Intravenous iron preparations have improved significantly over the years. The newer second-generation formulations, such as iron sucrose and ferric gluconate, have been marketed as safe, effective agents for the management of iron deficiency. This has resulted in widespread use of iron infusions for a range of medical conditions. However, there have been an increasing number of case reports of hypophosphatemia following iron infusions. We report the case of a 46 year-old lady with long standing Crohn’s disease who became iron transfusion dependent in the context of haemorrhagic ulcers and malabsorption. Subsequently she developed several episodes of hypophosphatemia with a clear temporal relationship to her iron infusions. Over time, the chronic hypophosphatemia resulted in osteomalacia with widespread insufficiency fractures involving the femoral head bilaterally, pelvis and right humerus. While the precise mechanism in which iron infusions cause hypophosphatemia is not completely understood, we demonstrate the probable mediation by FGF-23, a phosphaturic peptide essential for phosphate homeostasis. We also show that phosphate and calcitriol replacement at the time of the iron infusion may ameliorate the hypophosphatemia.
Based on these findings, we conclude iron infusions may cause severe asymptomatic hypophosphatemia. We hypothesise that due to the lack of symptoms and post infusion monitoring, hypophosphatemia is a more common complication of iron infusions than currently recognised. Furthermore, as our case illustrates, failure to recognise and treat the hypophosphatemia in the context of multiple iron infusions, can lead to osteomalacia in the long term.