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Background Obesity is a chronic inflammatory disorder in which leptin, adiponectin and C-reactive protein (CRP) play an important role. This study aimed to investigate the relationship between markers of adiposity such as leptin, adiponectin and high sensitivity C-reactive protein (hs-CRP) in obese children, and to determine whether these adipokines are significant markers in defining metabolic syndrome (MetS) in pediatric population. Methods A cross-sectional study was conducted over a period of 1 year, between July 2013 and June 2014, on 122 cases of obesity in children diagnosed at the Louis Ţurcanu Emergency Hospital for Children Timişoara, in the departments of Diabetes and Nutritional Diseases, Endocrinology and Cardiology. The patients were divided into two groups, according to the presence of MetS. Results MetS was present in 27% of obese children. The groups were homogenous with respect to age, sex and body mass index (BMI). Adiponectin, leptin and hs-CRP were significantly modified in the group with MetS (p=0.04, p=0.04, p=0.01, respectively). Conclusions hs-CRP, leptin and adiponectin can be used as predictors of cardiovascular risk in pediatric population.

Maternal PIH has a strong influence on the development of newborn hematologic abnormalities, such as neutropenia and thrombocytopenia. The incidence and severity of these hematological changes are increased in neonates of mothers with PIH, that are born preterm and/or SGA.

The present study reports the case of a 3-h old male with a de novo unbalanced t(15;22) translocation and velo-cardio-facial syndrome (VCFS), with other abnormalities. The manifestations of the condition observed in the patient included cleft palate with feeding difficulties, respiratory infection, dysmorphic face with almond-shaped eyes, a long and wide nose, small and low-set ears, tetralogy of Fallot, cryptorchidism and varus equinus. Standard lymphocyte cytogenetic analysis using G-banding demonstrated a 45,XY,-22,der (15),t(15;22)(q26.2;q12) karyotype. Fluorescent in situ hybridization with DiGeorge/VCFS TUPLE 1 confirmed 22q11 deletions. These cytogenetic aspects appear to be rare in the etiology of VCFS, as >1% of all 22q11 deletions are the result of an unbalanced translocation, which involves chromosomes 22 and another chromosome. To the best of our knowledge, this is the second reported case where the clinical features associated with VCFS are combined with an unbalanced (15;22) translocation involving the critical 22q11.2 region.