Minimizing therapeutically induced anemia.

A model for erythroid production based on a continuous maturation-proliferation scheme is developed. The model includes a simple control mechanism operating at the proliferating cell level, and analytic solutions for the time dependent response of the model are derived. Using this model, the response of the erythron to a massive depletion of the proliferating cell compartment (due for example to cytostatic drugs or radiation) is calculated.