ObjectiveTo define nomograms for blood pressure in Egyptian children and adolescents.Methods and study designA total of 60 025 Egyptian children from birth to 19 years were enrolled in this cross-sectional randomised study from December 2015 to March 2017. They were selected from diverse geographical districts in Egypt. Healthy children who fulfilled the inclusion criteria, which included good nutritional history, absence of fever or documented underlying disease at the time of examination, no evidence of haemodynamically significant illness, and no antihypertensive drugs or other chronic drug administration, were included in the study. Body weight, recumbent length (for less than 24 months) and height (from 2 years to 19 years), and blood pressure were measured using standard mercury sphygmomanometers.ResultsBlood pressure increases with age in both boys and girls. The 90th percentile of systolic and diastolic blood pressure among Egyptian children was different from other ethnic populations (American and Turkish children) in both sexes. Systolic and diastolic blood pressure showed a positive correlation with weight and height in both sexes (p<0.001).ConclusionWe assumed that normal blood pressure curves should be used cautiously during childhood, and it is recommended that every population have its own normal standard curve to define measured blood pressure levels in children. These centiles increased our knowledge and awareness of normal blood pressure among Egyptian children and adolescents. The percentiles will distinguish children and young adolescents with increased blood pressure and will be of value to both medical practice and scientific research.

Critically ill children frequently develop CIP/CIM, mostly of axonal polyneuropathy pattern, which compromises rehabilitation and recovery and is associated with a number of comorbidities.

Attention deficit hyperactivity disorder (ADHD) is among the most prevalent neurobehavioral disorders affecting children worldwide. The prevalence of ADHD is higher in children with epilepsy. Despite the plethora of conducted work, the precise cause of ADHD is not identified yet. We studied here the sociodemographic, clinical, electrophysiological, and biochemical profiles of children with ADHD, epilepsy, and ADHD with epilepsy. Subjects were divided into 4 groups (25 child/group): I—control, II—ADHD, III—epilepsy, and IV—ADHD with epilepsy. Male to female ratio was significantly (p < 0.05) higher in the ADHD (3.1) and ADHD with epilepsy (2.1) groups when compared to the control (1.08) or epilepsy (1.08) groups. Positive family history was significantly evident in patients with epilepsy and ADHD with epilepsy, but not in the control or ADHD groups. Speech development was significantly delayed in the ADHD and ADHD with epilepsy groups. EEG abnormalities were detected in patients with ADHD (12%) and ADHD with epilepsy (68%). Focal frontal activities were significantly detectable in the ADHD (100%) and ADHD with epilepsy (77.8%) groups, whereas focal temporal activity was significantly present in the epilepsy (83.3%) group. Serum ferritin was significantly lower in the ADHD group (110.27 ± 6.64 ηg/ml) when compared to the control (134.23 ± 14.82 ηg/ml), epilepsy (159.66 ± 33.17 ηg/ml), and ADHD with epilepsy (203.04 ± 50.64 ηg/ml) groups. Serum zinc was significantly higher in the ADHD, epilepsy, and ADHD with epilepsy groups (236.63 ± 20.89, 286.74 ± 43.84, and 229.95 ± 67.34 μg/dl, respectively), when compared to the control group (144.21 ± 17.40 μg/dl). Serum adenosine deaminase was insignificantly different among the groups. Our results indicate that gender and family history are significant moderators in the aetiology of ADHD and epilepsy or their comorbidity. We also demonstrated that EEG could be central in the assessment of ADHD with epilepsy cases. Serum ferritin and zinc alteration may contribute significantly in ADHD and epilepsy pathophysiology.

Background: A good survival rate among patients with beta thalassemia major (beta-TM) has led to the appearance of an unrecognized renal disease. Therefore, we aimed to assess the role of serum cystatin-C as a promising marker for the detection of renal glomerular dysfunction and N-acetyl beta-D-glucosaminidase (NAG) and kidney injury molecule 1 (KIM-1) as potential markers for the detection of renal tubular injury in beta-TM children. Methods: This case-control study was implemented on 100 beta-TM children receiving regular blood transfusions and undergoing iron chelation therapy and 100 healthy children as a control group. Detailed histories of complete physical and clinical examinations were recorded. All subjected children underwent blood and urinary investigations. Results: There was a significant increase in serum cystatin-C (p < 0.001) and a significant decrease in eGFR in patients with beta-TM compared with controls (p = 0.01). There was a significant increase in urinary NAG, KIM-1, UNAG/Cr, and UKIM-1/Cr (p < 0.001) among thalassemic children, with a significant positive correlation between serum cystatin-C, NAG and KIM-1 as regards serum ferritin, creatinine, and urea among thalassemic patients. A negative correlation between serum cystatin-C and urinary markers with eGFR was noted. Conclusion: Serum cystatin-C is a good marker for detection of glomerular dysfunction. NAG and KIM-1 may have a predictive role in the detection of kidney injury in beta-TM children.

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Background: Patients with chronic kidney disease (CKD) on maintenance hemodialysis frequently present with neurological complications. These complications include peripheral neuropathy, encephalopathy, and stroke. Objectives: To detect the prevalence of neurological manifestations and complications in children with CKD through neurophysiological and neuro-radiological findings. Methods: The study included 50 patients with CKD admitted to a pediatric nephrology unit. Their history and complete physical and neurological examination findings had been recorded. All patients underwent nerve conduction, electromyography, electroencephalography, and magnetic resonance imaging of the brain. Results: Fifty children of both sexes (23 males and 27 females) with a mean age of (12.08 ± 3.46 year) were studied. Eleven (22%) patients with CKD developed polyneuropathy, mostly of an axonal polyneuropathy pattern, while 39 (78%) of them showed normal electrophysiological studies. No myopathy was detected. Abnormal electroencephalography findings were detected in 18% of patients, mostly generalized and focal (temporal, occipital, and frontal) epileptogenic activity. Abnormal MRI brain findings were detected in 16% of patients, mostly of encephalomalacia. Conclusion: Uremic neuropathy was highly prevalent in children with CKD on maintenance hemodialysis. They developed polyneuropathy, mostly of an axonal polyneuropathy pattern. EEG is a useful method for early recognition of subclinical uremic encephalopathy and/or epileptogenic activity. Early demonstration and management of uremic neurological conditions may decrease the physical disability of CKD patients.

<P>Background: Autism Spectrum Disorders (ASD) as a considerable health obstacle in kids is characterized by compromised social collaboration and stereotyped behavior. Autism is triggered by an interactive impact of environmental and genetic influences. Presumably, some inborn errors of metabolism are implicated in a sector of developmental disabilities. Also, several trace elements may have an important role in human behavior and neurological development. This study was designed to verify the frequency of inherited metabolic disorders and/or trace element abnormalities in children with ASD. </P><P> Methods: In a retrospective analytical study, 320 children diagnosed with ASD according to the DSM-V criteria and Childhood Autism Rating Scale criteria were enrolled in this study. Serum ammonia, blood lactate, and arterial blood gases, plasma amino acid profile by tandem mass spectrophotometry, and a urinary organic acid assay were performed in all the patients. Likewise, the estimation of a number of trace elements in the form of serum lead, mercury, copper, and plasma zinc was done in all the patients. </P><P> Results: A total of 320 children with ASD, inherited metabolic disorders were identified in eight (2.5%) patients as follows: seven (2.19%) patients with phenylketonuria, and one (0.31%) patient with glutaric aciduria type 1. Regarding the trace element deficiency, sixteen (5%) patients presented low plasma zinc level, five (1.56%) children presented a high serum copper level, two (0.62%) children presented a high serum lead level and only one (0.31%) autistic child presented high serum mercury level. Electroencephalogram (EEG) abnormalities were reported in 13.12% and Magnetic Resonant Imaging (MRI) abnormalities in 8.43% of cases. </P><P> Conclusion: Screening for metabolic diseases and trace elements is required in all children diagnosed with ASD irrespective of any apparent clinical attributes of metabolic complaints and trace elements discrepancies.</P>

Background The risk of neurological complications is increased in children with sickle cell disease (SCD), such as silent cerebral infarction (SCI) and stroke. Brain-Derived Neurotrophic Factor (BDNF) is a nerve growth factor associated with elevated transcranial Doppler (TCD) velocities and increased risk of stroke in SCD patients. So, we assessed the BDNF level in children with SCD and its relation to neurological complication as silent stroke. Methods A comparative cross-sectional study was conducted on 40 patients with SCD, recruited from the Hematology Unit, Pediatric Department, Menoufia University Hospital, and 40 healthy children as controls. Laboratory investigations including BDNF were done. TCD was done for all patients and Magnetic Resonance Imaging (MRI) was done on high-risk patients. Results BDNF levels were significantly higher in children with SCD than in controls with a significant relation to TCD findings. There was a statistically significant diagnostic ability of BDNF in the prediction of SCD complications as its sensitivity was 89.5%, specificity (95% CI) was 80% with a cut-off point >0.69, AUC = 0.702, and p = 0.004). Conclusion Serum BDNF levels were higher in sickle disease patients who had abnormal transcranial Doppler. BDNF had a significant diagnostic ability in the detection of SCD complications. Impact Silent stroke is a very serious complication in children with sickle cell disease, so regular follow up should be every six months. BDNF is considered a potential biomarker for stroke risk prediction in patients unable to receive TCD.