![]() ![]() Bilirubin is formed mainly in the liver and spleen through two steps which include:.The heme is a component of various biological molecules and enzymes but, it is mainly incorporated in the hemoglobin which is the primary component of the red blood cells. Bilirubin is the final catabolic product of the heme.Pathophysiology Bilirubin formation and metabolism ![]() Inherited neonatal jaundice include Gilbert's syndrome, Crigler-Najjar syndrome type I and II, Lucey-Driscoll syndrome, Dubin-Johnson syndrome, and Rotor syndrome. Inherited neonatal jaundice is due to defect of one of the processes of bilirubin metabolism and it concludes some inherited syndromes. Acquired neonatal jaundice include Rh hemolytic disease, ABO incompatibility disease, and hemolytic disease due to G6PD enzyme deficiency. The pathological jaundice may be acquired or inherited. Pathogenesis of neonatal jaundice includes physiologic process of bilirubin accumulation or pathological mechanism. Jaundice develops due to increase the level of bilirubin and deposition under the skin and cause the yellow discoloration of the skin. Metabolism processes include hepatic uptake, conjugation, clearance and excretion of the bilirubin in the bile. Bilirubin is formed in the liver and spleen then it passes through several process in order to be metabolized. ![]() Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH Overviewīilirubin is the catabolic product of the heme which is the main component of the red blood cells. Risk calculators and risk factors for Neonatal jaundice pathophysiologyĮditor-In-Chief: C. Neonatal jaundice pathophysiology in the newsīlogs on Neonatal jaundice pathophysiologyĭirections to Hospitals Treating Neonatal jaundice Neonatal jaundice pathophysiology On the WebĪmerican Roentgen Ray Society Images of Neonatal jaundice pathophysiologyĪll Images X-rays Echo & Ultrasound CT Images MRI Natural History, Complications and Prognosis Differentiating Neonatal jaundice from other Diseases ![]()
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