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18-01: Jaundice & Evaluation of Abnormal Liver Biochemical Tests

Lawrence S. Friedman

ESSENTIALS OF DIAGNOSIS

ESSENTIALS OF DIAGNOSIS

  • Jaundice results from accumulation of bilirubin in body tissues; the cause may be hepatic or nonhepatic.

  • Hyperbilirubinemia may be due to abnormalities in the formation, transport, metabolism, or excretion of bilirubin.

  • Persistent mild elevations of aminotransferase levels are common in clinical practice and caused most often by metabolic dysfunction–associated steatotic liver disease (MASLD) (formerly nonalcoholic fatty liver disease, NAFLD).

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

GENERAL CONSIDERATIONS

Jaundice (icterus) results from the accumulation of bilirubin—a product of heme metabolism—in body tissues (eFigure 18–1). Hyperbilirubinemia may be due to abnormalities in the formation, transport, metabolism, or excretion of bilirubin. Total serum bilirubin is normally 0.2–1.2 mg/dL (3.42–20.52 mcmol/L). Mean levels are higher in men than women, are higher in White persons and Latinx persons than Black persons, and correlate with an increased risk of symptomatic gallstone disease and inversely with the risk of stroke, respiratory disease, CVD, and mortality, presumably because of antioxidant and intestinal anti-inflammatory effects. Jaundice may not be recognizable until serum bilirubin levels are about 3 mg/dL (51.3 mcmol/L). Jaundice may be caused by increases in predominantly unconjugated or conjugated bilirubin in the serum (Table 18–1).

eFigure 18–1.

Jaundice. (Reproduced, with permission, from Sherlock S, Summerfield JA. Color Atlas of Liver Disease. Mosby, 1991.)

A photo shows a patient with yellow-colored skin and sclera.
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Table 18–1.Classification of jaundice.
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Table 18–1. Classification of jaundice.
Type of Hyperbilirubinemia Location and Cause
Unconjugated hyperbilirubinemia (predominantly indirect bilirubin)

Increased bilirubin production (eg, hemolytic anemias, hemolytic reactions, hematoma, pulmonary infarction)

Impaired bilirubin uptake and storage (eg, posthepatitis hyperbilirubinemia, Gilbert syndrome, Crigler-Najjar syndrome, drug reactions)
Conjugated hyperbilirubinemia (predominantly direct bilirubin) Hereditary Cholestatic Syndromes (see also Table 18–2)
Faulty excretion of bilirubin conjugates (eg, Dubin-Johnson syndrome, Rotor syndrome) or pathogenic variant in genes coding for bile salt transport proteins (eg, progressive familial intrahepatic cholestasis syndromes, benign recurrent intrahepatic cholestasis, and some cases of intrahepatic cholestasis of pregnancy)
Hepatocellular Injury

Biliary epithelial and hepatocyte damage (eg, hepatitis, hepatic cirrhosis)

Intrahepatic cholestasis (eg, certain drugs, biliary cirrhosis, sepsis, postoperative jaundice)

Hepatocellular damage or intrahepatic cholestasis resulting from miscellaneous causes (eg, spirochetal infections, infectious mononucleosis, cholangitis, sarcoidosis, lymphomas, hyperthyroidism, industrial toxins)
Biliary Obstruction
Choledocholithiasis, biliary atresia, carcinoma of biliary duct, sclerosing cholangitis, IgG4-related cholangitis, ischemic cholangiopathy, COVID cholangiopathy, choledochal cyst, external pressure on bile duct, pancreatitis, pancreatic neoplasms

Ig, immunoglobulin.

CLINICAL FINDINGS

A. Unconjugated Hyperbilirubinemia

Unconjugated hyperbilirubinemia may result from overproduction of bilirubin because of hemolysis; impaired hepatic uptake of bilirubin due to certain drugs; or impaired conjugation of bilirubin by glucuronide, due to mild decreases in uridine diphosphate (UDP) glucuronyl transferase (Gilbert syndrome), or moderate decreases (type II) or absence (type ...

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