Intravenous Iron–Induced Hypophosphatemia in Surgical Patients

Intravenous (IV) iron has become a standard treatment for iron deficiency and anemia. Modern formulations of IV iron enable a large dose to be administered safely with a low complication rate comparable to other infusions.1 However, ferric carboxymaltose (FCM) can cause hypophosphatemia mediated by fibroblast growth factor 23 (FGF23) that increases urinary excretion of bone phosphate.2 While this is often an asymptomatic laboratory finding, concern has arisen from reports of osteomalacia and bone fractures.3

PREVENTT was a multicenter randomized clinical trial that compared IV FCM (1000 mg; n = 244) to placebo (saline; n = 243) to treat anemia before major open abdominal surgery.4 As the main clinical end points of blood transfusion, death, or perioperative complications were not different between the groups in the main trial, we hypothesized that if FCM caused hypophosphatemia, it was clinically asymptomatic. The aim of this study was to explore the incidence of preoperative hypophosphatemia in PREVENTT and, in the cohort of patients who received FCM, whether hypophosphatemia may have affected patient or trial outcomes.