An excess hemolysis was found in subjects with iron deficiency anemia associated with hookworm infection. Red cell survival, measured with Cr51 and DFP32 in the subjects before deworming, showed a marked disproportion between the decrease of the survival and the amount of daily intestinal blood loss in most cases. Excess of hemolysis was still present after more than 90 per cent of the parasites were removed. Red cell survival became normal after correction of anemia through iron treatment. Excess of hemolysis was also present in noninfected subjects with iron deficiency anemia due to other causes.
The reduction in the survival of the erythrocytes from infected subjects transfused into normal recipients shows that the hemolytic process is due to an intrinsic defect of the red cells. The low values of hemoglobinemia and the presence of haptoglobins in the plasma indicate that hemoglobin has not been liberated in excess intravascularly. Finally, the fact that the red cells from an infected patient taken after deworming survived normally in splenectomized recipients indicates that the spleen is probably the principal site of the red cell destruction. The clinical and autopsy findings suggest that splenic function is not pathologically increased, but rather that this organ is acting physiologically at a more rapid rate, "culling" the abnormal circulating red cells and thus leading to a decrease in red cell survival.
The studies presented here also indicate that the hookworm infection per se does not induce hemolysis.