Trace elements have a major role as both oxidants and antioxidants, promoting and protecting from tissue damage respectively. As the liver has a pivotal role in trace elements metabolism and consequenyly their bioavailability, we aimed to measure serum levels of essential trace elements in children with chronic liver diseases (CLDs) regardless the etiology and to study their correlation with liver function tests. Serum zinc (Zn), copper (Cu) and iron (Fe); together with other trace elements parameters; were measured in 50 children with CLDs using spectrophotometry and their levels were compared with those age and sex matched healthy children as controls. Serum Cu, Fe, ferritin and transferrin saturation (TS) were significantly higher in the CLDs group than that in the control group; while serum Zn and total iron binding capacity (TIBC) were significantly lower in the CLDs than that in the control group. Serum Fe, Cu, TS and ferritin were positively correlated with biochemical parameters of liver damage; while serum Zn and TIBC were negatively correlated with biochemical parameters of liver damage. These results encourage inclusion of serum Zn, Cu and Fe as biomarkers for monitoring the severity of liver damage during routine assessment of children with CLDs. We recommended caution to avoid excess Fe and Cu intake in children with CLDs. Moreover, Zn supplementation could be encouraged in children with CLDs regardless its etiology.

Biliary atresia (BA) is a necroinflammatory occlusive cholangiopathy that affects infants. Genetic and environmental factors has been proposed for its occurrence. The objectives of this study was to investigate the protein expression of 2 important genes regulating ductal plate remodeling, hepatocyte nuclear factor 1-beta (Hnf1β) and the fork head box protein A2 (FoxA2) in liver tissue from patients with BA and to compare their expression with other causes of neonatal cholestasis (NC). This retrospective study included 60 pediatric patients, 30 with BA and 30 with NC. Immunohistochemistry of Hnf1β and FoxA2 was performed on liver tissues from studied patients as well as 20 healthy subjects. Statistical analysis between immunohistochemistry results and other parameters was performed. Liver tissue from patients with BA revealed reduced Hnf1β and FoxA2 immunoexpression. A strong significant statistical difference between BA and NC group (P<0.0001) with regard to Hnf1β and FoxA2 immunoexpression was evident. Moreover, Hnf1β was significantly correlated with FoxA2 immunoexpression, stage of fibrosis, bile ductular proliferation, and bile plugs in bile ductules. Hnf1β immunoreaction in BA cases showed 76.7% sensitivity, 90% specificity, 88.5% positive predictive value, 79.4% negative predictive value, and 83.4% accuracy. FoxA2 expression in BA cases revealed 70.0% sensitivity, 80.0% specificity, 77.8% positive predictive value, 72.7% negative predictive value, 75.0% accuracy. Hnf1β and FoxA2 immunoexpression could differentiate between BA from other cause of NC.

Tumor necrosis factor (TNF or TNF-α) was formerly suggested as a circulating factor which can cause necrosis of tumors, before it has been known as a key regulator of some pleiotropic functions such as apoptosis, cell survival, inflammation, and immunity acting via two receptors (TNFR-1, TNFR-2). TNF-β or lymphotoxin (LT) has similar biologic effects as TNF-α; however it is produced in much smaller quantities and is a locally acting cytokine. This article discusses the biological function of TNF focusing on its role in cancer and autoimmune diseases via classical activation pathway of nuclear factor kappa-B (NF-κB).

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