Osteomalacia and Insufficiency Fractures Secondary to Intravenous Iron Therapy: A Case Report

INTRODUCTION: Intravenous (IV) iron therapy is associated with hypophosphatemia, and long-term administration may lead to osteomalacia and insufficiency fracture. Awareness of this complication could severely reduce patient morbidity. Our patient continued her iron therapy for 17 months after her initial complaint. After switching iron medications, the patient’s fractures healed completely and she is now pain free. CASE REPORT: A 61-year-old woman presented with a fracture in her right femoral neck and a non-displaced fracture in her left femoral neck. After total hip arthroplasty and pinning, the patient returned with bilateral insufficiency fractures of the medial tibial plateau. The fractures were secondary to her iron medication, ferric carboxymaltose (FCM). CONCLUSION: Fibroblast growth factor 23 (FGF23) is a protein that increases renal phosphate wasting and certain parenteral iron therapies may increase the activity of FGF23. Most IV iron medications have been shown to cause hypophosphatemia, but literature has indicated that FCM is associated with the highest risk of developing hypophosphatemia and possibly osteomalacia.