Bilirubin

Provides indication of hepatic uptake, metabolic (conjugation) and excretory functions; conjugated fraction (direct) distinguished from unconjugated by chemical assay (Table 44-1 Causes of Isolated Hyperbilirubinemia).

Aminotransferases (Transaminases)

Aspartate aminotransferase (AST; SGOT) and alanine aminotransferase (ALT; SGPT); sensitive indicators of liver cell injury; greatest elevations seen in hepatocellular necrosis (e.g., viral hepatitis, toxic or ischemic liver injury, acute hepatic vein obstruction), occasionally with sudden, complete biliary obstruction (e.g., from gallstone); milder abnormalities in cholestatic, cirrhotic, and infiltrative disease; poor correlation between degree of liver cell damage and level of aminotransferases; ALT more specific measure of liver injury, because AST also found in striated muscle and other organs; ethanol-induced liver injury usually produces modest increases with more prominent elevation of AST than ALT.

Alkaline Phosphatase

Sensitive indicator of cholestasis, biliary obstruction (enzyme increases more quickly than serum bilirubin), and liver infiltration; mild elevations in other forms of liver disease; limited specificity because of wide tissue distribution; elevations also seen in normal childhood, pregnancy, and bone diseases; tissue-specific isoenzymes can be distinguished by fractionation or by differences in heat stability (liver enzyme activity stable under conditions that destroy bone enzyme activity).

5′;-NUCLEOTIDASE (5′;-NT)

Pattern of elevation in hepatobiliary disease similar to alkaline phosphatase; has greater specificity for liver disorders; used to determine whether liver is source of elevation in serum alkaline phosphatase, esp. in children, pregnant women, pts with possible concomitant bone disease.

γ;-GLUTAMYL TRANSPEPTIDASE (GGT)

Correlates with serum alkaline phosphatase activity. Elevation is less specific for cholestasis than alkaline phosphatase or 5'-NT.

Coagulation Factors

Measure of clotting factor activity; prolongation results from clotting factor deficiency or inactivity; all clotting factors except factor VIII are synthesized in the liver, and deficiency can occur rapidly from widespread liver disease as in hepatitis, toxic injury, or cirrhosis; single best acute measure of hepatic synthetic function; helpful in diagnosis and prognosis of acute liver disease (See also Chap. 65 Bleeding and Thrombotic Disorders). Clotting factors II, VII, IX, X function only in the presence of the fat-soluble vitamin K; PT prolongation from fat malabsorption distinguished from hepatic disease by rapid and complete response to vitamin K replacement.

Albumin

Decreased serum levels result from decreased hepatic synthesis (chronic liver disease or prolonged malnutrition) or excessive losses in urine or stool; insensitive indicator of acute hepatic dysfunction, because serum half-life is 2-3 weeks; in pts with chronic liver disease, degree of hypoalbuminemia correlates with severity of liver dysfunction.

Globulin

Mild polyclonal hyperglobulinemia often seen in chronic liver diseases; marked elevation frequently seen in autoimmune chronic active hepatitis.

Ammonia

Elevated blood levels result from deficiency of hepatic detoxification pathways and portal-systemic shunting, as in fulminant hepatitis, hepatotoxin exposure, and severe portal hypertension (e.g., from cirrhosis); elevation of blood ammonia does not correlate well with hepatic function or the presence or degree of acute encephalopathy.