Hyperbilirubinemia and cholestasis.
Although the morphologist continues to describe cholestasis on the basis of precipitated bile seen on light microscopic sections of the liver or dilated canaliculi with loss of microvilli seen by electron microscopy, the physiologist can distinguish clearly between hyperbilirubinemia and cholestasis. Both bilirubin and bile acids are specifically removed from sinusoidal plasma by the normal hepatocyte and appear in bile in high concentration. Bilirubin conjugation and excretion appear to be governed by hepatocellular mechanisms that are, for the most part, separate from the conjugation and excretion of bile acids. Disturbances in bilirubin transport are recognized by hyperbilirubinemia which represents a number of clinical syndromes that can be classified by the nature of the block in the transport system. Serum bile acids appear to remain normal in hyperbilirubinemic syndromes. By contrast, cholestatic syndromes are characterized by marked bile acidemia with normal to slightly elevated bilirubin levels. Severe cholestasis, because of the marked reduction in bile flow, can however, engender jaundice. Further exploration of these excretory pathways will provide interesting new insights on the numerous cholestatic and hyperbilirubinemic syndromes that occur in nature.
D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D001663:Bilirubin / Q000097:blood / Q000378:metabolism*; D001665:Binding Sites; D002779:Cholestasis / Q000175:diagnosis / Q000378:metabolism*; D004997:Ethinyl Estradiol / Q000378:metabolism; D014453:Glucuronosyltransferase / Q000378:metabolism; D006801:Humans; D006932:Hyperbilirubinemia / Q000175:diagnosis / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D011485:Protein Binding; D011506:Proteins / Q000502:physiology; D013577:Syndrome
D001647:Bile Acids and Salts; D011506:Proteins; D004997:Ethinyl Estradiol; D014453:Glucuronosyltransferase; D001663:Bilirubin