Abstract
FOUR cases of jaundice were previously reported from this laboratory in which the hyperbilirubinæmia was not related to the breakdown of circulating erythrocytes nor to a defect in hepatic function1. The hyperbilirubinæmia was familial, the serum bilirubin predominantly indirect-reacting pigment and the total urobilinogen excretion in urine and stool increased. The bone marrows showed erythroid hyperplasia and the increased marrow activity was reflected in a peripheral reticulocytosis. Erythrocyte destruction, as measured by chromium-51 red cell survival, was not a causative factor. It was suggested that the excess bile pigments were derived from marrow erythrocytes or their precursors—either by their destruction or by a direct synthesis of bilirubin from hæm or its precursors. This short cut in bilirubin production was termed ‘shunt hyperbilirubinæmia’ and was thought to represent a marked exaggeration of the normal pathway in which at least 11 per cent of bile pigments (stercobilin) are derived from sources other than the hæm of the circulating red cell2. To test this postulate we have since studied four normals and one of the affected patients (A. P., case II)1, using 2-14C-glycine as an index of hæm and stercobilin formation.
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ISRAELS, L., ZIPURSKY, A. Primary Shunt Hyperbilirubinæmia. Nature 193, 73–74 (1962). https://doi.org/10.1038/193073a0
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DOI: https://doi.org/10.1038/193073a0
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