters, serum IGF-1, basal GH, and peak GH after stimulation with insulin.Results: PEM patients had higher basal GH levels than CP-N, CP-R and REF groups (p = 0.026, p < 0.001, and p < 0.001 respectively). After insulin stimulation, CP-N, CP-R, and PEM patients had lower GH levels compared to the REF group (p = 0.04, p = 0.007, and p = 0.036 respectively). IGF-1 levels were lower in CP-R group compared to CP-N and REF groups (p = 0.037 and p < 0.001 respectively), and in PEM group compared to CP-N and REF groups (p < 0.001 and p < 0.001 respectively). Conclusions:CP-R patients failed to demonstrate the same high basal GH response as PEM patients, and responded inadequately to the insulin stimulation test, but they had IGF-1 levels comparable to those of PEM patients. On the other hand, CP-N patients behaved as controls regarding their basal GH and IGF-1 levels, but failed to respond adequately to the insulin stimulation test. The PEM group presented high basal GH and low IGF-1 levels. These findings suggest that nonnutritional factors contribute to growth retardation in CP children. J Pediatr (Rio J). 2012;88(3):267-74:GH, IGF-1, cerebral palsy, children. ResumoObjetivo: Avaliar o eixo hormônio de crescimento (GH)/fator de crescimento semelhante à insulina 1 (IGF-1) como possível fator não nutricional para o retardo de crescimento em crianças com paralisia cerebral (PC). Conclusões:Os pacientes com PC-R não demonstraram a mesma resposta basal elevada do GH apresentada pelos pacientes com DPE, e responderam de forma inadequada ao estímulo com insulina, mas apresentaram níveis de IGF-1 comparáveis aos dos pacientes com DPE. Por outro lado, os pacientes com PC-N tiveram comportamento semelhante ao dos controles com relação aos níveis basais de GH e IGF-1, mas não responderam adequadamente ao estímulo com insulina. O grupo DPE apresentou GH basal elevado e IGF-1 baixo. Esses achados sugerem que fatores não nutricionais contribuem para o retardo de crescimento em crianças com PC. Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy Não foram declarados conflitos de interesse associados à publicação deste artigo.Como citar este artigo: Hegazi MA, Soliman OE, Hasaneen BM, El-Arman M, El-Galel NA, El-Deek BS. Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy. J Pediatr (Rio J). 2012;88(3):267-74.Artigo submetido em 27.11.11, aceito em 14.03.12.http://dx

Clinical asthma phenotypes have an impact on myocardial function especially those presented with shortness of breath. Thus, measurement of MPI by TDI can detect subclinical changes in the cardiac performance in asthmatic children.

Fibrodysplasia ossificans progressiva (FOP) is an autosomal dominant severe musculoskeletal disease characterized by extensive new bone formation within soft connective tissues and unique skeletal malformations of the big toes which represent a birth hallmark for the disease. Most of the isolated classic cases of FOP showed heterozygous mutation in the ACVR1 gene on chromosome 2q23 that encodes a bone morphogenetic protein BMP (ALK2). The most common mutation is (c.617G > A) leading to the amino acid substitution of arginine by histidine (p.Arg206His). We currently report on an Egyptian infant with a sporadic classic FOP in whom c.617G > A mutation had been documented. The patient presented with the unique congenital malformation of big toe and radiological evidence of heterotopic ossification in the back muscles. The triggering trauma was related to the infant's head, however; neither neck region nor sites of routine intramuscular vaccination given during the first year showed any ossifications. Characterization of the big toe malformation is detailed to serve as an early diagnostic marker for this rare disabling disease.