Brugada syndrome is a type of arrhythmia disorder, which is characterised by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death. The most frequent sign is a persistent ST elevation in the electrocardiographic leads V 1 -V 3 with a right bundle branch block (RBBB).We present a case of 12 years old healthy child, without any complains until then. He had 2 episodes of collapse/syncope, which lasted long and spontaneously disappeared. The collapses were provoked by physical activity. On ECG we found sinus rhythm 62 bpm, RBBB (right bundle brunch block) and Brugada signs in V 2 and V 3 channel-ST elevation ³ 2 mm. The child was sent in electrophysiological centre abroad where the electrophysiological study was performed. They did not found any accessory pathway. The atrioventricular (AV) conduction was normal. Long lasting polymorphic ventricular tachycardia/fibrillation was induced with programed stimulation with 3 extrastimuli in right ventricular outflow tract. Performing one defibrillation the rhythm turned in sinus way. Then they performed ECG with translocation of electrodes V 1-3 in 2 nd intercostal space and the Brugada I type findings was discovered. After confirming of presence of Brugada type -1 syndrome the implantable cardioverter-defibrillator (ICD) was applied on child heart.
Introduction: Pediatric obesity is a common nutritional disorder that affects more than a third of the young population and predis-poses individuals to greater future morbidity and mortality. Materials and methods: Sixty-two children were recruited in the study. Demographic and clinical information regarding the pa-tients and their parents was collected. Data about the weight, height, systolic (SP) and diastolic (DP) blood pressure, lipid metabolic profile, thyroid hormone levels, glucose and insulin levels before and after oral glucose tolerance test (OGTT) of participants were also collected. Body mass index (BMI) was calculated and patients were classified into groups according to the International Obesity Task Force criteria. Descriptive, comparative parametric, non-parametric tests and Spearman’s ranked correlations were used in the statistical analysis. Results: The study sample consisted of 34 males and 28 females aged 11.6 and 11.8 years, respectively (p=0.781). The mean BMI was 30.5 (SD 5.5): 8 of participant had normal weight (≤25 BMI), 22 were overweight (25-30 BMI), and 32 were obese (≥30 BMI). The chil-dren’s BMIs were significantly associated with parental BMIs (r=0.395, p=0.004). Both SP and DP were significantly different between BMI subgroups (p=0.005 and p=0.001, respectively) with the obese group having the highest values (post-hoc Benjamini, p=0.004). Obese children had lower average T4 levels when compared to the comparators (7.5 µg/dL vs. 9.9 µg/dL, p=0.021). Obese children had significantly lower baseline glucose levels and higher insulin levels when compared to the overweight/normal BMI children (73.8 mg/dL vs. 86.4 mg/dL, p<0.001 and 21.8 µgU/mL vs. 132 µgU/mL, p=0.003). Obese children had the greatest numerical increase in glucose levels during the OGTT (Δ63.0 mg/dL vs. Δ43.2 mg/dL, p=0.063) and numerically smaller absolute insulin response (Δ86.1 µIU/mL vs. Δ125.7 µIU/mL, p=0.307). Conclusions: Pediatric patients demonstrate familial type of obesity and premorbid asymptomatic endocrine impairments. In order to maintain normal glucose levels, obese pediatric patients demonstrate high levels of resting insulin levels and diminished response after OGTT load.
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