BACKGROUND:Visfatin is an intracellular enzyme, known as nicotinamide phosphoribosyltransferase (Nampt) and pre-B-cell colony-enhancing factor (PBEF-1). It has insulin-mimetic effects and lowers plasma glucose levels.AIM:The aim of the work was to assess serum concentration of Visfatin in type 1 diabetic children and adolescents and study its relationships with duration of diabetes, body mass index (BMI), glycemic control, insulin dosage, lipid profile and microvascular complications.MATERIAL AND METHODS:Fifty children and adolescents with type 1 diabetes mellitus were recruited with 30 ages and gender-matched healthy subjects. They were subjected to history taking; anthropometric measurements and chronic diabetic complications were recorded if present. Laboratory analysis included urinary microalbumin, serum triglycerides, HDL, LDL, cholesterol, fasting blood glucose, glycosylated Hb (HbA1c) and serum visfatin which was measured with enzyme-linked immunosorbent assay.RESULTS:Diabetic patients showed highly significant decrease in the level of visfatin compared to the control group (P = 0.0001). There was significant further decrease in visfatin level in diabetics with microalbuminuria (n = 13) compared to normoalbuminuric patients (n = 37) (P = 0.015). There was highly significant inverse correlation between visfatin level with age (r = -0.379, p = 0.007), BMI (r = -0.418, p = 0.003), waist circumference (r = -0.430, p = 0.002), hip circumference (r = -0.389, p = 0.005) and microalbuminuria (r = -0.323, p = 0.022).CONCLUSIONS:Type 1 diabetic children and adolescents had a significantly lower visfatin level compared to controls. A marked decrease in the level of visfatin was shown in patients with microalbuminuria with an inverse correlation with BMI suggesting an important role of visfatin in the pathogenesis of type 1 diabetics and type 1 diabetic nephropathy.

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Background: Transfusion-related immunomodulation (TRIM) has been described in adults; however, its existence in neonates is not confirmed. The generation of TRIM is attributed to increased concentrations of IL-8, sICAM-1 and other pro-inflammatory cytokines. This study aimed to monitor changes in IL-8, sICAM-1 as markers for TRIM in premature infants at different postnatal ages. Methods: Preterm infants with a gestational age between 28 and 32 weeks who were receiving PRBC transfusion during the first 28 days of life were included in the study. Infants were stratified into two groups according to their postnatal age: Group 1 with postnatal ages of (0e14) days and Group 2 of (15e28) days. The concentrations of IL-8 and sICAM-1 were measured by enzyme-linked immunosorbent assay (ELISA) before transfusion, 6 h after the end of transfusion and in the donor's PRBCs bag immediately before infusion into the baby. Results: IL-8 concentration in the PRBCs bags correlated with post-transfusion level in Group 2 (r Z 0.59, p Z 0.002) but not in Group 1 (r Z 0.39, p Z 0.06). sICAM-1 concentration in the bag correlated with infants'concentrations in neither group. In Group 1, pre-transfusion

Background: Cardiovascular disease (CVD) is considered a major cause of death in renal insufficiency (RI). Contributing genetic factors is a recent focus of research. This study aims to elucidate apolipoprotein E (APO-E) and plasminogen activator inhibitor 1 (PAI-1) gene polymorphisms in RI children associated with CVD. Methods: We studied 50 cases with chronic kidney disease (CKD) associated with CVD, and 30 healthy controls. Study sample was grouped as one on conservative treatment, the second on hemodialysis and the third was posttransplant. PAI-1 and APO-E gene polymorphisms were investigated using allele-specific polymerase chain reaction (AS-PCR) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) respectively. Results: 4G4G and 4G5G were the most common PAI-1 polymorphism denoting high association of 4 G allele in renal insufficiency associated with CVD with absent link to dyslipidemia, echocardiography changes or thrombosis. E3E3 was the most common among APO-E polymorphism without relation to dyslipidemia or thrombosis. Dyslipidemia was significantly linked to thrombosis. The study confirmed the role of dyslipidemia and hemodialysis in promoting thrombosis. Conclusion: Although PAI 4G Genotyping did not show significant association with echocardiography severity or thrombotic severity, yet genetic expression for high levels of PAI in plasma is expected in response to CRI factors known to trigger its release, in addition to those related to dialysis. APO-E3E3 genotyping showed a significant association with echocardiography severity as it enhances APO-A which contributes to CVD. The current study confirmed a significant association between dyslipidemia and CVD; however, the prevalent patterns 4G and E3E3 did not show a significant association with dyslipidemia. The genetic role for APO-A, B, O, or even other isomers for APO-E should be further studied as well.

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