Abstract
Bilirubin-induced neurologic dysfunction (BIND): appearances are fairly often deceptive
Highlights
More than 8 million Americans and 450 million peoples across the globe are affected by neurological disorders
Our hypothesis addresses the medical necessity of chelation therapy in the neonatal period [4] as it is feasible that unconjugated bilirubin (UCB) molecule reviels particular affinity to copper stored in basal ganglia (BG) of the neonatal brain, where copper-bilirubin complex can be formed together with the production of hydroxyl radical (OH–)
Especially preterm infants, are vulnerable to reactive reactive oxygen species (ROS) because they exhibit accelerated production of free radical and limited antioxidant protection, which increases the susceptibility of rapidly growing tissues to damage.There is a large body of literature demonstrating that free or weakly bound iron and copper ions may exert their toxic action on BG
Summary
More than 8 million Americans and 450 million peoples across the globe are affected by neurological disorders (including birth defects and BIND). Interest in bilirubin damage of the brain has been reawakened by an increase in its prevalence, owing to failure to closely observe infants discharged from the hospital well before the peak of NHBI. (underlying diseases or comorbidities) are comprised as risk factors, so, the UCB levels and neurological abnormalities are not strictly correlated. Our hypothesis addresses the medical necessity of chelation therapy (with D-PA) in the neonatal period [4] as it is feasible that UCB molecule reviels particular affinity to copper stored in BG of the neonatal brain, where copper-bilirubin complex can be formed together with the production of hydroxyl radical (OH–). Various amount of free metal ions can be accumulated in the intravascular space and in the tissues (especially in BG) during hemolytic processes
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