Abstract
Cell proliferation studies, utilizing 3H-thymidine radioautography combined with quantitative DNA microdensitometry, demonstrated a gross disturbance of bone marrow cell proliferation in a 17-yr-old youth with primary shunt hyperbilirubinemia. Early erythroid and myeloid cells were arrested at the S, G2 and mitotic phases of the cell cycle, but late normoblasts were not affected. Intramedullary death of the abnormal early erythrmoid cells probably results and is compensated by increased hemopoiesis with a hyperplastic marrow, which 59Fe studies suggest leads to the production and early release of "stress" reticulocytes. The increased early bilirubin production that characterizes this disorder is considered to be derived primarily from intramedullary death of early normoblasts and secondarily from hemolysis in the marrow and spleen of stress reticulocytes.