Liver Iron Retention Estimated from Utilization of Oral and Intravenous Radioiron in Various Anemias and Hemochromatosis in Humans.

Patients with hereditary hemochromatosis and non-transfusion-dependent hereditary anemia develop predominantly liver iron-overload. We present a unique method allowing quantification of liver iron retention in humans during first-pass of Fe-59-labeled iron through the portal system, using standard ferrokinetic techniques measuring red cell iron uptake after oral and intravenous Fe-59 administration. We present data from patients with iron deficiency (ID; N = 47), hereditary hemochromatosis (HH; N = 121) and non-transfusion-dependent hereditary anemia (HA; N = 40). Mean mucosal iron uptake and mucosal iron transfer (+/-SD) were elevated in patients with HH (59 +/- 18%, 80 +/- 15% respectively), HA (65 +/- 17%, 74 +/- 18%) and ID (84 +/- 14%, 94 +/- 6%) compared to healthy controls (43 +/- 19%, 64 +/- 18%) (p < 0.05) resulting in increased iron retention after 14 days compared to healthy controls in all groups (p < 0.01). The fraction of retained iron utilized for red cell production was 0.37 +/- 0.17 in untreated HA, 0.55 +/- 0.20 in untreated HH and 0.99 +/- 0.22 in ID (p < 0.01). Interestingly, compared to red blood cell iron utilization after oral iron administration, red blood cell iron utilization was higher after injection of transferrin-bound iron in HA and HH. Liver iron retention was considerably higher in HH and HA compared to ID. We hypothesize that albumin serves as a scavenger of absorbed Fe(II) for delivering albumin-bound Fe(III) to hepatocytes.