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Key Features

Essentials of Diagnosis

  • Jaundice results from accumulation of bilirubin in body tissues; the cause may be hepatic or nonhepatic (Table 16–1)

  • Hyperbilirubinemia may be due to abnormalities in the formation, transport, metabolism, or excretion of bilirubin (Table 16–2)

  • Persistent mild elevations of the aminotransferase levels are common in clinical practice and caused most often by nonalcoholic fatty liver disease

  • Evaluation of obstructive jaundice begins with ultrasonography and is usually followed by cholangiography

General Considerations

  • May be caused by predominantly unconjugated or conjugated bilirubin in the serum (Table 16–1)

  • In the absence of liver disease, hemolysis rarely elevates the serum bilirubin level to more than 7 mg/dL (119.7 mcmol/L)

  • "Cholestasis" denotes retention of bile in the liver, and "cholestatic jaundice" implies conjugated hyperbilirubinemia from impaired bile flow

  • Mediators of pruritus due to cholestasis have been identified to be

    • Lysophosphatidic acid (LPA)

    • Autotaxin, the enzyme that forms LPA

    • Mas-related G-protein coupled receptor X4

Table 16–1.Classification of jaundice.
Table 16–2.Hyperbilirubinemic disorders.

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