The systems controlling the number, size, and hemoglobin concentrations of populations of human red blood cells (RBCs), and
their dysregulation in anemia, are poorly understood. After release
from the bone marrow, RBCs undergo reduction in both volume
and total hemoglobin content by an unknown mechanism [Lew
VL, et al. (1995) Blood 86:334–341; Waugh RE, et al. (1992) Blood
79:1351–1358]; after ∼120 d, responding to an unknown trigger,
they are removed. We used theory from statistical physics and
data from the hospital clinical laboratory [d’Onofrio G, et al. (1995)
Blood 85:818–823] to develop a master equation model for RBC
maturation and clearance. The model accurately identifies patients
with anemia and distinguishes thalassemia-trait anemia from irondeficiency anemia. Strikingly, it also identifies many pre-anemic
patients several weeks before anemia becomes clinically detectable. More generally we illustrate how clinical laboratory data can
be used to develop and to test a dynamic model of human pathophysiology with potential clinical utility.