ANAEMIA is a frequent complication of thyroid dysfunction in man, and often remains unexplained, responding only to thyroid hormone replacement therapy1,2. Thyroid hormone has recently been shown to influence the rate of red blood cell and haemoglobin production3-7. In addition to stimulating erythropoietin (Ep) production3, thyroid hormone has been reported to act directly on haematopoietic precursors4,5. The enhancement of murine and canine in vitro erythroid colony growth by thyroid hormone6,7 suggests that this hormone may have a direct role in the modulation of erythroid proliferation. Studies of murine erythropoiesis support the existence of two distinct, age-structured, Ep responsive populations of committed erythroid precursor cells: the early committed erythroid burst forming unit (BFU-E) and the late committed erythroid colony forming unit (CFU-E) 8. These populations are distinguished by cell volume, responsiveness to Ep, and proliferative capacity. The BFU-E, a cell which arises from the pluripotent stem cell soon after its commitment to the erythroid line and which has a high Ep-responsive proliferative capacity, seems to be the precursor of the CFU-E, a cell of lower proliferative capacity. Thyroid hormone has been shown to enhance in vitro erythroid colony formation by canine marrow cells, an effect that may be mediated by a receptor with β2-adrenergic properties7. Velocity sedimentation analysis revealed that colony-forming cells stimulated by this hormone sedimented more slowly than colony-forming cells responding to Ep alone7. Here, we have extended these studies to human marrow cells and have shown that the ability of thyroid hormone to stimulate the erythroid committed progenitor cell does not seem to be a function of the state of differentiation of this cell. Both CFU-E-derived and BFU-E-derived colony formation were enhanced by the hormone. © 1978 Nature Publishing Group.
