Worldwide, the incidence and mortality rates of childhood cancers differ. The study of incidence patterns and survival rates in childhood malignancies is important in aiding in the planning of treatment centers and in obtaining further information with regard to the etiology. Few studies have investigated the survival in cases of childhood solid tumors in Egypt. The aim of the current study was to evaluate the patterns, frequency and outcome of solid tumors and lymphomas in children admitted to and followed up at the Pediatric Oncology Department of Zagazig University Hospital (Zagazig, Egypt) over a duration of 5 years (January 2004 to December 2008). A retrospective study was conducted, which included 155 children with solid tumors and lymphomas. The medical records were reviewed and the relevant data collected, in particular, those concerning demographic, clinical, histopathological, laboratory and imaging data as well as the treatment plans and outcomes. The mean age of patients was 5.6±3.04 years at diagnosis. The patients comprised 94 males and 61 females. Non-Hodgkin lymphoma (NHL) was the most common tumor type, followed by neuroblastoma (31.0 and 29.0%, respectively). When patients were stratified in terms of age (<5, ≥5 but <10, and ≥10 years), the <5-years-of-age group exhibited the greatest number of patients. Fever, pallor and pain were the most frequent initial clinical presentations among the patients and stage II was the most common stage (39.1%) followed by stage IV, III and I (35.0, 20.3 and 5.6% respectively). The overall 5-year survival rate in the study group was 66.7%. The survival rate was significantly higher in patients with Wilm’s tumor and Hodgkin lymphoma, followed by NHL (92.0, 88.0 and 72.0%, respectively; P<0.001), while the mortality rate was significantly higher in patients with neuroblastoma (P<0.001). In conclusion, NHL and neuroblastoma were the most common tumors; the survival rates were higher in patients with Wilm’s tumor and Hodgkin lymphoma and lower in patients with neuroblastoma. A larger multicenter study is required to further investigate the conclusions drawn from this study.

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Objectives There is a lack of information regarding thiamine status in children with diabetic ketoacidosis (DKA). This study was designed to assess the thiamine status upon admission and 24 h after treatment initiation of DKA, whether newly diagnosed children or with established T1DM diagnosis, who presented with DKA. Methods We enrolled 90 children (mean age, 9.8 ± 2.6 years; 58 females and 32 males) with type 1 diabetes mellitus (T1DM), whether newly diagnosed or with an established T1DM diagnosis (from 1 to 5.2 years ago), who presented with DKA. We observed the initial Glasgow Coma Scale (GCS) and recovery time. The whole blood thiamine diphosphate levels were measured upon admission (baseline point) and 24 h after initiation of the DKA treatment (second-time point). Results The mean blood thiamine levels at the second-time point (90.11 ± 15.76 nmol/L) significantly decreased compared with their levels at baseline (108.8 ± 17.6 nmol/L) (p<0.001). We compared thiamine levels with the initial GCS, patient’s age, and recovery time. Thiamine levels at the second-time point were positively correlated with baseline thiamine levels (r=0.86, p=0.0001) and the initial GCS (r=0.68, p=0.001) but were negatively correlated with patient’s age (r=−0.61, p=0.001) and recovery time (r=−0.724, p=0.001). Based on multiple regression analysis, thiamine levels at the second-time point were directly related to the initial GCS and inversely related to the patient’s age. Conclusions The current study indicates that blood thiamine diphosphate levels significantly decreased after 24 h of DKA treatment initiation compared to pre-treatment levels. After 24 h of treatment initiation, blood thiamine levels are directly related to the initial GCS and inversely related to the patient’s age.

Background Osteoporosis and neurological complications are consequences of acute lymphoblastic leukemia (ALL). Collagen type I alpha 1 gene (COL1A1) polymorphism is associated with osteoporosis. This study aimed to detect the COL1A1 polymorphism and the neurological complications in ALL patients and their association with decreased lumbar spine bone mineral density (BMDLS). This study included 100 pediatric ALL patients and 100 controls. All participants were subjected to laboratory assessment and assessment of BMDLS at the start of the study and 3 years later. COLIA1 genotyping was done once for all participants. Results At the start of the study, there was a significant decrease in osteocalcin (OC), alkaline phosphatase (ALP), and BMDLS levels in the patients. G/T variants and “T” alleles were significantly more detected in the patients (34% and 35% respectively); also, significant differences were detected between patients with polymorphism (G/T and T/T) and those without polymorphism (G/G) regarding OC, ALP, and BMDLS. After 3 years, significant decrement in BMDLS, OC, and ALP was detected in the patients. Twenty-four patients had neurological complications and seven patients had bone fractures. Those patients had significant decrement in BMDLS, OC, and ALP levels. As regards COL1A1 gene polymorphism, the GT and TT variants were significantly detected in fractured patients, while there was no significant difference regarding GT and TT variants in the patients with neurological complications. T allele, neurological complications, high-risk stratification, and age were significantly associated with decreased BMDLS. T allele was the most significant risk factor. Conclusion COLIA1 gene polymorphism, decreased BMDLS, and neurological complications were significantly detected in pediatric ALL patients. COLIA1 gene polymorphism is a significant risk factor for decreased BMDLS in pediatric ALL patients. There is no significant relation between COLIA1 gene polymorphism and the development of neurologic complications.

Background: Diabetes ketoacidosis (DKA) is the leading cause of death in children with diabetes, especially when it is complicated by cerebral edema. The predictors of CNS dysfunction/injury are largely unknown. In many neurological disorders, neuron-specific enolase (NSE) is a marker of neuronal damage.Objective: This study aimed to investigate the role of serum neuron-specific enolase as a marker of neuronal damage in patients with DKA. Patients and methods: A cross-sectional study with 90 DKA patients (aged 9.58 ± 2.89 years) presenting to Pediatric Intensive Care Unit (PICU), Children Hospital Zagazig University. Patients subjected to clinical history and examination including Glasco coma scale (GCS), blood glucose, serum electrolytes, blood PH and computed tomography of the brain for children with disturbed consciousness. Blood NSE at admission (baseline point) and after 24 hours of starting treatment of DKA (2-time points). Results: There was a significant difference between NSE level on admission and NSE level 24 hours after start of treatment. Patients with low GCS scores had higher serum NSE at baseline and 2-time points than those with normal CGS (P=0.001; P=0.053). Patients with moderate and severe DKA had higher NSE at baseline and 2-time points in comparison with those with mild DKA (P=0.001; P=0.098). Conclusions: Children with moderate to severe DKA and impaired consciousness had higher serum NSE. The high levels of NSE in patients with abnormal GCS, in the absence of cerebral edema on brain imaging indicate that NSE is a reliable marker of neuronal injury.