Abstract
Current concepts of bilirubin metabolism have been reviewed. Free bilirubin is conjugated in the liver with glucuronic acid, sulfates, and perhaps other compounds rendering it water-soluble and facilitating its excretion into the bile. With experimental extrahepatic obstruction or hepatocellular damage, alterations in the pattern of bilirubin conjugates in serum and bile may be demonstrated; but these patterns cannot be explained solely in terms of conjugation deficiency. Abnormalities in the uptake of free bilirubin by the hepatic cell and in its storage and excretion by the liver may contribute to the pigment patterns observed in most states of clinical jaundice. However, a few unusual conditions of clinical jaundice seem to represent pure defects of conjugation or excretion of bile pigments, and these have been discussed.
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