We appreciate Van De Bruaene et al’s interest in this topic and our report. The multiple relations that govern red cell production in cyanotic congenital heart disease are not well characterized in our opinion. Our own data are congruous with Van De Bruaene et al’s in showing that hematocrit is maintained in iron deficiency, whereas hemoglobin decreases. In other words, iron deficiency invokes production of smaller, hypochromatic cells, but red cell mass is unchanged, as are hematocrit and thus viscosity.

We appreciate the authors’ point that because of this shift, theoretical viscosity for a given hemoglobin will be higher, although in practical terms, the same hemoglobin cannot be maintained if iron stores are low, and hence viscosity will likely be unchanged. The observation made by Van De Bruaene et al highlights the fact that cyanosis invokes a relative macrocytosis, as also shown by others. We fully agree with the authors’ point that hemoglobin and hematocrit have potential clinical impact, for different reasons, and should be considered separately.