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Background. Allergic rhinitis (AR) is an inflammatory state categorized by a disturbance of immunoregulatory mechanisms. MicroRNA-155 (miRNA-155) has an essential role in regulating gene expression and can mediate the allergic TH2 process. Objective. In this study, we aimed to evaluate the role of miR-155 as a biomarker in AR and correlate its level with the total nasal symptom score (TNSS) and the levels of serum interleukin-4 (IL-4). Methods. This study included 90 children: 45 with pollen-induced AR and 45 healthy controls. Serum miR-155 expression levels were measured using quantitative real-time PCR. Human IL-4 ELIZA kits were used for the semiquantitative detection of the serum levels of IL-4. Receiver operating characteristic (ROC) curves were used to determine the best cutoff values for the studied parameters for the diagnosis of AR. Results. The demographic characteristics of the two groups were matched with respect to age and sex. The AR case group included 23 (51.1%) males and 22 (48.9%) females, while the control group included 24 (53.3%) males and 21 (46.7%) females. The miR-155 level was increased in the serum of children with pollen-induced AR compared with controls (mean difference = 2.8, p < 0.001 ). A significant positive correlation between the serum expression level of miR-155 and TNSS in children with AR was detected (r = 0.494, p < 0.001 ). However, no significant correlation was identified between the expression of miR-155 and that of IL-4. At a cutoff value of 1.09, the sensitivity of miR-155 as a biomarker for AR was 100%, and the specificity was 71.1%. Conclusion. MiR-155 expression levels were elevated in the serum of AR children. Therefore, miR-155 could be used as a biomarker in AR diagnosis.

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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.

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.