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- Dinesh Pashankar, MD*
- Richard A. Schreiber, MD†
- *Clinical Assistant Professor of Pediatrics, Division of Gastroenterology, Children’s Hospital of Iowa, Iowa City, IA
- †Clinical Associate Professor of Pediatrics, University of British Columbia, Division of Gastroenterology, British Columbia’s Children’s Hospital, Vancouver, BC, Canada.
Objectives After completing this article, readers should be able to:
Describe the basic physiology of bilirubin metabolism, the two standard laboratory methods for its fractionation, and the classification of jaundice.
Characterize the features of Gilbert disease.
Identify the leading infectious cause of acute jaundice in older children and adolescents.
Delineate the clinical and biochemical features of Wilson disease and autoimmune hepatitis.
Compare and contrast liver function tests and tests of liver function.
Describe the “worrisome” clinical and laboratory signs of hepatic synthetic dysfunction in jaundiced patients that should prompt an immediate referral to a center whHere liver transplantation is available.
Introduction
Jaundice is defined as the presence of a yellow or yellow-greenish hue to the skin, sclera, and mucous membranes due to an elevation of serum bilirubin. In healthy individuals, the total serum bilirubin is less than 1 mg/dL (17 mcmol/L). Jaundice can be readily detected clinically when the total serum bilirubin is greater than 5 mg/dL (85 mcmol/L). Clinical jaundice occurs much less frequently in older children and adolescents than in neonates. Moreover, the differential diagnosis in this older age group differs markedly from that in newborns and young infants. This review provides a practical approach to the clinical evaluation of jaundice in the older child or adolescent. Because jaundice may be the presenting feature of life-threatening conditions such as fulminant liver failure, a prompt and logical evaluation is necessary to identify the more serious disorders that require urgent management.
Bilirubin Metabolism
Bilirubin is a product of heme metabolism. Heme is converted in the reticuloendothelial (RE) system to biliverdin and then to bilirubin by heme oxygenase and biliverdin reductase, respectively. Bilirubin is lipophylic and is bound to serum albumin in circulation from the RE system to the liver. The liver takes up the bilirubin-albumin complex through an albumin receptor. Bilirubin, but not …
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