Intravenous iron administration is typically indicated in individuals who have iron deficiency refractory to oral iron. However, in certain chronic disease states such as heart failure, it may be beneficial to administer intravenous iron to individuals who are not strictly iron deficient. The purpose of this study was to define a dose-response relationship between clinical indices of iron status and modest loading with intravenous iron in healthy, iron-replete participants. This was a double-blind, controlled study involving 18 male participants. Participants were block-randomized 2:1 to the iron and saline (control) groups. Participants in the iron group received 3.75 mg/kg body wt up to a maximum of 250 mg of intravenous iron, once a month for 6 mo, provided that their ferritin remained measured 300 g/l within the week before a dose was due and their transferrin saturation remained 45%. Otherwise they received a saline infusion, as did the control participants. Iron indices were measured monthly during the study. The pulmonary vascular response to sustained hypoxia and total hemoglobin mass were measured before, at 3 mo (hemoglobin mass only), and at 6 mo as variables that may be affected by iron loading. Serum ferritin was robustly elevated by intravenous iron by 0.21 g·l1·mg1 of iron delivered (95% confidence interval: 0.15– 0.26 g·l1·mg1), but the effects on all other iron indices did not reach statistical significance. The pulmonary vascular response to sustained hypoxia was significantly suppressed by iron loading at 6 mo, but the hemoglobin mass was unaffected. We conclude that the robust effect on ferritin provides a quantitative measure for the degree of iron loading in iron-replete individuals.
Bibliographical noteFunding Information:
The research was funded by the Colt Foundation. N. K. Bart received additional support from the Sir John Monash Scholarship and Avant Scholarship. N. Petousi was supported by an National Institute of Health Research Clinical Lectureship. K. L. Dorrington was supported by the Dunhill Medical Trust (Grant No. R178/1110).
The authors thank the participants for their involvement in this research and David O’Connor for technical help and support. The research was funded by the Colt Foundation. N. K. Bart received additional support from the Sir John Monash Scholarship and Avant Scholarship. N. Petousi was supported by an National Institute of Health Research Clinical Lectureship. K. L. Dorrington was supported by the Dunhill Medical Trust (Grant No. R178/1110).
Copyright © 2018 the American Physiological Society.
- Iron loading
- Pulmonary circulation