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Chapter 12 - Neonatal jaundice and disorders of bilirubin metabolism

from Section II - Cholestatic liver disease

Published online by Cambridge University Press:  05 March 2014

By
Mark Bartlett  and
Glenn R. Gourley
Edited by
Frederick J. Suchy ,
Ronald J. Sokol  and
William F. Balistreri
Mark Bartlett
Affiliation:
University of Minnesota, Minneapolis, MN, USA
Glenn R. Gourley
Affiliation:
Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA
Frederick J. Suchy
Affiliation:
University of Colorado Medical Center
Ronald J. Sokol
Affiliation:
University of Colorado Medical Center
William F. Balistreri
Affiliation:
University of Cincinnati College of Medicine
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Summary

Introduction

Elevation of the serum bilirubin level is a common finding during the first week of life. This can be a transient phenomenon that will resolve spontaneously or it can signify a serious or even potentially life-threatening condition. There are many causes of hyperbilirubinemia and each has its own therapeutic and prognostic implications. Independent of the cause, elevated serum bilirubin levels can be potentially toxic to the newborn infant. This chapter will review perinatal bilirubin metabolism and address assessment, etiology, toxicity, and therapy for neonatal jaundice. Finally, the diseases in which there is a primary disorder in the metabolism of bilirubin will be reviewed regarding their clinical presentation, pathophysiology, diagnosis, and treatment. For more extensive referencing, see this chapter in the third edition of this textbook [1].

Production and circulation

Bilirubin (from Latin, bilis, bile; rube, red) is formed from the degradation of heme-containing compounds (Figure 12.1). The largest source for the production of bilirubin is hemoglobin. However, other heme-containing proteins are also degraded to bilirubin, including the cytochromes, catalases, tryptophane pyrrolase, and muscle myoglobin.

Type
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Information
Liver Disease in Children , pp. 177 - 198
Publisher: Cambridge University Press
Print publication year: 2014

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References

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